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#Clinical #Clinique #Meningo-encephalite #Meningoencephalitis
Meningitis is an inflammatory disease of the leptomeninges, the tissues surrounding the brain and spinal cord, and is characterized by an abnormal number of white blood cells (WBCs) in the cerebrospinal fluid (CSF) in the majority of patients [1].
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opics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Apr 2022. | This topic last updated: Mar 07, 2022. INTRODUCTION — <span>Meningitis is an inflammatory disease of the leptomeninges, the tissues surrounding the brain and spinal cord, and is characterized by an abnormal number of white blood cells (WBCs) in the cerebrospinal fluid (CSF) in the majority of patients [1]. The meninges consist of three parts: the pia, arachnoid, and dura maters (figure 1). Bacterial meningitis reflects infection of the arachnoid mater and the CSF in both the subarachnoid




#Clinical #Clinique #Meningo-encephalite #Meningoencephalitis
The meninges consist of three parts: the pia, arachnoid, and dura maters ( figure 1)
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nges, the tissues surrounding the brain and spinal cord, and is characterized by an abnormal number of white blood cells (WBCs) in the cerebrospinal fluid (CSF) in the majority of patients [1]. <span>The meninges consist of three parts: the pia, arachnoid, and dura maters (figure 1). Bacterial meningitis reflects infection of the arachnoid mater and the CSF in both the subarachnoid space and the cerebral ventricles. The clinical and laboratory features of acute bac




#Clinical #Clinique #Meningo-encephalite #Meningoencephalitis
Bacterial meningitis reflects infection of the arachnoid mater and the CSF in both the subarachnoid space and the cerebral ventricles.
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bnormal number of white blood cells (WBCs) in the cerebrospinal fluid (CSF) in the majority of patients [1]. The meninges consist of three parts: the pia, arachnoid, and dura maters (figure 1). <span>Bacterial meningitis reflects infection of the arachnoid mater and the CSF in both the subarachnoid space and the cerebral ventricles. The clinical and laboratory features of acute bacterial meningitis in adults will be reviewed here. The pathogenesis, epidemiology, treatment, prognosis, and prevention of acute bacteri




#Clinical #Clinique #Meningo-encephalite #Meningoencephalitis
The major causes of community-acquired bacterial meningitis in adults in developed countries are Streptococcus pneumoniae, Neisseria meningitidis, and, primarily in patients over 50 years of age or those who have deficiencies in cell-mediated immunity, Listeria monocytogenes (table 1).
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h to the adult with recurrent infections", section on 'Meningitis' and "Aseptic meningitis in adults".) EPIDEMIOLOGY — Bacterial meningitis can be community acquired or health care associated. ●<span>The major causes of community-acquired bacterial meningitis in adults in developed countries are Streptococcus pneumoniae, Neisseria meningitidis, and, primarily in patients over 50 years of age or those who have deficiencies in cell-mediated immunity, Listeria monocytogenes (table 1). ●The major causes of health care-associated ventriculitis and meningitis are different (usually staphylococci and aerobic gram-negative bacilli) and occur more commonly after neurosurgi




#Clinical #Clinique #Meningo-encephalite #Meningoencephalitis
The major causes of health care-associated ventriculitis and meningitis are different (usually staphylococci and aerobic gram-negative bacilli) and occur more commonly after neurosurgical procedures (eg, post-craniotomy, ventriculoperitoneal shunts, lumbar shunts, external ventricular drains or following head trauma such as basilar skull fracture with or without clinical evidence of leak of cerebrospinal fluid) [2]
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re Streptococcus pneumoniae, Neisseria meningitidis, and, primarily in patients over 50 years of age or those who have deficiencies in cell-mediated immunity, Listeria monocytogenes (table 1). ●<span>The major causes of health care-associated ventriculitis and meningitis are different (usually staphylococci and aerobic gram-negative bacilli) and occur more commonly after neurosurgical procedures (eg, post-craniotomy, ventriculoperitoneal shunts, lumbar shunts, external ventricular drains or following head trauma such as basilar skull fracture with or without clinical evidence of leak of cerebrospinal fluid) [2]. A more detailed discussion of the epidemiology of and risk factors for bacterial meningitis is presented elsewhere. (See "Epidemiology of bacterial meningitis in adults".) CLINICAL FEA




#Clinical #Clinique #Meningo-encephalite #Meningoencephalitis
In the largest prospective study of 1412 episodes of bacterial meningitis, for example, approximately half of the patients presented less than 24 hours after onset of illness [3].
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ented elsewhere. (See "Epidemiology of bacterial meningitis in adults".) CLINICAL FEATURES — Patients with bacterial meningitis are usually quite ill and often present soon after symptom onset. <span>In the largest prospective study of 1412 episodes of bacterial meningitis, for example, approximately half of the patients presented less than 24 hours after onset of illness [3]. Determinants of the pace of bacterial meningitis are related to both host and microbial virulence factors. Any form of bacterial meningitis that is untreated or treated very late in its




#Clinical #Clinique #Meningo-encephalite #Meningoencephalitis
Any form of bacterial meningitis that is untreated or treated very late in its course is almost uniformly fatal.
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ximately half of the patients presented less than 24 hours after onset of illness [3]. Determinants of the pace of bacterial meningitis are related to both host and microbial virulence factors. <span>Any form of bacterial meningitis that is untreated or treated very late in its course is almost uniformly fatal. (See "Initial therapy and prognosis of bacterial meningitis in adults", section on 'Avoidance of delay'.) Presenting manifestations — The classic triad of acute bacterial meningitis, wh




#Clinical #Clinique #Meningo-encephalite #Meningoencephalitis
The classic triad of acute bacterial meningitis, which occurs in 41 percent of patients, consists of fever, nuchal rigidity, and a change in mental status, usually of sudden onset [3,4]. Older patients (age >60 years) more commonly present with the triad than younger patients (58 versus 36 percent) [5].
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treated very late in its course is almost uniformly fatal. (See "Initial therapy and prognosis of bacterial meningitis in adults", section on 'Avoidance of delay'.) Presenting manifestations — <span>The classic triad of acute bacterial meningitis, which occurs in 41 percent of patients, consists of fever, nuchal rigidity, and a change in mental status, usually of sudden onset [3,4]. Older patients (age >60 years) more commonly present with the triad than younger patients (58 versus 36 percent) [5]. The most common clinical features include a severe headache (84 percent), fever greater than 38°C (74 percent), stiff neck (74 percent), a Glasgow Coma scale <14 (71 percent), and na




#Clinical #Clinique #Meningo-encephalite #Meningoencephalitis
The most common clinical features include a severe headache (84 percent), fever greater than 38°C (74 percent), stiff neck (74 percent), a Glasgow Coma scale <14 (71 percent), and nausea (62 percent) [3,4,6]
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rigidity, and a change in mental status, usually of sudden onset [3,4]. Older patients (age >60 years) more commonly present with the triad than younger patients (58 versus 36 percent) [5]. <span>The most common clinical features include a severe headache (84 percent), fever greater than 38°C (74 percent), stiff neck (74 percent), a Glasgow Coma scale <14 (71 percent), and nausea (62 percent) [3,4,6]. In a 2004 prospective study of 696 cases of community-acquired bacterial meningitis, almost all patients (95 percent) presented with at least two of four symptoms (ie, headache, fever,




#Clinical #Clinique #Meningo-encephalite #Meningoencephalitis
In a 2004 prospective study of 696 cases of community-acquired bacterial meningitis, almost all patients (95 percent) presented with at least two of four symptoms (ie, headache, fever, stiff neck, and altered mental status) [ 4]. The absence of all of these findings essentially excludes the presence of bacterial meningitis [7].
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inical features include a severe headache (84 percent), fever greater than 38°C (74 percent), stiff neck (74 percent), a Glasgow Coma scale <14 (71 percent), and nausea (62 percent) [3,4,6]. <span>In a 2004 prospective study of 696 cases of community-acquired bacterial meningitis, almost all patients (95 percent) presented with at least two of four symptoms (ie, headache, fever, stiff neck, and altered mental status) [4]. The absence of all of these findings essentially excludes the presence of bacterial meningitis [7]. In addition to the classic findings, less common manifestations are seizures (23 percent), aphasia or hemi- or monoparesis (22 percent), coma (13 percent), cranial nerve palsy (9 percen




#Clinical #Clinique #Meningo-encephalite #Meningoencephalitis
Concomitant infections may include sinusitis or otitis (34 percent), pneumonia (9 percent), and endocarditis (1 percent) [3]
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ifestations are seizures (23 percent), aphasia or hemi- or monoparesis (22 percent), coma (13 percent), cranial nerve palsy (9 percent), rash (8 percent), and papilledema (4 percent) [3,4,8,9]. <span>Concomitant infections may include sinusitis or otitis (34 percent), pneumonia (9 percent), and endocarditis (1 percent) [3]. Some findings may be suggestive of a particular bacterial etiology: ●In an observational study of 696 patients with community-acquired bacterial meningitis, cerebral infarction occurre




#Clinical #Clinique #Meningo-encephalite #Meningoencephalitis
In addition to the classic findings, less common manifestations are seizures (23 percent), aphasia or hemi- or monoparesis (22 percent), coma (13 percent), cranial nerve palsy (9 percent), rash (8 percent), and papilledema (4 percent) [3,4,8,9].
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least two of four symptoms (ie, headache, fever, stiff neck, and altered mental status) [4]. The absence of all of these findings essentially excludes the presence of bacterial meningitis [7]. <span>In addition to the classic findings, less common manifestations are seizures (23 percent), aphasia or hemi- or monoparesis (22 percent), coma (13 percent), cranial nerve palsy (9 percent), rash (8 percent), and papilledema (4 percent) [3,4,8,9]. Concomitant infections may include sinusitis or otitis (34 percent), pneumonia (9 percent), and endocarditis (1 percent) [3]. Some findings may be suggestive of a particular bacterial e




#Clinical #Clinique #Meningo-encephalite #Meningoencephalitis
In an observational study of 696 patients with community-acquired bacterial meningitis, cerebral infarction occurred in 25 percent of episodes and in 36 percent of patients with pneumococcal meningitis [10]. Delayed cerebral infarctions have been described in 1 to 4 percent of patients with bacterial meningitis with a possible association with adjunctive dexamethasone [11]
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oncomitant infections may include sinusitis or otitis (34 percent), pneumonia (9 percent), and endocarditis (1 percent) [3]. Some findings may be suggestive of a particular bacterial etiology: ●<span>In an observational study of 696 patients with community-acquired bacterial meningitis, cerebral infarction occurred in 25 percent of episodes and in 36 percent of patients with pneumococcal meningitis [10]. Delayed cerebral infarctions have been described in 1 to 4 percent of patients with bacterial meningitis with a possible association with adjunctive dexamethasone [11]. ●Patients with Listeria meningitis have an increased tendency to have seizures and focal neurologic deficits early in the course of infection. In addition, some patients may present wi




#Clinical #Clinique #Meningo-encephalite #Meningoencephalitis
Patients with Listeria meningitis have an increased tendency to have seizures and focal neurologic deficits early in the course of infection. In addition, some patients may present with rhombencephalitis affecting the brainstem and cerebellum, manifested as ataxia, cranial nerve palsies, and/or nystagmus.
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coccal meningitis [10]. Delayed cerebral infarctions have been described in 1 to 4 percent of patients with bacterial meningitis with a possible association with adjunctive dexamethasone [11]. ●<span>Patients with Listeria meningitis have an increased tendency to have seizures and focal neurologic deficits early in the course of infection. In addition, some patients may present with rhombencephalitis affecting the brainstem and cerebellum, manifested as ataxia, cranial nerve palsies, and/or nystagmus. In a review of 367 episodes of central nervous system infections caused by L. monocytogenes [12], the most common findings were fever (92 percent) and altered sensorium (65 percent). A




#Clinical #Clinique #Meningo-encephalite #Meningoencephalitis
Certain bacteria, particularly N. meningitidis, can cause characteristic skin manifestations, such as petechiae and palpable purpura. In two large series of patients with community-acquired bacterial meningitis, rash was present in 11 and 26 percent; among those with rash, 75 and 92 percent were associated with meningococcal meningitis [4,8].
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scussion of clinical manifestations of central nervous system (CNS) listeriosis are discussed elsewhere [13]. (See "Clinical manifestations and diagnosis of Listeria monocytogenes infection".) ●<span>Certain bacteria, particularly N. meningitidis, can cause characteristic skin manifestations, such as petechiae and palpable purpura. In two large series of patients with community-acquired bacterial meningitis, rash was present in 11 and 26 percent; among those with rash, 75 and 92 percent were associated with meningococcal meningitis [4,8]. In another study of 258 adults with meningococcal meningitis [14], rash was present in 64 percent and characterized as petechial in 91 percent of patients. However, others have observed




#Clinical #Clinique #Meningo-encephalite #Meningoencephalitis
However, others have observed a rash in ≤26 percent of cases of meningococcal meningitis and, if present, the rash was more likely to be scanty or more atypical appearing than the rash seen in patients with meningococcal septicemia [15]. A petechial rash is not specific for meningococcal infection, and some patients with meningococcal meningitis have a maculopapular rash [8]
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with meningococcal meningitis [4,8]. In another study of 258 adults with meningococcal meningitis [14], rash was present in 64 percent and characterized as petechial in 91 percent of patients. <span>However, others have observed a rash in ≤26 percent of cases of meningococcal meningitis and, if present, the rash was more likely to be scanty or more atypical appearing than the rash seen in patients with meningococcal septicemia [15]. A petechial rash is not specific for meningococcal infection, and some patients with meningococcal meningitis have a maculopapular rash [8]. (See "Clinical manifestations of meningococcal infection".) ●Arthritis occurs in some patients with bacterial meningitis. In a case series of 696 episodes of community-acquired bacteri




#Clinical #Clinique #Meningo-encephalite #Meningoencephalitis
Arthritis occurs in some patients with bacterial meningitis. In a case series of 696 episodes of community-acquired bacterial meningitis, arthritis was diagnosed in 48 (7 percent) of the episodes, with N. meningitidis the etiologic agent in two-thirds of these joint infections [16]. Joint fluid aspiration was performed in 23 patients and was positive by culture in 6 (26 percent). Recognition of the concurrent arthritis is important since prolonged antibiotic therapy is necessary. (See "Septic arthritis in adults".)
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ial rash is not specific for meningococcal infection, and some patients with meningococcal meningitis have a maculopapular rash [8]. (See "Clinical manifestations of meningococcal infection".) ●<span>Arthritis occurs in some patients with bacterial meningitis. In a case series of 696 episodes of community-acquired bacterial meningitis, arthritis was diagnosed in 48 (7 percent) of the episodes, with N. meningitidis the etiologic agent in two-thirds of these joint infections [16]. Joint fluid aspiration was performed in 23 patients and was positive by culture in 6 (26 percent). Recognition of the concurrent arthritis is important since prolonged antibiotic therapy is necessary. (See "Septic arthritis in adults".) Examination for meningeal irritation — Although patients may not complain specifically of a stiff neck, it is important to assess for meningeal irritation. Passive or active flexion of




#Clinical #Clinique #Meningo-encephalite #Meningoencephalitis
Although patients may not complain specifically of a stiff neck, it is important to assess for meningeal irritation. Passive or active flexion of the neck will usually result in an inability to touch the chin to the chest. Difficulty in lateral motion of the neck is a less reliable finding.
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6 (26 percent). Recognition of the concurrent arthritis is important since prolonged antibiotic therapy is necessary. (See "Septic arthritis in adults".) Examination for meningeal irritation — <span>Although patients may not complain specifically of a stiff neck, it is important to assess for meningeal irritation. Passive or active flexion of the neck will usually result in an inability to touch the chin to the chest. Difficulty in lateral motion of the neck is a less reliable finding. Tests to illustrate meningismus (such as Kernig and Brudzinski signs) were originally developed and tested in patients with severe, late-stage untreated bacterial and tuberculous mening




#Clinical #Clinique #Meningo-encephalite #Meningoencephalitis
Tests to illustrate meningismus (such as Kernig and Brudzinski signs) were originally developed and tested in patients with severe, late-stage untreated bacterial and tuberculous meningitis in the preantibiotic era (table 2)
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ingeal irritation. Passive or active flexion of the neck will usually result in an inability to touch the chin to the chest. Difficulty in lateral motion of the neck is a less reliable finding. <span>Tests to illustrate meningismus (such as Kernig and Brudzinski signs) were originally developed and tested in patients with severe, late-stage untreated bacterial and tuberculous meningitis in the preantibiotic era (table 2). ●The classic Brudzinski sign refers to spontaneous flexion of the hips during attempted passive flexion of the neck. ●The Kernig sign refers to the inability or reluctance to allow ful




#Clinical #Clinique #Meningo-encephalite #Meningoencephalitis

● The classic Brudzinski sign refers to spontaneous flexion of the hips during attempted passive flexion of the neck.

● The Kernig sign refers to the inability or reluctance to allow full extension of the knee when the hip is flexed 90 degrees. The Kernig test is usually performed in the supine position, but it can be tested in the seated patient.

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(such as Kernig and Brudzinski signs) were originally developed and tested in patients with severe, late-stage untreated bacterial and tuberculous meningitis in the preantibiotic era (table 2). <span>●The classic Brudzinski sign refers to spontaneous flexion of the hips during attempted passive flexion of the neck. ●The Kernig sign refers to the inability or reluctance to allow full extension of the knee when the hip is flexed 90 degrees. The Kernig test is usually performed in the supine position, but it can be tested in the seated patient. Nuchal rigidity and the Kernig and Brudzinski signs were described over a century ago. These tests may be less sensitive in modern day community-acquired bacterial meningitis. As an exa




#Clinical #Clinique #Meningo-encephalite #Meningoencephalitis
Nuchal rigidity and the Kernig and Brudzinski signs were described over a century ago. These tests may be less sensitive in modern day community-acquired bacterial meningitis. As an example, in a large, well-designed prospective study of 297 patients with suspected meningitis, the sensitivity was extremely low (5 percent for each sign and 30 percent for nuchal rigidity); the specificity was 95 percent for each sign and 68 percent for nuchal rigidity [17]
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ity or reluctance to allow full extension of the knee when the hip is flexed 90 degrees. The Kernig test is usually performed in the supine position, but it can be tested in the seated patient. <span>Nuchal rigidity and the Kernig and Brudzinski signs were described over a century ago. These tests may be less sensitive in modern day community-acquired bacterial meningitis. As an example, in a large, well-designed prospective study of 297 patients with suspected meningitis, the sensitivity was extremely low (5 percent for each sign and 30 percent for nuchal rigidity); the specificity was 95 percent for each sign and 68 percent for nuchal rigidity [17]. Jolt accentuation of headache may be a more sensitive maneuver for the diagnosis of meningitis. A positive test consists of accentuation of headache by horizontal rotation of the head




#Clinical #Clinique #Meningo-encephalite #Meningoencephalitis

Jolt accentuation of headache may be a more sensitive maneuver for the diagnosis of meningitis. A positive test consists of accentuation of headache by horizontal rotation of the head at a frequency of two to three times per second.

The diagnostic value of this maneuver has been evaluated in several studies with mixed results [18-20]. Although one study showed a sensitivity of jolt accentuation for the diagnosis of meningitis of 97 percent, other studies have revealed lower sensitivity and specificity highlighting the limited predictive value of the test in the diagnosis of meningitis.

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meningitis, the sensitivity was extremely low (5 percent for each sign and 30 percent for nuchal rigidity); the specificity was 95 percent for each sign and 68 percent for nuchal rigidity [17]. <span>Jolt accentuation of headache may be a more sensitive maneuver for the diagnosis of meningitis. A positive test consists of accentuation of headache by horizontal rotation of the head at a frequency of two to three times per second. The diagnostic value of this maneuver has been evaluated in several studies with mixed results [18-20]. Although one study showed a sensitivity of jolt accentuation for the diagnosis of meningitis of 97 percent, other studies have revealed lower sensitivity and specificity highlighting the limited predictive value of the test in the diagnosis of meningitis. LABORATORY EVALUATION Blood tests — Initial blood tests should include a complete blood count with differential and platelet count and two aerobic blood cultures of appropriate volume (




#Clinical #Clinique #Meningo-encephalite #Meningoencephalitis
Serum electrolytes and glucose, blood urea nitrogen, and creatinine concentrations are helpful in determining the cerebrospinal fluid- (CSF) to-blood glucose ratio. It is important to draw the serum glucose within one hour of obtaining the lumbar puncture to have a reliable ratio [21].
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ests should include a complete blood count with differential and platelet count and two aerobic blood cultures of appropriate volume (ideally, prior to the initiation of antimicrobial therapy). <span>Serum electrolytes and glucose, blood urea nitrogen, and creatinine concentrations are helpful in determining the cerebrospinal fluid- (CSF) to-blood glucose ratio. It is important to draw the serum glucose within one hour of obtaining the lumbar puncture to have a reliable ratio [21]. In addition, coagulation studies may be indicated, especially if petechiae or purpuric lesions are noted [22]. ●The white blood cell (WBC) count is usually elevated, with a shift toward




#Clinical #Clinique #Meningo-encephalite #Meningoencephalitis
In addition, coagulation studies may be indicated, especially if petechiae or purpuric lesions are noted [ 22]
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l in determining the cerebrospinal fluid- (CSF) to-blood glucose ratio. It is important to draw the serum glucose within one hour of obtaining the lumbar puncture to have a reliable ratio [21]. <span>In addition, coagulation studies may be indicated, especially if petechiae or purpuric lesions are noted [22]. ●The white blood cell (WBC) count is usually elevated, with a shift toward immature forms; however, severe infection can be associated with leukopenia. The platelet count may also be r




#Clinical #Clinique #Meningo-encephalite #Meningoencephalitis
The white blood cell (WBC) count is usually elevated, with a shift toward immature forms; however, severe infection can be associated with leukopenia. The platelet count may also be reduced. Leukopenia and thrombocytopenia have correlated with a poor outcome in patients with bacterial meningitis [23,24].
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e within one hour of obtaining the lumbar puncture to have a reliable ratio [21]. In addition, coagulation studies may be indicated, especially if petechiae or purpuric lesions are noted [22]. ●<span>The white blood cell (WBC) count is usually elevated, with a shift toward immature forms; however, severe infection can be associated with leukopenia. The platelet count may also be reduced. Leukopenia and thrombocytopenia have correlated with a poor outcome in patients with bacterial meningitis [23,24]. ●Coagulation studies may be consistent with disseminated intravascular coagulation. ●Serum chemistry results are usually commensurate with the severity of the overall process and may re




#Clinical #Clinique #Meningo-encephalite #Meningoencephalitis
Coagulation studies may be consistent with disseminated intravascular coagulation
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on can be associated with leukopenia. The platelet count may also be reduced. Leukopenia and thrombocytopenia have correlated with a poor outcome in patients with bacterial meningitis [23,24]. ●<span>Coagulation studies may be consistent with disseminated intravascular coagulation. ●Serum chemistry results are usually commensurate with the severity of the overall process and may reveal an anion gap metabolic acidosis or hyponatremia; in one series, hyponatremia w




#Clinical #Clinique #Meningo-encephalite #Meningoencephalitis
Serum chemistry results are usually commensurate with the severity of the overall process and may reveal an anion gap metabolic acidosis or hyponatremia; in one series, hyponatremia was present in 30 percent of patients but was usually mild and did not require specific treatment [25]
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enia and thrombocytopenia have correlated with a poor outcome in patients with bacterial meningitis [23,24]. ●Coagulation studies may be consistent with disseminated intravascular coagulation. ●<span>Serum chemistry results are usually commensurate with the severity of the overall process and may reveal an anion gap metabolic acidosis or hyponatremia; in one series, hyponatremia was present in 30 percent of patients but was usually mild and did not require specific treatment [25]. ●Blood cultures are often positive and can be useful in the event that CSF cannot be obtained before the administration of antimicrobials. Approximately 50 to 90 percent of patients wi




#Clinical #Clinique #Meningo-encephalite #Meningoencephalitis
Initial blood tests should include a complete blood count with differential and platelet count and two aerobic blood cultures of appropriate volume (ideally, prior to the initiation of antimicrobial therapy).
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percent, other studies have revealed lower sensitivity and specificity highlighting the limited predictive value of the test in the diagnosis of meningitis. LABORATORY EVALUATION Blood tests — <span>Initial blood tests should include a complete blood count with differential and platelet count and two aerobic blood cultures of appropriate volume (ideally, prior to the initiation of antimicrobial therapy). Serum electrolytes and glucose, blood urea nitrogen, and creatinine concentrations are helpful in determining the cerebrospinal fluid- (CSF) to-blood glucose ratio. It is important to d




#Clinical #Clinique #Meningo-encephalite #Meningoencephalitis
Blood cultures are often positive and can be useful in the event that CSF cannot be obtained before the administration of antimicrobials. Approximately 50 to 90 percent of patients with bacterial meningitis have positive blood cultures [3,4,6]; lower yields have been reported in some studies in patients with meningococcal infection [26]
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may reveal an anion gap metabolic acidosis or hyponatremia; in one series, hyponatremia was present in 30 percent of patients but was usually mild and did not require specific treatment [25]. ●<span>Blood cultures are often positive and can be useful in the event that CSF cannot be obtained before the administration of antimicrobials. Approximately 50 to 90 percent of patients with bacterial meningitis have positive blood cultures [3,4,6]; lower yields have been reported in some studies in patients with meningococcal infection [26]. Cultures obtained after antimicrobial therapy are much less likely to be positive, particularly for meningococcus [26-28]. In health care-associated ventriculitis and meningitis, previ




#Clinical #Clinique #Meningo-encephalite #Meningoencephalitis
Tests of serum and urine for bacterial antigens, as well as cultures of mucosal surfaces for the causative pathogen, are not generally helpful
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y for meningococcus [26-28]. In health care-associated ventriculitis and meningitis, previous antibiotic therapy can significantly reduce the sensitivity of the CSF Gram stain and culture [28]. <span>Tests of serum and urine for bacterial antigens, as well as cultures of mucosal surfaces for the causative pathogen, are not generally helpful. Cerebrospinal fluid examination — Every patient with suspected meningitis should have CSF obtained unless lumbar puncture (LP) is contraindicated. Examination of the CSF is crucial for




#Clinical #Clinique #Meningo-encephalite #Meningoencephalitis
Every patient with suspected meningitis should have CSF obtained unless lumbar puncture (LP) is contraindicated
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d culture [28]. Tests of serum and urine for bacterial antigens, as well as cultures of mucosal surfaces for the causative pathogen, are not generally helpful. Cerebrospinal fluid examination — <span>Every patient with suspected meningitis should have CSF obtained unless lumbar puncture (LP) is contraindicated. Examination of the CSF is crucial for establishing the diagnosis of bacterial meningitis, identifying the causative organism, and performing in vitro susceptibility testing [29]. Preca




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Although there are no absolute contraindications to performing the procedure, caution should be used in patients with (see "Lumbar puncture: Technique, indications, contraindications, and complications in adults", section on 'Contraindications'):

● Possible raised intracranial pressure with risk for cerebral herniation due to obstructive hydrocephalus, cerebral edema, or space-occupying lesion

● Thrombocytopenia or other bleeding diathesis, including ongoing anticoagulant therapy

● Suspected spinal epidural abscess

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Examination of the CSF is crucial for establishing the diagnosis of bacterial meningitis, identifying the causative organism, and performing in vitro susceptibility testing [29]. Precautions — <span>Although there are no absolute contraindications to performing the procedure, caution should be used in patients with (see "Lumbar puncture: Technique, indications, contraindications, and complications in adults", section on 'Contraindications'): ●Possible raised intracranial pressure with risk for cerebral herniation due to obstructive hydrocephalus, cerebral edema, or space-occupying lesion ●Thrombocytopenia or other bleeding diathesis, including ongoing anticoagulant therapy ●Suspected spinal epidural abscess Indications for CT scan before LP — An important early decision relates to whether a head computed tomography (CT) should be performed prior to LP to exclude a mass lesion or increased




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A head CT should be performed before LP in adults with suspected bacterial meningitis who have one or more of the following risk factors (algorithm 1) [30-32]:

● Immunocompromised state (eg, HIV infection, immunosuppressive therapy, solid organ or hematopoietic cell transplantation)

● History of central nervous system (CNS) disease (mass lesion, stroke, or focal infection)

● New onset seizure (within one week of presentation)

● Papilledema

● Abnormal level of consciousness

● Focal neurologic deficit

Patients without these indications should not undergo a CT scan as it is of no clinical benefit and delays therapy [33]

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ncreased intracranial pressure. These abnormalities might rarely lead to cerebral herniation during removal of large amounts of CSF, and cerebral herniation could have devastating consequences. <span>A head CT should be performed before LP in adults with suspected bacterial meningitis who have one or more of the following risk factors (algorithm 1) [30-32]: ●Immunocompromised state (eg, HIV infection, immunosuppressive therapy, solid organ or hematopoietic cell transplantation) ●History of central nervous system (CNS) disease (mass lesion, stroke, or focal infection) ●New onset seizure (within one week of presentation) ●Papilledema ●Abnormal level of consciousness ●Focal neurologic deficit Patients without these indications should not undergo a CT scan as it is of no clinical benefit and delays therapy [33]. The bacterial meningitis guidelines in Sweden were revised in 2009 to remove impaired mental status as a contraindication to LP without prior CT scan, and the effect of this change was




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It has been suggested that a normal CT scan does not always mean that performance of an LP is safe and that certain clinical signs of impending herniation (ie, deteriorating level of consciousness, particularly a Glasgow Coma scale <11; brainstem signs including pupillary changes, posturing, or irregular respirations; or a very recent seizure) may be predictive of patients in whom an LP should be delayed irrespective of CT findings (table 3) [36]. (See "Lumbar puncture: Technique, indications, contraindications, and complications in adults", section on 'Cerebral herniation'.)
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e, patients who have a CT before LP are sicker [33] or often not started on antibiotics before neuroimaging, despite recommendations to the contrary. (See 'If LP is delayed or deferred' below.) <span>It has been suggested that a normal CT scan does not always mean that performance of an LP is safe and that certain clinical signs of impending herniation (ie, deteriorating level of consciousness, particularly a Glasgow Coma scale <11; brainstem signs including pupillary changes, posturing, or irregular respirations; or a very recent seizure) may be predictive of patients in whom an LP should be delayed irrespective of CT findings (table 3) [36]. (See "Lumbar puncture: Technique, indications, contraindications, and complications in adults", section on 'Cerebral herniation'.) If LP is delayed or deferred — It is essential that antimicrobial therapy not be delayed if there is a contraindication to or inability to perform an LP, or if the LP is delayed by the




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If LP is delayed or deferred — It is essential that antimicrobial therapy not be delayed if there is a contraindication to or inability to perform an LP, or if the LP is delayed by the need for cranial imaging. In any of these situations, blood cultures should be obtained and empiric antibiotics administered as soon as is possible (before the imaging study in patients who require imaging).
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should be delayed irrespective of CT findings (table 3) [36]. (See "Lumbar puncture: Technique, indications, contraindications, and complications in adults", section on 'Cerebral herniation'.) <span>If LP is delayed or deferred — It is essential that antimicrobial therapy not be delayed if there is a contraindication to or inability to perform an LP, or if the LP is delayed by the need for cranial imaging. In any of these situations, blood cultures should be obtained and empiric antibiotics administered as soon as is possible (before the imaging study in patients who require imaging). (See "Initial therapy and prognosis of bacterial meningitis in adults", section on 'Empiric regimens'.) In addition, dexamethasone (0.15 mg/kg intravenously every 6 hours) should be giv




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In addition, dexamethasone (0.15 mg/kg intravenously every 6 hours) should be given shortly before or at the same time as the antimicrobial agents if the preponderance of clinical and laboratory evidence suggests bacterial meningitis with a plan to stop therapy, if indicated, when the evaluation is complete.
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stered as soon as is possible (before the imaging study in patients who require imaging). (See "Initial therapy and prognosis of bacterial meningitis in adults", section on 'Empiric regimens'.) <span>In addition, dexamethasone (0.15 mg/kg intravenously every 6 hours) should be given shortly before or at the same time as the antimicrobial agents if the preponderance of clinical and laboratory evidence suggests bacterial meningitis with a plan to stop therapy, if indicated, when the evaluation is complete. Adjunctive dexamethasone should not be given to patients who have already received antimicrobial therapy because it is unlikely to improve patient outcome even though the European and U




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Adjunctive dexamethasone should not be given to patients who have already received antimicrobial therapy because it is unlikely to improve patient outcome even though the European and United Kingdom guidelines recommend administering dexamethasone up to 4 and 12 hours after receipt of antimicrobial therapy, respectively [ 37]. Indications for adjunctive dexamethasone are discussed in greater detail separately. (See "Dexamethasone to prevent neurologic complications of bacterial meningitis in adults" and "Initial therapy and prognosis of bacterial meningitis in adults", section on 'Avoidance of delay'.)
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me as the antimicrobial agents if the preponderance of clinical and laboratory evidence suggests bacterial meningitis with a plan to stop therapy, if indicated, when the evaluation is complete. <span>Adjunctive dexamethasone should not be given to patients who have already received antimicrobial therapy because it is unlikely to improve patient outcome even though the European and United Kingdom guidelines recommend administering dexamethasone up to 4 and 12 hours after receipt of antimicrobial therapy, respectively [37]. Indications for adjunctive dexamethasone are discussed in greater detail separately. (See "Dexamethasone to prevent neurologic complications of bacterial meningitis in adults" and "Initial therapy and prognosis of bacterial meningitis in adults", section on 'Avoidance of delay'.) Prior administration of antimicrobials tends to have minimal effects on the chemistry and cytology findings [28,38] but can reduce the yield of Gram stain and culture [26-28]. However,




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Prior administration of antimicrobials tends to have minimal effects on the chemistry and cytology findings [28,38] but can reduce the yield of Gram stain and culture [26-28].
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ee "Dexamethasone to prevent neurologic complications of bacterial meningitis in adults" and "Initial therapy and prognosis of bacterial meningitis in adults", section on 'Avoidance of delay'.) <span>Prior administration of antimicrobials tends to have minimal effects on the chemistry and cytology findings [28,38] but can reduce the yield of Gram stain and culture [26-28]. However, a pathogen can still be cultured from the CSF in most patients up to several hours after the administration of antimicrobial agents [27,28], with the possible exception of the




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However, a pathogen can still be cultured from the CSF in most patients up to several hours after the administration of antimicrobial agents [ 27,28], with the possible exception of the meningococcus
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dance of delay'.) Prior administration of antimicrobials tends to have minimal effects on the chemistry and cytology findings [28,38] but can reduce the yield of Gram stain and culture [26-28]. <span>However, a pathogen can still be cultured from the CSF in most patients up to several hours after the administration of antimicrobial agents [27,28], with the possible exception of the meningococcus. This issue was addressed in a review of 128 children with bacterial meningitis in whom LP was first performed after initiation of therapy and serial LPs were obtained [27]. Among patie




