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Flashcard 7089102130444

Question

The issues you face all stem from how you’re trying to achieve it. If you’re trying to obtain your certainty from things that are out of your control, like women, or validation, or money, then you’re going to be fighting a losing battle to keep your certainty from leaving your life.

But if you’re trying to get your certainty through things that are within your control, like challenging yourself in activities, doing things you love, or creating a more beautiful world, then you’re going to be able to stop the endless chase for more and more and be able to really start to enjoy life.

Answer
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Normal CSF is crystal clear. Turbid CSF is due to hyperleuko- cytosis. The detection threshold for turbid CSF is approximately 200 leukocytes/mm 3
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Cytological examination. The first step consists in counting the number of leukocytes and red blood cells (RBC) in CSF. Normal CSF is devoid of cells (< 5 cells/mm 3 ). Bac- teria may be detected during microscopic examination, in the absence of cellular reaction, even though very rarely. This test may only be performed with a minimum of 10 leukocytes/mm 3
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
In case of traumatic lumbar puncture, it is impossible to rely on the cytological analysis. The meningitis diagnosis is unlikely when the leukocytes/RBC ratio is < 1/700.
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
In the absence of a dedicated tube and if the total CSF volume is sufficient, 500 L (10 drops) should be stocked by the laboratory at −20 ◦ C before performing any test, for potential microbiological test using gene amplification (PCR)
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Turbid CSF usually indicates cellular reaction of at least 200 leukocytes/mm 3 with a predominance of more or less altered neutrophils.
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Even after antibiotic administration, bacterial meningitis is associated with a leukocyte count > 1000 cells/mm 3 in 87% of patients and > 100 cells/mm 3 in 99% of patients. Patients presenting with viral meningitis usually have < 100 cells/mm 3 .
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
There is a correlation between the number of neutrophils and bacterial inoculum: 67% of CSF samples with high cellularity have a bacterial inoculum > 10 3 CFU/ml (P < 0.01) [19].
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
the cytological analysis of CSF may be normal if the lum- bar puncture is performed early on. A mixed count or even lymphocytic predominance may be observed if the lumbar puncture is performed very early on, especially in case of N. meningitidis [20,21]
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
viral meningitis is usually associated with lymphocytic predominance. However, polymorphonuclear leukocyte pre- dominance or a mixed count may be observed in case of enteroviral meningitis when the lumbar puncture is performed early on
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Direct microbiological examination following Gram staining. This is a simple and rapid examination. Its sensitivity is improved when the CSF is concentrated using centrifugation. Its sensitivity ranges from 60 to 97% for a specificity close to 100% in the absence of antibiotic therapy [22]. It depends on the causative agent and on transportation time to the laboratory, but also on the health professional’s experience in collecting samples. Its sensitivity rapidly drops to 40–60% — or even lower — when antibiotics are initiated before lumbar puncture [23].
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
A minimum inoculum of 10 5 bacteria/ml is required to be detected by Gram staining. Gram staining sensitivity is 25% when the inoculum is < 10 3 bacteria/ml, 60% when the inoculum is between 10 3 and 10 4 bacteria/ml, and 97% when the inoculum is > 10 5 bacteria/ml [19].
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Gram staining is always performed, irrespective of the cytological and biochemical results.
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
in case of S. pneumoniae suspicion, Etest ® assays should be performed (MIC determination) at least for cefotaxime or ceftriaxone. When the MIC of the tested cephalosporin is > 0.5 mg/l, the MIC of the second cephalosporin should be subsequently determined.
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
when the Gram staining direct examination is positive, an antimicrobial susceptibility test should be performed to deter- mine the minimum inhibitory concentrations (MIC) (Etest ® method) directly from the samples if the remaining volume of CSF is sufficient and if the quantity of bacteria observed at direct examination indicates sufficient inoculum
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Latex agglutination tests are no longer recommended.
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Soluble antigen detection. The conventional latex agglutination test should be distinguished from the more recent immunochromatographic test.