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Opening pressure — The opening pressure with the patient lying in the lateral decubitus position should be measured and documented. The opening pressure is typically elevated in patients with bacterial meningitis. In the series of 301 adults cited above, the mean opening pressure was approximately 350 mm H2O (normal up to 200 mm H2O) [3]. However, there is a wide range of values as illustrated in a report of 296 episodes of community-acquired bacterial meningitis: 39 percent had values ≥300 mm H2O, while 9 percent had values below 140 mm H2O [8]
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fection, CSF culture was negative in 3 of 9 samples obtained within one hour. In contrast, 4 to 10 hours were required before CSF cultures were sterile in patients with pneumococcal meningitis. <span>Opening pressure — The opening pressure with the patient lying in the lateral decubitus position should be measured and documented. The opening pressure is typically elevated in patients with bacterial meningitis. In the series of 301 adults cited above, the mean opening pressure was approximately 350 mm H2O (normal up to 200 mm H2O) [3]. However, there is a wide range of values as illustrated in a report of 296 episodes of community-acquired bacterial meningitis: 39 percent had values ≥300 mm H2O, while 9 percent had values below 140 mm H2O [8]. Cerebrospinal fluid analysis Overview — CSF should be sent for: •Cell count and differential •Glucose concentration •Protein concentration •Gram stain and bacterial culture •Other appr




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Characteristic findings in bacterial meningitis include a CSF glucose concentration <40 mg/dL (<2.22 mmol/L), a CSF to serum glucose ratio of ≤0.4, a protein concentration >200 mg/dL (>2000 mg/L), and a WBC count above 1000/microL, with a percentage of neutrophils usually greater than 80 percent [3,32,39]
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and bacterial culture •Other appropriate tests (eg, rapid tests, polymerase chain reaction [PCR]), depending upon the level of concern for other etiologies of meningitis or meningoencephalitis <span>Characteristic findings in bacterial meningitis include a CSF glucose concentration <40 mg/dL (<2.22 mmol/L), a CSF to serum glucose ratio of ≤0.4, a protein concentration >200 mg/dL (>2000 mg/L), and a WBC count above 1000/microL, with a percentage of neutrophils usually greater than 80 percent [3,32,39]. The spectrum of CSF values in bacterial meningitis is so wide, however, that the absence of one or more of the typical findings is of little value [4,8]. For example, in a prospective




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he spectrum of CSF values in bacterial meningitis is so wide, however, that the absence of one or more of the typical findings is of little value [ 4,8].
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rum glucose ratio of ≤0.4, a protein concentration >200 mg/dL (>2000 mg/L), and a WBC count above 1000/microL, with a percentage of neutrophils usually greater than 80 percent [3,32,39]. T<span>he spectrum of CSF values in bacterial meningitis is so wide, however, that the absence of one or more of the typical findings is of little value [4,8]. For example, in a prospective study of 1412 adults with bacterial meningitis, a CSF WBC >1000/microL was seen in only 66 percent of patients [3]. Why some patients have milder CSF ab




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For example, in a prospective study of 1412 adults with bacterial meningitis, a CSF WBC >1000/microL was seen in only 66 percent of patients [ 3].
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ally greater than 80 percent [3,32,39]. The spectrum of CSF values in bacterial meningitis is so wide, however, that the absence of one or more of the typical findings is of little value [4,8]. <span>For example, in a prospective study of 1412 adults with bacterial meningitis, a CSF WBC >1000/microL was seen in only 66 percent of patients [3]. Why some patients have milder CSF abnormalities cannot usually be identified. Potential causes include early presentation, recent prior antimicrobial therapy, and neutropenia. (See "Cer




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Why some patients have milder CSF abnormalities cannot usually be identified. Potential causes include early presentation, recent prior antimicrobial therapy, and neutropenia. (See "Cerebrospinal fluid: Physiology and utility of an examination in disease states", section on 'CSF in CNS infection'.)
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e typical findings is of little value [4,8]. For example, in a prospective study of 1412 adults with bacterial meningitis, a CSF WBC >1000/microL was seen in only 66 percent of patients [3]. <span>Why some patients have milder CSF abnormalities cannot usually be identified. Potential causes include early presentation, recent prior antimicrobial therapy, and neutropenia. (See "Cerebrospinal fluid: Physiology and utility of an examination in disease states", section on 'CSF in CNS infection'.) An observational study found that bacterial meningitis was highly probable (≥99 percent certainty) when any one of the following parameters was present: a CSF glucose concentration belo




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An observational study found that bacterial meningitis was highly probable (≥99 percent certainty) when any one of the following parameters was present: a CSF glucose concentration below 34 mg/dL (1.9 mmol/L), a protein concentration above 220 mg/dL (2200 mg/L), a WBC count above 2000/microL, or a neutrophil count more than 1180/microL [40]. However, clinicians must recognize that many exceptions exist and that empiric antimicrobial therapy is warranted when bacterial meningitis is suspected clinically even if the CSF abnormalities are not diagnostic
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ly presentation, recent prior antimicrobial therapy, and neutropenia. (See "Cerebrospinal fluid: Physiology and utility of an examination in disease states", section on 'CSF in CNS infection'.) <span>An observational study found that bacterial meningitis was highly probable (≥99 percent certainty) when any one of the following parameters was present: a CSF glucose concentration below 34 mg/dL (1.9 mmol/L), a protein concentration above 220 mg/dL (2200 mg/L), a WBC count above 2000/microL, or a neutrophil count more than 1180/microL [40]. However, clinicians must recognize that many exceptions exist and that empiric antimicrobial therapy is warranted when bacterial meningitis is suspected clinically even if the CSF abnormalities are not diagnostic. A false-positive elevation of the CSF WBC count can be found after traumatic LP or in patients with intracerebral or subarachnoid hemorrhage in which both red blood cells (RBCs) and WB




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A false-positive elevation of the CSF WBC count can be found after traumatic LP or in patients with intracerebral or subarachnoid hemorrhage in which both red blood cells (RBCs) and WBCs are introduced into the subarachnoid space. If a traumatic LP is suspected and the peripheral WBC count is not abnormally low or high, a good rule of thumb for estimating the adjusted WBC count is to subtract one WBC for every 500 to 1000 RBCs measured in the CSF. This "corrected" CSF WBC has better diagnostic accuracy in differentiating culture-positive bacterial meningitis than patients with intracerebral hemorrhage alone [41]. The formula in the following calculator can also be used to determine the adjusted WBC count in the presence of CSF RBCs (calculator 1) [41,42]
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must recognize that many exceptions exist and that empiric antimicrobial therapy is warranted when bacterial meningitis is suspected clinically even if the CSF abnormalities are not diagnostic. <span>A false-positive elevation of the CSF WBC count can be found after traumatic LP or in patients with intracerebral or subarachnoid hemorrhage in which both red blood cells (RBCs) and WBCs are introduced into the subarachnoid space. If a traumatic LP is suspected and the peripheral WBC count is not abnormally low or high, a good rule of thumb for estimating the adjusted WBC count is to subtract one WBC for every 500 to 1000 RBCs measured in the CSF. This "corrected" CSF WBC has better diagnostic accuracy in differentiating culture-positive bacterial meningitis than patients with intracerebral hemorrhage alone [41]. The formula in the following calculator can also be used to determine the adjusted WBC count in the presence of CSF RBCs (calculator 1) [41,42]. Determination of the CSF lactate concentration has been suggested as a useful test to differentiate bacterial from viral meningitis. Two meta-analyses that included 25 studies (1692 pa




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Two meta-analyses that included 25 studies (1692 patients) and 31 studies (1885 patients) concluded that the diagnostic accuracy of CSF lactate was superior to that of CSF WBC count, glucose, and protein concentration in differentiating bacterial from aseptic meningitis [43,44], although sensitivity was lower in patients who received antimicrobial treatment prior to LP [43], and CSF lactate may be elevated in patients with other CNS diseases.
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BC count in the presence of CSF RBCs (calculator 1) [41,42]. Determination of the CSF lactate concentration has been suggested as a useful test to differentiate bacterial from viral meningitis. <span>Two meta-analyses that included 25 studies (1692 patients) and 31 studies (1885 patients) concluded that the diagnostic accuracy of CSF lactate was superior to that of CSF WBC count, glucose, and protein concentration in differentiating bacterial from aseptic meningitis [43,44], although sensitivity was lower in patients who received antimicrobial treatment prior to LP [43], and CSF lactate may be elevated in patients with other CNS diseases. A CSF lactate may help differentiate health care-associated ventriculitis from chemical meningitis in patients with recent neurosurgical procedures, but it is only performed in approxim




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A CSF lactate may help differentiate health care-associated ventriculitis from chemical meningitis in patients with recent neurosurgical procedures, but it is only performed in approximately 50 percent of the patients [ 45]
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septic meningitis [43,44], although sensitivity was lower in patients who received antimicrobial treatment prior to LP [43], and CSF lactate may be elevated in patients with other CNS diseases. <span>A CSF lactate may help differentiate health care-associated ventriculitis from chemical meningitis in patients with recent neurosurgical procedures, but it is only performed in approximately 50 percent of the patients [45]. Gram stain — A Gram stain should be obtained whenever there is suspicion of bacterial meningitis. It has the advantage of suggesting the bacterial etiology one day or more before cultu




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● Gram-positive diplococci suggest pneumococcal infection (picture 1).

● Gram-negative diplococci suggest meningococcal infection (picture 2).

● Small pleomorphic gram-negative coccobacilli suggest Haemophilus influenzae infection (picture 3).

● Gram-positive rods and coccobacilli suggest listerial infection (picture 4).

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re is suspicion of bacterial meningitis. It has the advantage of suggesting the bacterial etiology one day or more before culture results are available [26]. The following findings may be seen: <span>●Gram-positive diplococci suggest pneumococcal infection (picture 1). ●Gram-negative diplococci suggest meningococcal infection (picture 2). ●Small pleomorphic gram-negative coccobacilli suggest Haemophilus influenzae infection (picture 3). ●Gram-positive rods and coccobacilli suggest listerial infection (picture 4). The reported sensitivity of Gram stain for bacterial meningitis has varied from 50 to 90 percent; however, the specificity approaches 100 percent [4,11,46]. In the report of 696 patient




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The Gram stain is positive in 10 to 15 percent of patients who have bacterial meningitis but negative CSF cultures [8]. As noted above, the yield of both Gram stain and culture may be reduced by prior antibiotic therapy [26-28]
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d a specificity of 97 percent [4]. In a trial of 301 adults with bacterial meningitis, for example, the Gram stain was positive in 74 percent and the CSF culture was positive in 78 percent [3]. <span>The Gram stain is positive in 10 to 15 percent of patients who have bacterial meningitis but negative CSF cultures [8]. As noted above, the yield of both Gram stain and culture may be reduced by prior antibiotic therapy [26-28]. Rapid tests — Several rapid diagnostic tests have been developed to aid in the diagnosis of bacterial meningitis. Latex agglutination tests detect the antigens of the common meningeal




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The reported sensitivity of Gram stain for bacterial meningitis has varied from 50 to 90 percent; however, the specificity approaches 100 percent [4,11,46]
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on (picture 2). ●Small pleomorphic gram-negative coccobacilli suggest Haemophilus influenzae infection (picture 3). ●Gram-positive rods and coccobacilli suggest listerial infection (picture 4). <span>The reported sensitivity of Gram stain for bacterial meningitis has varied from 50 to 90 percent; however, the specificity approaches 100 percent [4,11,46]. In the report of 696 patients with community-acquired bacterial meningitis, CSF Gram stain had a sensitivity of 80 percent and a specificity of 97 percent [4]. In a trial of 301 adults




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A rapid multiplex PCR that tests for the most common viruses, bacteria, and fungi is now widely available and has been shown to be useful, especially in those with a negative-CSF Gram stain or culture, or in those who have received prior antimicrobial therapy.
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Nucleic acid amplification tests, such as the polymerase chain reaction (PCR), have been evaluated in patients with bacterial meningitis and have shown high sensitivity and specificity [49,50]. <span>A rapid multiplex PCR that tests for the most common viruses, bacteria, and fungi is now widely available and has been shown to be useful, especially in those with a negative-CSF Gram stain or culture, or in those who have received prior antimicrobial therapy. Use of PCR for the two most common meningeal pathogens (S. pneumoniae and N. meningitidis) is routinely recommended in the United Kingdom guidelines for patients presenting with meningi




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Problems with false-positive results have been reported with PCR but false negatives are very uncommon [52]
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tis [51]. Studies evaluating the multiplex PCR assay for detection of N. meningitidis, S. pneumoniae, and H. influenzae type b have shown sensitivities and specificities of 100 percent [49,50]. <span>Problems with false-positive results have been reported with PCR but false negatives are very uncommon [52]. Molecular diagnosis of bacterial meningitis is discussed in greater detail separately. (See "Molecular diagnosis of central nervous system infections", section on 'Meningitis'.) DIAGNO




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Molecular diagnosis of bacterial meningitis is discussed in greater detail separately. (See "Molecular diagnosis of central nervous system infections", section on 'Meningitis'.)
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influenzae type b have shown sensitivities and specificities of 100 percent [49,50]. Problems with false-positive results have been reported with PCR but false negatives are very uncommon [52]. <span>Molecular diagnosis of bacterial meningitis is discussed in greater detail separately. (See "Molecular diagnosis of central nervous system infections", section on 'Meningitis'.) DIAGNOSIS — Acute bacterial meningitis should be promptly suspected in adults who present with fever, headache, stiff neck, and/or altered mental status. Late diagnosis is associated wi




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Isolation of bacteria from blood cultures in a patient with CSF pleocytosis also confirms the diagnosis, even if the CSF culture remains negative
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ids, and a higher mortality [53]. Isolation of a bacterial pathogen from the cerebrospinal fluid (CSF; by culture or other diagnostic techniques) confirms the diagnosis of bacterial meningitis. <span>Isolation of bacteria from blood cultures in a patient with CSF pleocytosis also confirms the diagnosis, even if the CSF culture remains negative. It may be difficult to definitively establish the diagnosis of bacterial meningitis in those patients who have received antibiotics prior to lumbar puncture which decreases the yield o




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Differentiation of these disorders from bacterial meningitis requires careful examination of cerebrospinal fluid (CSF) parameters (table 4) and neuroimaging (when indicated), as well as consideration of any epidemiologic factors that would raise the possibility of specific bacterial or nonbacterial central nervous system infections
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inal fluid culture'.) DIFFERENTIAL DIAGNOSIS — The clinical and laboratory findings of bacterial meningitis overlap with those of meningitis caused by viruses, mycobacteria, fungi, or protozoa. <span>Differentiation of these disorders from bacterial meningitis requires careful examination of cerebrospinal fluid (CSF) parameters (table 4) and neuroimaging (when indicated), as well as consideration of any epidemiologic factors that would raise the possibility of specific bacterial or nonbacterial central nervous system infections. For patients with abnormal CSF findings, the differential diagnosis includes the following: ●Viral meningitis – Aseptic (usually viral) meningitis is a less severe disease that is ofte




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Viral meningitis – Aseptic (usually viral) meningitis is a less severe disease that is often monitored in the outpatient setting without antimicrobial therapy, whereas bacterial meningitis is a life-threatening illness that requires hospital admission. Similar to bacterial meningitis, viral meningitis presents acutely with classic signs and symptoms of meningitis. Unlike bacterial meningitis, the CSF normally has a lymphocytic pleocytosis, normal glucose, moderate elevation of protein, and negative-CSF Gram stain and culture. Definitive diagnosis of viral meningitis is generally made by CSF polymerase chain reaction (PCR), although serologies are typically used for the diagnosis of meningitis due to arboviruses (eg, West Nile virus).
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would raise the possibility of specific bacterial or nonbacterial central nervous system infections. For patients with abnormal CSF findings, the differential diagnosis includes the following: ●<span>Viral meningitis – Aseptic (usually viral) meningitis is a less severe disease that is often monitored in the outpatient setting without antimicrobial therapy, whereas bacterial meningitis is a life-threatening illness that requires hospital admission. Similar to bacterial meningitis, viral meningitis presents acutely with classic signs and symptoms of meningitis. Unlike bacterial meningitis, the CSF normally has a lymphocytic pleocytosis, normal glucose, moderate elevation of protein, and negative-CSF Gram stain and culture. Definitive diagnosis of viral meningitis is generally made by CSF polymerase chain reaction (PCR), although serologies are typically used for the diagnosis of meningitis due to arboviruses (eg, West Nile virus). (See "Aseptic meningitis in adults" and "Clinical manifestations and diagnosis of West Nile virus infection", section on 'Diagnosis'.) ●TB meningitis – Patients with tuberculous (TB) me




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TB meningitis – Patients with tuberculous (TB) meningitis may have classic signs and symptoms of meningitis at presentation, however, it is generally a subacute process. CSF exam typically reveals a lymphocyte predominant pleocytosis with elevated protein and decreased glucose. Certain scoring systems (eg, the Lancet consensus scoring system and the Thwaites system) have been developed to help differentiate bacterial from TB meningitis [54]; these are based primarily on clinical and CSF findings. A definitive diagnosis of TB meningitis is made by identification of mycobacterium from the CSF either by culture or PCR.
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s of meningitis due to arboviruses (eg, West Nile virus). (See "Aseptic meningitis in adults" and "Clinical manifestations and diagnosis of West Nile virus infection", section on 'Diagnosis'.) ●<span>TB meningitis – Patients with tuberculous (TB) meningitis may have classic signs and symptoms of meningitis at presentation, however, it is generally a subacute process. CSF exam typically reveals a lymphocyte predominant pleocytosis with elevated protein and decreased glucose. Certain scoring systems (eg, the Lancet consensus scoring system and the Thwaites system) have been developed to help differentiate bacterial from TB meningitis [54]; these are based primarily on clinical and CSF findings. A definitive diagnosis of TB meningitis is made by identification of mycobacterium from the CSF either by culture or PCR. (See "Central nervous system tuberculosis: An overview".) ●Fungal meningitis – Several fungal species may cause meningitis including Candida, Cryptococcus, Histoplasma, Blastomyces, and




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Fungal meningitis – Several fungal species may cause meningitis including Candida, Cryptococcus, Histoplasma, Blastomyces, and Coccidioides. Although fungal meningitis may present with classic symptoms of meningitis, it often is a subacute process in patients with epidemiologic risk factors for fungal disease (eg, immunocompromise, HIV).
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SF findings. A definitive diagnosis of TB meningitis is made by identification of mycobacterium from the CSF either by culture or PCR. (See "Central nervous system tuberculosis: An overview".) ●<span>Fungal meningitis – Several fungal species may cause meningitis including Candida, Cryptococcus, Histoplasma, Blastomyces, and Coccidioides. Although fungal meningitis may present with classic symptoms of meningitis, it often is a subacute process in patients with epidemiologic risk factors for fungal disease (eg, immunocompromise, HIV). (See "Candida infections of the central nervous system" and "Epidemiology, clinical manifestations, and diagnosis of Cryptococcus neoformans meningoencephalitis in patients with HIV" an




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Generalized seizures without meningitis – Generalized seizures may also induce a mild transient CSF pleocytosis, although this has not been well studied [55-57]. However, CSF pleocytosis should not be ascribed to seizure activity alone unless the fluid is clear and colorless, the opening pressure and CSF glucose are normal, the CSF Gram stain is negative, and the patient has no clinical evidence of bacterial meningitis
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negative patients" and "Coccidioidal meningitis" and "Diagnosis and treatment of disseminated histoplasmosis in HIV-uninfected patients" and "Approach to the patient with chronic meningitis".) ●<span>Generalized seizures without meningitis – Generalized seizures may also induce a mild transient CSF pleocytosis, although this has not been well studied [55-57]. However, CSF pleocytosis should not be ascribed to seizure activity alone unless the fluid is clear and colorless, the opening pressure and CSF glucose are normal, the CSF Gram stain is negative, and the patient has no clinical evidence of bacterial meningitis. When the Gram stain is negative, studies in both adults and children have concluded that, in the setting of an elevated CSF white blood cell (WBC) count, no single CSF biochemical vari




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When the Gram stain is negative, studies in both adults and children have concluded that, in the setting of an elevated CSF white blood cell (WBC) count, no single CSF biochemical variable can reliably exclude bacterial meningitis [40,46,58]
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alone unless the fluid is clear and colorless, the opening pressure and CSF glucose are normal, the CSF Gram stain is negative, and the patient has no clinical evidence of bacterial meningitis. <span>When the Gram stain is negative, studies in both adults and children have concluded that, in the setting of an elevated CSF white blood cell (WBC) count, no single CSF biochemical variable can reliably exclude bacterial meningitis [40,46,58]. (See "Cerebrospinal fluid: Physiology and utility of an examination in disease states", section on 'CSF in CNS infection' and "Aseptic meningitis in adults".) SOCIETY GUIDELINE LINKS —




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The number of definite indications for LP has decreased with the advent of better neuroimaging procedures including computed tomography (CT) scans and magnetic resonance imaging (MRI), but urgent LP is still indicated to diagnose two serious conditions [1,2]:

● Suspected CNS infection (with the exception of brain abscess or a parameningeal process).

● Suspected SAH in a patient with a negative CT scan [3]. The use of cerebrospinal fluid (CSF) examination in the evaluation of a patient with suspected SAH is discussed in detail separately. (See "Aneurysmal subarachnoid hemorrhage: Clinical manifestations and diagnosis", section on 'Lumbar puncture'.)

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ous system (CNS) infections and, in certain settings, for help in the diagnosis of subarachnoid hemorrhage (SAH), CNS malignancies, demyelinating diseases, and Guillain-Barré syndrome. Urgent — <span>The number of definite indications for LP has decreased with the advent of better neuroimaging procedures including computed tomography (CT) scans and magnetic resonance imaging (MRI), but urgent LP is still indicated to diagnose two serious conditions [1,2]: ●Suspected CNS infection (with the exception of brain abscess or a parameningeal process). ●Suspected SAH in a patient with a negative CT scan [3]. The use of cerebrospinal fluid (CSF) examination in the evaluation of a patient with suspected SAH is discussed in detail separately. (See "Aneurysmal subarachnoid hemorrhage: Clinical manifestations and diagnosis", section on 'Lumbar puncture'.) The most common use of the LP is to diagnose or exclude meningitis in patients presenting with some combination of fever, altered mental status, headache, or meningeal signs. Examinatio




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A nonurgent LP is indicated in the diagnosis of many other conditions. The findings are discussed in the appropriate topic reviews:

● Idiopathic intracranial hypertension (pseudotumor cerebri)

● Carcinomatous meningitis

● Normal pressure hydrocephalus

● CNS syphilis

● CNS lymphoma

● Autoimmune encephalitis

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bacterial meningitis from viral infections of the CNS. However, there is often substantial overlap. (See "Viral encephalitis in adults", section on 'Cerebrospinal fluid findings'.) Nonurgent — <span>A nonurgent LP is indicated in the diagnosis of many other conditions. The findings are discussed in the appropriate topic reviews: ●Idiopathic intracranial hypertension (pseudotumor cerebri) ●Carcinomatous meningitis ●Normal pressure hydrocephalus ●CNS syphilis ●CNS lymphoma ●Autoimmune encephalitis Conditions in which LP is rarely diagnostic but still useful include: ●Multiple sclerosis ●Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy ●Paraneoplastic




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Conditions in which LP is rarely diagnostic but still useful include:

● Multiple sclerosis

● Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy

● Paraneoplastic syndromes

● Neurosarcoidosis

● CNS vasculitis

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ropriate topic reviews: ●Idiopathic intracranial hypertension (pseudotumor cerebri) ●Carcinomatous meningitis ●Normal pressure hydrocephalus ●CNS syphilis ●CNS lymphoma ●Autoimmune encephalitis <span>Conditions in which LP is rarely diagnostic but still useful include: ●Multiple sclerosis ●Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy ●Paraneoplastic syndromes ●Neurosarcoidosis ●CNS vasculitis LP is also required as a therapeutic or diagnostic maneuver in the following situations [1,2,4,5]: ●Spinal anesthesia ●Intrathecal administration of chemotherapy ●Intrathecal administra




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In many situations, high-risk patients can be identified and risks can be mitigated. These are discussed in detail in relation to the complications with which they are associated. (See 'Complications' below.)
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to obstructive hydrocephalus, cerebral edema, or space-occupying lesion ●Thrombocytopenia or other bleeding diathesis, including ongoing anticoagulant therapy ●Suspected spinal epidural abscess <span>In many situations, high-risk patients can be identified and risks can be mitigated. These are discussed in detail in relation to the complications with which they are associated. (See 'Complications' below.) When the LP is delayed or deferred in the setting of suspected bacterial meningitis, it is important to obtain blood cultures (which reveal the pathogen in more than half of patients) a




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The choice of needle type (cutting versus atraumatic) and bore size can influence the risk of a post-LP headache, but also may increase the technical difficulty of the procedure. This is discussed in detail separately. (See "Post dural puncture headache", section on 'Prevention of PDPH after dural puncture'.)
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mptly when this is suspected. Specific treatments are discussed separately. (See "Initial therapy and prognosis of bacterial meningitis in adults", section on 'Avoidance of delay'.) TECHNIQUE — <span>The choice of needle type (cutting versus atraumatic) and bore size can influence the risk of a post-LP headache, but also may increase the technical difficulty of the procedure. This is discussed in detail separately. (See "Post dural puncture headache", section on 'Prevention of PDPH after dural puncture'.) Positioning — An LP can be performed with the patient in the lateral recumbent or prone positions or sitting upright. The lateral recumbent or prone positions are preferred over the upr




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The correct level of entry of the spinal needle is most easily determined with the patient sitting upright or standing. The highest points of the iliac crests should be identified visually and confirmed by palpation; a direct line joining these is a guide to the fourth lumbar vertebral body. However, this line may intersect the spine at points ranging from L1-L2 to L4-L5 [6], and tends to point to a higher spinal level in females and in patients with obesity [7].
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osition because they allow more accurate measurement of the opening pressure. The prone position is generally used for LPs performed under fluoroscopic guidance. (See 'Imaging guidance' below.) <span>The correct level of entry of the spinal needle is most easily determined with the patient sitting upright or standing. The highest points of the iliac crests should be identified visually and confirmed by palpation; a direct line joining these is a guide to the fourth lumbar vertebral body. However, this line may intersect the spine at points ranging from L1-L2 to L4-L5 [6], and tends to point to a higher spinal level in females and in patients with obesity [7]. The lumbar spinous processes of L3, L4, and L5, and the interspaces between, can usually be directly identified by palpation. The spinal needle can be safely inserted into the subarachn




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The lumbar spinous processes of L3, L4, and L5, and the interspaces between, can usually be directly identified by palpation. The spinal needle can be safely inserted into the subarachnoid space at the L3-4 or L4-5 interspace, since this is well below the termination of the spinal cord in most patients.
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ar vertebral body. However, this line may intersect the spine at points ranging from L1-L2 to L4-L5 [6], and tends to point to a higher spinal level in females and in patients with obesity [7]. <span>The lumbar spinous processes of L3, L4, and L5, and the interspaces between, can usually be directly identified by palpation. The spinal needle can be safely inserted into the subarachnoid space at the L3-4 or L4-5 interspace, since this is well below the termination of the spinal cord in most patients. Spinal cord imaging is not considered necessary prior to LP, but, if performed, images should be reviewed to confirm the position of the conus prior to LP. An alternate approach to obta




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An alternate approach to obtaining cerebrospinal fluid (CSF) with a paramedian needle insertion through the L5-S1 space (Taylor approach) (figure 1) has been successfully used in a patient with advanced ankylosing spondylitis [8]
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of the spinal cord in most patients. Spinal cord imaging is not considered necessary prior to LP, but, if performed, images should be reviewed to confirm the position of the conus prior to LP. <span>An alternate approach to obtaining cerebrospinal fluid (CSF) with a paramedian needle insertion through the L5-S1 space (Taylor approach) (figure 1) has been successfully used in a patient with advanced ankylosing spondylitis [8]. Correct patient positioning is an important determinant of success in obtaining CSF. The patient is instructed to remain in the fetal position with the neck, back, and limbs held in fl




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Correct patient positioning is an important determinant of success in obtaining CSF. The patient is instructed to remain in the fetal position with the neck, back, and limbs held in flexion. The lower lumbar spine should be flexed with the back perfectly perpendicular to the edge of a bed or examining table. The hips and legs should be parallel to each other and perpendicular to the table. Pillows placed under the head and between the knees may improve patient comfort
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rebrospinal fluid (CSF) with a paramedian needle insertion through the L5-S1 space (Taylor approach) (figure 1) has been successfully used in a patient with advanced ankylosing spondylitis [8]. <span>Correct patient positioning is an important determinant of success in obtaining CSF. The patient is instructed to remain in the fetal position with the neck, back, and limbs held in flexion. The lower lumbar spine should be flexed with the back perfectly perpendicular to the edge of a bed or examining table. The hips and legs should be parallel to each other and perpendicular to the table. Pillows placed under the head and between the knees may improve patient comfort. Aseptic technique — The overlying skin should be cleaned with alcohol and a disinfectant such as povidone-iodine or chlorhexidine (0.5 percent in alcohol 70 percent); the antiseptic sh




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The overlying skin should be cleaned with alcohol and a disinfectant such as povidone-iodine or chlorhexidine (0.5 percent in alcohol 70 percent); the antiseptic should be allowed to dry before the procedure is begun.
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ng table. The hips and legs should be parallel to each other and perpendicular to the table. Pillows placed under the head and between the knees may improve patient comfort. Aseptic technique — <span>The overlying skin should be cleaned with alcohol and a disinfectant such as povidone-iodine or chlorhexidine (0.5 percent in alcohol 70 percent); the antiseptic should be allowed to dry before the procedure is begun. Many product inserts of chlorhexidine-containing solutions warn against use of chlorhexidine prior to LP because of a concern that it can cause arachnoiditis. The evidence that it does




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Many product inserts of chlorhexidine-containing solutions warn against use of chlorhexidine prior to LP because of a concern that it can cause arachnoiditis. The evidence that it does so is very limited, and many experts believe that chlorhexidine has an advantage over povidone-iodine because of its onset, efficacy, and potency [ 9-13].
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d be cleaned with alcohol and a disinfectant such as povidone-iodine or chlorhexidine (0.5 percent in alcohol 70 percent); the antiseptic should be allowed to dry before the procedure is begun. <span>Many product inserts of chlorhexidine-containing solutions warn against use of chlorhexidine prior to LP because of a concern that it can cause arachnoiditis. The evidence that it does so is very limited, and many experts believe that chlorhexidine has an advantage over povidone-iodine because of its onset, efficacy, and potency [9-13]. Due to specific labeling prohibiting use, a formal institutional policy to support such use may be indicated. After the skin is cleaned and allowed to dry, a sterile drape with an openi




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After the skin is cleaned and allowed to dry, a sterile drape with an opening over the lumbar spine is placed on the patient
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advantage over povidone-iodine because of its onset, efficacy, and potency [9-13]. Due to specific labeling prohibiting use, a formal institutional policy to support such use may be indicated. <span>After the skin is cleaned and allowed to dry, a sterile drape with an opening over the lumbar spine is placed on the patient. Face masks should be used by individuals who place a catheter or inject material into the spinal canal as recommended by the Healthcare Infection Control Practices Advisory Committee a




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Face masks should be used by individuals who place a catheter or inject material into the spinal canal as recommended by the Healthcare Infection Control Practices Advisory Committee and the Centers for Disease Control and Prevention (CDC) [14]. While routine use of face masks during diagnostic LP and neuroradiologic imaging procedures involving LP has been recommended by some [15-17], others question the practicality and necessity of the use of face masks since infections are rare and there is no proof that face masks prevent such infections [18,19]
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a formal institutional policy to support such use may be indicated. After the skin is cleaned and allowed to dry, a sterile drape with an opening over the lumbar spine is placed on the patient. <span>Face masks should be used by individuals who place a catheter or inject material into the spinal canal as recommended by the Healthcare Infection Control Practices Advisory Committee and the Centers for Disease Control and Prevention (CDC) [14]. While routine use of face masks during diagnostic LP and neuroradiologic imaging procedures involving LP has been recommended by some [15-17], others question the practicality and necessity of the use of face masks since infections are rare and there is no proof that face masks prevent such infections [18,19]. However, we believe a face mask should be used for diagnostic procedures if the procedure is likely to be prolonged or difficult, or if the person carrying out the procedure has an upp




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Local anesthesia (eg, lidocaine) is infiltrated into the previously identified lumbar intervertebral space and a 20- or 22-gauge spinal needle containing a stylet is inserted into the lumbar intervertebral space
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, or if the person carrying out the procedure has an upper respiratory tract infection. (See "Infection prevention: Precautions for preventing transmission of infection".) Procedure technique — <span>Local anesthesia (eg, lidocaine) is infiltrated into the previously identified lumbar intervertebral space and a 20- or 22-gauge spinal needle containing a stylet is inserted into the lumbar intervertebral space. The spinal needle may be advanced slowly, angling slightly toward the head, as if aiming towards the umbilicus. The flat surface of the bevel of the needle should be positioned to face




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The spinal needle may be advanced slowly, angling slightly toward the head, as if aiming towards the umbilicus. The flat surface of the bevel of the needle should be positioned to face the patient's flanks to allow the needle to spread rather than cut the dural sac (the fibers of which run parallel to the spinal axis). The approximate distance of the epidural space from the skin is 45 to 55 mm on average but is variable and may be longer in patients with obesity [7,20,21]
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g, lidocaine) is infiltrated into the previously identified lumbar intervertebral space and a 20- or 22-gauge spinal needle containing a stylet is inserted into the lumbar intervertebral space. <span>The spinal needle may be advanced slowly, angling slightly toward the head, as if aiming towards the umbilicus. The flat surface of the bevel of the needle should be positioned to face the patient's flanks to allow the needle to spread rather than cut the dural sac (the fibers of which run parallel to the spinal axis). The approximate distance of the epidural space from the skin is 45 to 55 mm on average but is variable and may be longer in patients with obesity [7,20,21]. Many clinicians choose to advance the needle incrementally, removing the stylet periodically to check for CSF flow, then reinserting the stylet until the subarachnoid space is entered




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Many clinicians choose to advance the needle incrementally, removing the stylet periodically to check for CSF flow, then reinserting the stylet until the subarachnoid space is entered [ 22]. Some report a higher rate of successful LP when the stylet is removed, just after the skin is punctured and before it is passed into the subarachnoid space in order to better observe the flow of CSF upon entry of the subarachnoid space [23,24]; however, this technique may be associated with a risk of epidermoid tumor, possibly infection, or failure to get flow of CSF. (See 'Epidermoid tumor' below.)
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ch run parallel to the spinal axis). The approximate distance of the epidural space from the skin is 45 to 55 mm on average but is variable and may be longer in patients with obesity [7,20,21]. <span>Many clinicians choose to advance the needle incrementally, removing the stylet periodically to check for CSF flow, then reinserting the stylet until the subarachnoid space is entered [22]. Some report a higher rate of successful LP when the stylet is removed, just after the skin is punctured and before it is passed into the subarachnoid space in order to better observe the flow of CSF upon entry of the subarachnoid space [23,24]; however, this technique may be associated with a risk of epidermoid tumor, possibly infection, or failure to get flow of CSF. (See 'Epidermoid tumor' below.) Once CSF appears and begins to flow through the needle, a manometer should be placed over the hub of the needle (figure 2). The patient should be instructed to slowly straighten or exte