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
A CSF immunochromatographic test is recommended to detect pneumococcal soluble antigens when the clinical signs and symptoms are highly indicative of bacterial meningitis even when the direct examination is negative
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Immunochromatographic test (BINAX Now Streptococcus pneumoniae ® test). This rapid (15 minutes) and simple test detects the C-polysaccharide molecules present in the wall of all S. pneumoniae strains, irrespective of the serotypes
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
On the basis of studies including more than 2000 patients (more than half being children), of whom 156 presented with pneumococcal meningitis, the specificity of the immunochro- matographic test was 100% and its sensitivity 95–99%.
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
However, cross-reactivity has been reported espe- cially with Streptococcus mitis and Streptococcus oralis. The immunochromatographic test has the advantage of not being impacted by prior antibiotic therapy administration
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
A positive culture confirms the diagnosis, identifies the causative agent, and determines its susceptibility to antibiotics. This examination may be faulted because of: • antibiotic intake before lumbar puncture performance; • the conditions and time required for transporting the sample to the laboratory, which may not be compatible with the survival of particularly fragile bacteria; • a very low bacterial inoculum
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Ceftriaxone MICs should be determined in case of reduced susceptibility to cefotaxime, or cefotaxime MICs should be determined in case of reduced susceptibility to ceftriaxone because the MICs of both of these molecules are sometimes different
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Accurate determination of MICs is required for amoxicillin and for one of the two 3GCs (cefotaxime or ceftriaxone). The use of strips impregnated with a predefined concentration gradient of antibiotics is recommended (Etest ® ).
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Tests targeting a specific bacterial or viral agent should be distinguished from those aiming at detecting the presence of any bacterial DNA (universal PCR) from a biological speci- men.
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Two amplification techniques have been developed and val- idated for the main microorganisms responsible for meningitis (multiplex PCR and real-time PCR)
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
When bacterial meningitis is highly suspected and when the direct examination is negative, physicians should perform the following before culture result availability whenever possible meningococcal PCR, pneumococcal PCR, and Listeria PCR (when patients have risk factors for the latter infection); • or universal PCR
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
When the direct examination is positive and the culture is negative at 24 hours, these PCR tests are also recommended
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
When the suspicion of a bacterial etiology is low, a PCR test is recommended in infants and children to detect an enterovirus (Genexpert ® test). Considering the high sensitivity (86–100%) and specificity (92–100%) of this test, the high prevalence of enteroviruses in pediatric acute meningitis, and the rapid time to results (two hours), a positive enterovirus PCR test rules out the need for a bacterial PCR and allows for discontinuing the antibiotic therapy if initiated [28]. However, several epidemic enteroviruses in infants such as parechoviruses, cannot be iden- tified with this technique and a specific PCR test should be performed
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Meningococcal blood PCR performed on EDTA and/or skin biopsy of purpuric lesions in case of purpura fulminans suspicion, allows for confirming the diagnosis when meningo- coccemia is suspected. Blood PCR is, however, useless when performed more than 24 hours after treatment initiation
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Blood cultures. At least one pair of blood culture bottles should be inoculated. A second blood culture may be performed in adults just before initiating the antibiotic therapy
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Blood cultures are positive in 50–75% of cases even when the CSF culture is negative
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
An association between CSF bacterial load and blood inoculum has been demonstrated.
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Skin biopsy. Patients presenting with purpura skin lesions should have a skin biopsy performed, even more so when the antibiotic therapy has already been initiated or when the CSF direct examination is negative or has not been performed. The causative agent may be isolated from culture of this type of sample in 60 to 80% of cases (most frequently N. meningitidis). N. meningitidis persists in skin lesions for at least 24 hours after antibiotic therapy initiation [29]
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
CSF glucose levels. CSF glucose levels should be interpreted according to blood glucose levels, which samples should be taken at the same time. Normal CSF glucose levels are usually two thirds (66%) of those of blood glucose. CSF glucose levels of patients presenting with bacterial meningitis are < 40% of those of blood glucose (sensitivity 80%, specificity 98% [30]).
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
CSF protein level. High CSF protein levels are significantly associated with bacterial meningitis. The CSF pro- tein level threshold associated with bacterial meningitis ranges from 0.5 to 1.2 g/l.
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
CSF lactate levels. The 2008 consensus confer- ence recommended routine measurement of CSF lactate levels for differentiating bacterial from viral meningitis using the 3.5 mmol/l threshold; CSF lactate levels above that threshold are indicative of bacterial meningitis in adults. Since 2008, two meta-analyses of 25 and 33 studies have been published on that topic in 2010 and 2011, respectively (22 studies similar to both meta-analyses) [31,32]. They demon- strated the excellent diagnostic performance of this biochemical marker, with a threshold ranging from 3.7 to 4 mmol/l to distin- guish bacterial from viral meningitis
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
The lowest CSF lactate level for bacterial meningitis was 3.2 mmol/l and the highest CSF lactate level for viral meningitis was 3.7 mmol/l [34].
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Lactate levels should always be interpreted alongside the CSF cytological and biochemical results. Lactate level measurement is only useful when the direct examination is negative and when the other CSF parameters do not point to a bacterial origin.
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Procalcitonin (PCT). In 2008 the jury recom- mended performing serum measurement of PCT levels to help diagnose bacterial meningitis, using 0.5 ng/ml as the discrimi- natory value. Several studies [35–37] and one meta-analysis of nine stud- ies (725 patients) [38] have since confirmed the effectiveness of this marker in discriminating bacterial and viral meningitis, with thresholds ranging between 0.5 and 1 ng/ml.
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
PCT level measurement is only use- ful when the direct examination is negative and when the other CSF parameters do not indicate a bacterial origin. When sepsis is observed in infants, PCT levels may be normal the first six hours; thus, the bacterial origin cannot be officially ruled out at that stage
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
The diagnos- tic effectiveness of serum PCT level measurement seems to be even better with the new version of the BRAHMS/Thermofisher diagnostic kit (Kryptor ® ), and the discriminatory value is lower (close to 0.25 ng/ml) [34].
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Hoen’s algorithm [43] combines the number of blood leuko- cytes, blood glucose levels, CSF protein levels, and the number of neutrophils in CSF in adults and children
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Bacterial Meningitis Score (BMS) is based on the presence of seizures, the number of blood neutrophils (≥ 10,000/mm 3 ), CSF protein levels (≥ 0.8 g/l), the number of neutrophils in CSF (≥ 1000/mm 3 ), and on a positive direct examination using CSF Gram staining [46] in children
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Meningitest ® , an improved version of BMS, is based on the presence of purpura, severe presentation in children (irritability, lethargy, prolonged time to skin recoloration), seizures, positive direct examination using CSF Gram stain- ing, CSF protein levels ≥ 0.5 g/l, or PCT levels ≥ 0.5 ng/ml [42] in children
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
In France and in other countries, brain imaging test — usually a CT-scan — is too often performed before lumbar puncture when confronted with meningitis suspicion [50].
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Removing consciousness disorders, recent seizures, and immunodeficiency (even severe) from the list of scenarios requiring brain CT scan to be performed before the lumbar puncture (besides those associated with brain herniation signs) led to performing the lumbar puncture earlier on and to better prognosis (case fatality and severity of sequelae) [52].
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
The contribution and compliance with indications for imaging tests before lumbar puncture recommended by the IDSA [30] in case of community-acquired bacterial meningitis suspicion were assessed in eight hospitals of Houston (Texas, United States) and its region between 2005 and 2010 [59]. A total of 614 cases of meningitis were included in this assessment. Imaging tests were performed in 549/614 cases (89%). They were not recommended in two-thirds of cases and only led to identifying two cases of minor abnormalities in this population. An imaging test was indicated in 193 cases and revealed major abnormalities requir- ing a change in clinical management in only 15 cases. Indication was based on isolated consciousness disorders in 17% of cases (5.8% overall). Two-thirds of the 119 patients presenting with consciousness disorders had a second contraindication to lum- bar puncture. Median times to lumbar puncture observed in this study were respectively 5.5 hours and 8.25 hours in patients who did not undergo or who underwent an imaging test before the lumbar puncture. This is not compatible with adequate mana- gement of bacterial meningitis, which only accounted for 46 of 614 cases (7.4%).
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
However, some factors may lead physicians to consider the likelihood of brain herniation such as the following contraindications to lumbar puncture without prior brain imag- ing: sus- and infratentorial focal neurological signs (with or without consciousness disorders or even direct signs of brain herniation) are absolute contraindications to the lumbar punc- ture; however, in case of brain herniation signs, normal imaging results do not allow the lumbar puncture to be performed.