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Once CSF appears and begins to flow through the needle, a manometer should be placed over the hub of the needle (figure 2). The patient should be instructed to slowly straighten or extend the legs to allow free flow of CSF within the subarachnoid space and the opening pressure should be measured
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of the subarachnoid space [23,24]; however, this technique may be associated with a risk of epidermoid tumor, possibly infection, or failure to get flow of CSF. (See 'Epidermoid tumor' below.) <span>Once CSF appears and begins to flow through the needle, a manometer should be placed over the hub of the needle (figure 2). The patient should be instructed to slowly straighten or extend the legs to allow free flow of CSF within the subarachnoid space and the opening pressure should be measured. While the pressure measurement is affected by the position of the legs, the available evidence suggests that the effect is likely to be small. In one review, pressures were elevated by




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While the pressure measurement is affected by the position of the legs, the available evidence suggests that the effect is likely to be small. In one review, pressures were elevated by only 1 to 2 cm H 2O in four of five studies studying this effect; however, in one study, changing position from a straight to a fully flexed position resulted in an increase in pressure of 6.4 mmHg (approximately 8.7 cm H2O) [25]
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needle (figure 2). The patient should be instructed to slowly straighten or extend the legs to allow free flow of CSF within the subarachnoid space and the opening pressure should be measured. <span>While the pressure measurement is affected by the position of the legs, the available evidence suggests that the effect is likely to be small. In one review, pressures were elevated by only 1 to 2 cm H2O in four of five studies studying this effect; however, in one study, changing position from a straight to a fully flexed position resulted in an increase in pressure of 6.4 mmHg (approximately 8.7 cm H2O) [25]. Opening pressure does not appear to be significantly different if measured in the prone or lateral recumbent position [26]. Fluid is then serially collected in sterile plastic tubes. A




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A total of 8 to 15 mL of CSF is typically removed during routine LP. However, when special studies are required, such as cytology or cultures for organisms that grow less readily (eg, fungi or mycobacteria), 40 mL of fluid can safely be removed
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H2O) [25]. Opening pressure does not appear to be significantly different if measured in the prone or lateral recumbent position [26]. Fluid is then serially collected in sterile plastic tubes. <span>A total of 8 to 15 mL of CSF is typically removed during routine LP. However, when special studies are required, such as cytology or cultures for organisms that grow less readily (eg, fungi or mycobacteria), 40 mL of fluid can safely be removed. Aspiration of CSF should not be attempted, as it may increase the risk of bleeding [22]. The stylet should be replaced before the spinal needle is removed, as this can reduce the risk




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Aspiration of CSF should not be attempted, as it may increase the risk of bleeding [ 22].
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ring routine LP. However, when special studies are required, such as cytology or cultures for organisms that grow less readily (eg, fungi or mycobacteria), 40 mL of fluid can safely be removed. <span>Aspiration of CSF should not be attempted, as it may increase the risk of bleeding [22]. The stylet should be replaced before the spinal needle is removed, as this can reduce the risk of post-LP headache. (See "Post dural puncture headache", section on 'Procedural risk fact




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The stylet should be replaced before the spinal needle is removed, as this can reduce the risk of post-LP headache.
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for organisms that grow less readily (eg, fungi or mycobacteria), 40 mL of fluid can safely be removed. Aspiration of CSF should not be attempted, as it may increase the risk of bleeding [22]. <span>The stylet should be replaced before the spinal needle is removed, as this can reduce the risk of post-LP headache. (See "Post dural puncture headache", section on 'Procedural risk factors'.) No trials have shown that bed rest following LP significantly decreases the risk of post-LP headache compared




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No trials have shown that bed rest following LP significantly decreases the risk of post-LP headache compared with immediate mobilization [27,28].
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. The stylet should be replaced before the spinal needle is removed, as this can reduce the risk of post-LP headache. (See "Post dural puncture headache", section on 'Procedural risk factors'.) <span>No trials have shown that bed rest following LP significantly decreases the risk of post-LP headache compared with immediate mobilization [27,28]. (See "Post dural puncture headache", section on 'Prevention of PDPH after dural puncture'.) The Queckenstedt maneuver can be used to demonstrate that there is free flow of fluid from th




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The Queckenstedt maneuver can be used to demonstrate that there is free flow of fluid from the ventricles to the lumbar space. This maneuver is performed by measuring the CSF pressure and then observing the change in pressure after manual compression of both jugular veins. However, this test is rarely useful in modern practice, since newer techniques such as magnetic resonance imaging (MRI) and computed tomography (CT) readily identify most obstructing spinal or basilar lesions
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LP significantly decreases the risk of post-LP headache compared with immediate mobilization [27,28]. (See "Post dural puncture headache", section on 'Prevention of PDPH after dural puncture'.) <span>The Queckenstedt maneuver can be used to demonstrate that there is free flow of fluid from the ventricles to the lumbar space. This maneuver is performed by measuring the CSF pressure and then observing the change in pressure after manual compression of both jugular veins. However, this test is rarely useful in modern practice, since newer techniques such as magnetic resonance imaging (MRI) and computed tomography (CT) readily identify most obstructing spinal or basilar lesions. Imaging guidance — Imaging guidance is typically reserved for patients with difficult anatomy and/or unsuccessful LP attempts. Fluoroscopy — Fluoroscopic guidance for LP may be require




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A subsequently published randomized trial involving 100 adult patients undergoing LP in the emergency department found no significant difference in outcomes with ultrasound guidance [34].
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d that ultrasound guidance reduced the risk of failed and traumatic procedures (risk ratio [RR] = 0.21 and 0.27, respectively), as well as the number of needle insertions and redirections [33]. <span>A subsequently published randomized trial involving 100 adult patients undergoing LP in the emergency department found no significant difference in outcomes with ultrasound guidance [34]. The use of ultrasound in spinal anesthesia is discussed separately. (See "Spinal anesthesia: Technique", section on 'Preprocedure ultrasonography'.) COMPLICATIONS — LP is a relatively s




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LP is a relatively safe procedure, but minor and major complications can occur even when standard infection control measures and good technique are used. These complications include:

● Post-LP headache

● Infection

● Bleeding

● Cerebral herniation

● Minor neurologic symptoms such as radicular pain or numbness

● Late onset of epidermoid tumors of the thecal sac

● Back pain

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th ultrasound guidance [34]. The use of ultrasound in spinal anesthesia is discussed separately. (See "Spinal anesthesia: Technique", section on 'Preprocedure ultrasonography'.) COMPLICATIONS — <span>LP is a relatively safe procedure, but minor and major complications can occur even when standard infection control measures and good technique are used. These complications include: ●Post-LP headache ●Infection ●Bleeding ●Cerebral herniation ●Minor neurologic symptoms such as radicular pain or numbness ●Late onset of epidermoid tumors of the thecal sac ●Back pain The risk of complications was studied in a cohort of 376 patients who underwent LP for evaluation of acute cerebrovascular disease [35]. The following frequency of complications was not




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The risk of complications was studied in a cohort of 376 patients who underwent LP for evaluation of acute cerebrovascular disease [35]. The following frequency of complications was noted: backache (25 percent), headache (22 percent), headache and backache (12 percent), severe radicular pain (15 percent), and paraparesis (1.5 percent). Severe pain or paraparesis occurred in 6.7 percent of patients receiving anticoagulants following the procedure and in none of the 34 patients who did not receive anticoagulants.
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include: ●Post-LP headache ●Infection ●Bleeding ●Cerebral herniation ●Minor neurologic symptoms such as radicular pain or numbness ●Late onset of epidermoid tumors of the thecal sac ●Back pain <span>The risk of complications was studied in a cohort of 376 patients who underwent LP for evaluation of acute cerebrovascular disease [35]. The following frequency of complications was noted: backache (25 percent), headache (22 percent), headache and backache (12 percent), severe radicular pain (15 percent), and paraparesis (1.5 percent). Severe pain or paraparesis occurred in 6.7 percent of patients receiving anticoagulants following the procedure and in none of the 34 patients who did not receive anticoagulants. Post-LP headache — Headache, which occurs in 10 to 30 percent of patients, is one of the most common complications following LP. Post-LP headache is caused by leakage of cerebrospinal f




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Headache, which occurs in 10 to 30 percent of patients, is one of the most common complications following LP. Post-LP headache is caused by leakage of cerebrospinal fluid (CSF) from the dura and traction on pain-sensitive structures. Patients characteristically present with frontal or occipital headache within 24 to 48 hours of the procedure, which is exacerbated in an upright position and improved in the supine position. Associated symptoms may include nausea, vomiting, dizziness, tinnitus, and visual changes.
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re pain or paraparesis occurred in 6.7 percent of patients receiving anticoagulants following the procedure and in none of the 34 patients who did not receive anticoagulants. Post-LP headache — <span>Headache, which occurs in 10 to 30 percent of patients, is one of the most common complications following LP. Post-LP headache is caused by leakage of cerebrospinal fluid (CSF) from the dura and traction on pain-sensitive structures. Patients characteristically present with frontal or occipital headache within 24 to 48 hours of the procedure, which is exacerbated in an upright position and improved in the supine position. Associated symptoms may include nausea, vomiting, dizziness, tinnitus, and visual changes. This risk factors, prevention, and treatment of post-LP headache are discussed separately. (See "Post dural puncture headache".) Infection — Infections are rare after LP; in typical pat




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Meningitis is an uncommon complication of LP. In a review of 179 cases of post-LP meningitis reported in the medical literature between 1952 and 2005, half of all cases occurred after spinal anesthesia; only 9 percent occurred after diagnostic LP. The most commonly isolated causative organisms were Streptococcus salivarius (30 percent), Streptococcus viridans (29 percent), alpha-hemolytic strep (11 percent), Staphylococcus aureus (9 percent), and Pseudomonas aeruginosa (8 percent) [36].
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. (See "Post dural puncture headache".) Infection — Infections are rare after LP; in typical patients no techniques beyond usual aseptic technique are required. (See 'Aseptic technique' above.) <span>Meningitis is an uncommon complication of LP. In a review of 179 cases of post-LP meningitis reported in the medical literature between 1952 and 2005, half of all cases occurred after spinal anesthesia; only 9 percent occurred after diagnostic LP. The most commonly isolated causative organisms were Streptococcus salivarius (30 percent), Streptococcus viridans (29 percent), alpha-hemolytic strep (11 percent), Staphylococcus aureus (9 percent), and Pseudomonas aeruginosa (8 percent) [36]. An LP through a spinal epidural abscess can result in the spread of bacteria into the subarachnoid space. Because an LP is not needed for diagnosis, the procedure should not be performe




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An LP through a spinal epidural abscess can result in the spread of bacteria into the subarachnoid space. Because an LP is not needed for diagnosis, the procedure should not be performed in most patients with suspected epidural abscess in the lumbar region [37].
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e Streptococcus salivarius (30 percent), Streptococcus viridans (29 percent), alpha-hemolytic strep (11 percent), Staphylococcus aureus (9 percent), and Pseudomonas aeruginosa (8 percent) [36]. <span>An LP through a spinal epidural abscess can result in the spread of bacteria into the subarachnoid space. Because an LP is not needed for diagnosis, the procedure should not be performed in most patients with suspected epidural abscess in the lumbar region [37]. (See "Spinal epidural abscess".) While some cases of post-LP meningitis due to staphylococci, pseudomonas, and other gram-negative bacilli have been attributed to contaminated instrumen




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We and other authors believe that theoretical concerns about inducing meningitis in patients with bacteremia should not be used as the basis to forego LP if meningitis is suspected [19]
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nce of spontaneous meningitis in children who underwent LP and subsequently developed meningitis was not statistically different from those who did not undergo LP (2.1 versus 0.8 percent) [44]. <span>We and other authors believe that theoretical concerns about inducing meningitis in patients with bacteremia should not be used as the basis to forego LP if meningitis is suspected [19]. There are rare case reports of discitis and vertebral osteomyelitis following LP. Most cases were due to normal skin flora such as Cutibacterium species and coagulase negative staphylo




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There are rare case reports of discitis and vertebral osteomyelitis following LP. Most cases were due to normal skin flora such as Cutibacterium species and coagulase negative staphylococci [45-47]. These complications presumably result from direct inoculation of bacteria into the vertebral bone.
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[44]. We and other authors believe that theoretical concerns about inducing meningitis in patients with bacteremia should not be used as the basis to forego LP if meningitis is suspected [19]. <span>There are rare case reports of discitis and vertebral osteomyelitis following LP. Most cases were due to normal skin flora such as Cutibacterium species and coagulase negative staphylococci [45-47]. These complications presumably result from direct inoculation of bacteria into the vertebral bone. Bleeding — The CSF is normally acellular, although up to five red blood cells (RBCs) are considered normal after LP due to incidental trauma to a capillary or venule. A higher number of




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The CSF is normally acellular, although up to five red blood cells (RBCs) are considered normal after LP due to incidental trauma to a capillary or venule. A higher number of RBCs is seen in some patients in whom calculation of the white blood cell (WBC)-to-RBC ratio and the presence or absence of xanthochromia may differentiate LP-induced from true central nervous system (CNS) bleeding.
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n flora such as Cutibacterium species and coagulase negative staphylococci [45-47]. These complications presumably result from direct inoculation of bacteria into the vertebral bone. Bleeding — <span>The CSF is normally acellular, although up to five red blood cells (RBCs) are considered normal after LP due to incidental trauma to a capillary or venule. A higher number of RBCs is seen in some patients in whom calculation of the white blood cell (WBC)-to-RBC ratio and the presence or absence of xanthochromia may differentiate LP-induced from true central nervous system (CNS) bleeding. (See "Cerebrospinal fluid: Physiology and utility of an examination in disease states", section on 'Cells'.) Incidence — Serious bleeding that results in spinal cord compromise is rare




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Serious bleeding that results in spinal cord compromise is rare in the absence of bleeding risk [48]. Patients who have thrombocytopenia or other bleeding disorders or those who received anticoagulant therapy prior to or immediately after undergoing LP have an increased risk of bleeding
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ifferentiate LP-induced from true central nervous system (CNS) bleeding. (See "Cerebrospinal fluid: Physiology and utility of an examination in disease states", section on 'Cells'.) Incidence — <span>Serious bleeding that results in spinal cord compromise is rare in the absence of bleeding risk [48]. Patients who have thrombocytopenia or other bleeding disorders or those who received anticoagulant therapy prior to or immediately after undergoing LP have an increased risk of bleeding. This risk may be further increased with other factors that increase bleeding risk, such as traumatic or repeated taps. In one series, spinal hematoma developed in 7 of 342 patients (2




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In one series, spinal hematoma developed in 7 of 342 patients (2 percent) who received anticoagulant therapy after undergoing LP; five of these patients developed paraparesis [35]. In one literature review, 47 percent of 21 published cases of spinal hematoma following LP occurred in patients with a coagulopathy [49]. Thus, a high index of suspicion of spinal hematoma should be maintained in all patients who develop neurologic symptoms after an LP, including those with no known coagulopathy. In rare cases, intraventricular, intracerebral, and subarachnoid hemorrhage (SAH) have also been reported as complications of LP [50,51]
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to or immediately after undergoing LP have an increased risk of bleeding. This risk may be further increased with other factors that increase bleeding risk, such as traumatic or repeated taps. <span>In one series, spinal hematoma developed in 7 of 342 patients (2 percent) who received anticoagulant therapy after undergoing LP; five of these patients developed paraparesis [35]. In one literature review, 47 percent of 21 published cases of spinal hematoma following LP occurred in patients with a coagulopathy [49]. Thus, a high index of suspicion of spinal hematoma should be maintained in all patients who develop neurologic symptoms after an LP, including those with no known coagulopathy. In rare cases, intraventricular, intracerebral, and subarachnoid hemorrhage (SAH) have also been reported as complications of LP [50,51]. Reducing risk — We are unaware of any study that has systematically examined interventions to reduce the risk of bleeding following LP based upon the degree of thrombocytopenia or clot




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We are unaware of any study that has systematically examined interventions to reduce the risk of bleeding following LP based upon the degree of thrombocytopenia or clotting study abnormalities. Thus, at present the only guidepost is "clinical judgment."

We generally advise not performing an LP in patients with coagulation defects who are actively bleeding, have severe thrombocytopenia (eg, platelet counts <50,000 to 80,000/microL), or an international normalized ratio (INR) >1.4, without correcting the underlying abnormalities [52,53]

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uding those with no known coagulopathy. In rare cases, intraventricular, intracerebral, and subarachnoid hemorrhage (SAH) have also been reported as complications of LP [50,51]. Reducing risk — <span>We are unaware of any study that has systematically examined interventions to reduce the risk of bleeding following LP based upon the degree of thrombocytopenia or clotting study abnormalities. Thus, at present the only guidepost is "clinical judgment." We generally advise not performing an LP in patients with coagulation defects who are actively bleeding, have severe thrombocytopenia (eg, platelet counts <50,000 to 80,000/microL), or an international normalized ratio (INR) >1.4, without correcting the underlying abnormalities [52,53]. When an LP is considered urgent and essential in a patient with an abnormal INR or platelet count in whom the cause is not obvious, consultation with a hematologist may provide the bes




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For elective procedures in a patient receiving systemic anticoagulation, observational studies and expert opinion have suggested stopping the agents for a specified time period prior to spinal anesthesia or LP (table 1) [55-57]:

● Unfractionated intravenous heparin drips – Two to four hours.

● Low-molecular-weight heparin – 12 to 24 hours.

Warfarin – Five to seven days.

● Newer oral anticoagulants (NOACs), apixaban, edoxaban, and rivaroxaban – 72 hours. Dabigatran should be held 48 to 96 hours based on renal function.

● Subcutaneous heparin – <10,000 units per day is not believed to pose a substantial risk for bleeding.

None of these approaches have been carefully assessed for efficacy or risk, and all presume that the underlying indications for anticoagulation therapy allow a temporary suspension of treatment

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ained thrombocytopenia", section on 'General management principles' and "Platelet transfusion: Indications, ordering, and associated risks", section on 'Preparation for an invasive procedure'.) <span>For elective procedures in a patient receiving systemic anticoagulation, observational studies and expert opinion have suggested stopping the agents for a specified time period prior to spinal anesthesia or LP (table 1) [55-57]: ●Unfractionated intravenous heparin drips – Two to four hours. ●Low-molecular-weight heparin – 12 to 24 hours. ●Warfarin – Five to seven days. ●Newer oral anticoagulants (NOACs), apixaban, edoxaban, and rivaroxaban – 72 hours. Dabigatran should be held 48 to 96 hours based on renal function. ●Subcutaneous heparin – <10,000 units per day is not believed to pose a substantial risk for bleeding. None of these approaches have been carefully assessed for efficacy or risk, and all presume that the underlying indications for anticoagulation therapy allow a temporary suspension of treatment. While the optimal timing of restarting anticoagulation after LP is not known, the incidence of spinal hematoma in one series was much lower when anticoagulation was started at least on




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While the optimal timing of restarting anticoagulation after LP is not known, the incidence of spinal hematoma in one series was much lower when anticoagulation was started at least one hour after the LP [35]. NOACs can be restarted six to eight hours after an atraumatic spinal or epidural anesthesia or clean LP; however, in traumatic procedures with increased risk of bleeding, the guidelines recommend restarting NOACs 48 to 72 hours after complete hemostasis [57]
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one of these approaches have been carefully assessed for efficacy or risk, and all presume that the underlying indications for anticoagulation therapy allow a temporary suspension of treatment. <span>While the optimal timing of restarting anticoagulation after LP is not known, the incidence of spinal hematoma in one series was much lower when anticoagulation was started at least one hour after the LP [35]. NOACs can be restarted six to eight hours after an atraumatic spinal or epidural anesthesia or clean LP; however, in traumatic procedures with increased risk of bleeding, the guidelines recommend restarting NOACs 48 to 72 hours after complete hemostasis [57]. Antiplatelet therapy with aspirin and nonsteroidal antiinflammatory agents has not been shown to increase the risk of serious bleeding following LP. In a prospective study of 924 patie




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Antiplatelet therapy with aspirin and nonsteroidal antiinflammatory agents has not been shown to increase the risk of serious bleeding following LP. In a prospective study of 924 patients who underwent orthopedic procedures with spinal or epidural anesthesia, 386 patients were taking antiplatelet therapy prior to surgery; 193 were taking aspirin [58]. Neither aspirin nor any other antiplatelet agents were associated with an increased risk of bleeding. However, none of these patients were taking clopidogrel, ticlopidine, or a GP IIb/IIIa receptor antagonist.
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al or epidural anesthesia or clean LP; however, in traumatic procedures with increased risk of bleeding, the guidelines recommend restarting NOACs 48 to 72 hours after complete hemostasis [57]. <span>Antiplatelet therapy with aspirin and nonsteroidal antiinflammatory agents has not been shown to increase the risk of serious bleeding following LP. In a prospective study of 924 patients who underwent orthopedic procedures with spinal or epidural anesthesia, 386 patients were taking antiplatelet therapy prior to surgery; 193 were taking aspirin [58]. Neither aspirin nor any other antiplatelet agents were associated with an increased risk of bleeding. However, none of these patients were taking clopidogrel, ticlopidine, or a GP IIb/IIIa receptor antagonist. Female sex, increased age, a history of excessive bruising/bleeding, hip surgery, continuous catheter anesthetic technique, large needle gauge, multiple needle passes, and moderate or d




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Given the unknown risk of bleeding with thienopyridine derivatives (clopidogrel, ticlopidine, prasugrel, ticagrelor), it may be reasonable to suspend treatment with these agents, when possible, for one to two weeks prior to an elective LP, while pharmacologic data suggest that for GP IIb/IIIa receptor antagonists, a shorter period of treatment cessation (8 hours for tirofiban and eptifibatide and 24 to 48 hours for abciximab) may be indicated [56]
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ic technique, large needle gauge, multiple needle passes, and moderate or difficult needle placement were all significant risk factors for minor bleeding at the site of catheter placement [58]. <span>Given the unknown risk of bleeding with thienopyridine derivatives (clopidogrel, ticlopidine, prasugrel, ticagrelor), it may be reasonable to suspend treatment with these agents, when possible, for one to two weeks prior to an elective LP, while pharmacologic data suggest that for GP IIb/IIIa receptor antagonists, a shorter period of treatment cessation (8 hours for tirofiban and eptifibatide and 24 to 48 hours for abciximab) may be indicated [56]. In all cases, the relative risk of performing an LP has to be weighed against the potential benefit (eg, diagnosing meningitis due to an unusual or difficult to treat pathogen). In cas




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Patients who have persistent back pain or neurologic findings (eg, weakness, decreased sensation, or incontinence) after undergoing LP require urgent evaluation (usually spinal magnetic resonance imaging [MRI]) for possible spinal hematoma [59]
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atelet medication".) Management of spinal hematoma — The diagnosis of spinal hematoma is complicated by the concealed nature of the bleeding; thus, a high index of suspicion must be maintained. <span>Patients who have persistent back pain or neurologic findings (eg, weakness, decreased sensation, or incontinence) after undergoing LP require urgent evaluation (usually spinal magnetic resonance imaging [MRI]) for possible spinal hematoma [59]. The appropriate treatment for patients with significant or progressing neurologic deficits is prompt surgical intervention, usually a laminectomy, and evacuation of the blood. Timely d




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The appropriate treatment for patients with significant or progressing neurologic deficits is prompt surgical intervention, usually a laminectomy, and evacuation of the blood. Timely decompression of the hematoma is essential to avoid permanent loss of neurologic function [60,61]. Patients with mild symptoms or early signs of recovery may be managed conservatively with vigilant monitoring; dexamethasone may be administered to mitigate neurologic injury [49,50].
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findings (eg, weakness, decreased sensation, or incontinence) after undergoing LP require urgent evaluation (usually spinal magnetic resonance imaging [MRI]) for possible spinal hematoma [59]. <span>The appropriate treatment for patients with significant or progressing neurologic deficits is prompt surgical intervention, usually a laminectomy, and evacuation of the blood. Timely decompression of the hematoma is essential to avoid permanent loss of neurologic function [60,61]. Patients with mild symptoms or early signs of recovery may be managed conservatively with vigilant monitoring; dexamethasone may be administered to mitigate neurologic injury [49,50]. (See "Disorders affecting the spinal cord", section on 'Spinal epidural hematoma'.) Cerebral herniation — The most serious complication of LP is cerebral herniation. Suspected increased




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The most serious complication of LP is cerebral herniation. Suspected increased intracranial pressure (ICP) due to an intracranial mass lesion, cerebral edema, or obstructive hydrocephalus is a relative contraindication to performance of an LP and also requires independent assessment and treatment
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nt monitoring; dexamethasone may be administered to mitigate neurologic injury [49,50]. (See "Disorders affecting the spinal cord", section on 'Spinal epidural hematoma'.) Cerebral herniation — <span>The most serious complication of LP is cerebral herniation. Suspected increased intracranial pressure (ICP) due to an intracranial mass lesion, cerebral edema, or obstructive hydrocephalus is a relative contraindication to performance of an LP and also requires independent assessment and treatment. Incidence — The magnitude of the risk was evaluated in a report of 129 patients with increased ICP: 15 patients (12 percent) had an unfavorable outcome within 48 hours of LP [62]. Simi




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In another series of 1533 patients with bacterial meningitis, 47 (3 percent) had a clinical deterioration after LP [64]. Cardiorespiratory collapse, loss of consciousness, and death may follow. (See "Evaluation and management of elevated intracranial pressure in adults".)
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re noted in a series of 55 patients with SAH: seven patients (13 percent) experienced neurologic deterioration during or soon after an LP, six of whom had evidence of cerebral dislocation [63]. <span>In another series of 1533 patients with bacterial meningitis, 47 (3 percent) had a clinical deterioration after LP [64]. Cardiorespiratory collapse, loss of consciousness, and death may follow. (See "Evaluation and management of elevated intracranial pressure in adults".) A 1969 study of 30 patients with increased ICP who deteriorated after LP attempted to identify the clinical features of patients who were at greatest risk for this complication [65]. Th




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A 1969 study of 30 patients with increased ICP who deteriorated after LP attempted to identify the clinical features of patients who were at greatest risk for this complication [65]. The following findings were noted: 73 percent had focal findings on neurologic examination (including dysphagia, hemiparesis, and cranial nerve palsies), 30 percent had documented papilledema prior to the LP, and 30 percent had evidence of increased ICP on plain skull films (erosion of the posterior clinoid processes). Deterioration occurred immediately in one-half of the patients, with the remainder declining within 12 hours
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d a clinical deterioration after LP [64]. Cardiorespiratory collapse, loss of consciousness, and death may follow. (See "Evaluation and management of elevated intracranial pressure in adults".) <span>A 1969 study of 30 patients with increased ICP who deteriorated after LP attempted to identify the clinical features of patients who were at greatest risk for this complication [65]. The following findings were noted: 73 percent had focal findings on neurologic examination (including dysphagia, hemiparesis, and cranial nerve palsies), 30 percent had documented papilledema prior to the LP, and 30 percent had evidence of increased ICP on plain skull films (erosion of the posterior clinoid processes). Deterioration occurred immediately in one-half of the patients, with the remainder declining within 12 hours. A more recent series compared patients who did and did not deteriorate after LP and found that interrater reliability regarding the presence of a contraindication on computed tomograph




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A more recent series compared patients who did and did not deteriorate after LP and found that interrater reliability regarding the presence of a contraindication on computed tomography (CT) was only moderate (kappa = 0.47) and that a similar proportion of patients in both groups had such a contraindication (14 versus 11 percent) [ 64].
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of increased ICP on plain skull films (erosion of the posterior clinoid processes). Deterioration occurred immediately in one-half of the patients, with the remainder declining within 12 hours. <span>A more recent series compared patients who did and did not deteriorate after LP and found that interrater reliability regarding the presence of a contraindication on computed tomography (CT) was only moderate (kappa = 0.47) and that a similar proportion of patients in both groups had such a contraindication (14 versus 11 percent) [64]. Indications for CT scan — The concern about this serious complication has resulted in routine CT scanning prior to LP being the standard of care in many emergency departments. At one in




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Moreover, CT scanning is not necessary in all patients prior to LP and may not be adequate to exclude elevated ICP in others [67,68].
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ith suspected bacterial meningitis, delays the performance of LP, which in turn may delay treatment or limit the diagnostic power of CSF analysis when performed after antibiotic administration. <span>Moreover, CT scanning is not necessary in all patients prior to LP and may not be adequate to exclude elevated ICP in others [67,68]. Some studies suggest that high-risk patients can be identified, allowing the majority of patients to safely undergo LP without screening CT [66,69]. This was best illustrated in a prosp




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This was best illustrated in a prospective study of 301 adults with suspected meningitis [66]. The following findings were noted:

● Among the 235 (78 percent) who underwent CT scan before LP, 24 percent had an abnormal finding but only 5 percent (11 patients) had a mass effect

● The risk of an abnormal CT scan was associated with specific clinical features (presence of impaired cellular immunity, history of previous CNS disease, or a seizure within the previous week), as well as certain findings on neurologic examination (reduced level of consciousness, and focal motor or cranial abnormalities)

● Among 96 patients with none of these abnormalities, only three had an abnormal CT scan; one of the three misclassified patients had a mild mass effect, but all three underwent LP without herniation

● Compared with patients who did not undergo CT scan before LP, those who underwent CT scan before LP had an average of a two-hour delay in diagnosis and a one-hour delay in therapy

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e to exclude elevated ICP in others [67,68]. Some studies suggest that high-risk patients can be identified, allowing the majority of patients to safely undergo LP without screening CT [66,69]. <span>This was best illustrated in a prospective study of 301 adults with suspected meningitis [66]. The following findings were noted: ●Among the 235 (78 percent) who underwent CT scan before LP, 24 percent had an abnormal finding but only 5 percent (11 patients) had a mass effect ●The risk of an abnormal CT scan was associated with specific clinical features (presence of impaired cellular immunity, history of previous CNS disease, or a seizure within the previous week), as well as certain findings on neurologic examination (reduced level of consciousness, and focal motor or cranial abnormalities) ●Among 96 patients with none of these abnormalities, only three had an abnormal CT scan; one of the three misclassified patients had a mild mass effect, but all three underwent LP without herniation ●Compared with patients who did not undergo CT scan before LP, those who underwent CT scan before LP had an average of a two-hour delay in diagnosis and a one-hour delay in therapy Based upon these observations, we do not perform a CT scan before an LP in patients with suspected bacterial meningitis unless one or more risk factors is present: ●Altered mentation ●F




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Based upon these observations, we do not perform a CT scan before an LP in patients with suspected bacterial meningitis unless one or more risk factors is present:

● Altered mentation

● Focal neurologic signs

● Papilledema

● Seizure within the previous week

● Impaired cellular immunity

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t herniation ●Compared with patients who did not undergo CT scan before LP, those who underwent CT scan before LP had an average of a two-hour delay in diagnosis and a one-hour delay in therapy <span>Based upon these observations, we do not perform a CT scan before an LP in patients with suspected bacterial meningitis unless one or more risk factors is present: ●Altered mentation ●Focal neurologic signs ●Papilledema ●Seizure within the previous week ●Impaired cellular immunity Patients with these clinical risk factors should have a CT scan to identify possible mass lesion and other causes of increased ICP. Mass lesions causing elevated ICP are usually easily




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However, the CT scan should also be scrutinized for more subtle signs including diffuse brain swelling as manifest by loss of differentiation between gray and white matter and effacement of sulci, as well as ventricular enlargement and effacement of the basal cisterns [70]
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these clinical risk factors should have a CT scan to identify possible mass lesion and other causes of increased ICP. Mass lesions causing elevated ICP are usually easily identified on CT scan. <span>However, the CT scan should also be scrutinized for more subtle signs including diffuse brain swelling as manifest by loss of differentiation between gray and white matter and effacement of sulci, as well as ventricular enlargement and effacement of the basal cisterns [70]. Management of elevated intracranial pressure — Independent of the decision to perform LP, patients with possible elevated ICP based upon the above clinical features may require urgent




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Management of elevated intracranial pressure — Independent of the decision to perform LP, patients with possible elevated ICP based upon the above clinical features may require urgent life-saving interventions to lower ICP that may include head elevation, hyperventilation to a partial pressure of carbon dioxide (PCO2) of 26 to 30 mmHg, and intravenous mannitol (1 to 1.5 g/kg). When indicated, these should not await CT scan. These same measures should be instituted if a patient develops signs of herniation after LP. The evaluation and management of patients with elevated ICP is discussed in detail separately. (See "Evaluation and management of elevated intracranial pressure in adults", section on 'Urgent situations'.)
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iffuse brain swelling as manifest by loss of differentiation between gray and white matter and effacement of sulci, as well as ventricular enlargement and effacement of the basal cisterns [70]. <span>Management of elevated intracranial pressure — Independent of the decision to perform LP, patients with possible elevated ICP based upon the above clinical features may require urgent life-saving interventions to lower ICP that may include head elevation, hyperventilation to a partial pressure of carbon dioxide (PCO2) of 26 to 30 mmHg, and intravenous mannitol (1 to 1.5 g/kg). When indicated, these should not await CT scan. These same measures should be instituted if a patient develops signs of herniation after LP. The evaluation and management of patients with elevated ICP is discussed in detail separately. (See "Evaluation and management of elevated intracranial pressure in adults", section on 'Urgent situations'.) Other complications Epidermoid tumor — The formation of an epidermoid spinal cord tumor is a rare complication of LP that may become evident years after the procedure is performed [71-7




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Epidermoid tumor — The formation of an epidermoid spinal cord tumor is a rare complication of LP that may become evident years after the procedure is performed [71-73]. Most reported cases are children ages 5 to 12 years who had an LP in infancy; however, this has also been described in adults [74-76]. It may be caused by epidermoid tissue that is transplanted into the spinal canal during LP without a stylet, or with one that is poorly fitting. This complication probably can be avoided by using spinal needles with tight-fitting stylets during LP [77,78]
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patients with elevated ICP is discussed in detail separately. (See "Evaluation and management of elevated intracranial pressure in adults", section on 'Urgent situations'.) Other complications <span>Epidermoid tumor — The formation of an epidermoid spinal cord tumor is a rare complication of LP that may become evident years after the procedure is performed [71-73]. Most reported cases are children ages 5 to 12 years who had an LP in infancy; however, this has also been described in adults [74-76]. It may be caused by epidermoid tissue that is transplanted into the spinal canal during LP without a stylet, or with one that is poorly fitting. This complication probably can be avoided by using spinal needles with tight-fitting stylets during LP [77,78]. Abducens palsy — Both unilateral and bilateral abducens palsy are reported complications of LP [79-81]. This is believed to result from intracranial hypotension and is generally accomp




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Abducens palsy — Both unilateral and bilateral abducens palsy are reported complications of LP [79-81]. This is believed to result from intracranial hypotension and is generally accompanied by other clinical features of post-LP headache. Most patients recover completely within days to weeks. Other cranial nerve palsies are rarely reported [82]
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the spinal canal during LP without a stylet, or with one that is poorly fitting. This complication probably can be avoided by using spinal needles with tight-fitting stylets during LP [77,78]. <span>Abducens palsy — Both unilateral and bilateral abducens palsy are reported complications of LP [79-81]. This is believed to result from intracranial hypotension and is generally accompanied by other clinical features of post-LP headache. Most patients recover completely within days to weeks. Other cranial nerve palsies are rarely reported [82]. Radicular symptoms and low back pain — It is not uncommon (13 percent in one series) for patients to experience transient electrical-type pain in one leg during the procedure [83]. How




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Radicular symptoms and low back pain — It is not uncommon (13 percent in one series) for patients to experience transient electrical-type pain in one leg during the procedure [83]. However, more sustained radicular symptoms or radicular injury appear to be rare [84].