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
However, the risks of brain herniation following lumbar punc- ture are very low even when performed in the presence of intracranial lesions with a mass effect. The authors of a study of 94 brain abscesses [61] reported that 55 patients (59%) had a lumbar puncture performed while — besides the abscess — mass effect had been observed at CT scan in 65% of them. Only one of these patients died from brain herniation within six hours following the lumbar puncture, but the authors could not establish the causative role of the lumbar puncture in the patient’s death. This figure is similar to those reported in brain abscesses.
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Post- critical state may hide neurological abnormalities indicative of focal neurological lesions because of the associated hypotonia and confusion. The neurological examination is not contribu- tory in case of status epilepticus and is a cause of intracranial hypertension. Children aged below 5 years often present with generalized seizures in case of fever, irrespective of the ori- gin. They are therefore not considered contraindications to the lumbar puncture, except for unilateral seizures, which should be considered a sign of localization
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Recent seizures may be manifestations of intracra- nial expansion; the lumbar puncture is in that case dangerous. A Dutch study of adult patients presenting with bacterial menin- gitis reported that 5% of the 666 patients experienced one or more seizures before hospital admission. Seventy per cent of these patients had a brain imaging performed before lumbar puncture, with focal lesions observed in 32% of them [62].
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Consciousness disorders associated with brain herniation (pupillary abnormalities [fixed unilateral or bilateral mydriasis], dysautonomia [blood pressure and bradycardia, respiratory rate abnormalities], cerebellar tonic seizures, no reaction to stimuli, decortication or decerebration symptoms) are absolute contraindications to lumbar puncture without prior imaging test.
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Isolated consciousness disorders are not considered con- traindications to an immediate lumbar puncture
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
When bacterial meningitis is suspected, brain imaging should be performed BEFORE lumbar puncture in the following situations only (neurological contraindications to the lumbar puncture): • presence of clinical signs potentially indicating intracranial expansion: ◦ signs of localization (Table 1), ◦ focal AND recent seizures (< 4 days); • signs of brain herniation: consciousness disorders AND one or more of the following signs: ◦ pupillary abnormalities (fixed unilateral or bilateral mydri- asis), ◦ dysautonomia (blood pressure and bradycardia, respiratory rate abnormalities), ◦ cerebellar tonic seizures, ◦ no reaction to stimuli, ◦ decortication or decerebration symptoms; • persisting seizures (i.e., generalized motor seizures) prevent- ing lumbar puncture
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[MENINGO-ENCEPHALITE] - Méningites SPILF 2019
#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation #has-images
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
The antibiotic therapy should be urgently initiated in patients presenting with bacterial meningitis. The immediate and mid- term prognoses depend on how early the antibiotic therapy is initiated [63]
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Proulx et al. studied prognostic factors in 123 patients [64]. The median time between arrival at the emergency department and antibiotic therapy initiation was 3.8 hours (IQR 1.4–6.1 hours). The multivariate analy- sis revealed that more than 6 hours between admission and administration of the first dose of antibiotics were significan- tly associated with a higher rate of deaths, with an adjusted odds ratio (OR) of 8.4 (95% CI 1.6–40.9, P < 0.01).
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Another study assessed the impact of a delayed antibiotic therapy initiation in 176 patients aged above 16 years and hospitalized for bacterial meningitis, includ- ing 40% caused by S. pneumoniae. Although the time between admission and antibiotic therapy initiation was short (median of 1 hour, mean of 1.2 ± 0.9 hours) and was not considered a risk factor for poor prognosis, the multivariate analysis revealed that a time interval > 24 hours between symptom onset and treat- ment initiation was associated with a higher risk of poor outcome (OR 2.8; 95% CI 1.13–7, P = 0.026) [66].
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
After adjustment based on age, sex, consciousness disorders, use of corticosteroids, and antibiotic choice, odds ratios for antibi- otic administration within one or two hours following admission were respectively 1.82 (95% CI 1.15–2.89, P < 0.05) and 2.07 (95% CI 1.34–3.20, P < 0.01) during the second period. The authors also reported a decreased case fatality between both periods, from 11.7% to 6.9% (P < 0.05), but the difference was not statistically significant after adjustment based on the above- mentioned criteria.