Up to one-third of patients complain of localized back pain after LP; this may persist for several days, but rarely beyond [83]

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tension and is generally accompanied by other clinical features of post-LP headache. Most patients recover completely within days to weeks. Other cranial nerve palsies are rarely reported [82]. <span>Radicular symptoms and low back pain — It is not uncommon (13 percent in one series) for patients to experience transient electrical-type pain in one leg during the procedure [83]. However, more sustained radicular symptoms or radicular injury appear to be rare [84]. Up to one-third of patients complain of localized back pain after LP; this may persist for several days, but rarely beyond [83]. SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline lin




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Post dural puncture headache (PDPH), also known as post lumbar puncture (LP) headache, is a common complication of diagnostic LP. It also can occur following spinal anesthesia or, more commonly, inadvertent dural puncture during attempted epidural catheter placement. The headache is usually positional (worse when upright, better when lying flat) and is often accompanied by neck stiffness, photophobia, nausea, or subjective hearing symptoms
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opics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Apr 2022. | This topic last updated: Jul 27, 2021. INTRODUCTION — <span>Post dural puncture headache (PDPH), also known as post lumbar puncture (LP) headache, is a common complication of diagnostic LP. It also can occur following spinal anesthesia or, more commonly, inadvertent dural puncture during attempted epidural catheter placement. The headache is usually positional (worse when upright, better when lying flat) and is often accompanied by neck stiffness, photophobia, nausea, or subjective hearing symptoms. This topic will review PDPH. Techniques for LP, spinal, epidural, and combined spinal-epidural (CSE) anesthesia are discussed separately. (See "Lumbar puncture: Technique, indications,




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The precise etiology of headache after dural puncture is unclear, but is thought to relate to leakage of cerebrospinal fluid (CSF) through the dural hole created by the needle.
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Technique, indications, contraindications, and complications in adults" and "Spinal anesthesia: Technique" and "Epidural and combined spinal-epidural anesthesia: Techniques".) PATHOPHYSIOLOGY — <span>The precise etiology of headache after dural puncture is unclear, but is thought to relate to leakage of cerebrospinal fluid (CSF) through the dural hole created by the needle. If CSF leaks at a rate greater than the rate of CSF production, low CSF pressure can result, accentuated at the level of the brain in the upright position. However, not all patients wit




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However, not all patients with PDPH have low CSF pressure, and not all patients with significant CSF leak develop a headache.
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the dural hole created by the needle. If CSF leaks at a rate greater than the rate of CSF production, low CSF pressure can result, accentuated at the level of the brain in the upright position. <span>However, not all patients with PDPH have low CSF pressure, and not all patients with significant CSF leak develop a headache. Three pathophysiologic mechanisms have been proposed: ●CSF hypotension results in compensatory meningeal venodilation and blood volume expansion, with headache caused by acute venous di




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hree pathophysiologic mechanisms have been proposed:

● CSF hypotension results in compensatory meningeal venodilation and blood volume expansion, with headache caused by acute venous distention. This mechanism is consistent with magnetic resonance imaging (MRI) in several reported cases of PDPH [1,2].

● Intracranial hypotension related to CSF leak may cause sagging of intracranial structures and stretch of sensory intracranial nerves, causing pain and cranial nerve palsies. In one study of seven patients with intracranial hypotension, MRI findings of downward displacement of the brain were associated with headache, and resolved along with the headache symptoms [3]. Traction of the upper cervical nerves may cause PDPH associated neck, back and shoulder pain [4].

● Altered craniospinal elasticity after lumbar puncture (LP) results in increased caudal compliance relative to intracranial compliance and acute intracranial venodilation in the upright position [5].

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lt, accentuated at the level of the brain in the upright position. However, not all patients with PDPH have low CSF pressure, and not all patients with significant CSF leak develop a headache. T<span>hree pathophysiologic mechanisms have been proposed: ●CSF hypotension results in compensatory meningeal venodilation and blood volume expansion, with headache caused by acute venous distention. This mechanism is consistent with magnetic resonance imaging (MRI) in several reported cases of PDPH [1,2]. ●Intracranial hypotension related to CSF leak may cause sagging of intracranial structures and stretch of sensory intracranial nerves, causing pain and cranial nerve palsies. In one study of seven patients with intracranial hypotension, MRI findings of downward displacement of the brain were associated with headache, and resolved along with the headache symptoms [3]. Traction of the upper cervical nerves may cause PDPH associated neck, back and shoulder pain [4]. ●Altered craniospinal elasticity after lumbar puncture (LP) results in increased caudal compliance relative to intracranial compliance and acute intracranial venodilation in the upright position [5]. INCIDENCE — The incidence of PDPH varies widely, depending on patient (eg, age, gender, pregnancy, body mass index [BMI]) and procedural (eg, needle size and type, bevel orientation for




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The incidence of PDPH varies widely, depending on patient (eg, age, gender, pregnancy, body mass index [BMI]) and procedural (eg, needle size and type, bevel orientation for cutting needles) risk factors.
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nal elasticity after lumbar puncture (LP) results in increased caudal compliance relative to intracranial compliance and acute intracranial venodilation in the upright position [5]. INCIDENCE — <span>The incidence of PDPH varies widely, depending on patient (eg, age, gender, pregnancy, body mass index [BMI]) and procedural (eg, needle size and type, bevel orientation for cutting needles) risk factors. The incidence of PDPH after spinal anesthesia is generally <3 percent, but may occur in up to 9 percent of cases, depending on the type and size of needle used [6-8]. PDPH after lumb




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PDPH after lumbar puncture (LP) occurs in approximately 11 percent of cases when a standard, traumatic needle is used [9].
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needles) risk factors. The incidence of PDPH after spinal anesthesia is generally <3 percent, but may occur in up to 9 percent of cases, depending on the type and size of needle used [6-8]. <span>PDPH after lumbar puncture (LP) occurs in approximately 11 percent of cases when a standard, traumatic needle is used [9]. PDPH related to neuraxial anesthesia is most common in obstetric patients. The reported incidence of PDPH after unintentional dural puncture (UDP) with an epidural needle (which is larg




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Patient risk factors — In various studies, common patient risk factors for PDPH have included female gender, pregnancy, age 18 to 50 years compared with older or younger ages, and a prior history of headache
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]. UDP occurs in <1 to as high as 6 percent of epidural placements [7,12-19], with 11 to 33 percent of UDP going unrecognized until the patient presents with PDPH [13,14,19-22]. RISK FACTORS <span>Patient risk factors — In various studies, common patient risk factors for PDPH have included female gender, pregnancy, age 18 to 50 years compared with older or younger ages, and a prior history of headache: ●Female gender – Several studies have found that women have a two to three times increased risk for PDPH compared with men [23-25]. ●Pregnancy – Pregnancy confers an additional risk fo




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Age – In most studies, extremes of age are associated with lower incidence of PDPH, with young adults (18 to 50 years of age) having the highest risk [23,24,31,37-39]. As an example, in one prospective study of patients who had spinal anesthesia with 25 or 27 gauge Quincke (ie, traumatic) needles, PDPH occurred in 11 percent of patients aged 31 to 50 years, compared with 4 percent of others [24].
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29,30]. ●Prior headaches – History of prior headaches (both PDPH and chronic headaches) may be a risk factor for PDPH [4,23,31-33]; although, this has not been observed in all studies [34-36]. ●<span>Age – In most studies, extremes of age are associated with lower incidence of PDPH, with young adults (18 to 50 years of age) having the highest risk [23,24,31,37-39]. As an example, in one prospective study of patients who had spinal anesthesia with 25 or 27 gauge Quincke (ie, traumatic) needles, PDPH occurred in 11 percent of patients aged 31 to 50 years, compared with 4 percent of others [24]. The incidence in very young children may be under-reported due to their inability to report headache and lack of behavioral documentation by parents and clinicians [40,41]. ●Low opening




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Prior headaches – History of prior headaches (both PDPH and chronic headaches) may be a risk factor for PDPH [4,23,31-33]; although, this has not been observed in all studies [34-36]
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; however, definitive evidence is lacking [27,28]. Second stage pushing in labor [28,29] and multiparity [16] have been associated with an increased PDPH risk in the postpartum period [29,30]. ●<span>Prior headaches – History of prior headaches (both PDPH and chronic headaches) may be a risk factor for PDPH [4,23,31-33]; although, this has not been observed in all studies [34-36]. ●Age – In most studies, extremes of age are associated with lower incidence of PDPH, with young adults (18 to 50 years of age) having the highest risk [23,24,31,37-39]. As an example,




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Pregnancy – Pregnancy confers an additional risk for PDPH, possibly due to increased cerebral vasodilation in response to cerebrospinal fluid (CSF) hypotension, related to high levels of circulating estrogen [24,26].
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with older or younger ages, and a prior history of headache: ●Female gender – Several studies have found that women have a two to three times increased risk for PDPH compared with men [23-25]. ●<span>Pregnancy – Pregnancy confers an additional risk for PDPH, possibly due to increased cerebral vasodilation in response to cerebrospinal fluid (CSF) hypotension, related to high levels of circulating estrogen [24,26]. It is also thought that increased CSF pressure during labor leads to a larger CSF leak and higher risk of PDPH; however, definitive evidence is lacking [27,28]. Second stage pushing in




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Female gender – Several studies have found that women have a two to three times increased risk for PDPH compared with men [23-25]
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tors — In various studies, common patient risk factors for PDPH have included female gender, pregnancy, age 18 to 50 years compared with older or younger ages, and a prior history of headache: ●<span>Female gender – Several studies have found that women have a two to three times increased risk for PDPH compared with men [23-25]. ●Pregnancy – Pregnancy confers an additional risk for PDPH, possibly due to increased cerebral vasodilation in response to cerebrospinal fluid (CSF) hypotension, related to high levels




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Low opening pressure – Low opening pressure during lumbar puncture (LP) may also predict an increased risk of PDPH [42]. However, a 2019 case-control retrospective study and systematic literature review found no association between either opening pressure or closing pressure and PDPH risk [43]
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ent of others [24]. The incidence in very young children may be under-reported due to their inability to report headache and lack of behavioral documentation by parents and clinicians [40,41]. ●<span>Low opening pressure – Low opening pressure during lumbar puncture (LP) may also predict an increased risk of PDPH [42]. However, a 2019 case-control retrospective study and systematic literature review found no association between either opening pressure or closing pressure and PDPH risk [43]. ●Volume of CSF removed – PDPH may have distinct temporal and prognostic profiles depending on the volume of CSF removed, particularly for high volume CSF removal. A systematic literatu




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Volume of CSF removed – PDPH may have distinct temporal and prognostic profiles depending on the volume of CSF removed, particularly for high volume CSF removal. A systematic literature review found that high volume CSF removal (ie, 20 to 30 mL) may be associated with increased risk of immediate PDPH, but decreased risk of PDPH at 24 hours, compared with lower volume CSF removal [43].
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isk of PDPH [42]. However, a 2019 case-control retrospective study and systematic literature review found no association between either opening pressure or closing pressure and PDPH risk [43]. ●<span>Volume of CSF removed – PDPH may have distinct temporal and prognostic profiles depending on the volume of CSF removed, particularly for high volume CSF removal. A systematic literature review found that high volume CSF removal (ie, 20 to 30 mL) may be associated with increased risk of immediate PDPH, but decreased risk of PDPH at 24 hours, compared with lower volume CSF removal [43]. In one retrospective study of over 300 LPs performed as part of an Alzheimer disease research trial, patients who had >30 mL CSF removed were more likely to have an immediate onset P




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High volume CSF removal with lowered closing pressure may help reduce further CSF leakage to heal the dural hole
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of an Alzheimer disease research trial, patients who had >30 mL CSF removed were more likely to have an immediate onset PDPH, but were less likely to need an epidural blood patch (EBP) [44]. <span>High volume CSF removal with lowered closing pressure may help reduce further CSF leakage to heal the dural hole. ●Low body mass index (BMI) – The literature on the effect of BMI on the risk of PDPH is inconclusive. Some studies have reported a higher risk of PDPH in patients with low BMI (≤25 kg/




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Low body mass index (BMI) – The literature on the effect of BMI on the risk of PDPH is inconclusive
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e onset PDPH, but were less likely to need an epidural blood patch (EBP) [44]. High volume CSF removal with lowered closing pressure may help reduce further CSF leakage to heal the dural hole. ●<span>Low body mass index (BMI) – The literature on the effect of BMI on the risk of PDPH is inconclusive. Some studies have reported a higher risk of PDPH in patients with low BMI (≤25 kg/m2) after diagnostic LP [45] and lower risk of PDPH after unintentional dural puncture (UDP) in obese




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Procedural risk factors — The choice of spinal needle and procedural factors can affect the risk of PDPH. We suggest the use of pencil point (atraumatic) needles for spinal anesthesia and diagnostic LP.
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k of PDPH after unintentional dural puncture (UDP) in obese parturients (BMI ≥31.5 kg/m2) [30,46]. In contrast, other studies have reported no effect of BMI on the incidence of PDPH [23,47-51]. <span>Procedural risk factors — The choice of spinal needle and procedural factors can affect the risk of PDPH. We suggest the use of pencil point (atraumatic) needles for spinal anesthesia and diagnostic LP. ●Needle tip – For both diagnostic LP and spinal anesthesia, we recommend the use of spinal needles with a pencil point tip, rather than needles with a sharp cutting tip. The use of penc




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Needle tip – For both diagnostic LP and spinal anesthesia, we recommend the use of spinal needles with a pencil point tip, rather than needles with a sharp cutting tip. The use of pencil point spinal needles reduces the risk of PDPH compared with cutting needles of the same size [8,52-54]
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risk factors — The choice of spinal needle and procedural factors can affect the risk of PDPH. We suggest the use of pencil point (atraumatic) needles for spinal anesthesia and diagnostic LP. ●<span>Needle tip – For both diagnostic LP and spinal anesthesia, we recommend the use of spinal needles with a pencil point tip, rather than needles with a sharp cutting tip. The use of pencil point spinal needles reduces the risk of PDPH compared with cutting needles of the same size [8,52-54]. Whitacre and Sprotte needles, which are the most commonly used pencil point needles, have a closed tip shaped like that of a pencil, with the hole on the side of the needle near the ti




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The incidence of PDPH was significantly lower in the atraumatic group compared with the conventional group (4.2 versus 11 percent, relative risk [RR] 0.40, 95% CI 0.34-0.47, absolute risk reduction 6.8 percent, number needed to treat to avoid one headache 15)
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-analysis of randomized controlled trials that compared pencil point and conventional (cutting) needles for LP [9]. The review identified 110 trials from 29 countries with over 31,000 subjects. <span>The incidence of PDPH was significantly lower in the atraumatic group compared with the conventional group (4.2 versus 11 percent, relative risk [RR] 0.40, 95% CI 0.34-0.47, absolute risk reduction 6.8 percent, number needed to treat to avoid one headache 15). In addition, use of atraumatic needles was associated with a significant reduction in the need for EBP (RR 0.5, 95% CI 0.33-0.75). There was no significant difference between groups fo




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In addition, use of atraumatic needles was associated with a significant reduction in the need for EBP (RR 0.5, 95% CI 0.33-0.75). There was no significant difference between groups for the success rate of LP on first attempt, LP failure rate, incidence of traumatic tap, or backache.
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up compared with the conventional group (4.2 versus 11 percent, relative risk [RR] 0.40, 95% CI 0.34-0.47, absolute risk reduction 6.8 percent, number needed to treat to avoid one headache 15). <span>In addition, use of atraumatic needles was associated with a significant reduction in the need for EBP (RR 0.5, 95% CI 0.33-0.75). There was no significant difference between groups for the success rate of LP on first attempt, LP failure rate, incidence of traumatic tap, or backache. ●Needle size – Larger conventional needle size (ie, lower needle gauge) is correlated with an increased incidence of PDPH, as demonstrated in a 2016 meta-analysis that included 12 studi




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Needle size – Larger conventional needle size (ie, lower needle gauge) is correlated with an increased incidence of PDPH, as demonstrated in a 2016 meta-analysis that included 12 studies with over 3100 patients who had neuraxial anesthesia with cutting needles [55]. As examples from the meta-analysis, the incidence of PDPH with a 22 or 23 gauge Quincke needle ranged from 8 to 25 percent, whereas the incidence of PDPH with a 27 gauge Quincke needle ranged from 0 to 14 percent
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ed for EBP (RR 0.5, 95% CI 0.33-0.75). There was no significant difference between groups for the success rate of LP on first attempt, LP failure rate, incidence of traumatic tap, or backache. ●<span>Needle size – Larger conventional needle size (ie, lower needle gauge) is correlated with an increased incidence of PDPH, as demonstrated in a 2016 meta-analysis that included 12 studies with over 3100 patients who had neuraxial anesthesia with cutting needles [55]. As examples from the meta-analysis, the incidence of PDPH with a 22 or 23 gauge Quincke needle ranged from 8 to 25 percent, whereas the incidence of PDPH with a 27 gauge Quincke needle ranged from 0 to 14 percent. In obstetric patients who undergo spinal anesthesia, there is little difference in the rate of PDPH or the need for EBP with the commonly used sizes of pencil point needles. The 2016 m




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Smaller spinal needles may be technically more difficult to use, as they tend to bend during insertion. Thus they are typically used with an introducer needle, which is inserted through the skin and along the desired needle path. Flow rate is slower than with larger bore needles; confirmatory CSF appears more slowly in the needle hub, and collection of CSF is slower. In our practice, spinal anesthesia is performed using a small gauge noncutting needle (ie, 25 gauge Whitacre).
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e of PDPH and pencil point needle size [55]. For patients who undergo diagnostic LP, the relationship between pencil point needle size and the risk of PDPH is less clear, as there are few data. <span>Smaller spinal needles may be technically more difficult to use, as they tend to bend during insertion. Thus they are typically used with an introducer needle, which is inserted through the skin and along the desired needle path. Flow rate is slower than with larger bore needles; confirmatory CSF appears more slowly in the needle hub, and collection of CSF is slower. In our practice, spinal anesthesia is performed using a small gauge noncutting needle (ie, 25 gauge Whitacre). (See "Spinal anesthesia: Technique", section on 'Choice of spinal needle'.) The optimal size of spinal needle may be different for spinal anesthesia versus diagnostic LP in which openin




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The optimal size of spinal needle may be different for spinal anesthesia versus diagnostic LP in which opening pressure and/or CSF sampling is required. In one laboratory study that compared flow rates and the rate of accurate pressure transduction for various cutting and pencil point spinal needles, the 20 gauge Sprotte needles provided rapid pressure transduction (>90 percent of true pressure within one minute) and an optimal flow rate, defined as 2 mL per minute. [56].
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lower. In our practice, spinal anesthesia is performed using a small gauge noncutting needle (ie, 25 gauge Whitacre). (See "Spinal anesthesia: Technique", section on 'Choice of spinal needle'.) <span>The optimal size of spinal needle may be different for spinal anesthesia versus diagnostic LP in which opening pressure and/or CSF sampling is required. In one laboratory study that compared flow rates and the rate of accurate pressure transduction for various cutting and pencil point spinal needles, the 20 gauge Sprotte needles provided rapid pressure transduction (>90 percent of true pressure within one minute) and an optimal flow rate, defined as 2 mL per minute. [56]. The technique of diagnostic LP is discussed in detail elsewhere. (See "Lumbar puncture: Technique, indications, contraindications, and complications in adults".) ●Needle orientation – P




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Needle orientation – PDPH is more than twice as likely if a cutting spinal or epidural needle is inserted with the bevel perpendicular, rather than parallel, to the long axis of the spine [31,57-59]. As an example, in one study, 218 patients who underwent nonobstetric surgery with spinal anesthesia using a 27 gauge Quincke needle were randomly assigned to have the needle inserted parallel or transverse to the long axis of the spine [59]. PDPH occurred in 4 percent of patients in the parallel group, and 23 percent of patients in the transverse group
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ined as 2 mL per minute. [56]. The technique of diagnostic LP is discussed in detail elsewhere. (See "Lumbar puncture: Technique, indications, contraindications, and complications in adults".) ●<span>Needle orientation – PDPH is more than twice as likely if a cutting spinal or epidural needle is inserted with the bevel perpendicular, rather than parallel, to the long axis of the spine [31,57-59]. As an example, in one study, 218 patients who underwent nonobstetric surgery with spinal anesthesia using a 27 gauge Quincke needle were randomly assigned to have the needle inserted parallel or transverse to the long axis of the spine [59]. PDPH occurred in 4 percent of patients in the parallel group, and 23 percent of patients in the transverse group. Since pencil point needles have no bevels, needle orientation is not a relevant issue when they are used. ●Reinsertion of stylet – Whether reinserting the stylet before removing the sp




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Reinsertion of stylet – Whether reinserting the stylet before removing the spinal needle reduces the risk of PDPH is unclear. Available data suggest that reinsertion does not reduce PDPH when a cutting needle is used, and the data regarding the use of pencil point needles is equivocal. Authors to this topic do not routinely reinsert the stylet before removing a spinal needle
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of patients in the parallel group, and 23 percent of patients in the transverse group. Since pencil point needles have no bevels, needle orientation is not a relevant issue when they are used. ●<span>Reinsertion of stylet – Whether reinserting the stylet before removing the spinal needle reduces the risk of PDPH is unclear. Available data suggest that reinsertion does not reduce PDPH when a cutting needle is used, and the data regarding the use of pencil point needles is equivocal. Authors to this topic do not routinely reinsert the stylet before removing a spinal needle. •Pencil point needles – Evidence of benefit for stylet reinsertion comes from a randomized trial of 600 patients undergoing diagnostic LP using a 21 gauge Sprotte needle, which found t




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Placement of spinal needle in the sitting as opposed to lateral position [66] and a higher number of needle passes may be associated with increased risk for PDPH in spinal anesthetics, but the evidence is conflicting [31,67].
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sthesia/analgesia are similar to the incidences after an epidural technique [63-65]. CSE is discussed separately. (See "Epidural and combined spinal-epidural anesthesia: Techniques".) ●Others – <span>Placement of spinal needle in the sitting as opposed to lateral position [66] and a higher number of needle passes may be associated with increased risk for PDPH in spinal anesthetics, but the evidence is conflicting [31,67]. Paramedian approach to the spinal space and decreased operator experience [68,69] may confer additional increased risk for PDPH, but results are limited and conflicting between the orth




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Paramedian approach to the spinal space and decreased operator experience [68,69] may confer additional increased risk for PDPH, but results are limited and conflicting between the orthopedic and obstetric populations [70,71].
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e sitting as opposed to lateral position [66] and a higher number of needle passes may be associated with increased risk for PDPH in spinal anesthetics, but the evidence is conflicting [31,67]. <span>Paramedian approach to the spinal space and decreased operator experience [68,69] may confer additional increased risk for PDPH, but results are limited and conflicting between the orthopedic and obstetric populations [70,71]. In epidural placements, studies have failed to show a difference in PDPH risk with the use of air versus saline for the loss of resistance technique to identify the epidural space acros




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In epidural placements, studies have failed to show a difference in PDPH risk with the use of air versus saline for the loss of resistance technique to identify the epidural space across all patient populations [72,73]. The onset of headache may be sooner in obstetric patients when air is used for loss of resistance, likely related to pneumocephalus rather than low pressure headache [20]
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space and decreased operator experience [68,69] may confer additional increased risk for PDPH, but results are limited and conflicting between the orthopedic and obstetric populations [70,71]. <span>In epidural placements, studies have failed to show a difference in PDPH risk with the use of air versus saline for the loss of resistance technique to identify the epidural space across all patient populations [72,73]. The onset of headache may be sooner in obstetric patients when air is used for loss of resistance, likely related to pneumocephalus rather than low pressure headache [20]. PREVENTION OF PDPH AFTER DURAL PUNCTURE — In addition to procedure modification, a number of strategies have been used to attempt to prevent PDPH after dural puncture. ●Bed rest – Desp




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Bed rest – Despite common recommendations for bed rest following dural puncture, this remedy has not been shown to significantly decrease the risk of PDPH [4,74-77].
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pressure headache [20]. PREVENTION OF PDPH AFTER DURAL PUNCTURE — In addition to procedure modification, a number of strategies have been used to attempt to prevent PDPH after dural puncture. ●<span>Bed rest – Despite common recommendations for bed rest following dural puncture, this remedy has not been shown to significantly decrease the risk of PDPH [4,74-77]. A meta-analysis of 16 randomized controlled trials of LP performed for anesthesia, myelography, or diagnostic purposes found no evidence in any trial that longer bed rest was superior t




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While of no use for prevention of PDPH, bed rest does decrease the intensity of the headache. (See 'Treatment' below.)
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ter bed rest [76]. The relative risk (RR) of headache among patients undergoing a diagnostic LP was 0.97 with longer bed rest. A similar lack of benefit was noted in a later meta-analysis [74]. <span>While of no use for prevention of PDPH, bed rest does decrease the intensity of the headache. (See 'Treatment' below.) ●Abdominal binder – Given the low risk of this intervention, some of the authors of this topic routinely offer abdominal binders to patients who have unintentional dural puncture (UDP)




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There is a theoretical role for abdominal compression with a tight abdominal binder for prevention and/or treatment of PDPH. The rationale for such treatment is that increased intra-abdominal pressure may be transmitted to the epidural space, may help to seal the dural puncture and decrease cerebrospinal fluid (CSF) leak, and may improve an existing headache
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erience, some patients enjoy wearing the binder in the immediate postpartum period. However, abdominal binders are not widely recommended [78], and there is little literature on their use [79]. <span>There is a theoretical role for abdominal compression with a tight abdominal binder for prevention and/or treatment of PDPH. The rationale for such treatment is that increased intra-abdominal pressure may be transmitted to the epidural space, may help to seal the dural puncture and decrease cerebrospinal fluid (CSF) leak, and may improve an existing headache. ●Prophylactic drug therapy – Based on the limited evidence available, we do not recommend administration of prophylactic medications after UDP or LP to prevent PDPH. Small trials have




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Prophylactic drug therapy – Based on the limited evidence available, we do not recommend administration of prophylactic medications after UDP or LP to prevent PDPH.
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reased intra-abdominal pressure may be transmitted to the epidural space, may help to seal the dural puncture and decrease cerebrospinal fluid (CSF) leak, and may improve an existing headache. ●<span>Prophylactic drug therapy – Based on the limited evidence available, we do not recommend administration of prophylactic medications after UDP or LP to prevent PDPH. Small trials have reported that prophylactic administration of epidural morphine [80] and intravenous (IV) cosyntropin [81] may reduce the incidence of PDPH after UDP during obstetric a




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In addition, ondansetron may reduce the risk of PDPH. In one randomized trial, 210 women were randomly assigned to receive ondansetron 0.15 mg/kg IV or saline during spinal anesthesia with a 25 gauge Quincke needle for cesarean delivery [84]. PDPH occurred in 5 percent of patients who received ondansetron, compared with 21 percent of patients who did not. Ondansetron may trigger migraine headache in susceptible patients [85]. Further research is needed to elucidate the role of these drugs in PDPH prevention.
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cosyntropin and epidural morphine was associated with decreased incidence of PDPH and need for epidural blood patch, compared with other prophylactic treatment or conservative management [83]. <span>In addition, ondansetron may reduce the risk of PDPH. In one randomized trial, 210 women were randomly assigned to receive ondansetron 0.15 mg/kg IV or saline during spinal anesthesia with a 25 gauge Quincke needle for cesarean delivery [84]. PDPH occurred in 5 percent of patients who received ondansetron, compared with 21 percent of patients who did not. Ondansetron may trigger migraine headache in susceptible patients [85]. Further research is needed to elucidate the role of these drugs in PDPH prevention. In obstetric and general surgical populations, oral caffeine has not been shown to prevent PDPH after dural puncture [86,87]. ●Prophylactic epidural blood patch – Epidural blood patch (




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In obstetric and general surgical populations, oral caffeine has not been shown to prevent PDPH after dural puncture [86,87].
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h 21 percent of patients who did not. Ondansetron may trigger migraine headache in susceptible patients [85]. Further research is needed to elucidate the role of these drugs in PDPH prevention. <span>In obstetric and general surgical populations, oral caffeine has not been shown to prevent PDPH after dural puncture [86,87]. ●Prophylactic epidural blood patch – Epidural blood patch (EBP) is an effective treatment for PDPH, and may also be performed prophylactically before a headache occurs for patients in w




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Epidural blood patch (EBP) is an effective treatment for PDPH, and may also be performed prophylactically before a headache occurs for patients in whom an epidural catheter is placed after an inadvertent dural puncture.
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hese drugs in PDPH prevention. In obstetric and general surgical populations, oral caffeine has not been shown to prevent PDPH after dural puncture [86,87]. ●Prophylactic epidural blood patch – <span>Epidural blood patch (EBP) is an effective treatment for PDPH, and may also be performed prophylactically before a headache occurs for patients in whom an epidural catheter is placed after an inadvertent dural puncture. For prophylactic EBP, blood is injected into the epidural catheter prior to its removal after anesthesia. (See 'Epidural blood patch' below.) We do not routinely perform prophylactic EB




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We do not routinely perform prophylactic EBP, since the efficacy is unclear [88-93].
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eter is placed after an inadvertent dural puncture. For prophylactic EBP, blood is injected into the epidural catheter prior to its removal after anesthesia. (See 'Epidural blood patch' below.) <span>We do not routinely perform prophylactic EBP, since the efficacy is unclear [88-93]. A review of the literature of prophylactic EBP in obstetric patients found that it does not appear to decrease the incidence of PDPH, but may decrease the intensity and/or duration of s




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Patients with PDPH typically present with frontal or occipital headache that is worse with sitting or standing, and relieved by lying flat. The headache tends to be worse if it occurs in the first 24 hours, and associated symptoms are more common with severe headaches. In some patients, the symptoms of PDPH are similar to their previously experienced migraine headaches, except that there is an added postural component
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anaged with either placement of an intrathecal catheter or replacement of an epidural catheter [94]. There was no difference in the incidence of PDPH between the two groups. CLINICAL FEATURES — <span>Patients with PDPH typically present with frontal or occipital headache that is worse with sitting or standing, and relieved by lying flat. The headache tends to be worse if it occurs in the first 24 hours, and associated symptoms are more common with severe headaches. In some patients, the symptoms of PDPH are similar to their previously experienced migraine headaches, except that there is an added postural component. Associated symptoms occur in up to 70 percent of patients [24], and may include nausea, neck stiffness, low back pain, vertigo, vision changes (diplopia, blurred vision, or photophobia




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Associated symptoms occur in up to 70 percent of patients [24], and may include nausea, neck stiffness, low back pain, vertigo, vision changes (diplopia, blurred vision, or photophobia), dizziness, or auditory disturbances (tinnitus, hearing loss) [42]. In one study of 133 patients who developed PDPH after diagnostic lumbar puncture (LP), neck stiffness was reported in 55.6 percent, shoulder stiffness in 46.6 percent, nausea and vomiting in 33 percent, tinnitus in 22 percent, and photophobia in 23 percent. [4].
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s are more common with severe headaches. In some patients, the symptoms of PDPH are similar to their previously experienced migraine headaches, except that there is an added postural component. <span>Associated symptoms occur in up to 70 percent of patients [24], and may include nausea, neck stiffness, low back pain, vertigo, vision changes (diplopia, blurred vision, or photophobia), dizziness, or auditory disturbances (tinnitus, hearing loss) [42]. In one study of 133 patients who developed PDPH after diagnostic lumbar puncture (LP), neck stiffness was reported in 55.6 percent, shoulder stiffness in 46.6 percent, nausea and vomiting in 33 percent, tinnitus in 22 percent, and photophobia in 23 percent. [4]. Approximately 90 percent of PDPHs occur within 72 hours after a dural puncture, though onset has rarely been reported up to two weeks later [42,98]. Without treatment, most headaches re




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Approximately 90 percent of PDPHs occur within 72 hours after a dural puncture, though onset has rarely been reported up to two weeks later [42,98].
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ar puncture (LP), neck stiffness was reported in 55.6 percent, shoulder stiffness in 46.6 percent, nausea and vomiting in 33 percent, tinnitus in 22 percent, and photophobia in 23 percent. [4]. <span>Approximately 90 percent of PDPHs occur within 72 hours after a dural puncture, though onset has rarely been reported up to two weeks later [42,98]. Without treatment, most headaches resolve within one week, and one-half resolve by four to five days after dural puncture [24,31,99]. Longer duration of PDPH has been associated with th




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Without treatment, most headaches resolve within one week, and one-half resolve by four to five days after dural puncture [ 24,31,99].
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percent, and photophobia in 23 percent. [4]. Approximately 90 percent of PDPHs occur within 72 hours after a dural puncture, though onset has rarely been reported up to two weeks later [42,98]. <span>Without treatment, most headaches resolve within one week, and one-half resolve by four to five days after dural puncture [24,31,99]. Longer duration of PDPH has been associated with the use of a cutting needle for dural puncture compared with a pencil point needle [100], dural puncture with the patient in the sitting




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Longer duration of PDPH has been associated with the use of a cutting needle for dural puncture compared with a pencil point needle [ 100], dural puncture with the patient in the sitting position compared with lateral decubitus, multiple attempts at dural puncture, and patient history of depression [36].
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set has rarely been reported up to two weeks later [42,98]. Without treatment, most headaches resolve within one week, and one-half resolve by four to five days after dural puncture [24,31,99]. <span>Longer duration of PDPH has been associated with the use of a cutting needle for dural puncture compared with a pencil point needle [100], dural puncture with the patient in the sitting position compared with lateral decubitus, multiple attempts at dural puncture, and patient history of depression [36]. DIAGNOSIS OF PDPH — The diagnosis of PDPH is made clinically by identifying the typical positional headache within 72 hours after a dural puncture. Other causes may need to be excluded




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The diagnosis of PDPH is made clinically by identifying the typical positional headache within 72 hours after a dural puncture. Other causes may need to be excluded if symptoms are atypical
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[100], dural puncture with the patient in the sitting position compared with lateral decubitus, multiple attempts at dural puncture, and patient history of depression [36]. DIAGNOSIS OF PDPH — <span>The diagnosis of PDPH is made clinically by identifying the typical positional headache within 72 hours after a dural puncture. Other causes may need to be excluded if symptoms are atypical. Neuroimaging with computed tomography (CT) or magnetic resonance imaging (MRI) is not indicated unless required to exclude alternative diagnoses. If imaging is performed, findings cons




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If imaging is performed, findings consistent with PDPH include small ventricles, downward displacement (sagging) of the brain, engorged cerebral venous sinuses, subdural fluid collections, pituitary enlargement, and diffuse meningeal enhancement [2,101,102]. These findings are analogous to those reported in patients with spontaneous intracranial hypotension. (See "Spontaneous intracranial hypotension: Pathophysiology, clinical features, and diagnosis".)
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y need to be excluded if symptoms are atypical. Neuroimaging with computed tomography (CT) or magnetic resonance imaging (MRI) is not indicated unless required to exclude alternative diagnoses. <span>If imaging is performed, findings consistent with PDPH include small ventricles, downward displacement (sagging) of the brain, engorged cerebral venous sinuses, subdural fluid collections, pituitary enlargement, and diffuse meningeal enhancement [2,101,102]. These findings are analogous to those reported in patients with spontaneous intracranial hypotension. (See "Spontaneous intracranial hypotension: Pathophysiology, clinical features, and diagnosis".) Diagnostic lumbar puncture (LP) should be avoided if possible, due to the risk of worsening an existing PDPH. If performed, however, a low cerebrospinal fluid (CSF) opening pressure or




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Diagnostic lumbar puncture (LP) should be avoided if possible, due to the risk of worsening an existing PDPH. If performed, however, a low cerebrospinal fluid (CSF) opening pressure or dry tap (indicative of intracranial hypotension) with increased CSF protein and lymphocyte count may be present [103].
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findings are analogous to those reported in patients with spontaneous intracranial hypotension. (See "Spontaneous intracranial hypotension: Pathophysiology, clinical features, and diagnosis".) <span>Diagnostic lumbar puncture (LP) should be avoided if possible, due to the risk of worsening an existing PDPH. If performed, however, a low cerebrospinal fluid (CSF) opening pressure or dry tap (indicative of intracranial hypotension) with increased CSF protein and lymphocyte count may be present [103]. DIFFERENTIAL DIAGNOSIS — The differential diagnosis of headache after dural puncture is broad, as outlined in the table (table 1), but a postural headache in this setting is most likely




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The differential diagnosis of headache after dural puncture is broad, as outlined in the table (table 1), but a postural headache in this setting is most likely related to the procedure.
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low cerebrospinal fluid (CSF) opening pressure or dry tap (indicative of intracranial hypotension) with increased CSF protein and lymphocyte count may be present [103]. DIFFERENTIAL DIAGNOSIS — <span>The differential diagnosis of headache after dural puncture is broad, as outlined in the table (table 1), but a postural headache in this setting is most likely related to the procedure. Serious and/or life-threatening etiologies (eg, hemorrhage, thrombosis, vasculopathy, meningitis), which may or may not be related to the dural puncture, must be ruled out in the presen




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Serious and/or life-threatening etiologies (eg, hemorrhage, thrombosis, vasculopathy, meningitis), which may or may not be related to the dural puncture, must be ruled out in the presence of focal or worsening neurologic deficits. Findings that should prompt further investigation are shown in a table ( table 2).
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OSIS — The differential diagnosis of headache after dural puncture is broad, as outlined in the table (table 1), but a postural headache in this setting is most likely related to the procedure. <span>Serious and/or life-threatening etiologies (eg, hemorrhage, thrombosis, vasculopathy, meningitis), which may or may not be related to the dural puncture, must be ruled out in the presence of focal or worsening neurologic deficits. Findings that should prompt further investigation are shown in a table (table 2). Subdural hematoma and other forms of intracranial hemorrhage are rare but potentially lethal complications of dural puncture. Intracranial hemorrhage should be suspected in patients wit




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Subdural hematoma and other forms of intracranial hemorrhage are rare but potentially lethal complications of dural puncture. Intracranial hemorrhage should be suspected in patients with prolonged headache (ie, beyond five to seven days), whose headaches become non-positional, who do not improve or worsen after an epidural blood patch (EBP), or who develop focal neurologic symptoms [104,105]
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be related to the dural puncture, must be ruled out in the presence of focal or worsening neurologic deficits. Findings that should prompt further investigation are shown in a table (table 2). <span>Subdural hematoma and other forms of intracranial hemorrhage are rare but potentially lethal complications of dural puncture. Intracranial hemorrhage should be suspected in patients with prolonged headache (ie, beyond five to seven days), whose headaches become non-positional, who do not improve or worsen after an epidural blood patch (EBP), or who develop focal neurologic symptoms [104,105]. Other possible causes of postural headache (eg, migraine, headache associated with postural orthostatic tachycardia) may occur coincidentally after dural puncture, and may be excluded




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Other possible causes of postural headache (eg, migraine, headache associated with postural orthostatic tachycardia) may occur coincidentally after dural puncture, and may be excluded based on history, symptoms, and physical examination. Some headaches may improve but are not completely abolished with rest, including in the supine position (eg, migraine)
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che (ie, beyond five to seven days), whose headaches become non-positional, who do not improve or worsen after an epidural blood patch (EBP), or who develop focal neurologic symptoms [104,105]. <span>Other possible causes of postural headache (eg, migraine, headache associated with postural orthostatic tachycardia) may occur coincidentally after dural puncture, and may be excluded based on history, symptoms, and physical examination. Some headaches may improve but are not completely abolished with rest, including in the supine position (eg, migraine). PDPH related to neuraxial anesthesia is most common in obstetric patients. Headache in the postpartum period is remarkably common, with a reported incidence as high as 39 percent in th




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Mild PDPH — Patients with PDPH who can tolerate an upright position and perform activities of daily living are considered to have mild PDPH; obstetric patients with mild PDPH are able to care for their baby. Patients with mild PDPH may benefit from an initial trial of conservative treatment including bed rest as needed, and a brief course of oral analgesics (see 'Drug therapy' below) and antiemetics as necessary. Vigorous oral and/or intravenous (IV) hydration are also routinely encouraged in postpartum patients as a noninvasive, low-risk therapy [108]
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cy and postpartum", section on 'Evaluation of postpartum patients'.) TREATMENT — The treatment of PDPH depends upon the severity of headache and its impact on the patient's ability to function. <span>Mild PDPH — Patients with PDPH who can tolerate an upright position and perform activities of daily living are considered to have mild PDPH; obstetric patients with mild PDPH are able to care for their baby. Patients with mild PDPH may benefit from an initial trial of conservative treatment including bed rest as needed, and a brief course of oral analgesics (see 'Drug therapy' below) and antiemetics as necessary. Vigorous oral and/or intravenous (IV) hydration are also routinely encouraged in postpartum patients as a noninvasive, low-risk therapy [108]. Debilitating PDPH — Patients with PDPH who are unable to tolerate sitting or standing, or are unable to perform activities of daily living (including obstetric patients unable to care




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Debilitating PDPH — Patients with PDPH who are unable to tolerate sitting or standing, or are unable to perform activities of daily living (including obstetric patients unable to care for their baby) and whose headache is refractory to a brief trial of conservative measures are considered to have moderate to severe PDPH. These patients should be offered an epidural blood patch (EBP), which may provide permanent symptomatic relief.
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Drug therapy' below) and antiemetics as necessary. Vigorous oral and/or intravenous (IV) hydration are also routinely encouraged in postpartum patients as a noninvasive, low-risk therapy [108]. <span>Debilitating PDPH — Patients with PDPH who are unable to tolerate sitting or standing, or are unable to perform activities of daily living (including obstetric patients unable to care for their baby) and whose headache is refractory to a brief trial of conservative measures are considered to have moderate to severe PDPH. These patients should be offered an epidural blood patch (EBP), which may provide permanent symptomatic relief. Epidural blood patch — EBP is considered the definitive treatment for PDPH. A systematic review published in 2010 noted that EBP reduced the duration and intensity of post-dural punctur




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Similar to epidural anesthesia, EBP is contraindicated in patients with coagulopathy or on anticoagulation, and in patients with systemic infection or infection at the site for epidural needle placement. Patients with HIV present a theoretical risk for developing central nervous system (CNS) infection after EBP. However, HIV is known to be a neurotropic virus, infecting the CNS in its earliest stages, and no adverse effects have been reported after either neuraxial anesthesia or EBP in HIV-infected patients [118].
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ate for a second EBP, if it is required [10,110,113-116]. The success rate for EBP may be lower if dural puncture occurs with a larger diameter needle (ie, ≥20 gauge) [117]. Contraindications — <span>Similar to epidural anesthesia, EBP is contraindicated in patients with coagulopathy or on anticoagulation, and in patients with systemic infection or infection at the site for epidural needle placement. Patients with HIV present a theoretical risk for developing central nervous system (CNS) infection after EBP. However, HIV is known to be a neurotropic virus, infecting the CNS in its earliest stages, and no adverse effects have been reported after either neuraxial anesthesia or EBP in HIV-infected patients [118]. Patients with PDPH after an initially challenging neuraxial anesthetic may benefit from fluoroscopically-guided EBP placement. The decision to place EBP must always be weighed against t




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Once the epidural space has been identified in this manner, a syringe of autologous venous blood is drawn by a second operator using aseptic technique; the blood is slowly injected through the epidural needle. Typically, headache symptoms will improve within seconds to minutes of the completion of the procedure, although a transient sensation of "fullness" in the back is common
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sistance to saline to identify the epidural space, without inserting a catheter (see "Epidural and combined spinal-epidural anesthesia: Techniques", section on 'Epidural anesthesia technique'). <span>Once the epidural space has been identified in this manner, a syringe of autologous venous blood is drawn by a second operator using aseptic technique; the blood is slowly injected through the epidural needle. Typically, headache symptoms will improve within seconds to minutes of the completion of the procedure, although a transient sensation of "fullness" in the back is common. Upon completion of the EBP, the patient is instructed to lie flat (or at a maximum 30 degree angle) for one to two hours with minimal movement. After this, the patient may stand and re




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Upon completion of the EBP, the patient is instructed to lie flat (or at a maximum 30 degree angle) for one to two hours with minimal movement. After this, the patient may stand and resume normal activities. It is reasonable to avoid heavy lifting and strenuous activity within the first 24 hours of EBP, although evidence is lacking to support this recommendation. Patients should also be instructed to taper analgesic medications (eg, butalbital-acetaminophen-caffeine) to avoid the possibility of a rebound headache from sudden medication withdrawal
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the epidural needle. Typically, headache symptoms will improve within seconds to minutes of the completion of the procedure, although a transient sensation of "fullness" in the back is common. <span>Upon completion of the EBP, the patient is instructed to lie flat (or at a maximum 30 degree angle) for one to two hours with minimal movement. After this, the patient may stand and resume normal activities. It is reasonable to avoid heavy lifting and strenuous activity within the first 24 hours of EBP, although evidence is lacking to support this recommendation. Patients should also be instructed to taper analgesic medications (eg, butalbital-acetaminophen-caffeine) to avoid the possibility of a rebound headache from sudden medication withdrawal. ●Optimal volume of blood for EBP – We aim to inject 20 mL of blood for blood patch, and stop injection if the patient complains of significant pain or pressure. A randomized trial that




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Mechanism of action — The mechanism by which EBP relieves PDPH is unclear, and may be multifactorial. It is thought that the injection of blood directly compresses the thecal sac, thereby increasing lumbar and intracranial cerebrospinal fluid (CSF) pressure. Once the injected blood clots, it may plug the CSF leak and/or initiate an inflammatory reaction that facilitates healing of the puncture site.
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performed with the patient in the lateral decubitus position [123]. The blood spread a mean of 4.6 interspaces, approximately 3.5 interspaces cephalad and 1 interspace caudad to the injection. <span>Mechanism of action — The mechanism by which EBP relieves PDPH is unclear, and may be multifactorial. It is thought that the injection of blood directly compresses the thecal sac, thereby increasing lumbar and intracranial cerebrospinal fluid (CSF) pressure. Once the injected blood clots, it may plug the CSF leak and/or initiate an inflammatory reaction that facilitates healing of the puncture site. Regardless of the mechanism, clotting appears to be important to the success of injectates used for EBP, as whole blood, fibrin glue, and possibly platelet-rich plasma more effectively




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Complications — The most common complication of EBP is back pain, which occurs in 25 to 35 percent of patients [113,126,127]. Back pain usually resolves within 48 hours of EBP.
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EBP, as whole blood, fibrin glue, and possibly platelet-rich plasma more effectively maintain CSF pressure than saline, anticoagulated blood, or dextran solutions in animal models [89,124,125]. <span>Complications — The most common complication of EBP is back pain, which occurs in 25 to 35 percent of patients [113,126,127]. Back pain usually resolves within 48 hours of EBP. However, in one prospective observational study of women who underwent EBP for PDPH, back pain lasted from 3 to 100 days (mean 28 days) in 16 percent of patients [113]. Rare complicatio




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Rare complications include misplacement of blood resulting in spinal subdural hematoma [128] or intrathecal injection and arachnoiditis [126,129]. Other rare complications include infection, subdural abscess [130], facial nerve paralysis [113,131-133], spastic paraparesis, and cauda equina syndrome [134,135].
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within 48 hours of EBP. However, in one prospective observational study of women who underwent EBP for PDPH, back pain lasted from 3 to 100 days (mean 28 days) in 16 percent of patients [113]. <span>Rare complications include misplacement of blood resulting in spinal subdural hematoma [128] or intrathecal injection and arachnoiditis [126,129]. Other rare complications include infection, subdural abscess [130], facial nerve paralysis [113,131-133], spastic paraparesis, and cauda equina syndrome [134,135]. Drug therapy — A number of drugs have been investigated for the treatment of PDPH in small trials and studies, but none have been proven beneficial for this specific indication. Neverth




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Drug therapy — A number of drugs have been investigated for the treatment of PDPH in small trials and studies, but none have been proven beneficial for this specific indication. Nevertheless, oral caffeine is a low-risk option for most patients, and caffeine and oral analgesics are options for the symptomatic treatment of PDPH.
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and arachnoiditis [126,129]. Other rare complications include infection, subdural abscess [130], facial nerve paralysis [113,131-133], spastic paraparesis, and cauda equina syndrome [134,135]. <span>Drug therapy — A number of drugs have been investigated for the treatment of PDPH in small trials and studies, but none have been proven beneficial for this specific indication. Nevertheless, oral caffeine is a low-risk option for most patients, and caffeine and oral analgesics are options for the symptomatic treatment of PDPH. ●Caffeine – Caffeine has commonly been used for treatment of PDPH (sometimes in combination with butalbital and/or acetaminophen), without high-quality supporting evidence [86]. We enco




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Caffeine – Caffeine has commonly been used for treatment of PDPH (sometimes in combination with butalbital and/or acetaminophen), without high-quality supporting evidence [86]. We encourage self-administered oral caffeine in patients who normally drink caffeinated beverages on a daily basis, in order to avoid headache and other symptoms of caffeine withdrawal.
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beneficial for this specific indication. Nevertheless, oral caffeine is a low-risk option for most patients, and caffeine and oral analgesics are options for the symptomatic treatment of PDPH. ●<span>Caffeine – Caffeine has commonly been used for treatment of PDPH (sometimes in combination with butalbital and/or acetaminophen), without high-quality supporting evidence [86]. We encourage self-administered oral caffeine in patients who normally drink caffeinated beverages on a daily basis, in order to avoid headache and other symptoms of caffeine withdrawal. A 2015 systematic review of the literature on drug therapy for PDPH found two small randomized trials (approximately 40 patients in each) that compared oral and IV caffeine with placebo




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Hearing loss may occur after dural puncture, and has been variably reported in up to 10 to 50 percent of patients after spinal anesthesia, though less than 25 percent of these patients are aware of the deficit [153,154]. It may be unilateral or bilateral, and may occur even in the absence of headache.
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ich are activated by dural stretch in PDPH [151,152]. OTHER COMPLICATIONS OF DURAL PUNCTURE — PDPH is the most common adverse outcome of dural puncture and is generally self-limited and benign. <span>Hearing loss may occur after dural puncture, and has been variably reported in up to 10 to 50 percent of patients after spinal anesthesia, though less than 25 percent of these patients are aware of the deficit [153,154]. It may be unilateral or bilateral, and may occur even in the absence of headache. Hearing loss is usually transient, but there are reported cases of hearing loss lasting for years after spinal anesthesia [155], unintentional dural puncture (UDP) [156], and diagnostic




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Injection of air into the subarachnoid space during placement of neuraxial block may result in acute onset of severe headache and other neurologic signs and symptoms [160,161]. This complication may occur with an UDP if air, rather than saline, is used for loss of resistance to identify the epidural space (see "Epidural and combined spinal-epidural anesthesia: Techniques", section on 'Epidural anesthesia technique'). A pneumocephalus headache can occur within a few seconds if the epidural is placed with the patient in the sitting position, but may be delayed until the patient sits up if the epidural is placed in the lateral decubitus position. Regardless of onset delay, the headache is usually maximal at onset (ie, "thunderclap") [162]
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r needle size [158] and cutting needles have been associated with increased incidence of hearing loss [159]. Epidural blood patch (EBP) has been performed with resolution of hearing loss [157]. <span>Injection of air into the subarachnoid space during placement of neuraxial block may result in acute onset of severe headache and other neurologic signs and symptoms [160,161]. This complication may occur with an UDP if air, rather than saline, is used for loss of resistance to identify the epidural space (see "Epidural and combined spinal-epidural anesthesia: Techniques", section on 'Epidural anesthesia technique'). A pneumocephalus headache can occur within a few seconds if the epidural is placed with the patient in the sitting position, but may be delayed until the patient sits up if the epidural is placed in the lateral decubitus position. Regardless of onset delay, the headache is usually maximal at onset (ie, "thunderclap") [162]. Treatment of pneumocephalus headache is symptomatic. Limited data suggest that normobaric oxygen therapy leads to more rapid resolution [163,164]; hyperbaric oxygen therapy may be indi




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In rare cases, dural puncture has been associated with reversible cerebral vasoconstriction syndrome (RCVS) [177,178] and posterior reversible encephalopathy syndrome (PRES) [179-181], but causation is uncertain; several of these reports involved obstetric patients with possible preeclampsia or eclampsia, which are also associated with RCVS and PRES.
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ent for any of these complications. (See "Subdural hematoma in adults: Etiology, clinical features, and diagnosis" and "Cerebral venous thrombosis: Etiology, clinical features, and diagnosis".) <span>In rare cases, dural puncture has been associated with reversible cerebral vasoconstriction syndrome (RCVS) [177,178] and posterior reversible encephalopathy syndrome (PRES) [179-181], but causation is uncertain; several of these reports involved obstetric patients with possible preeclampsia or eclampsia, which are also associated with RCVS and PRES. (See "Reversible cerebral vasoconstriction syndrome", section on 'Risk factors and associated conditions' and "Reversible posterior leukoencephalopathy syndrome", section on 'Related co




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Risk factors – Risk factors for PDPH include patient age (highest among adults 18 to 50 years of age), female gender, pregnancy, possibly prior history of headache, the use of cutting versus pencil point spinal needles, and the use of larger needles. For patients undergoing LP or spinal anesthesia, we recommend performing the procedure with spinal needles that have a pencil point (atraumatic) tip, rather than needles with a sharp cutting tip (Grade 1A).
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approximately 10 percent of patients after dural puncture with a spinal needle, and up to approximately 85 percent of patients who have an UDP with an epidural needle. (See 'Incidence' above.) ●<span>Risk factors – Risk factors for PDPH include patient age (highest among adults 18 to 50 years of age), female gender, pregnancy, possibly prior history of headache, the use of cutting versus pencil point spinal needles, and the use of larger needles. For patients undergoing LP or spinal anesthesia, we recommend performing the procedure with spinal needles that have a pencil point (atraumatic) tip, rather than needles with a sharp cutting tip (Grade 1A). (See 'Risk factors' above.) ●Prevention – Measures to prevent PDPH after dural puncture (eg, bed rest, placement of a spinal catheter after UDP, medications) have not been proven effect




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Prevention – Measures to prevent PDPH after dural puncture (eg, bed rest, placement of a spinal catheter after UDP, medications) have not been proven effective.
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hesia, we recommend performing the procedure with spinal needles that have a pencil point (atraumatic) tip, rather than needles with a sharp cutting tip (Grade 1A). (See 'Risk factors' above.) ●<span>Prevention – Measures to prevent PDPH after dural puncture (eg, bed rest, placement of a spinal catheter after UDP, medications) have not been proven effective. (See 'Prevention of PDPH after dural puncture' above.) ●Clinical features – PDPH is a postural headache (ie, worse when upright, improved when supine) that usually occurs within 72 hour




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Clinical features – PDPH is a postural headache (ie, worse when upright, improved when supine) that usually occurs within 72 hours of dural puncture. In most cases, PDPH resolves within one week, even without treatment. Other causes of headache must be ruled out (table 1).
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o prevent PDPH after dural puncture (eg, bed rest, placement of a spinal catheter after UDP, medications) have not been proven effective. (See 'Prevention of PDPH after dural puncture' above.) ●<span>Clinical features – PDPH is a postural headache (ie, worse when upright, improved when supine) that usually occurs within 72 hours of dural puncture. In most cases, PDPH resolves within one week, even without treatment. Other causes of headache must be ruled out (table 1). (See 'Clinical Features' above and 'Differential diagnosis' above.) ●Diagnosis – The diagnosis of PDPH is made clinically by identifying the typical positional headache within 72 hours




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Treatment – Conservative treatment for patients with mild PDPH includes bed rest and a brief course of oral caffeine and/or oral analgesics. (See 'Mild PDPH' above and 'Drug therapy' above.)

For patients with moderate to severe PDPH that is prolonged (>24 hours) and refractory to conservative measures, we recommend treatment with epidural blood patch (EBP) (Grade 1B).

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ours after a dural puncture. In patients with atypical features, other causes may need to be excluded (table 1 and table 2). (See 'Diagnosis of PDPH' above and 'Differential diagnosis' above.) ●<span>Treatment – Conservative treatment for patients with mild PDPH includes bed rest and a brief course of oral caffeine and/or oral analgesics. (See 'Mild PDPH' above and 'Drug therapy' above.) For patients with moderate to severe PDPH that is prolonged (>24 hours) and refractory to conservative measures, we recommend treatment with epidural blood patch (EBP) (Grade 1B). EBP is performed by injecting autologous blood through an epidural needle immediately after drawing the blood under sterile conditions. (See 'Debilitating PDPH' above and 'Epidural bloo




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Cerebrospinal fluid (CSF) is produced by the choroid plexus in the lateral, third, and fourth ventricles and circulates through the subarachnoid space between the arachnoid mater and the pia mater. The choroid plexus consists of projections of vessels and pia mater that protrude into the ventricular cavities as frond-like villi containing capillaries in loose connective stroma. A specialized layer of ependymal cells called the choroidal epithelium overlies these villi (figure 1)
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ldren is presented elsewhere. (See "Bacterial meningitis in children older than one month: Clinical features and diagnosis", section on 'Interpretation'.) PHYSIOLOGY OF CSF FORMATION AND FLOW — <span>Cerebrospinal fluid (CSF) is produced by the choroid plexus in the lateral, third, and fourth ventricles and circulates through the subarachnoid space between the arachnoid mater and the pia mater. The choroid plexus consists of projections of vessels and pia mater that protrude into the ventricular cavities as frond-like villi containing capillaries in loose connective stroma. A specialized layer of ependymal cells called the choroidal epithelium overlies these villi (figure 1). CSF is formed in the choroid plexus by both filtration and active transport. In normal adults, the CSF volume is 90 to 200 mL [1]; approximately 20 percent of the CSF is contained in t




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In normal adults, the CSF volume is 90 to 200 mL [1]; approximately 20 percent of the CSF is contained in the ventricles; the rest is contained in the subarachnoid space in the cranium and spinal cord. The normal rate of CSF production is approximately 20 mL per hour
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tive stroma. A specialized layer of ependymal cells called the choroidal epithelium overlies these villi (figure 1). CSF is formed in the choroid plexus by both filtration and active transport. <span>In normal adults, the CSF volume is 90 to 200 mL [1]; approximately 20 percent of the CSF is contained in the ventricles; the rest is contained in the subarachnoid space in the cranium and spinal cord. The normal rate of CSF production is approximately 20 mL per hour. CSF circulates from the lateral ventricles though the interventricular foramina of Monro into the third ventricle and then the fourth ventricle via the cerebral aqueduct. Thereafter, C




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CSF circulates from the lateral ventricles though the interventricular foramina of Monro into the third ventricle and then the fourth ventricle via the cerebral aqueduct. Thereafter, CSF passes through median (foramen of Magendie) and lateral (foramina of Luschka) apertures in the fourth ventricle into the subarachnoid space at the base of the brain and then flows over the convexities of the brain and down the length of the spinal cord.
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ent of the CSF is contained in the ventricles; the rest is contained in the subarachnoid space in the cranium and spinal cord. The normal rate of CSF production is approximately 20 mL per hour. <span>CSF circulates from the lateral ventricles though the interventricular foramina of Monro into the third ventricle and then the fourth ventricle via the cerebral aqueduct. Thereafter, CSF passes through median (foramen of Magendie) and lateral (foramina of Luschka) apertures in the fourth ventricle into the subarachnoid space at the base of the brain and then flows over the convexities of the brain and down the length of the spinal cord. The CSF is propelled along the neuroaxis by a cranio-caudal pulsatile wave induced by flow in the cerebral arteries and by the associated expansions of the vascular compartment in the c




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The CSF is propelled along the neuroaxis by a cranio-caudal pulsatile wave induced by flow in the cerebral arteries and by the associated expansions of the vascular compartment in the cranial vault
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amina of Luschka) apertures in the fourth ventricle into the subarachnoid space at the base of the brain and then flows over the convexities of the brain and down the length of the spinal cord. <span>The CSF is propelled along the neuroaxis by a cranio-caudal pulsatile wave induced by flow in the cerebral arteries and by the associated expansions of the vascular compartment in the cranial vault. CSF is reabsorbed in the arachnoid villi, located along the superior sagittal and intracranial venous sinuses and around the spinal nerve roots. Each arachnoid villus functions as a on




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CSF is reabsorbed in the arachnoid villi, located along the superior sagittal and intracranial venous sinuses and around the spinal nerve roots. Each arachnoid villus functions as a one-way valve permitting unidirectional flow of CSF into the blood.
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SF is propelled along the neuroaxis by a cranio-caudal pulsatile wave induced by flow in the cerebral arteries and by the associated expansions of the vascular compartment in the cranial vault. <span>CSF is reabsorbed in the arachnoid villi, located along the superior sagittal and intracranial venous sinuses and around the spinal nerve roots. Each arachnoid villus functions as a one-way valve permitting unidirectional flow of CSF into the blood. Arachnoid villi and venous sinuses are separated by endothelial cells connected by tight junctions (figure 1). Arachnoid villi normally allow the passage of particles less than 7.5 micr




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Arachnoid villi and venous sinuses are separated by endothelial cells connected by tight junctions ( figure 1). Arachnoid villi normally allow the passage of particles less than 7.5 micron in diameter from the CSF into the blood
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the superior sagittal and intracranial venous sinuses and around the spinal nerve roots. Each arachnoid villus functions as a one-way valve permitting unidirectional flow of CSF into the blood. <span>Arachnoid villi and venous sinuses are separated by endothelial cells connected by tight junctions (figure 1). Arachnoid villi normally allow the passage of particles less than 7.5 micron in diameter from the CSF into the blood. Movement of CSF and cellular components across arachnoid villi occurs via transport within giant vesicles. These vesicles may become obstructed by bacteria or cells as a result of an i




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Movement of CSF and cellular components across arachnoid villi occurs via transport within giant vesicles. These vesicles may become obstructed by bacteria or cells as a result of an inflammatory process or by red blood cells during subarachnoid hemorrhage
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are separated by endothelial cells connected by tight junctions (figure 1). Arachnoid villi normally allow the passage of particles less than 7.5 micron in diameter from the CSF into the blood. <span>Movement of CSF and cellular components across arachnoid villi occurs via transport within giant vesicles. These vesicles may become obstructed by bacteria or cells as a result of an inflammatory process or by red blood cells during subarachnoid hemorrhage. Lipid-soluble molecules or drugs readily diffuse across the vascular endothelium and epithelium of the choroid plexus into the interstitial fluid and CSF. In contrast, ionically charge




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Lipid-soluble molecules or drugs readily diffuse across the vascular endothelium and epithelium of the choroid plexus into the interstitial fluid and CSF. In contrast, ionically charged molecules generally require active transport for entry into the CSF. Drug entry also may be altered in patients with meningitis by the accompanying inflammation, and this may subsequently rapidly change with regression of this inflammation with therapy.
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ccurs via transport within giant vesicles. These vesicles may become obstructed by bacteria or cells as a result of an inflammatory process or by red blood cells during subarachnoid hemorrhage. <span>Lipid-soluble molecules or drugs readily diffuse across the vascular endothelium and epithelium of the choroid plexus into the interstitial fluid and CSF. In contrast, ionically charged molecules generally require active transport for entry into the CSF. Drug entry also may be altered in patients with meningitis by the accompanying inflammation, and this may subsequently rapidly change with regression of this inflammation with therapy. (See 'CSF in CNS infection' below.) In addition to these well-described transport mechanisms, newer studies have documented the existence of other pathways involved in the movement of C




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The finding of dura-associated lymphatic vessels is contrary to long-held beliefs about the absence of meningeal lymphatics. The role of these lymphatic pathways, however, in the clearance of interstitial and CSF solutes has not yet been elucidated
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tes from the brain to the CSF and extra-axial meningeal lymphatic vessels associated with the dural sinuses that facilitate the movement of solutes in the CSF into the systemic vascular system. <span>The finding of dura-associated lymphatic vessels is contrary to long-held beliefs about the absence of meningeal lymphatics. The role of these lymphatic pathways, however, in the clearance of interstitial and CSF solutes has not yet been elucidated. CSF PRESSURE — Cerebrospinal fluid (CSF) secretion and reabsorption remain in balance in most healthy individuals to maintain a CSF pressure less than 15 cmH2O. The normal CSF pressure




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Cerebrospinal fluid (CSF) secretion and reabsorption remain in balance in most healthy individuals to maintain a CSF pressure less than 15 cmH2O. The normal CSF pressure as measured with a manometer in a patient lying flat in the lateral decubitus position with the legs extended is between 6 and 25 cmH2O [3]; however, some experts consider the upper limit of normal CSF pressure to be 20 cmH2O (figure 2) [4].
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ld beliefs about the absence of meningeal lymphatics. The role of these lymphatic pathways, however, in the clearance of interstitial and CSF solutes has not yet been elucidated. CSF PRESSURE — <span>Cerebrospinal fluid (CSF) secretion and reabsorption remain in balance in most healthy individuals to maintain a CSF pressure less than 15 cmH2O. The normal CSF pressure as measured with a manometer in a patient lying flat in the lateral decubitus position with the legs extended is between 6 and 25 cmH2O [3]; however, some experts consider the upper limit of normal CSF pressure to be 20 cmH2O (figure 2) [4]. A variety of factors, such as the patient's position, the skill of the person performing the lumbar puncture, and the patient’s degree of relaxation, can affect the measurement of the o




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A variety of factors, such as the patient's position, the skill of the person performing the lumbar puncture, and the patient’s degree of relaxation, can affect the measurement of the opening pressure
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flat in the lateral decubitus position with the legs extended is between 6 and 25 cmH2O [3]; however, some experts consider the upper limit of normal CSF pressure to be 20 cmH2O (figure 2) [4]. <span>A variety of factors, such as the patient's position, the skill of the person performing the lumbar puncture, and the patient’s degree of relaxation, can affect the measurement of the opening pressure. Patients with obesity tend to have higher opening pressures; however, the correlation between opening pressure and body mass index was weak in a study involving 242 outpatients with a




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Slow-growing masses, such as abscesses or tumors, may allow time for compensation between CSF secretion and absorption to occur; thus, a rise in CSF pressure may not occur until the normal compliance of the intracranial structures is overcome. In contrast, acute infections, such as meningitis, typically lead to rapid increases in CSF pressure due to alterations in either production or reabsorption of CSF, or as a result of cerebral edema.
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atory mechanisms develop. Processes, such as infection, bleeding, or a tumor, can alter the balance between CSF secretion and reabsorption and have potential to cause intracranial hypertension. <span>Slow-growing masses, such as abscesses or tumors, may allow time for compensation between CSF secretion and absorption to occur; thus, a rise in CSF pressure may not occur until the normal compliance of the intracranial structures is overcome. In contrast, acute infections, such as meningitis, typically lead to rapid increases in CSF pressure due to alterations in either production or reabsorption of CSF, or as a result of cerebral edema. (See "Neurologic complications of bacterial meningitis in adults", section on 'Increased intracranial pressure'.) Intracranial hypertension may cause downward and backward shifting of t




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There are actually two barriers: a blood-brain barrier and a blood-CSF barrier.
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hat separate the brain and the cerebrospinal fluid (CSF) from the blood and prevent entry by simple diffusion of fluids, electrolytes, and other substances from blood into the CSF or brain [6]. <span>There are actually two barriers: a blood-brain barrier and a blood-CSF barrier. Both barriers separate the central nervous system (CNS) from systemic immune responses and affect the composition of the brain interstitial fluid and CSF. The blood-brain and the blood-




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The blood-brain and the blood-CSF barriers are not precisely equivalent [ 6].
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brain barrier and a blood-CSF barrier. Both barriers separate the central nervous system (CNS) from systemic immune responses and affect the composition of the brain interstitial fluid and CSF. <span>The blood-brain and the blood-CSF barriers are not precisely equivalent [6]. Blood-brain barrier — The blood-brain barrier controls the content of brain interstitial fluid. It has a 5000-fold greater surface area than the blood-CSF barrier [6]. The anatomic basi




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Blood-brain barrier — The blood-brain barrier controls the content of brain interstitial fluid. It has a 5000-fold greater surface area than the blood-CSF barrier [6]. The anatomic basis for the blood-brain barrier is a series of high-resistance, tight junctions between endothelial cells as well as astrocytes with processes that terminate in overlapping fashion on capillary walls.

Lipid-soluble small molecules with a molecular mass less than 400 to 600 Da are transported readily through the blood-brain barrier. In contrast, many drugs and other small molecules cannot cross this barrier system [7].