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
One of the key findings of this study was that time to treat- ment administration was significantly associated with the risk of death, with a relative increase of 12.6% (95% CI 3.1–23.1%, P < 0.01) per delayed hour of administration of the first dose of antibiotics.
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Recommendations: The antibiotic therapy (and the admin- istration of dexamethasone when indicated) should ideally be initiated within the hour following hospital admission, irrespec- tive of the presumed time since meningitis onset. Any delay in antibiotic therapy initiation is associated with a poorer progno- sis
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Recommendations: The antibiotic therapy should be initiated before lumbar puncture (but after blood culture) in the three following situations: • purpura fulminans; • patients who cannot be admitted to hospital within 90 minutes [54] ; • contraindication to the immediate lumbar puncture (Question 1)
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
The lumbar puncture should be performed as soon as possi- ble following correction of abnormalities — whenever possible. Several experts do not recommend performing the lumbar punc- ture in patients presenting with purpura fulminans, even when abnormalities have been corrected.
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Bacterial menin- gitis case fatality is highly reduced if the antibiotic therapy is initially adapted to the causative agent in terms of in vitro sus- ceptibility [74–84], and sequelae are less common when CSF sterilization is rapidly obtained [85,86].
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Since April 2013 vacci- nation with PCV13 followed by the 23-valent polysaccharid pneumococcal vaccine is recommended in older children and adults at higher risk of pneumococcal invasive infection [91]. High vaccination coverage with PCV13 is currently observed among children aged below 2 years (> 90% since 2010).
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Although vaccination coverage for group C meningococcal infections is still too low to induce the required herd immu- nity, these new recommendations — especially those relating to pneumococcal vaccination — led to substantial changes in the epidemiology of bacterial meningitis [93]
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
The latest data published by GPIP/ACTIV indicates that group B Streptococcus is the leading cause of meningi- tis (57.2%) in infants aged below 2 months, while the leading cause is S. pneumoniae in infants aged between 2 and 12 months (44%). N. meningitidis and S. pneumoniae respectively account for half and a third of meningitis cases in infants aged above 1 year.
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
The case fatality of pediatric bacterial meningitis remains stable at approximately 7% with variations depending on the pathogen and age, with a higher case fatality in infants aged below 2 months (11%) (Table 2).
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
S. pneumoniae. A reduced incidence of pneumococ- cal meningitis and of all pneumococcal invasive infections is being observed in France and abroad [97–100]. The incidence of pneumococcal meningitis has indeed significantly decreased in France between 2009 and 2014 in all age groups (Table 3) and especially among children aged < 2 years (66% decrease) [88]
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
N. meningitidis. The 2015 incidence of meningo- coccal invasive infections was 8.5/100,000 (64 cases) among newborns aged < 1 year. It ranged from 3 to 1/100,000 among children aged between 1 and 4 years (64 cases) and was approxi- mately 0.9/100,000 among children aged between 5 and 14 years (50 cases). Serogroup B is predominant in all age groups and accounts for more than 60% of pediatric cases. The proportion of serogroup C ranges from 22% among newborns aged < 1 year to 36% among children between 5 and 14 years of age. Serogroup Y accounts for < 10% of cases among children and serogroup W remains rare (< 5%) [88,101].
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
The end of the mandatory BCG vaccination did not lead to an increase in tuberculous meningitis cases, which account for 0.9% of pediatric meningitis cases (Table 2) [102,103] .