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vous system (CNS) from systemic immune responses and affect the composition of the brain interstitial fluid and CSF. The blood-brain and the blood-CSF barriers are not precisely equivalent [6]. <span>Blood-brain barrier — The blood-brain barrier controls the content of brain interstitial fluid. It has a 5000-fold greater surface area than the blood-CSF barrier [6]. The anatomic basis for the blood-brain barrier is a series of high-resistance, tight junctions between endothelial cells as well as astrocytes with processes that terminate in overlapping fashion on capillary walls. Lipid-soluble small molecules with a molecular mass less than 400 to 600 Da are transported readily through the blood-brain barrier. In contrast, many drugs and other small molecules cannot cross this barrier system [7]. Blood-CSF barrier — The blood-CSF barrier controls the composition of the CSF, which, as noted above, is primarily dependent upon secretion in the choroid plexus. The blood-CSF barrier




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Blood-CSF barrier — The blood-CSF barrier controls the composition of the CSF, which, as noted above, is primarily dependent upon secretion in the choroid plexus. The blood-CSF barrier is formed by tight junctions between choroid epithelial cells.

Both barrier systems are dynamic. Endothelial cells and astrocytes that compose the blood-brain barrier and cells forming the blood-CSF barrier are capable of producing cytokines such as tumor necrosis factor and interleukins. In addition, astrocytes can act as antigen-presenting cells that modulate the immunologic response to CNS infections. Release of cytokines from endothelial cells and astrocytes probably mediate or generate much of the CNS inflammatory response in infectious and noninfectious conditions.

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es with a molecular mass less than 400 to 600 Da are transported readily through the blood-brain barrier. In contrast, many drugs and other small molecules cannot cross this barrier system [7]. <span>Blood-CSF barrier — The blood-CSF barrier controls the composition of the CSF, which, as noted above, is primarily dependent upon secretion in the choroid plexus. The blood-CSF barrier is formed by tight junctions between choroid epithelial cells. Both barrier systems are dynamic. Endothelial cells and astrocytes that compose the blood-brain barrier and cells forming the blood-CSF barrier are capable of producing cytokines such as tumor necrosis factor and interleukins. In addition, astrocytes can act as antigen-presenting cells that modulate the immunologic response to CNS infections. Release of cytokines from endothelial cells and astrocytes probably mediate or generate much of the CNS inflammatory response in infectious and noninfectious conditions. A brain-CSF barrier also exists in the pia mater. A continuous layer of astrocytes overlies the basement membrane of cells in the pia mater. These astrocytes are separated by gap juncti




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Normal cerebrospinal fluid (CSF) is clear and colorless. Both infectious and noninfectious processes can alter the appearance of the CSF.
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ion of the pathogenesis of bacterial meningitis is presented in a separate topic review. (See "Pathogenesis and pathophysiology of bacterial meningitis".) COMPOSITION OF THE CSF Xanthochromia — <span>Normal cerebrospinal fluid (CSF) is clear and colorless. Both infectious and noninfectious processes can alter the appearance of the CSF. As few as 200 white blood cells (WBCs)/microL or 400 red blood cells (RBCs)/microL will cause CSF to appear turbid. CSF will appear grossly bloody if ≥6000 RBCs/microL are present [4].




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As few as 200 white blood cells (WBCs)/microL or 400 red blood cells (RBCs)/microL will cause CSF to appear turbid. CSF will appear grossly bloody if ≥6000 RBCs/microL are present [ 4]
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al meningitis".) COMPOSITION OF THE CSF Xanthochromia — Normal cerebrospinal fluid (CSF) is clear and colorless. Both infectious and noninfectious processes can alter the appearance of the CSF. <span>As few as 200 white blood cells (WBCs)/microL or 400 red blood cells (RBCs)/microL will cause CSF to appear turbid. CSF will appear grossly bloody if ≥6000 RBCs/microL are present [4]. Red blood cells rapidly lyse after entry into CSF. The breakdown of hemoglobin first to oxyhemoglobin (pink) and later to bilirubin (yellow) leads to a yellow or pink discoloration of




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Red blood cells rapidly lyse after entry into CSF. The breakdown of hemoglobin first to oxyhemoglobin (pink) and later to bilirubin (yellow) leads to a yellow or pink discoloration of the CSF known as xanthochromia. Spectrophotometry can be used to analyze blood breakdown products as they progress from oxyhemoglobin to methemoglobin and finally to bilirubin, thereby ruling out traumatic blood [13-15].
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the CSF. As few as 200 white blood cells (WBCs)/microL or 400 red blood cells (RBCs)/microL will cause CSF to appear turbid. CSF will appear grossly bloody if ≥6000 RBCs/microL are present [4]. <span>Red blood cells rapidly lyse after entry into CSF. The breakdown of hemoglobin first to oxyhemoglobin (pink) and later to bilirubin (yellow) leads to a yellow or pink discoloration of the CSF known as xanthochromia. Spectrophotometry can be used to analyze blood breakdown products as they progress from oxyhemoglobin to methemoglobin and finally to bilirubin, thereby ruling out traumatic blood [13-15]. Although xanthochromia is generally confirmed visually [16], laboratory confirmation with spectrophotometry may be more sensitive and, if available, is recommended by some experts [13,1




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Xanthochromia can be detected as soon as two to four hours after RBCs have entered the subarachnoid space, and therefore this is often used in the diagnosis of subarachnoid hemorrhage (SAH). Xanthochromia is present in over 90 percent of patients with a subarachnoid hemorrhage within 12 hours of the onset of bleeding, and it may persist thereafter for two to four weeks [13,19-21].
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. Although xanthochromia is generally confirmed visually [16], laboratory confirmation with spectrophotometry may be more sensitive and, if available, is recommended by some experts [13,17,18]. <span>Xanthochromia can be detected as soon as two to four hours after RBCs have entered the subarachnoid space, and therefore this is often used in the diagnosis of subarachnoid hemorrhage (SAH). Xanthochromia is present in over 90 percent of patients with a subarachnoid hemorrhage within 12 hours of the onset of bleeding, and it may persist thereafter for two to four weeks [13,19-21]. The use of xanthochromia and RBC count to distinguish SAH from traumatic tap is discussed separately. (See "Aneurysmal subarachnoid hemorrhage: Clinical manifestations and diagnosis", s




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The use of xanthochromia and RBC count to distinguish SAH from traumatic tap is discussed separately. (See "Aneurysmal subarachnoid hemorrhage: Clinical manifestations and diagnosis", section on 'Lumbar puncture'.)
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Xanthochromia is present in over 90 percent of patients with a subarachnoid hemorrhage within 12 hours of the onset of bleeding, and it may persist thereafter for two to four weeks [13,19-21]. <span>The use of xanthochromia and RBC count to distinguish SAH from traumatic tap is discussed separately. (See "Aneurysmal subarachnoid hemorrhage: Clinical manifestations and diagnosis", section on 'Lumbar puncture'.) Xanthochromia can also occur with increased CSF concentrations of protein (≥150 mg/dL) or systemic hyperbilirubinemia (serum bilirubin >10 to 15 mg/dL) [4]. Cells Normal findings — T




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Xanthochromia can also occur with increased CSF concentrations of protein (≥150 mg/dL) or systemic hyperbilirubinemia (serum bilirubin >10 to 15 mg/dL) [4].
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mia and RBC count to distinguish SAH from traumatic tap is discussed separately. (See "Aneurysmal subarachnoid hemorrhage: Clinical manifestations and diagnosis", section on 'Lumbar puncture'.) <span>Xanthochromia can also occur with increased CSF concentrations of protein (≥150 mg/dL) or systemic hyperbilirubinemia (serum bilirubin >10 to 15 mg/dL) [4]. Cells Normal findings — The CSF is normally acellular. However, up to 5 WBCs and 5 RBCs are considered normal in adults when the CSF is sampled by lumbar puncture (LP). More than 3 poly




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Normal findings — The CSF is normally acellular. However, up to 5 WBCs and 5 RBCs are considered normal in adults when the CSF is sampled by lumbar puncture (LP). More than 3 polymorphonuclear leukocytes (PMNs)/microL are abnormal in adults. The CSF cell profiles in neonates and children are discussed separately.
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tion on 'Lumbar puncture'.) Xanthochromia can also occur with increased CSF concentrations of protein (≥150 mg/dL) or systemic hyperbilirubinemia (serum bilirubin >10 to 15 mg/dL) [4]. Cells <span>Normal findings — The CSF is normally acellular. However, up to 5 WBCs and 5 RBCs are considered normal in adults when the CSF is sampled by lumbar puncture (LP). More than 3 polymorphonuclear leukocytes (PMNs)/microL are abnormal in adults. The CSF cell profiles in neonates and children are discussed separately. (See "Bacterial meningitis in the neonate: Clinical features and diagnosis", section on 'Cell count' and "Bacterial meningitis in children older than one month: Clinical features and di




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The CSF cell count determination should be performed promptly since the count may be falsely low if measured more than 60 minutes after the LP is performed. This spuriously low cell count may be due to settling of the cells in the CSF over time and/or adherence of RBCs or PMNs to plastic tubes
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he neonate: Clinical features and diagnosis", section on 'Cell count' and "Bacterial meningitis in children older than one month: Clinical features and diagnosis", section on 'Interpretation'.) <span>The CSF cell count determination should be performed promptly since the count may be falsely low if measured more than 60 minutes after the LP is performed. This spuriously low cell count may be due to settling of the cells in the CSF over time and/or adherence of RBCs or PMNs to plastic tubes. Pleocytosis — An elevated CSF WBC concentration does not diagnose an infection, since increases in the CSF WBC concentration can occur in infectious and noninfectious inflammatory stat




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The CSF cell count must always be correlated with clinical findings. PMNs, for example, predominate in the CSF of as many as two-thirds of patients with meningitis due to enteroviruses; a shift to lymphocytic predominance usually occurs within 12 to 24 hours [22,23]. On the other hand, lymphocytes rarely predominate in the early phases of bacterial meningitis
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on, since increases in the CSF WBC concentration can occur in infectious and noninfectious inflammatory states. The following truisms about the interpretation of CSF cell counts may be useful: ●<span>The CSF cell count must always be correlated with clinical findings. PMNs, for example, predominate in the CSF of as many as two-thirds of patients with meningitis due to enteroviruses; a shift to lymphocytic predominance usually occurs within 12 to 24 hours [22,23]. On the other hand, lymphocytes rarely predominate in the early phases of bacterial meningitis. (See "Aseptic meningitis in adults" and 'CSF in CNS infection' below.) ●The presence of eosinophils in the CSF has limited diagnostic utility. CSF eosinophilia may occur in parasitic i




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The presence of eosinophils in the CSF has limited diagnostic utility. CSF eosinophilia may occur in parasitic infestations but also in infections due to other microorganisms, including Mycobacterium tuberculosis, Mycoplasma pneumoniae, Rickettsia rickettsii, some fungi, and in noninfectious conditions, such as lymphomas, leukemias of various types, subarachnoid hemorrhage, and obstructive hydrocephalus
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in 12 to 24 hours [22,23]. On the other hand, lymphocytes rarely predominate in the early phases of bacterial meningitis. (See "Aseptic meningitis in adults" and 'CSF in CNS infection' below.) ●<span>The presence of eosinophils in the CSF has limited diagnostic utility. CSF eosinophilia may occur in parasitic infestations but also in infections due to other microorganisms, including Mycobacterium tuberculosis, Mycoplasma pneumoniae, Rickettsia rickettsii, some fungi, and in noninfectious conditions, such as lymphomas, leukemias of various types, subarachnoid hemorrhage, and obstructive hydrocephalus. Predicted WBC count after traumatic tap — Accidental trauma to a capillary or venule may occur during performance of an LP, increasing the number of both RBCs and WBCs in the CSF. If a




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If a traumatic lumbar puncture is suspected and the peripheral WBC count is not abnormally low or high, a good rule of thumb for estimating the adjusted WBC count is to subtract 1 WBC for every 500 to 1500 RBCs measured in the CSF. The formula in the following Calculator can also be used to determine the adjusted WBC count in the presence of CSF RBCs (calculator 1) [24,25].
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ydrocephalus. Predicted WBC count after traumatic tap — Accidental trauma to a capillary or venule may occur during performance of an LP, increasing the number of both RBCs and WBCs in the CSF. <span>If a traumatic lumbar puncture is suspected and the peripheral WBC count is not abnormally low or high, a good rule of thumb for estimating the adjusted WBC count is to subtract 1 WBC for every 500 to 1500 RBCs measured in the CSF. The formula in the following Calculator can also be used to determine the adjusted WBC count in the presence of CSF RBCs (calculator 1) [24,25]. The interpretation of CSF pleocytosis in the setting of bacterial meningitis is discussed in detail separately. The presence or absence of otherwise unexplained xanthochromia also may h




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The presence or absence of otherwise unexplained xanthochromia also may help distinguish a traumatic tap from subarachnoid hemorrhage as long as the LP is performed at least six hours after the onset of headache.
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ermine the adjusted WBC count in the presence of CSF RBCs (calculator 1) [24,25]. The interpretation of CSF pleocytosis in the setting of bacterial meningitis is discussed in detail separately. <span>The presence or absence of otherwise unexplained xanthochromia also may help distinguish a traumatic tap from subarachnoid hemorrhage as long as the LP is performed at least six hours after the onset of headache. (See 'Xanthochromia' above.) Interpretation of traumatic LPs in children is discussed separately. (See "Bacterial meningitis in children older than one month: Clinical features and diag




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Proteins are largely excluded from the CSF by the blood-CSF barrier. Proteins gaining access to the CSF primarily reach the CSF by transport within pinocytotic vesicles traversing capillary endothelial cells.
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diagnosis", section on 'Interpretation'.) Chemical composition — Determination of CSF protein and glucose concentrations are routinely done and may reveal useful clinical information. Protein — <span>Proteins are largely excluded from the CSF by the blood-CSF barrier. Proteins gaining access to the CSF primarily reach the CSF by transport within pinocytotic vesicles traversing capillary endothelial cells. The normal CSF protein concentration ranges from 23 to 38 mg/dL (0.23 to 0.38 g/L) in adults [4]; in one report, the extreme upper and lower CSF protein concentrations in normal individ




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The normal CSF protein concentration ranges from 23 to 38 mg/dL (0.23 to 0.38 g/L) in adults [ 4]; in one report, the extreme upper and lower CSF protein concentrations in normal individuals were 58 and 9 mg/dL (0.58 and 0.09 g/L), respectively [21]
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rgely excluded from the CSF by the blood-CSF barrier. Proteins gaining access to the CSF primarily reach the CSF by transport within pinocytotic vesicles traversing capillary endothelial cells. <span>The normal CSF protein concentration ranges from 23 to 38 mg/dL (0.23 to 0.38 g/L) in adults [4]; in one report, the extreme upper and lower CSF protein concentrations in normal individuals were 58 and 9 mg/dL (0.58 and 0.09 g/L), respectively [21]. CSF protein concentrations in premature and term neonates normally range between 20 and 170 mg/dL (0.2 and 1.7 g/L) [26]. The CSF protein concentration may be mildly elevated in patien




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The CSF protein concentration may be mildly elevated in patients with diabetes mellitus
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individuals were 58 and 9 mg/dL (0.58 and 0.09 g/L), respectively [21]. CSF protein concentrations in premature and term neonates normally range between 20 and 170 mg/dL (0.2 and 1.7 g/L) [26]. <span>The CSF protein concentration may be mildly elevated in patients with diabetes mellitus. CSF protein can also be elevated by a subarachnoid hemorrhage or a traumatic LP. The presence of CSF bleeding results in approximately 1 mg of protein/dL per 1000 RBCs/microL. When ass




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The presence of CSF bleeding results in approximately 1 mg of protein/dL per 1000 RBCs/microL
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(0.2 and 1.7 g/L) [26]. The CSF protein concentration may be mildly elevated in patients with diabetes mellitus. CSF protein can also be elevated by a subarachnoid hemorrhage or a traumatic LP. <span>The presence of CSF bleeding results in approximately 1 mg of protein/dL per 1000 RBCs/microL. When assessing the potential effect of CSF bleeding on an elevated CSF protein concentration, the CSF protein concentration and RBC count should be performed on the same tube of CSF. E




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CSF protein elevations may persist for weeks or months following recovery from meningitis and have little utility in assessing cure or the response to therapy [27].
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med on the same tube of CSF. Elevations in the CSF protein concentration can occur in both infectious and noninfectious conditions, including conditions associated with obstruction of CSF flow. <span>CSF protein elevations may persist for weeks or months following recovery from meningitis and have little utility in assessing cure or the response to therapy [27]. (See 'CSF in CNS infection' below.) Immunoglobulins and oligoclonal bands — Immunoglobulins are almost totally excluded from the CSF in healthy individuals. The blood to CSF ratio of Ig




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Elevations in the CSF protein concentration can occur in both infectious and noninfectious conditions, including conditions associated with obstruction of CSF flow.
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Cs/microL. When assessing the potential effect of CSF bleeding on an elevated CSF protein concentration, the CSF protein concentration and RBC count should be performed on the same tube of CSF. <span>Elevations in the CSF protein concentration can occur in both infectious and noninfectious conditions, including conditions associated with obstruction of CSF flow. CSF protein elevations may persist for weeks or months following recovery from meningitis and have little utility in assessing cure or the response to therapy [27]. (See 'CSF in CNS inf




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Immunoglobulins are almost totally excluded from the CSF in healthy individuals. The blood to CSF ratio of IgG is normally 500:1 or more.
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months following recovery from meningitis and have little utility in assessing cure or the response to therapy [27]. (See 'CSF in CNS infection' below.) Immunoglobulins and oligoclonal bands — <span>Immunoglobulins are almost totally excluded from the CSF in healthy individuals. The blood to CSF ratio of IgG is normally 500:1 or more. Elevations in oligoclonally expanded immunoglobulin concentrations in the CSF, termed oligoclonal bands, may occur in any disorder that disrupts the blood-brain barrier. Oligoclonal ban




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Elevations in oligoclonally expanded immunoglobulin concentrations in the CSF, termed oligoclonal bands, may occur in any disorder that disrupts the blood-brain barrier.
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ection' below.) Immunoglobulins and oligoclonal bands — Immunoglobulins are almost totally excluded from the CSF in healthy individuals. The blood to CSF ratio of IgG is normally 500:1 or more. <span>Elevations in oligoclonally expanded immunoglobulin concentrations in the CSF, termed oligoclonal bands, may occur in any disorder that disrupts the blood-brain barrier. Oligoclonal bands may also be caused by intrathecal production of IgG, and the presence of such bands is a diagnostic criterion for multiple sclerosis [28]. Examples of other diseases t




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Oligoclonal bands may also be caused by intrathecal production of IgG, and the presence of such bands is a diagnostic criterion for multiple sclerosis [ 28]. Examples of other diseases that can cause oligoclonal bands in the CSF include infections (eg, nervous system Lyme disease), autoimmune diseases, brain tumors, and lymphoproliferative diseases. Given how many diseases can result in oligoclonal bands in the CSF, the diagnostic utility of this finding is limited.
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normally 500:1 or more. Elevations in oligoclonally expanded immunoglobulin concentrations in the CSF, termed oligoclonal bands, may occur in any disorder that disrupts the blood-brain barrier. <span>Oligoclonal bands may also be caused by intrathecal production of IgG, and the presence of such bands is a diagnostic criterion for multiple sclerosis [28]. Examples of other diseases that can cause oligoclonal bands in the CSF include infections (eg, nervous system Lyme disease), autoimmune diseases, brain tumors, and lymphoproliferative diseases. Given how many diseases can result in oligoclonal bands in the CSF, the diagnostic utility of this finding is limited. (See "Nervous system Lyme disease", section on 'Cerebrospinal fluid analysis' and "Evaluation and diagnosis of multiple sclerosis in adults", section on 'CSF analysis and oligoclonal ba




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Low CSF glucose concentration (hypoglycorrhachia) may occur in a variety of infectious and noninfectious pathologic conditions. Elevated CSF glucose concentrations only occur in the setting of hyperglycemia
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rvous system Lyme disease", section on 'Cerebrospinal fluid analysis' and "Evaluation and diagnosis of multiple sclerosis in adults", section on 'CSF analysis and oligoclonal bands'.) Glucose — <span>Low CSF glucose concentration (hypoglycorrhachia) may occur in a variety of infectious and noninfectious pathologic conditions. Elevated CSF glucose concentrations only occur in the setting of hyperglycemia. ●CSF glucose concentrations less than 18 mg/dL (1.0 mmol/L) are strongly predictive of bacterial meningitis [27]. Abnormally low CSF glucose concentrations can also occur in mycobacter




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CSF glucose concentrations less than 18 mg/dL (1.0 mmol/L) are strongly predictive of bacterial meningitis [27]. Abnormally low CSF glucose concentrations can also occur in mycobacterial, mycoplasmal (M. pneumoniae), treponemal, and fungal CNS infections (table 1). During recovery from meningitis, CSF glucose concentration tends to normalize more rapidly than the CSF cell count and protein concentration.
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concentration (hypoglycorrhachia) may occur in a variety of infectious and noninfectious pathologic conditions. Elevated CSF glucose concentrations only occur in the setting of hyperglycemia. ●<span>CSF glucose concentrations less than 18 mg/dL (1.0 mmol/L) are strongly predictive of bacterial meningitis [27]. Abnormally low CSF glucose concentrations can also occur in mycobacterial, mycoplasmal (M. pneumoniae), treponemal, and fungal CNS infections (table 1). During recovery from meningitis, CSF glucose concentration tends to normalize more rapidly than the CSF cell count and protein concentration. (See 'CSF in CNS infection' below.) In contrast, the CSF glucose concentration is typically normal during most viral CNS infections, although low concentrations have been reported in pa




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In contrast, the CSF glucose concentration is typically normal during most viral CNS infections, although low concentrations have been reported in patients with meningoencephalitis due to mumps, enteroviruses, lymphocytic choriomeningitis (LCM), herpes simplex, and herpes zoster viruses
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ions (table 1). During recovery from meningitis, CSF glucose concentration tends to normalize more rapidly than the CSF cell count and protein concentration. (See 'CSF in CNS infection' below.) <span>In contrast, the CSF glucose concentration is typically normal during most viral CNS infections, although low concentrations have been reported in patients with meningoencephalitis due to mumps, enteroviruses, lymphocytic choriomeningitis (LCM), herpes simplex, and herpes zoster viruses. ●Low CSF glucose concentrations can also occur in noninfectious conditions; patients with leptomeningeal carcinomatosis, leukemia, CNS lymphoma, severe subarachnoid hemorrhages, or neu




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Low CSF glucose concentrations can also occur in noninfectious conditions; patients with leptomeningeal carcinomatosis, leukemia, CNS lymphoma, severe subarachnoid hemorrhages, or neurosarcoidosis may have hypoglycorrhachia because of cellular or inflammatory infiltrates that disrupt the active transport of glucose into the CSF (table 1) [29].
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although low concentrations have been reported in patients with meningoencephalitis due to mumps, enteroviruses, lymphocytic choriomeningitis (LCM), herpes simplex, and herpes zoster viruses. ●<span>Low CSF glucose concentrations can also occur in noninfectious conditions; patients with leptomeningeal carcinomatosis, leukemia, CNS lymphoma, severe subarachnoid hemorrhages, or neurosarcoidosis may have hypoglycorrhachia because of cellular or inflammatory infiltrates that disrupt the active transport of glucose into the CSF (table 1) [29]. Salicylate poisoning has been reported to cause low CSF glucose concentration, but this has not been well-documented, and this association is speculative [30-32]. Also, hypoglycemic pat




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The normal CSF-to-serum glucose ratio ranges from 0.5 to 0.8 [33-35], and shows large hourly diurnal variations related to timing of food intake [36]
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ellitus: Clinical manifestations, diagnosis, and causes"). In the setting of hyperglycemia, a low CSF glucose may not be recognized if only the absolute CSF glucose concentration is considered. <span>The normal CSF-to-serum glucose ratio ranges from 0.5 to 0.8 [33-35], and shows large hourly diurnal variations related to timing of food intake [36]. Attempts to "correct" the CSF glucose concentration for hyperglycemia should take into account the fact that it takes several hours for the serum glucose to equilibrate with the CSF gl




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Attempts to "correct" the CSF glucose concentration for hyperglycemia should take into account the fact that it takes several hours for the serum glucose to equilibrate with the CSF glucose; thus the timing of the last meal and/or administration of insulin or oral hypoglycemic may be relevant [ 36].
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e CSF glucose concentration is considered. The normal CSF-to-serum glucose ratio ranges from 0.5 to 0.8 [33-35], and shows large hourly diurnal variations related to timing of food intake [36]. <span>Attempts to "correct" the CSF glucose concentration for hyperglycemia should take into account the fact that it takes several hours for the serum glucose to equilibrate with the CSF glucose; thus the timing of the last meal and/or administration of insulin or oral hypoglycemic may be relevant [36]. Other considerations include that CSF-to-serum glucose ratios in neonates are highly variable and also that ventricular CSF glucose concentration is 6 to 18 mg/dL (0.33 to 1.0 mmol/L) h




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Other considerations include that CSF-to-serum glucose ratios in neonates are highly variable and also that ventricular CSF glucose concentration is 6 to 18 mg/dL (0.33 to 1.0 mmol/L) higher than in the lumbar CSF [ 37]
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at it takes several hours for the serum glucose to equilibrate with the CSF glucose; thus the timing of the last meal and/or administration of insulin or oral hypoglycemic may be relevant [36]. <span>Other considerations include that CSF-to-serum glucose ratios in neonates are highly variable and also that ventricular CSF glucose concentration is 6 to 18 mg/dL (0.33 to 1.0 mmol/L) higher than in the lumbar CSF [37]. In addition, CSF glucose levels rarely exceed 300 mg/dL (16.7 mmol/L) even in patients with severe hyperglycemia. Lactate — Determination of the CSF lactate concentration has been sugg




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In addition, CSF glucose levels rarely exceed 300 mg/dL (16.7 mmol/L) even in patients with severe hyperglycemia
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de that CSF-to-serum glucose ratios in neonates are highly variable and also that ventricular CSF glucose concentration is 6 to 18 mg/dL (0.33 to 1.0 mmol/L) higher than in the lumbar CSF [37]. <span>In addition, CSF glucose levels rarely exceed 300 mg/dL (16.7 mmol/L) even in patients with severe hyperglycemia. Lactate — Determination of the CSF lactate concentration has been suggested as a useful test to differentiate bacterial from viral meningitis. Two meta-analyses that included 25 studie




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Cytology is occasionally useful for the diagnosis of malignancy involving the CNS [40]. In such instances, at least 10 to 15 mL of fluid should be sent to the pathology laboratory for prompt examination. Cytology should be performed within one hour of collection in specialized laboratories with experienced staff [41].
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], although sensitivity was lower in patients who received antimicrobial treatment prior to lumbar puncture [39], and CSF lactate may be elevated in patients with other CNS diseases. Cytology — <span>Cytology is occasionally useful for the diagnosis of malignancy involving the CNS [40]. In such instances, at least 10 to 15 mL of fluid should be sent to the pathology laboratory for prompt examination. Cytology should be performed within one hour of collection in specialized laboratories with experienced staff [41]. CSF IN CNS INFECTION — Chemical analysis and Gram stain of the cerebrospinal fluid (CSF) are an integral part of the evaluation of patients with suspected meningitis or encephalitis. Al




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Among patients with viral meningitis, the typical findings include:

● The CSF white blood cell (WBC) count is usually less than 250/microL and almost always less than 2000/microL [27]. The differential typically shows a predominance of lymphocytes, although early infection may reveal a predominance of neutrophils that, within the next 24 hours, generally shows a shift from neutrophils to lymphocytes [23].

● The CSF protein concentration is typically less than 150 mg/dL; it has been estimated that CSF protein concentrations greater than 220 mg/dL reduce the probability of viral infection to 1 percent or less [27].

● The CSF glucose concentration is usually more than 50 percent of serum concentration, but moderately reduced values are occasionally seen with herpes simplex virus (HSV), mumps, some enteroviruses, and lymphocytic choriomeningitis virus

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bacterial and viral infections (table 2). (See "Clinical features and diagnosis of acute bacterial meningitis in adults" and "Viral encephalitis in adults" and "Aseptic meningitis in adults".) <span>Among patients with viral meningitis, the typical findings include: ●The CSF white blood cell (WBC) count is usually less than 250/microL and almost always less than 2000/microL [27]. The differential typically shows a predominance of lymphocytes, although early infection may reveal a predominance of neutrophils that, within the next 24 hours, generally shows a shift from neutrophils to lymphocytes [23]. ●The CSF protein concentration is typically less than 150 mg/dL; it has been estimated that CSF protein concentrations greater than 220 mg/dL reduce the probability of viral infection to 1 percent or less [27]. ●The CSF glucose concentration is usually more than 50 percent of serum concentration, but moderately reduced values are occasionally seen with herpes simplex virus (HSV), mumps, some enteroviruses, and lymphocytic choriomeningitis virus. Among patients with bacterial meningitis, the classic findings are (table 2): ●A CSF WBC count above 1000/microL, usually with a neutrophilic predominance ●A CSF protein concentration




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Among patients with bacterial meningitis, the classic findings are (table 2):

● A CSF WBC count above 1000/microL, usually with a neutrophilic predominance

● A CSF protein concentration above 250 mg/dL

● A CSF glucose concentration below 45 mg/dL (2.5 mmol/L)

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e than 50 percent of serum concentration, but moderately reduced values are occasionally seen with herpes simplex virus (HSV), mumps, some enteroviruses, and lymphocytic choriomeningitis virus. <span>Among patients with bacterial meningitis, the classic findings are (table 2): ●A CSF WBC count above 1000/microL, usually with a neutrophilic predominance ●A CSF protein concentration above 250 mg/dL ●A CSF glucose concentration below 45 mg/dL (2.5 mmol/L) However, the spectrum of CSF values in bacterial meningitis is so wide that there is substantial overlap with the findings in viral infection (table 2). This was illustrated in a review




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However, the spectrum of CSF values in bacterial meningitis is so wide that there is substantial overlap with the findings in viral infection (table 2). This was illustrated in a review of 296 episodes of community-acquired bacterial meningitis: 50 percent had a CSF glucose above 40 mg/dL (2.2 mmol/L), 44 percent had a CSF protein below 200 mg/dL, and 13 percent had a CSF white cell count below 100/microL [42]
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are (table 2): ●A CSF WBC count above 1000/microL, usually with a neutrophilic predominance ●A CSF protein concentration above 250 mg/dL ●A CSF glucose concentration below 45 mg/dL (2.5 mmol/L) <span>However, the spectrum of CSF values in bacterial meningitis is so wide that there is substantial overlap with the findings in viral infection (table 2). This was illustrated in a review of 296 episodes of community-acquired bacterial meningitis: 50 percent had a CSF glucose above 40 mg/dL (2.2 mmol/L), 44 percent had a CSF protein below 200 mg/dL, and 13 percent had a CSF white cell count below 100/microL [42]. (See "Clinical features and diagnosis of acute bacterial meningitis in adults", section on 'Cerebrospinal fluid analysis'.) SUMMARY ●Cerebrospinal fluid pressure – The normal cerebrosp




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Cerebrospinal fluid pressure – The normal cerebrospinal fluid (CSF) pressure is 6 to 20 cmH2O; patients with obesity may have CSF pressures up to 25 cmH2O.
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13 percent had a CSF white cell count below 100/microL [42]. (See "Clinical features and diagnosis of acute bacterial meningitis in adults", section on 'Cerebrospinal fluid analysis'.) SUMMARY ●<span>Cerebrospinal fluid pressure – The normal cerebrospinal fluid (CSF) pressure is 6 to 20 cmH2O; patients with obesity may have CSF pressures up to 25 cmH2O. (See 'Physiology of CSF formation and flow' above.) Infection, bleeding, or a tumor can alter the balance between CSF secretion and reabsorption, resulting in intracranial hypertension.




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A CSF–blood glucose ratio of 0.4 or less (likelihood ratio [LR], 18; 95% CI, 12-27]), CSF white blood cell count of 500/µL or higher (LR, 15; 95% CI, 10-22), and CSF lactate level of 31.53 mg/dL or more (!3.5 mmol/L; LR, 21; 95% CI, 14-32) accurately diag- nosed bacterial meningitis
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In a prospective study, 113 patients were examined by internal medicine residents (overseen by emergency physicians) prior to under- going computed tomography (CT) of the brain and subsequent LP. 12 The me- dian age of patients was 42 years, 36% were immunocompromised, and 46% of patients had altered mentation. Altered mentation (likelihood ratio [LR], 2.2; 95% confidence interval [CI], 1.5-3.2), focal neurological finding (LR, 4.3; 95% CI, 1.9-10), and papilledema (LR, 11; 95% CI, 1.1-115) increased the likeli- hood of an intracranial lesion. 12 Over- all clinical impression (not defined in the study) was able to identify patients with aCT-definedcontraindicationtoLP(LR, 19; 95% CI, 4.8-43).
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In a second pro- spective study of 301 patients with sus- pected meningitis, 235 underwent a CT scan prior to LP. 13 The mean age of pa- tients was 40 years (16% were ! 60 years), 25% were immunocompro- mised, and 27% of patients had a Charl- son comorbidity score of more than 1. Patients were assessed clinically by an emergency physician or general inter- nist.

The absence of a number of clinical features at baseline was able to identify those who were unlikely to have an abnormal CT result (LR, 0.10; 95% CI, 0.03-0.31).

The absence of all of the fol- lowing baseline characteristics was associated with this low LR: age 60 years or older, immunocompromised state, history of central nervous system disease, and seizure within 1 week of presentation.

In addition, there could be none of the following physical examination findings: abnormal level of consciousness, inability to answer 2 questions correctly, inability to follow 2 consecutive commands correctly, gaze palsy, abnormal visual fields, facial palsy, arm drift, leg drift, and abnormal language.

Using the pretest probability of an abnormal CT finding from this study (23.8%), the absence of all of these features would reduce the probability of an abnormal finding to 3.0%.

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More frequently, clinicians are concerned about coagulation defects and use of anticoagulants, which may increase the risk of epidural hemor- rhage. In 1 study of post-LP complica- tions, outcomes were compared in 166 patients receiving anticoagulation with 171 of those who were not receiving therapy. There was a trend toward in- creased risk of paraparesis in the anti- coagulated patients (relative risk, 11.0; 95% CI, 0.60-199) with 5 patients in the anticoagulation group experienc- ing an adverse event compared with none in the control group. In all pa- tients who experienced paraparesis, an- ticoagulation had been started within an hour of the procedure. 14
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Recently published guidelines from the American Academy of Neurology support the use of atraumatic needles when completing diagnostic LPs to re- duce the risk of post-LP headache. 35 In an earlier version of this guideline, they reported that LP trays containing the Sprotte needle are the same price as those containing the Quincke. 36
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The risk of headache was sig- nificantly reduced with a smaller needle (ARR, 26%; 95% CI, 11%-40%)
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Fewer pa- tients who underwent LP with reinser- tion of the stylet experienced headache (ARR, 11%; 95% CI, 6.5%-16%). It is postulated that a strand of arachnoid could enter the needle along with the out flowing CSF and if the stylet is not re- placed, the strand may be threaded back through the dura during removal of the needle, producing prolonged leakage of the CSF. By replacing the stylet before removing the needle, the strand would be pushed out and cut, reducing the risk of continued leakage and the resulting headache. 38
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In the single identified study, CSF pressur e changed little ("1.1 mm of water) with flexion of the lower extremities. 49
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Various maneuvers, such as compressing the abdomen or the jugular vein (Queckenstedt’s maneu- ver 50 ), can increase CSF pressure. 51 An obstruction to CSF flow prevents the normal rise and fall in pressure (posi- tive Queckenstedt), but we were un- able to find any studies describing the accuracy of this maneuver for detec- tion of CSF outflow obstruction.
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Steele and col- leagues suggest rapid analysis of CSF and noted that neutrophil counts can decrease by 50% within 2 hours of collection. 59
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2 He also states that a single polymorphonuclear cell in the CSF with a white blood cell count of less than 5 µL is considered normal.
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A CSF lactate level of 31.53 mg/dL or more (!3.5 mmol/L) was accurate for diagnosing bacterial meningitis (LR, 21; 95% CI, 14-32 55-57 ; Table 4), whereas aCSFlactateleveloflessthan31.53 mg/dL ("3.5 mmol/L) makes the di- agnosis of bacterial meningitis less likely (LR, 0.12; 95% CI, 0.07-0.23).
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Spanos and colleagues 60 developed a prediction rule for diagnosing bacte- rial meningitis. This rule (TABLE 5)was derived from a retrospective chart re- view of patients with a final diagnosis of acute meningitis
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In another retrospec- tive review of patients with meningitis, Leblebicioglu and colleagues 62 assessed the rules by Hoen and Spanos and the AUC was 0.99 and 0.95, respectively. McKinney and colleagues 63 obtained similar results in their retrospective review
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In the only prospective validation that we were able to identify, Baty and colleagues 64 assessed Hoen’s rule in a sample of 109 patients aged 1 to 85 years with acute community-acquired meningitis. Data are only available in patients with bacterial and viral men- ingitis, and thus the specificity of the model cannot be calculated. The sen- sitivity of their computed model was 80% for the diagnosis of bacterial men- ingitis.
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[unknown IMAGE 7088533015820]
[MENINGO-ENCEPHALITE] - JAMA - How do I perform a LP and interpret
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Ideally, a successful LP should meet the following criteria: (1) obtain suffi- cient CSF on the first attempt, (2) oc- curs without trauma (ie, CSF contain- ing "1000 red blood cells per high powered field), (3) occurs with mini- mal discomfort to the patient during and after the procedure, and, (4) oc- curs without serious adverse events such as cerebral herniation
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For the anxious patient, some experts suggest that a small dose of anxiolytic (eg, lorazepam) may be given prior to the procedure if the pa- tient wishes
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The LP is usually completed with the patient in the lateral recumbent posi- tion with his/her back at the edge of the bed to minimize curving of the spine (F IGURE 4). Both legs should be flexed toward the chest and the neck should also be slightly flexed. The patient’s shoulders and pelvis should be verti- cal to the bed. In this position, an imagi- nary line connecting the patient’s pos- terior superior iliac crests would cross the L4-L5 interspace (Figure 4)
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Lum- bar puncture can occur in the L3-L4, L4-L5, or L5-S1 interspace. 67
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The performance of LP may occur at L5-S1 because there are fewer nerve roots and arelativelylargerinterspace
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The spinous process superior to the cho- sen interspace should be palpated. The needle should be inserted about 1 cm inferior to the tip of this process. 68
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Wearing sterile gloves and a mask, the clinician should cleanse the punc- ture site with an antiseptic solution by applying it in a circular motion that starts at the center of where the punc- ture will occur. Sterile drapes can be applied, leaving the puncture site exposed
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Palpate the identified spinous process again and with 2 to 3 mL of local anesthetic (eg, lidocaine), infiltrate the patient’s skin and deeper tissues allowing 1 to 2 minutes for this to take effect.
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An atraumatic needle does not have the same cutting edge as astandardneedlesoitmaybeprefer- able to use an introducer to puncture the skin prior to insertion of the needle if this needle type is used. Introduce the spinal needle (using the same track that was used for the anes- thetic) and advance it horizontally while aiming toward the umbilicus to adepthofabout2cm.Ifboneis encountered, withdraw the needle to the subcutaneous position and reinsert at a slightly different angle. Continue to advance the needle until a pop is felt, indicating penetration of the liga- mentum flavum. The needle should now be in the subarachnoid space.
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When the stylet is withdrawn, clear fluid should drip. If no fluid emerges, rotate the needle to ensure that no flap of dura is blocking flow of CSF. If there is still no fluid, reinsert the stylet and advance the needle slightly, with- drawing the stylet after each move- ment.
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Pain radiating down either leg indicates that the needle is too lateral and has touched nerve roots. If this occurs, immediately withdraw the needle almost to the skin, recheck the patient’s position, and reinsert the needle in the mid line. If this process fails, move down 1 interspace and try again. If this fails, the procedure should be attempted by another person; alternatively it can be done under fluoroscopic guidance
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If the LP attempt is unsuccessful with the patient in the lateral position, it may be attempted with the patient sitting upright. 50 However, this position does not permit accurate measurement of the CSF pressure. 50,69
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When flow of CSF is seen, pressure can be measured by connecting a manom- eter directly to the needle or via a 2- or 3-way stopcock. The 0 mark on the manometer should be held at the level of the spinal needle and the tube held ver- tically. Normally, there will be variation in the pressure with respiration
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The manometer contents can be re- leased for collection and analysis. Ad- ditional CSF can be collected for the re- quired investigations. Typically, the examiner prepares 3 to 4 collection tubes. The initial CSF sample is placed into a tube labeled for biochemistry, and tube number 2 is for bacterial studies (Gram stain, culture, and sensitivity). Cell counts can be done on tube num- ber 3, and the fourth tube can be used for cytology or for other tests that might be done when considering other diag- noses.
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These tests will vary depending on the differential diagnosis for the in- dividual patient. Once CSF collection has been completed, the stylet should be reinserted prior to removal of the needle. A bandage may be applied to the puncture site and the patient allowed to ambulate
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[MENINGO-ENCEPHALITE] - JAMA - How do I perform a LP and interpret
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The term aseptic meningitis refers to patients who have clinical and laboratory evidence for meningeal inflammation with negative routine bacterial cultures. The most common causes are the enteroviruses [1]. Additional etiologies include other infections (mycobacteria, fungi, spirochetes), parameningeal infections, medications, and malignancies (table 1) [2]
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opics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Apr 2022. | This topic last updated: Sep 26, 2018. INTRODUCTION — <span>The term aseptic meningitis refers to patients who have clinical and laboratory evidence for meningeal inflammation with negative routine bacterial cultures. The most common causes are the enteroviruses [1]. Additional etiologies include other infections (mycobacteria, fungi, spirochetes), parameningeal infections, medications, and malignancies (table 1) [2]. Aseptic meningitis often has a similar presentation to that of bacterial meningitis (ie, fever, headache, altered mental status, stiff neck, photophobia), which can be a life-threateni




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Aseptic meningitis often has a similar presentation to that of bacterial meningitis (ie, fever, headache, altered mental status, stiff neck, photophobia), which can be a life-threatening illness. However, in contrast to bacterial meningitis, many patients with aseptic meningitis (particularly those who have disease caused by viruses or medications) have a self-limited course that will resolve without specific therapy
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ommon causes are the enteroviruses [1]. Additional etiologies include other infections (mycobacteria, fungi, spirochetes), parameningeal infections, medications, and malignancies (table 1) [2]. <span>Aseptic meningitis often has a similar presentation to that of bacterial meningitis (ie, fever, headache, altered mental status, stiff neck, photophobia), which can be a life-threatening illness. However, in contrast to bacterial meningitis, many patients with aseptic meningitis (particularly those who have disease caused by viruses or medications) have a self-limited course that will resolve without specific therapy. The assessment of patients with probable aseptic meningitis is complicated by the large number of potential etiologic agents and the relatively limited diagnostic tools for identifying




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The assessment of patients with probable aseptic meningitis is complicated by the large number of potential etiologic agents and the relatively limited diagnostic tools for identifying specific pathogens. (See "Clinical features and diagnosis of acute bacterial meningitis in adults" and "Herpes simplex virus type 1 encephalitis".)
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l meningitis, many patients with aseptic meningitis (particularly those who have disease caused by viruses or medications) have a self-limited course that will resolve without specific therapy. <span>The assessment of patients with probable aseptic meningitis is complicated by the large number of potential etiologic agents and the relatively limited diagnostic tools for identifying specific pathogens. (See "Clinical features and diagnosis of acute bacterial meningitis in adults" and "Herpes simplex virus type 1 encephalitis".) The symptoms, signs, and cerebrospinal fluid (CSF) findings for various etiologies of aseptic meningitis will be reviewed here. Each diagnostic entity is discussed in detail separately




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Patients with meningitis may be lethargic or distracted by headache, but their cerebral function remains normal. In contrast, patients with encephalitis commonly present with abnormalities in brain function such as altered mental status, motor or sensory deficits, altered behavior and personality changes, and speech or movement disorders.
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on the appropriate topic reviews. MENINGITIS VERSUS ENCEPHALITIS — The presence or absence of normal brain function is the important distinguishing feature between encephalitis and meningitis. <span>Patients with meningitis may be lethargic or distracted by headache, but their cerebral function remains normal. In contrast, patients with encephalitis commonly present with abnormalities in brain function such as altered mental status, motor or sensory deficits, altered behavior and personality changes, and speech or movement disorders. Seizures and postictal states can be seen with meningitis alone and should not be construed as definitive evidence of encephalitis. Other neurologic manifestations include hemiparesis,




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Seizures and postictal states can be seen with meningitis alone and should not be construed as definitive evidence of encephalitis. Other neurologic manifestations include hemiparesis, flaccid paralysis, and paresthesias
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litis commonly present with abnormalities in brain function such as altered mental status, motor or sensory deficits, altered behavior and personality changes, and speech or movement disorders. <span>Seizures and postictal states can be seen with meningitis alone and should not be construed as definitive evidence of encephalitis. Other neurologic manifestations include hemiparesis, flaccid paralysis, and paresthesias. However, the distinction between the two entities is frequently blurred since some patients may have both a parenchymal and meningeal process with clinical features of both. The patien




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However, the distinction between the two entities is frequently blurred since some patients may have both a parenchymal and meningeal process with clinical features of both. The patient is usually labeled as having meningitis or encephalitis based upon which features predominate in the illness although meningoencephalitis is also a common term that recognizes the overlap.
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s can be seen with meningitis alone and should not be construed as definitive evidence of encephalitis. Other neurologic manifestations include hemiparesis, flaccid paralysis, and paresthesias. <span>However, the distinction between the two entities is frequently blurred since some patients may have both a parenchymal and meningeal process with clinical features of both. The patient is usually labeled as having meningitis or encephalitis based upon which features predominate in the illness although meningoencephalitis is also a common term that recognizes the overlap. (See "Viral encephalitis in adults".) VIRAL MENINGITIS — A number of viruses produce aseptic meningitis including enteroviruses, herpes simplex virus (HSV), human immunodeficiency virus




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A number of viruses produce aseptic meningitis including enteroviruses, herpes simplex virus (HSV), human immunodeficiency virus (HIV), West Nile virus (WNV), varicella-zoster virus (VZV), mumps, and lymphocytic choriomeningitis virus (LCM)
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tis based upon which features predominate in the illness although meningoencephalitis is also a common term that recognizes the overlap. (See "Viral encephalitis in adults".) VIRAL MENINGITIS — <span>A number of viruses produce aseptic meningitis including enteroviruses, herpes simplex virus (HSV), human immunodeficiency virus (HIV), West Nile virus (WNV), varicella-zoster virus (VZV), mumps, and lymphocytic choriomeningitis virus (LCM) [3]. (See "Viral encephalitis in adults".) Enteroviruses — Aseptic meningitis occurring during the summer or fall is most likely to be caused by enteroviruses (eg, Coxsackievirus, echov




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Enteroviruses — Aseptic meningitis occurring during the summer or fall is most likely to be caused by enteroviruses (eg, Coxsackievirus, echovirus, other non-poliovirus enteroviruses), the most common causes of viral meningitis [3]. However, seasonal variation of certain CNS viral infections is relative and not absolute. Enteroviruses continue to cause 6 to 10 percent of cases of viral meningitis in the winter and spring despite their predilection for inciting illness in the late summer and fall [4]
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us (HSV), human immunodeficiency virus (HIV), West Nile virus (WNV), varicella-zoster virus (VZV), mumps, and lymphocytic choriomeningitis virus (LCM) [3]. (See "Viral encephalitis in adults".) <span>Enteroviruses — Aseptic meningitis occurring during the summer or fall is most likely to be caused by enteroviruses (eg, Coxsackievirus, echovirus, other non-poliovirus enteroviruses), the most common causes of viral meningitis [3]. However, seasonal variation of certain CNS viral infections is relative and not absolute. Enteroviruses continue to cause 6 to 10 percent of cases of viral meningitis in the winter and spring despite their predilection for inciting illness in the late summer and fall [4]. The presenting signs and symptoms of enteroviral meningitis are not distinctive. The onset of symptoms is characteristically abrupt and typically includes headache, fever, nausea or vo




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The presenting signs and symptoms of enteroviral meningitis are not distinctive. The onset of symptoms is characteristically abrupt and typically includes headache, fever, nausea or vomiting, malaise, photophobia, and meningismus. Rash, diarrhea, and upper respiratory symptoms may also be present
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absolute. Enteroviruses continue to cause 6 to 10 percent of cases of viral meningitis in the winter and spring despite their predilection for inciting illness in the late summer and fall [4]. <span>The presenting signs and symptoms of enteroviral meningitis are not distinctive. The onset of symptoms is characteristically abrupt and typically includes headache, fever, nausea or vomiting, malaise, photophobia, and meningismus. Rash, diarrhea, and upper respiratory symptoms may also be present. Cerebrospinal fluid (CSF) findings are typical of other viral meningitides and include a white blood cell (WBC) count that is generally less than 250 cells/microL, a modest elevation i




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Cerebrospinal fluid (CSF) findings are typical of other viral meningitides and include a white blood cell (WBC) count that is generally less than 250 cells/microL, a modest elevation in CSF protein concentration (generally less than 150 mg/dL), and a normal glucose concentration (table 2).
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characteristically abrupt and typically includes headache, fever, nausea or vomiting, malaise, photophobia, and meningismus. Rash, diarrhea, and upper respiratory symptoms may also be present. <span>Cerebrospinal fluid (CSF) findings are typical of other viral meningitides and include a white blood cell (WBC) count that is generally less than 250 cells/microL, a modest elevation in CSF protein concentration (generally less than 150 mg/dL), and a normal glucose concentration (table 2). (See "Cerebrospinal fluid: Physiology and utility of an examination in disease states".) Up to two-thirds of patients with enteroviral meningitis have a polymorphonuclear predominance i




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Up to two-thirds of patients with enteroviral meningitis have a polymorphonuclear predominance in the CSF when examined early in the course of the illness. Repeat lumbar puncture after 12 to 24 hours, if performed, generally shows an evolution to a lymphocytic predominance
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CSF protein concentration (generally less than 150 mg/dL), and a normal glucose concentration (table 2). (See "Cerebrospinal fluid: Physiology and utility of an examination in disease states".) <span>Up to two-thirds of patients with enteroviral meningitis have a polymorphonuclear predominance in the CSF when examined early in the course of the illness. Repeat lumbar puncture after 12 to 24 hours, if performed, generally shows an evolution to a lymphocytic predominance. Polymerase chain reaction (PCR) testing for enteroviruses can be considered if a definitive diagnosis is desired, or in the setting of an outbreak situation, but is not necessary in al




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Polymerase chain reaction (PCR) testing for enteroviruses can be considered if a definitive diagnosis is desired, or in the setting of an outbreak situation, but is not necessary in all patients.
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predominance in the CSF when examined early in the course of the illness. Repeat lumbar puncture after 12 to 24 hours, if performed, generally shows an evolution to a lymphocytic predominance. <span>Polymerase chain reaction (PCR) testing for enteroviruses can be considered if a definitive diagnosis is desired, or in the setting of an outbreak situation, but is not necessary in all patients. CSF nucleic acid amplification tests (NAATs) for enteroviruses yield sensitivities that range from 86 to 100 percent and specificities that range from 92 to 100 percent [5]. Among patie




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CSF nucleic acid amplification tests (NAATs) for enteroviruses yield sensitivities that range from 86 to 100 percent and specificities that range from 92 to 100 percent [ 5]. Among patients with CNS manifestations and a negative CSF NAAT, upper respiratory tract and gastrointestinal tract specimens for enterovirus may be useful to establish a diagnosis of enterovirus infection [6]. However, detection of enterovirus from the throat or stool of an individual with aseptic meningitis may represent an infection that occurred weeks previously and is unrelated to the present syndrome [5].

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lymerase chain reaction (PCR) testing for enteroviruses can be considered if a definitive diagnosis is desired, or in the setting of an outbreak situation, but is not necessary in all patients. <span>CSF nucleic acid amplification tests (NAATs) for enteroviruses yield sensitivities that range from 86 to 100 percent and specificities that range from 92 to 100 percent [5]. Among patients with CNS manifestations and a negative CSF NAAT, upper respiratory tract and gastrointestinal tract specimens for enterovirus may be useful to establish a diagnosis of enterovirus infection [6]. However, detection of enterovirus from the throat or stool of an individual with aseptic meningitis may represent an infection that occurred weeks previously and is unrelated to the present syndrome [5]. Additional discussions of enterovirus infections are found elsewhere. (See "Enterovirus and parechovirus infections: Clinical features, laboratory diagnosis, treatment, and prevention"




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HIV infection — Primary infection with HIV frequently presents as a mononucleosis-like syndrome manifested by fever, malaise, lymphadenopathy, rash, and pharyngitis. A subset of these patients will develop meningitis or meningoencephalitis, manifested by headache, confusion, seizures or cranial nerve palsies.
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(See "Enterovirus and parechovirus infections: Clinical features, laboratory diagnosis, treatment, and prevention" and "Enterovirus and parechovirus infections: Epidemiology and pathogenesis".) <span>HIV infection — Primary infection with HIV frequently presents as a mononucleosis-like syndrome manifested by fever, malaise, lymphadenopathy, rash, and pharyngitis. A subset of these patients will develop meningitis or meningoencephalitis, manifested by headache, confusion, seizures or cranial nerve palsies. (See "Acute and early HIV infection: Pathogenesis and epidemiology".) In most patients with HIV-1 meningitis, the clinical findings resolve without treatment, and patients may be errone




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In most patients with HIV-1 meningitis, the clinical findings resolve without treatment, and patients may be erroneously assumed to have a benign cause of viral meningitis. Thus, clinicians should have a high index of suspicion for primary HIV infection in patients at increased risk for acquisition of this virus. The identification of the patient with acute HIV infection is also important from a public health viewpoint since the risk of transmission is facilitated by high levels of viremia
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ients will develop meningitis or meningoencephalitis, manifested by headache, confusion, seizures or cranial nerve palsies. (See "Acute and early HIV infection: Pathogenesis and epidemiology".) <span>In most patients with HIV-1 meningitis, the clinical findings resolve without treatment, and patients may be erroneously assumed to have a benign cause of viral meningitis. Thus, clinicians should have a high index of suspicion for primary HIV infection in patients at increased risk for acquisition of this virus. The identification of the patient with acute HIV infection is also important from a public health viewpoint since the risk of transmission is facilitated by high levels of viremia. The CSF profile characteristically has a lymphocytic pleocytosis, an elevated protein concentration, and normal glucose concentration (table 2). Documentation of primary HIV infection




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The CSF profile characteristically has a lymphocytic pleocytosis, an elevated protein concentration, and normal glucose concentration (table 2). Documentation of primary HIV infection is accomplished by demonstration of seroconversion or detection of HIV-1 viremia in the absence of HIV antibody.
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this virus. The identification of the patient with acute HIV infection is also important from a public health viewpoint since the risk of transmission is facilitated by high levels of viremia. <span>The CSF profile characteristically has a lymphocytic pleocytosis, an elevated protein concentration, and normal glucose concentration (table 2). Documentation of primary HIV infection is accomplished by demonstration of seroconversion or detection of HIV-1 viremia in the absence of HIV antibody. (See "Techniques and interpretation of HIV-1 RNA quantitation" and "Screening and diagnostic testing for HIV infection".) Herpes simplex meningitis — Primary HSV has been increasingly r




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Herpes simplex meningitis — Primary HSV has been increasingly recognized as a cause of viral meningitis in adults. In contrast to HSV encephalitis, which is almost exclusively due to HSV-1, viral meningitis in immunocompetent adults is generally caused by HSV-2 [3].
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onversion or detection of HIV-1 viremia in the absence of HIV antibody. (See "Techniques and interpretation of HIV-1 RNA quantitation" and "Screening and diagnostic testing for HIV infection".) <span>Herpes simplex meningitis — Primary HSV has been increasingly recognized as a cause of viral meningitis in adults. In contrast to HSV encephalitis, which is almost exclusively due to HSV-1, viral meningitis in immunocompetent adults is generally caused by HSV-2 [3]. (See "Epidemiology, clinical manifestations, and diagnosis of genital herpes simplex virus infection".) Between 13 and 36 percent of patients presenting with primary genital herpes have




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Between 13 and 36 percent of patients presenting with primary genital herpes have clinical findings consistent with meningeal involvement, including headache, photophobia and meningismus. On the other hand, genital lesions are present in approximately 85 percent of patients with primary HSV-2 meningitis and generally precede the onset of CNS symptoms by approximately seven days. The CSF profile includes a pleocytosis with a predominance of lymphocytes, and a normal CSF glucose concentration (table 2). HSV meningitis can also occur without evidence of genital lesions, although this is less common [3,7]. Thus, the absence of genital lesions should not deter the clinician from testing for HSV-2 infection in a patient with aseptic meningitis.
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ue to HSV-1, viral meningitis in immunocompetent adults is generally caused by HSV-2 [3]. (See "Epidemiology, clinical manifestations, and diagnosis of genital herpes simplex virus infection".) <span>Between 13 and 36 percent of patients presenting with primary genital herpes have clinical findings consistent with meningeal involvement, including headache, photophobia and meningismus. On the other hand, genital lesions are present in approximately 85 percent of patients with primary HSV-2 meningitis and generally precede the onset of CNS symptoms by approximately seven days. The CSF profile includes a pleocytosis with a predominance of lymphocytes, and a normal CSF glucose concentration (table 2). HSV meningitis can also occur without evidence of genital lesions, although this is less common [3,7]. Thus, the absence of genital lesions should not deter the clinician from testing for HSV-2 infection in a patient with aseptic meningitis. (See "PCR testing for the diagnosis of herpes simplex virus in patients with encephalitis or meningitis".) There is no standard approach to the treatment of HSV meningitis [8]. For hosp




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There is no standard approach to the treatment of HSV meningitis [8]. For hospitalized patients, intravenous acyclovir at 10 mg/kg administered every eight hours is reasonable. The dose should be adjusted for individuals with reduced kidney function, and recommendations are provided in the Lexicomp drug information topic within UpToDate. Patients can be switched to an oral agent on discharge for a total of 10 to 14 days of treatment.
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r the clinician from testing for HSV-2 infection in a patient with aseptic meningitis. (See "PCR testing for the diagnosis of herpes simplex virus in patients with encephalitis or meningitis".) <span>There is no standard approach to the treatment of HSV meningitis [8]. For hospitalized patients, intravenous acyclovir at 10 mg/kg administered every eight hours is reasonable. The dose should be adjusted for individuals with reduced kidney function, and recommendations are provided in the Lexicomp drug information topic within UpToDate. Patients can be switched to an oral agent on discharge for a total of 10 to 14 days of treatment. However, the role of antiviral therapy for HSV meningitis remains unclear, especially in immunocompetent hosts. As an example, a retrospective observational study that evaluated forty-t




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However, the role of antiviral therapy for HSV meningitis remains unclear, especially in immunocompetent hosts. As an example, a retrospective observational study that evaluated forty-two patient episodes of HSV meningitis found that immunocompromised patients had fewer neurologic sequelae when treated with a short course of antiviral therapy [9]. By contrast, this benefit was not seen in the 27 patient episodes that occurred in immunocompetent patients. More studies are needed to help guide management decisions.
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ction, and recommendations are provided in the Lexicomp drug information topic within UpToDate. Patients can be switched to an oral agent on discharge for a total of 10 to 14 days of treatment. <span>However, the role of antiviral therapy for HSV meningitis remains unclear, especially in immunocompetent hosts. As an example, a retrospective observational study that evaluated forty-two patient episodes of HSV meningitis found that immunocompromised patients had fewer neurologic sequelae when treated with a short course of antiviral therapy [9]. By contrast, this benefit was not seen in the 27 patient episodes that occurred in immunocompetent patients. More studies are needed to help guide management decisions. Recurrent (Mollaret's) meningitis — Mollaret's meningitis is a form of recurrent benign lymphocytic meningitis (RBLM), an uncommon illness characterized by greater than three episodes o




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Recurrent (Mollaret's) meningitis — Mollaret's meningitis is a form of recurrent benign lymphocytic meningitis (RBLM), an uncommon illness characterized by greater than three episodes of fever and meningismus lasting two to five days, followed by spontaneous resolution [10]. There is a large patient-to-patient variation in the time course to recurrence that can vary from weeks to years. One-half of patients can also exhibit transient neurological manifestations, including seizures, hallucinations, diplopia, cranial nerve palsies, or altered consciousness
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, this benefit was not seen in the 27 patient episodes that occurred in immunocompetent patients. More studies are needed to help guide management decisions. Recurrent (Mollaret's) meningitis — <span>Mollaret's meningitis is a form of recurrent benign lymphocytic meningitis (RBLM), an uncommon illness characterized by greater than three episodes of fever and meningismus lasting two to five days, followed by spontaneous resolution [10]. There is a large patient-to-patient variation in the time course to recurrence that can vary from weeks to years. One-half of patients can also exhibit transient neurological manifestations, including seizures, hallucinations, diplopia, cranial nerve palsies, or altered consciousness. The most common etiologic agent in Mollaret's meningitis is HSV-2, although some patients do not have evidence of genital lesions at the time of presentation [11]. Studies suggest that




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The most common etiologic agent in Mollaret's meningitis is HSV-2, although some patients do not have evidence of genital lesions at the time of presentation [11]. Studies suggest that recurrent meningitis occurs in approximately 20 percent of patients who present with primary HSV-2 infection with meningitis [12,13]. The diagnosis can be made by PCR testing for HSV DNA in the CSF.
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from weeks to years. One-half of patients can also exhibit transient neurological manifestations, including seizures, hallucinations, diplopia, cranial nerve palsies, or altered consciousness. <span>The most common etiologic agent in Mollaret's meningitis is HSV-2, although some patients do not have evidence of genital lesions at the time of presentation [11]. Studies suggest that recurrent meningitis occurs in approximately 20 percent of patients who present with primary HSV-2 infection with meningitis [12,13]. The diagnosis can be made by PCR testing for HSV DNA in the CSF. A randomized controlled trial evaluated whether suppressive therapy with valacyclovir (500 mg twice daily for one year) was more effective than placebo in preventing recurrent HSV-2-rel




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Noninfectious etiologies for Mollaret's meningitis have also been proposed. As an example, patients with an intracranial epidermoid cyst or other cystic abnormalities in the brain can develop meningeal irritation due to intermittent leakage of irritating squamous material into the CSF [15,16]. This may be detected acutely by polarizing microscopy of CSF. Imaging studies should be performed subsequently when the patient is asymptomatic, since the epidermoid cyst is often collapsed immediately after leaking its contents
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by several factors, including: inclusion of patients without a clear etiologic diagnosis at study entry, use of symptoms alone for the diagnosis of recurrent meningitis, and small sample size. <span>Noninfectious etiologies for Mollaret's meningitis have also been proposed. As an example, patients with an intracranial epidermoid cyst or other cystic abnormalities in the brain can develop meningeal irritation due to intermittent leakage of irritating squamous material into the CSF [15,16]. This may be detected acutely by polarizing microscopy of CSF. Imaging studies should be performed subsequently when the patient is asymptomatic, since the epidermoid cyst is often collapsed immediately after leaking its contents. Lymphocytic choriomeningitis virus — Lymphocytic choriomeningitis virus (LCMV) is a human zoonosis caused by a rodent-borne arenavirus. LCMV is excreted in the urine and feces of roden




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Lymphocytic choriomeningitis virus — Lymphocytic choriomeningitis virus (LCMV) is a human zoonosis caused by a rodent-borne arenavirus. LCMV is excreted in the urine and feces of rodents, including mice, rats, and hamsters, and is transmitted to humans by exposure to secretions or excretions (by direct contact or aerosol) of infected animals or contaminated environmental surfaces [17-19]. Infection is more common during winter months.

Affected patients generally present with an influenza-like systemic illness accompanied by headache and meningismus. A minority of patients develop orchitis, parotitis, myopericarditis, or arthritis

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rizing microscopy of CSF. Imaging studies should be performed subsequently when the patient is asymptomatic, since the epidermoid cyst is often collapsed immediately after leaking its contents. <span>Lymphocytic choriomeningitis virus — Lymphocytic choriomeningitis virus (LCMV) is a human zoonosis caused by a rodent-borne arenavirus. LCMV is excreted in the urine and feces of rodents, including mice, rats, and hamsters, and is transmitted to humans by exposure to secretions or excretions (by direct contact or aerosol) of infected animals or contaminated environmental surfaces [17-19]. Infection is more common during winter months. Affected patients generally present with an influenza-like systemic illness accompanied by headache and meningismus. A minority of patients develop orchitis, parotitis, myopericarditis, or arthritis. CSF findings are typical of other causes of viral meningitis except that low glucose concentrations are observed in 20 to 30 percent of patients with LCMV meningitis and CSF WBC counts




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CSF findings are typical of other causes of viral meningitis except that low glucose concentrations are observed in 20 to 30 percent of patients with LCMV meningitis and CSF WBC counts of greater than 1000/microL are not unusual [20]. The diagnosis is established by documentation of seroconversion to the virus in paired serum samples; in addition, cell culture of CSF usually detects the presence of LCMV [5]. There is no specific antiviral therapy for LCMV
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ed patients generally present with an influenza-like systemic illness accompanied by headache and meningismus. A minority of patients develop orchitis, parotitis, myopericarditis, or arthritis. <span>CSF findings are typical of other causes of viral meningitis except that low glucose concentrations are observed in 20 to 30 percent of patients with LCMV meningitis and CSF WBC counts of greater than 1000/microL are not unusual [20]. The diagnosis is established by documentation of seroconversion to the virus in paired serum samples; in addition, cell culture of CSF usually detects the presence of LCMV [5]. There is no specific antiviral therapy for LCMV. Mumps — Aseptic meningitis is the most frequent extrasalivary complication of mumps virus infection. Prior to the introduction of the mumps vaccine in 1967, this paramyxovirus was a re




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Mumps — Aseptic meningitis is the most frequent extrasalivary complication of mumps virus infection. Prior to the introduction of the mumps vaccine in 1967, this paramyxovirus was a relatively common cause of viral meningitis, accounting for between 10 and 20 percent of all cases [4,20].

The most frequent manifestations are headache, low-grade fever, and mild nuchal rigidity. The onset of meningitis is variable and can occur before, during, or after an episode of mumps parotitis, although salivary gland enlargement is only present in about 50 percent of patients with mumps CNS disease. (See "Mumps".)

The CSF profile typically reveals fewer than 500 WBC/microL with a lymphocytic predominance, but more than 1000 WBC/microL and an early neutrophil predominance can occasionally be seen. The CSF total protein is generally normal or mildly elevated and the CSF glucose levels may be mildly depressed.

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documentation of seroconversion to the virus in paired serum samples; in addition, cell culture of CSF usually detects the presence of LCMV [5]. There is no specific antiviral therapy for LCMV. <span>Mumps — Aseptic meningitis is the most frequent extrasalivary complication of mumps virus infection. Prior to the introduction of the mumps vaccine in 1967, this paramyxovirus was a relatively common cause of viral meningitis, accounting for between 10 and 20 percent of all cases [4,20]. The most frequent manifestations are headache, low-grade fever, and mild nuchal rigidity. The onset of meningitis is variable and can occur before, during, or after an episode of mumps parotitis, although salivary gland enlargement is only present in about 50 percent of patients with mumps CNS disease. (See "Mumps".) The CSF profile typically reveals fewer than 500 WBC/microL with a lymphocytic predominance, but more than 1000 WBC/microL and an early neutrophil predominance can occasionally be seen. The CSF total protein is generally normal or mildly elevated and the CSF glucose levels may be mildly depressed. Miscellaneous viruses — A number of other viruses can infrequently be associated with viral meningitis. In certain areas of the United States, arthropod-borne viruses can cause aseptic




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Miscellaneous viruses — A number of other viruses can infrequently be associated with viral meningitis. In certain areas of the United States, arthropod-borne viruses can cause aseptic meningitis. West Nile virus, St. Louis encephalitis virus, and California encephalitis group of viruses all can cause aseptic meningitis but more frequently are associated with encephalitis. (See "Epidemiology and pathogenesis of West Nile virus infection" and "St. Louis encephalitis" and "Viral encephalitis in adults".)
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n 1000 WBC/microL and an early neutrophil predominance can occasionally be seen. The CSF total protein is generally normal or mildly elevated and the CSF glucose levels may be mildly depressed. <span>Miscellaneous viruses — A number of other viruses can infrequently be associated with viral meningitis. In certain areas of the United States, arthropod-borne viruses can cause aseptic meningitis. West Nile virus, St. Louis encephalitis virus, and California encephalitis group of viruses all can cause aseptic meningitis but more frequently are associated with encephalitis. (See "Epidemiology and pathogenesis of West Nile virus infection" and "St. Louis encephalitis" and "Viral encephalitis in adults".) Aseptic meningitis can also be associated with varicella zoster virus infection [21], Epstein-Barr virus, cytomegalovirus, human herpes virus-6, and adenoviruses. (See "Epidemiology, cl




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Aseptic meningitis can also be associated with varicella zoster virus infection [21], Epstein-Barr virus, cytomegalovirus, human herpes virus-6, and adenoviruses.
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ingitis but more frequently are associated with encephalitis. (See "Epidemiology and pathogenesis of West Nile virus infection" and "St. Louis encephalitis" and "Viral encephalitis in adults".) <span>Aseptic meningitis can also be associated with varicella zoster virus infection [21], Epstein-Barr virus, cytomegalovirus, human herpes virus-6, and adenoviruses. (See "Epidemiology, clinical manifestations, and diagnosis of herpes zoster", section on 'Aseptic meningitis' and "Human herpesvirus 6 infection in children: Clinical manifestations, di




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Spirochetes — The two major spirochetes that need to be considered in the differential diagnosis of aseptic meningitis are Treponema pallidum, the causative agent of syphilis, and Borrelia burgdorferi, the spirochete that causes Lyme disease. Leptospirosis can also cause an aseptic meningitis syndrome.
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nocompetent adults", section on 'Neurologic manifestations' and "Pathogenesis, epidemiology, and clinical manifestations of adenovirus infection", section on 'Nervous system'.) OTHER INFECTIONS <span>Spirochetes — The two major spirochetes that need to be considered in the differential diagnosis of aseptic meningitis are Treponema pallidum, the causative agent of syphilis, and Borrelia burgdorferi, the spirochete that causes Lyme disease. Leptospirosis can also cause an aseptic meningitis syndrome. (See "Leptospirosis: Epidemiology, microbiology, clinical manifestations, and diagnosis", section on 'Clinical manifestations'.) Syphilis — Treponema pallidum, the causative agent of sy




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Syphilis — Treponema pallidum, the causative agent of syphilis, disseminates to the central nervous system during early infection. Syphilitic meningitis can present in the setting of secondary syphilis with headache, malaise, and disseminated rash. (See "Syphilis: Epidemiology, pathophysiology, and clinical manifestations in patients without HIV", section on 'Neurologic/ocular findings'.)

Cerebrospinal fluid (CSF) findings include a lymphocytic pleocytosis with an elevated protein concentration; occasionally a depressed glucose concentration may also be seen. Specific serum treponemal tests are almost always positive. The CSF venereal disease research laboratory test (VDRL) has a generally accepted sensitivity of 30 to 70 percent, but is highly specific in the absence of visible blood contamination.

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se. Leptospirosis can also cause an aseptic meningitis syndrome. (See "Leptospirosis: Epidemiology, microbiology, clinical manifestations, and diagnosis", section on 'Clinical manifestations'.) <span>Syphilis — Treponema pallidum, the causative agent of syphilis, disseminates to the central nervous system during early infection. Syphilitic meningitis can present in the setting of secondary syphilis with headache, malaise, and disseminated rash. (See "Syphilis: Epidemiology, pathophysiology, and clinical manifestations in patients without HIV", section on 'Neurologic/ocular findings'.) Cerebrospinal fluid (CSF) findings include a lymphocytic pleocytosis with an elevated protein concentration; occasionally a depressed glucose concentration may also be seen. Specific serum treponemal tests are almost always positive. The CSF venereal disease research laboratory test (VDRL) has a generally accepted sensitivity of 30 to 70 percent, but is highly specific in the absence of visible blood contamination. A more detailed discussion of how to diagnose neurosyphilis is found elsewhere. (See "Neurosyphilis", section on 'Diagnosis'.) Lyme disease — Lyme meningitis typically occurs in the lat




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Lyme disease — Lyme meningitis typically occurs in the late summer and early fall, the same time as the peak incidence of enteroviral meningitis. During the acute primary infection, some patients develop headache, neck stiffness, and photophobia. Fever is usually mild; Kernig and Brudzinski signs are usually absent on physical examination, and neurologic features can include cranial nerve palsies, especially involving the facial nerve which may be bilateral.

The diagnosis of aseptic meningitis due to Lyme disease is facilitated when other characteristic findings are present, such as erythema migrans. When Lyme meningitis occurs alone, the diagnosis can be missed unless the clinician considers other risk factors, such as potential exposure to ticks or travel history. (See "Epidemiology of Lyme disease" and "Diagnosis of Lyme disease".)

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is highly specific in the absence of visible blood contamination. A more detailed discussion of how to diagnose neurosyphilis is found elsewhere. (See "Neurosyphilis", section on 'Diagnosis'.) <span>Lyme disease — Lyme meningitis typically occurs in the late summer and early fall, the same time as the peak incidence of enteroviral meningitis. During the acute primary infection, some patients develop headache, neck stiffness, and photophobia. Fever is usually mild; Kernig and Brudzinski signs are usually absent on physical examination, and neurologic features can include cranial nerve palsies, especially involving the facial nerve which may be bilateral. The diagnosis of aseptic meningitis due to Lyme disease is facilitated when other characteristic findings are present, such as erythema migrans. When Lyme meningitis occurs alone, the diagnosis can be missed unless the clinician considers other risk factors, such as potential exposure to ticks or travel history. (See "Epidemiology of Lyme disease" and "Diagnosis of Lyme disease".) Fungal infections — The two major fungal infections that should be considered in the differential diagnosis of aseptic meningitis include cryptococcus and coccidioidomycosis. Cryptococc




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Fungal infections — The two major fungal infections that should be considered in the differential diagnosis of aseptic meningitis include cryptococcus and coccidioidomycosis.
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sis can be missed unless the clinician considers other risk factors, such as potential exposure to ticks or travel history. (See "Epidemiology of Lyme disease" and "Diagnosis of Lyme disease".) <span>Fungal infections — The two major fungal infections that should be considered in the differential diagnosis of aseptic meningitis include cryptococcus and coccidioidomycosis. Cryptococcal infection — Cryptococcus neoformans produces infection following inhalation through the respiratory tract. The organism disseminates hematogenously and has a propensity to




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Cryptococcal infection — Cryptococcus neoformans produces infection following inhalation through the respiratory tract. The organism disseminates hematogenously and has a propensity to localize to the CNS, particularly in patients with severe deficiencies in cell-mediated immunity. (See "Clinical manifestations and diagnosis of Cryptococcus neoformans meningoencephalitis in HIV-seronegative patients" and "Epidemiology, clinical manifestations, and diagnosis of Cryptococcus neoformans meningoencephalitis in patients with HIV".)

Symptoms typically begin in an indolent fashion, usually over a period of one to two weeks. The three most common symptoms are fever, malaise, and headache. Stiff neck, photophobia, and vomiting are seen in one-fourth to one-third of patients.

The CSF WBC count is typically low (<50/microL) with a mononuclear predominance and the protein and glucose concentrations are usually only slightly abnormal.

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of Lyme disease".) Fungal infections — The two major fungal infections that should be considered in the differential diagnosis of aseptic meningitis include cryptococcus and coccidioidomycosis. <span>Cryptococcal infection — Cryptococcus neoformans produces infection following inhalation through the respiratory tract. The organism disseminates hematogenously and has a propensity to localize to the CNS, particularly in patients with severe deficiencies in cell-mediated immunity. (See "Clinical manifestations and diagnosis of Cryptococcus neoformans meningoencephalitis in HIV-seronegative patients" and "Epidemiology, clinical manifestations, and diagnosis of Cryptococcus neoformans meningoencephalitis in patients with HIV".) Symptoms typically begin in an indolent fashion, usually over a period of one to two weeks. The three most common symptoms are fever, malaise, and headache. Stiff neck, photophobia, and vomiting are seen in one-fourth to one-third of patients. The CSF WBC count is typically low (<50/microL) with a mononuclear predominance and the protein and glucose concentrations are usually only slightly abnormal. Coccidioidal infection — Coccidioides immitis is endemic in desert regions of the southwestern United States and Central and South America. This infection has protean manifestations, an




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Coccidioidal infection — Coccidioides immitis is endemic in desert regions of the southwestern United States and Central and South America. This infection has protean manifestations, and primary infection is frequently unrecognized. Meningitis is the most lethal complication of coccidioidomycosis and is therefore crucial to recognize.

Symptoms of meningitis, including persistent and severe headache, usually develop within several months of the initial infection. Abnormal neurologic findings on physical examination are frequently absent early in the course of coccidioidal meningitis.

The CSF WBC counts ranges from one to several hundred cells. A significant numbers of eosinophils may be present, but this finding is not specific for coccidioidal meningitis. The CSF glucose concentration may be depressed and is occasionally profoundly low in association with an elevation of the CSF protein concentration. (See "Coccidioidal meningitis".)

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ourth to one-third of patients. The CSF WBC count is typically low (<50/microL) with a mononuclear predominance and the protein and glucose concentrations are usually only slightly abnormal. <span>Coccidioidal infection — Coccidioides immitis is endemic in desert regions of the southwestern United States and Central and South America. This infection has protean manifestations, and primary infection is frequently unrecognized. Meningitis is the most lethal complication of coccidioidomycosis and is therefore crucial to recognize. Symptoms of meningitis, including persistent and severe headache, usually develop within several months of the initial infection. Abnormal neurologic findings on physical examination are frequently absent early in the course of coccidioidal meningitis. The CSF WBC counts ranges from one to several hundred cells. A significant numbers of eosinophils may be present, but this finding is not specific for coccidioidal meningitis. The CSF glucose concentration may be depressed and is occasionally profoundly low in association with an elevation of the CSF protein concentration. (See "Coccidioidal meningitis".) Tuberculous meningitis — Patients with tuberculous meningitis frequently have protracted headache, vomiting, confusion, and varying degrees of cranial nerve signs. Mental status changes




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Tuberculous meningitis — Patients with tuberculous meningitis frequently have protracted headache, vomiting, confusion, and varying degrees of cranial nerve signs. Mental status changes can occur, leading to coma, seizures, and at times hemiparesis. Signs of disseminated TB are of diagnostic importance, but are often absent.

CSF analysis typically shows elevated protein and lowered glucose concentrations with a mononuclear pleocytosis. (See "Central nervous system tuberculosis: An overview".)

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meningitis. The CSF glucose concentration may be depressed and is occasionally profoundly low in association with an elevation of the CSF protein concentration. (See "Coccidioidal meningitis".) <span>Tuberculous meningitis — Patients with tuberculous meningitis frequently have protracted headache, vomiting, confusion, and varying degrees of cranial nerve signs. Mental status changes can occur, leading to coma, seizures, and at times hemiparesis. Signs of disseminated TB are of diagnostic importance, but are often absent. CSF analysis typically shows elevated protein and lowered glucose concentrations with a mononuclear pleocytosis. (See "Central nervous system tuberculosis: An overview".) Bacterial infections — There are a variety of ways in which bacterial infections can lead to a clinical picture of aseptic meningitis with a CSF pleocytosis: ●Parameningeal sources, suc




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Bacterial infections — There are a variety of ways in which bacterial infections can lead to a clinical picture of aseptic meningitis with a CSF pleocytosis:

● Parameningeal sources, such as an epidural abscess or subdural empyema, sinus, or ear infection, can occasionally lead to meningitis. A thorough history and physical examination can lead to appropriate imaging and the correct diagnosis. (See "Spinal epidural abscess" and "Intracranial epidural abscess" and "Acute sinusitis and rhinosinusitis in adults: Clinical manifestations and diagnosis" and "Acute otitis media in children: Epidemiology, microbiology, and complications", section on 'Complications and sequelae'.)

● Bacterial endocarditis can lead to brain abscesses and seeding of the cerebrospinal fluid via hematogenous seeding. (See "Complications and outcome of infective endocarditis", section on 'Neurologic complications'.)

● A lymphocytic CSF profile and sterile cultures may be seen in partially treated bacterial meningitis. (See "Clinical features and diagnosis of acute bacterial meningitis in adults".)

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but are often absent. CSF analysis typically shows elevated protein and lowered glucose concentrations with a mononuclear pleocytosis. (See "Central nervous system tuberculosis: An overview".) <span>Bacterial infections — There are a variety of ways in which bacterial infections can lead to a clinical picture of aseptic meningitis with a CSF pleocytosis: ●Parameningeal sources, such as an epidural abscess or subdural empyema, sinus, or ear infection, can occasionally lead to meningitis. A thorough history and physical examination can lead to appropriate imaging and the correct diagnosis. (See "Spinal epidural abscess" and "Intracranial epidural abscess" and "Acute sinusitis and rhinosinusitis in adults: Clinical manifestations and diagnosis" and "Acute otitis media in children: Epidemiology, microbiology, and complications", section on 'Complications and sequelae'.) ●Bacterial endocarditis can lead to brain abscesses and seeding of the cerebrospinal fluid via hematogenous seeding. (See "Complications and outcome of infective endocarditis", section on 'Neurologic complications'.) ●A lymphocytic CSF profile and sterile cultures may be seen in partially treated bacterial meningitis. (See "Clinical features and diagnosis of acute bacterial meningitis in adults".) Angiostrongylus infection — Angiostrongylus cantonensis, the rat lungworm, is a parasite that is endemic in Southeast Asia and Pacific that can also cause an aseptic meningitis. Symptom




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Angiostrongylus infection — Angiostrongylus cantonensis, the rat lungworm, is a parasite that is endemic in Southeast Asia and Pacific that can also cause an aseptic meningitis. Symptoms include severe headache, stiff neck, paresthesias, and uncommonly facial nerve palsy [22,23].

The diagnosis of cerebral angiostrongyliasis is generally based upon the clinical presentation, CSF eosinophilia, and an epidemiologic history of known or possible exposure to infective A. cantonensis larvae. The CSF protein concentration is usually elevated, but the glucose concentration is normal or only minimally reduced. Peripheral blood and CSF eosinophilia frequently occur. (See "Eosinophilic meningitis".)

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ations'.) ●A lymphocytic CSF profile and sterile cultures may be seen in partially treated bacterial meningitis. (See "Clinical features and diagnosis of acute bacterial meningitis in adults".) <span>Angiostrongylus infection — Angiostrongylus cantonensis, the rat lungworm, is a parasite that is endemic in Southeast Asia and Pacific that can also cause an aseptic meningitis. Symptoms include severe headache, stiff neck, paresthesias, and uncommonly facial nerve palsy [22,23]. The diagnosis of cerebral angiostrongyliasis is generally based upon the clinical presentation, CSF eosinophilia, and an epidemiologic history of known or possible exposure to infective A. cantonensis larvae. The CSF protein concentration is usually elevated, but the glucose concentration is normal or only minimally reduced. Peripheral blood and CSF eosinophilia frequently occur. (See "Eosinophilic meningitis".) NEOPLASMS OF THE LEPTOMENINGES — Hematologic malignancies, have a particular propensity to seed the CNS, especially large cell lymphomas and acute leukemias. Solid tumors frequently cau




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Hematologic malignancies, have a particular propensity to seed the CNS, especially large cell lymphomas and acute leukemias. Solid tumors frequently causing carcinomatous meningitis include breast cancer, lung cancer, melanoma, gastrointestinal malignancies, and cancers of unknown primary origin
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ted, but the glucose concentration is normal or only minimally reduced. Peripheral blood and CSF eosinophilia frequently occur. (See "Eosinophilic meningitis".) NEOPLASMS OF THE LEPTOMENINGES — <span>Hematologic malignancies, have a particular propensity to seed the CNS, especially large cell lymphomas and acute leukemias. Solid tumors frequently causing carcinomatous meningitis include breast cancer, lung cancer, melanoma, gastrointestinal malignancies, and cancers of unknown primary origin. (See "Treatment of leptomeningeal disease from solid tumors".) Meningeal signs caused by tumor invasion of the leptomeninges and secondary inflammation are common. Headache, nausea, an




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Meningeal signs caused by tumor invasion of the leptomeninges and secondary inflammation are common. Headache, nausea, and vomiting may be presenting symptoms of increased intracranial pressure.
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ous meningitis include breast cancer, lung cancer, melanoma, gastrointestinal malignancies, and cancers of unknown primary origin. (See "Treatment of leptomeningeal disease from solid tumors".) <span>Meningeal signs caused by tumor invasion of the leptomeninges and secondary inflammation are common. Headache, nausea, and vomiting may be presenting symptoms of increased intracranial pressure. The diagnosis of neoplastic meningitis is the cytologic identification of malignant cells within the cerebrospinal fluid (CSF). The CSF profile may include an elevated protein concentra




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The diagnosis of neoplastic meningitis is the cytologic identification of malignant cells within the cerebrospinal fluid (CSF). The CSF profile may include an elevated protein concentration and a lymphocytic pleocytosis; a very high protein concentration suggests a CSF block. There may be a low glucose concentration, sometimes close to zero. CSF eosinophilia can be seen in Hodgkin lymphoma.
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eningeal signs caused by tumor invasion of the leptomeninges and secondary inflammation are common. Headache, nausea, and vomiting may be presenting symptoms of increased intracranial pressure. <span>The diagnosis of neoplastic meningitis is the cytologic identification of malignant cells within the cerebrospinal fluid (CSF). The CSF profile may include an elevated protein concentration and a lymphocytic pleocytosis; a very high protein concentration suggests a CSF block. There may be a low glucose concentration, sometimes close to zero. CSF eosinophilia can be seen in Hodgkin lymphoma. DRUG-INDUCED MENINGITIS — Drug-induced meningitis is an unusual adverse reaction that is usually a diagnosis of exclusion [24-26]. A number of drugs can induce symptoms and signs of ase




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Drug-induced meningitis is an unusual adverse reaction that is usually a diagnosis of exclusion [24-26]. A number of drugs can induce symptoms and signs of aseptic meningitis including nonsteroidal anti-inflammatory drugs (NSAIDs) [24-28], certain antibiotics (eg, trimethoprim-sulfamethoxazole) [29], intravenous immune globulin [24,25,30], rofecoxib, cetuximab [31], antiepileptic drugs [32,33], infliximab [34], and OKT3 antibodies.

Two mechanisms have been proposed for drug-induced meningitis: a delayed hypersensitivity type reaction and direct meningeal irritation [26].

The cerebrospinal fluid (CSF) profile typically has a neutrophilic pleocytosis. Symptoms often resolve a few days after drug discontinuation [24,30,31].

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y high protein concentration suggests a CSF block. There may be a low glucose concentration, sometimes close to zero. CSF eosinophilia can be seen in Hodgkin lymphoma. DRUG-INDUCED MENINGITIS — <span>Drug-induced meningitis is an unusual adverse reaction that is usually a diagnosis of exclusion [24-26]. A number of drugs can induce symptoms and signs of aseptic meningitis including nonsteroidal anti-inflammatory drugs (NSAIDs) [24-28], certain antibiotics (eg, trimethoprim-sulfamethoxazole) [29], intravenous immune globulin [24,25,30], rofecoxib, cetuximab [31], antiepileptic drugs [32,33], infliximab [34], and OKT3 antibodies. Two mechanisms have been proposed for drug-induced meningitis: a delayed hypersensitivity type reaction and direct meningeal irritation [26]. The cerebrospinal fluid (CSF) profile typically has a neutrophilic pleocytosis. Symptoms often resolve a few days after drug discontinuation [24,30,31]. There are also multiple reports of drug-induced meningitis in patients with autoimmune disease [27,29,35]. Many of these reports implicate use of NSAIDs. It is unclear whether these pat




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There are also multiple reports of drug-induced meningitis in patients with autoimmune disease [27,29,35]. Many of these reports implicate use of NSAIDs. It is unclear whether these patients are inherently at increased risk or whether the incidence is greater as a result of the prevalent usage of nonsteroidal anti-inflammatory drugs [36]. (See "Manifestations of systemic lupus erythematosus affecting the peripheral nervous system".)
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on and direct meningeal irritation [26]. The cerebrospinal fluid (CSF) profile typically has a neutrophilic pleocytosis. Symptoms often resolve a few days after drug discontinuation [24,30,31]. <span>There are also multiple reports of drug-induced meningitis in patients with autoimmune disease [27,29,35]. Many of these reports implicate use of NSAIDs. It is unclear whether these patients are inherently at increased risk or whether the incidence is greater as a result of the prevalent usage of nonsteroidal anti-inflammatory drugs [36]. (See "Manifestations of systemic lupus erythematosus affecting the peripheral nervous system".) APPROACH TO THE PATIENT — The clinical presentation of aseptic meningitis is generally nonspecific, with fever, headache, nausea and vomiting, occasionally accompanied by photophobia an




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APPROACH TO THE PATIENT — The clinical presentation of aseptic meningitis is generally nonspecific, with fever, headache, nausea and vomiting, occasionally accompanied by photophobia and a stiff neck. Physical examination typically reveals signs of nuchal rigidity.

As noted above, the approach to patients with aseptic meningitis is complicated by the diverse range of etiologic agents and relatively limited available diagnostic tools

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dence is greater as a result of the prevalent usage of nonsteroidal anti-inflammatory drugs [36]. (See "Manifestations of systemic lupus erythematosus affecting the peripheral nervous system".) <span>APPROACH TO THE PATIENT — The clinical presentation of aseptic meningitis is generally nonspecific, with fever, headache, nausea and vomiting, occasionally accompanied by photophobia and a stiff neck. Physical examination typically reveals signs of nuchal rigidity. As noted above, the approach to patients with aseptic meningitis is complicated by the diverse range of etiologic agents and relatively limited available diagnostic tools. Historical clues — Clinicians should bear in mind the following points: ●Obtain a comprehensive travel and exposure history, including exposure to rodents (LCMV), ticks (Lyme), and tub




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Historical clues — Clinicians should bear in mind the following points:

● Obtain a comprehensive travel and exposure history, including exposure to rodents (LCMV), ticks (Lyme), and tuberculosis, sexual activity (HSV-2, HIV, syphilis), and contact with other individuals with similar symptoms or viral exanthems (enteroviruses).

● Consider potential nonviral etiologies. Patients should be specifically questioned about preceding use of drugs associated with meningitis (eg, NSAIDs, intravenous immune globulin, trimethoprim-sulfamethoxazole).

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s of nuchal rigidity. As noted above, the approach to patients with aseptic meningitis is complicated by the diverse range of etiologic agents and relatively limited available diagnostic tools. <span>Historical clues — Clinicians should bear in mind the following points: ●Obtain a comprehensive travel and exposure history, including exposure to rodents (LCMV), ticks (Lyme), and tuberculosis, sexual activity (HSV-2, HIV, syphilis), and contact with other individuals with similar symptoms or viral exanthems (enteroviruses). ●Consider potential nonviral etiologies. Patients should be specifically questioned about preceding use of drugs associated with meningitis (eg, NSAIDs, intravenous immune globulin, trimethoprim-sulfamethoxazole). Clues on physical examination — Physical examination may reveal findings suggestive of a specific agent: ●A diffuse maculopapular exanthem in a mildly ill patient may be consistent with




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Clues on physical examination — Physical examination may reveal findings suggestive of a specific agent:

● A diffuse maculopapular exanthem in a mildly ill patient may be consistent with enteroviral infection, primary HIV, or syphilis.

● Parotitis suggests mumps meningitis in an unvaccinated patient.

● Severe vesicular and ulcerative genital lesions suggests a primary episode of HSV-2 infection.

● Oropharyngeal thrush and cervical lymphadenopathy is consistent with primary HIV infection.

● Asymmetric flaccid paralysis strongly suggests the possibility of West Nile virus meningitis [26]. (See "Clinical manifestations and diagnosis of West Nile virus infection".)

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nonviral etiologies. Patients should be specifically questioned about preceding use of drugs associated with meningitis (eg, NSAIDs, intravenous immune globulin, trimethoprim-sulfamethoxazole). <span>Clues on physical examination — Physical examination may reveal findings suggestive of a specific agent: ●A diffuse maculopapular exanthem in a mildly ill patient may be consistent with enteroviral infection, primary HIV, or syphilis. ●Parotitis suggests mumps meningitis in an unvaccinated patient. ●Severe vesicular and ulcerative genital lesions suggests a primary episode of HSV-2 infection. ●Oropharyngeal thrush and cervical lymphadenopathy is consistent with primary HIV infection. ●Asymmetric flaccid paralysis strongly suggests the possibility of West Nile virus meningitis [26]. (See "Clinical manifestations and diagnosis of West Nile virus infection".) Management — Based upon the history, physical examination, and cerebrospinal fluid (CSF) findings, patients can be classified as having probable bacterial meningitis, probable viral men




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Management — Based upon the history, physical examination, and cerebrospinal fluid (CSF) findings, patients can be classified as having probable bacterial meningitis, probable viral meningitis, or indeterminant (table 2).
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ry HIV infection. ●Asymmetric flaccid paralysis strongly suggests the possibility of West Nile virus meningitis [26]. (See "Clinical manifestations and diagnosis of West Nile virus infection".) <span>Management — Based upon the history, physical examination, and cerebrospinal fluid (CSF) findings, patients can be classified as having probable bacterial meningitis, probable viral meningitis, or indeterminant (table 2). (See "Cerebrospinal fluid: Physiology and utility of an examination in disease states".) ●For patients with suspected bacterial meningitis (eg, WBC count >1000/microL, glucose concen




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For patients with suspected bacterial meningitis (eg, WBC count >1000/microL, glucose concentration <40 mg/dL [2.2 mmol/L], protein concentration >100 mg/dL), antibiotics should be initiated promptly.
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ssified as having probable bacterial meningitis, probable viral meningitis, or indeterminant (table 2). (See "Cerebrospinal fluid: Physiology and utility of an examination in disease states".) ●<span>For patients with suspected bacterial meningitis (eg, WBC count >1000/microL, glucose concentration <40 mg/dL [2.2 mmol/L], protein concentration >100 mg/dL), antibiotics should be initiated promptly. (See "Initial therapy and prognosis of bacterial meningitis in adults".) ●Patients with probable viral meningitis include those with CSF findings of cell count <500/microL, >50 pe




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Patients with probable viral meningitis include those with CSF findings of cell count <500/microL, >50 percent CSF lymphocytes, protein concentration less than 80 to 100 mg/dL, normal glucose concentration, and negative Gram stain. Patients who are elderly, immunocompromised, or have received antibiotics prior to presentation should be given antibiotics even if viral meningitis is the suspected diagnosis. Otherwise, the clinician can consider observing the patient without antibiotic therapy.
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oncentration <40 mg/dL [2.2 mmol/L], protein concentration >100 mg/dL), antibiotics should be initiated promptly. (See "Initial therapy and prognosis of bacterial meningitis in adults".) ●<span>Patients with probable viral meningitis include those with CSF findings of cell count <500/microL, >50 percent CSF lymphocytes, protein concentration less than 80 to 100 mg/dL, normal glucose concentration, and negative Gram stain. Patients who are elderly, immunocompromised, or have received antibiotics prior to presentation should be given antibiotics even if viral meningitis is the suspected diagnosis. Otherwise, the clinician can consider observing the patient without antibiotic therapy. ●When it is not clear whether the patient has a viral or bacterial process, the treating physician can choose empiric antibiotics after obtaining blood and CSF cultures or observation w




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When it is not clear whether the patient has a viral or bacterial process, the treating physician can choose empiric antibiotics after obtaining blood and CSF cultures or observation with repeat lumbar puncture (LP) in 6 to 24 hours. The majority of clinicians opt for empiric antibiotics until culture results are available in 24 to 48 hours. If the patient is symptomatically improved and culture results are negative, then antibiotics can generally be stopped without a repeat LP if the suspicion for bacterial meningitis is unlikely. However, repeat LP may be indicated in patients with persistent symptoms who do not have a clear diagnosis
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s prior to presentation should be given antibiotics even if viral meningitis is the suspected diagnosis. Otherwise, the clinician can consider observing the patient without antibiotic therapy. ●<span>When it is not clear whether the patient has a viral or bacterial process, the treating physician can choose empiric antibiotics after obtaining blood and CSF cultures or observation with repeat lumbar puncture (LP) in 6 to 24 hours. The majority of clinicians opt for empiric antibiotics until culture results are available in 24 to 48 hours. If the patient is symptomatically improved and culture results are negative, then antibiotics can generally be stopped without a repeat LP if the suspicion for bacterial meningitis is unlikely. However, repeat LP may be indicated in patients with persistent symptoms who do not have a clear diagnosis. Many patients fall into the indeterminate category because of the lack of specificity of presenting symptoms and signs and because each CSF finding taken in isolation often displays si




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Many patients fall into the indeterminate category because of the lack of specificity of presenting symptoms and signs and because each CSF finding taken in isolation often displays significant overlap among patients with viral and bacterial meningitis.
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be stopped without a repeat LP if the suspicion for bacterial meningitis is unlikely. However, repeat LP may be indicated in patients with persistent symptoms who do not have a clear diagnosis. <span>Many patients fall into the indeterminate category because of the lack of specificity of presenting symptoms and signs and because each CSF finding taken in isolation often displays significant overlap among patients with viral and bacterial meningitis. (See "Clinical features and diagnosis of acute bacterial meningitis in adults", section on 'Cerebrospinal fluid analysis'.) Examination of multiple parameters with the use of a nomogram




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Thus, in view of the serious consequences if treatment of bacterial meningitis is delayed, the threshold to initiate empiric antibiotic therapy pending the results of cultures should be relatively low.
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e prediction rules should not be used to make clinical decisions in individual patients [38]. These guidelines can be accessed through the Infectious Diseases Society of America's website [39]. <span>Thus, in view of the serious consequences if treatment of bacterial meningitis is delayed, the threshold to initiate empiric antibiotic therapy pending the results of cultures should be relatively low. (See "Initial therapy and prognosis of bacterial meningitis in adults".) For patients with suspected viral meningitis or indeterminate CSF results, the CSF should be sent for virus dete




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For patients with suspected viral meningitis or indeterminate CSF results, the CSF should be sent for virus detection assay (eg, polymerase chain reaction [PCR] for HSV and enteroviruses), as well as for bacterial culture and routine CSF studies. In patients with cutaneous clues as to the etiology (eg, genital herpes or herpes zoster), PCR testing is preferred. Other tests to consider in selected patients include: serum treponemal and nontreponemal tests and CSF Venereal Disease Research Laboratory (VDRL) and fluorescent treponemal antibody absorption (FTA-ABS) tests, HIV antigen/antibody or RNA tests, Lyme serology, and acute/convalescent serologic testing for specific viruses (LCMV, mumps, measles).
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delayed, the threshold to initiate empiric antibiotic therapy pending the results of cultures should be relatively low. (See "Initial therapy and prognosis of bacterial meningitis in adults".) <span>For patients with suspected viral meningitis or indeterminate CSF results, the CSF should be sent for virus detection assay (eg, polymerase chain reaction [PCR] for HSV and enteroviruses), as well as for bacterial culture and routine CSF studies. In patients with cutaneous clues as to the etiology (eg, genital herpes or herpes zoster), PCR testing is preferred. Other tests to consider in selected patients include: serum treponemal and nontreponemal tests and CSF Venereal Disease Research Laboratory (VDRL) and fluorescent treponemal antibody absorption (FTA-ABS) tests, HIV antigen/antibody or RNA tests, Lyme serology, and acute/convalescent serologic testing for specific viruses (LCMV, mumps, measles). (See "Syphilis: Screening and diagnostic testing" and "Diagnosis of Lyme disease".) The differential diagnosis should be broadened for the patient with lymphocytic predominance in the C




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The differential diagnosis should be broadened for the patient with lymphocytic predominance in the CSF and negative bacterial cultures if symptoms worsen or persist. Evaluation should include a repeat CSF analysis with removal of large volume of fluid (3 to 5 mL, if possible) for fungal and mycobacterial cultures, and imaging of the CNS and sinuses with magnetic resonance imaging (MRI) or computed tomography (CT). Potential noninfectious etiologies should also be considered (table 1)
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A tests, Lyme serology, and acute/convalescent serologic testing for specific viruses (LCMV, mumps, measles). (See "Syphilis: Screening and diagnostic testing" and "Diagnosis of Lyme disease".) <span>The differential diagnosis should be broadened for the patient with lymphocytic predominance in the CSF and negative bacterial cultures if symptoms worsen or persist. Evaluation should include a repeat CSF analysis with removal of large volume of fluid (3 to 5 mL, if possible) for fungal and mycobacterial cultures, and imaging of the CNS and sinuses with magnetic resonance imaging (MRI) or computed tomography (CT). Potential noninfectious etiologies should also be considered (table 1). INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, “The Basics” and “Beyond the Basics.” The Basics patient education pieces are written in plain lang




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Management — A careful history should include travel and exposure history, including exposure to rodents (LCMV), ticks (Lyme disease), mosquitoes (West Nile virus, St. Louis encephalitis virus) and patients with tuberculosis, sexual activity (HSV-2, HIV, syphilis), travel (C. immitis, A. cantonensis) and contact with other individuals with similar symptoms or viral exanthems (enteroviruses). The patient should also be questioned about medications and other comorbidities.
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h aseptic meningitis may be difficult because of the large variety of potential etiologic agents and the overlap between self-limited viral illnesses and potentially fatal bacterial infections. <span>Management — A careful history should include travel and exposure history, including exposure to rodents (LCMV), ticks (Lyme disease), mosquitoes (West Nile virus, St. Louis encephalitis virus) and patients with tuberculosis, sexual activity (HSV-2, HIV, syphilis), travel (C. immitis, A. cantonensis) and contact with other individuals with similar symptoms or viral exanthems (enteroviruses). The patient should also be questioned about medications and other comorbidities. The opening cerebrospinal fluid (CSF) pressure should be noted and CSF should be sent for cell count, glucose, protein and culture or specific antigen or nucleic acid tests for viruses,




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Patients who are elderly, immunocompromised, or have received antibiotics prior to presentation may be considered for empiric therapy for 48 hours, even if viral meningitis is the suspected diagnosis. Otherwise, the clinician can consider observing the patient without antibiotic therapy.
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viral meningitis — The approach to empiric antibiotic therapy in the patient with suspected viral meningitis will depend upon the clinical appearance of the patient and underlying host factors. <span>Patients who are elderly, immunocompromised, or have received antibiotics prior to presentation may be considered for empiric therapy for 48 hours, even if viral meningitis is the suspected diagnosis. Otherwise, the clinician can consider observing the patient without antibiotic therapy. If HIV is a diagnostic consideration, then blood testing for HIV RNA and HIV antibody should be performed. (See "Techniques and interpretation of HIV-1 RNA quantitation" and "Screening




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If aseptic meningitis due to HSV is suspected (eg, concomitant genital lesions), empiric therapy with acyclovir (10 mg/kg intravenously every eight hours) can be considered for hospitalized patients.
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n, then blood testing for HIV RNA and HIV antibody should be performed. (See "Techniques and interpretation of HIV-1 RNA quantitation" and "Screening and diagnostic testing for HIV infection".) <span>If aseptic meningitis due to HSV is suspected (eg, concomitant genital lesions), empiric therapy with acyclovir (10 mg/kg intravenously every eight hours) can be considered for hospitalized patients. (See "Acyclovir: An overview".) Unclear etiology — When it is not clear whether the patient has a viral or bacterial process, we recommend empiric antibiotics after obtaining blood and




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Unclear etiology — When it is not clear whether the patient has a viral or bacterial process, we recommend empiric antibiotics after obtaining blood and CSF cultures or observation with repeat lumbar puncture in 6 to 24 hours. If the patient is symptomatically improved and culture results are negative, then antibiotics can generally be stopped without a repeat LP. However, repeat LPs may be indicated in patients with persistent symptoms who do not have a clear diagnosis.
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spected (eg, concomitant genital lesions), empiric therapy with acyclovir (10 mg/kg intravenously every eight hours) can be considered for hospitalized patients. (See "Acyclovir: An overview".) <span>Unclear etiology — When it is not clear whether the patient has a viral or bacterial process, we recommend empiric antibiotics after obtaining blood and CSF cultures or observation with repeat lumbar puncture in 6 to 24 hours. If the patient is symptomatically improved and culture results are negative, then antibiotics can generally be stopped without a repeat LP. However, repeat LPs may be indicated in patients with persistent symptoms who do not have a clear diagnosis. ACKNOWLEDGMENT — The editorial staff at UpToDate would like to acknowledge R Paul Johnson, MD, who contributed to an earlier version of this topic review. Use of UpToDate is subject to