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Group B streptococcus is responsible for slightly more than 10% of pediatric meningitis cases (excluding new- borns) and the EPIBAC data reported 16 patients aged between 2 and 11 months in 2014 [88]
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
H. influenzae meningitis accounts for 3.7% of pediatric meningitis cases and the EPIBAC network reported 20 cases in 2014 [88]
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Escherichia coli is observed in 4.3% of cases and Listeria meningitis (nine cases reported by EPIBAC in 2014) and group A streptococcal meningitis remain rare in children (Table 2)
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[unknown IMAGE 7089224551692]
[MENINGO-ENCEPHALITE] - Méningites SPILF 2019
#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation #has-images
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Irrespective of the etiology, the incidence of bacterial menin- gitis in adults was 1.74 cases per 100,000 inhabitants aged 15 years or above in 2013–2014
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
A decreased incidence (−19%, P < 10 −4 ) has therefore been observed compared with that of 2008–2009 (1.93 cases per 100,000 inhabitants aged 15 years or above). This is due to the decreased incidence of pneumococcal and meningococcal meningitis as well as to a stable incidence of other types of bacterial meningitis [88]
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
The incidence of meningococcal meningitis decreased by 24% (P = 0.007) among adults between 2008–2009 and 2013–2014 [88]. This decreased incidence was mainly observed among young adults aged 15–24 years, and was mainly due to the decreased incidence of group B meningo- coccal infections [101]. No decrease in the incidence of group C meningococcal invasive infections in adults was observed because of the insufficient vaccination coverage for group C meningococcal infections [93]
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
The introduction of the PCV7 vaccine was associated with a paradoxical increase in adult pneumococcal meningitis between 2001–2002 and 2008–2009 [10], but the incidence of pneumococcal meningitis decreased following the introduc- tion of the PCV13: by 23% (P < 10 −4 ) among individuals aged above 15 years [88]. This decreased incidence was observed in all age groups, except in the 15–24-year age group.
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
These changes did not substantially change the epidemiology of adult bacterial meningitis. S. pneumoniae and N. meningitidis are still mostly responsible for adult bacterial meningitis. They respectively account for 55% and 24% of cases, i.e. 500 and 220 cases per year in 2013–2014. L. monocytogenes is the third cause of bacterial meningitis
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
N. meningitidis is most common in adolescents and young adults, accounting for 79% of cases among the 15–24-year age group and for 60% of cases among the 25–29-year age group
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
S. pneumoniae is responsible for 64% of meningitis cases in adults aged above 30 years.
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Etiologies are slightly more diverse among elderly patients: S. pneumoniae accounts for 59% of adult bacterial meningitis cases, L. monocytogenes for 16% of cases, N. meningitidis for 9% of cases, H. influenzae for 9% of cases, and group A and B streptococci for less than 5% of cases
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
To sum up, despite a decreased incidence of pneumococ- cal meningitis due to the indirect effect of infant vaccination with PCV13, S. pneumoniae remains the leading cause of bac- terial meningitis in adults. N. meningitidis is the leading cause of meningitis in adults aged below 30 years. L. monocytogenes is the second cause of bacterial meningitis in elderly individu- als
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
The most recent 2016 data reports the following rates of pneumococci responsible for meningitis with reduced susceptibility to beta-lactams: 26% for penicillin, 6.2% for amoxicillin, and 2% for cefotaxime
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Irrespective of age, 1.5% of strains had reduced susceptibility to cefotaxime (MIC > 0.5 mg/l) but no strain was resistant to the molecule (all have MICs < 2 mg/l). The highest cefotaxime MIC measured in 2014 was 1 mg/l.
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[unknown IMAGE 7089245261068]
[MENINGO-ENCEPHALITE] - Méningites SPILF 2019
#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation #has-images
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
The highest amoxicillin MIC measured in 2014 was 4 mg/l. This was observed in two strains isolated from adults (Fig. 4).
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
The proportion of pneumococci with reduced susceptibility to amoxicillin or cefotaxime has therefore not really been differ- ent between children and adults since 2012 (Fig. 5). Antibiotic susceptibility of S. pneumoniae strains isolated from patients presenting with meningitis in 2016 is displayed in Table 5
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Most strains with reduced susceptibility to beta-lactams were represented by vaccine serotypes (6B, 9V, 14, 19F, 23F, 19A, and 6A) no longer observed in pediatric meningitis (< 2 years) and which incidence has significantly decreased in the rest of the population (Fig. 6) [104,106]
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
The incidence of pneumococcal meningitis with reduced sus- ceptibility to beta-lactams has now bottomed out since the start of the surveillance in 2001 — in all age groups (Figs. 7 and 8).
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
N. meningitidis. Susceptibility profiles of N. menin- gitidis strains isolated from patients presenting with invasive meningococcal infections were defined by the national reference center for meningococci for the antibiotics of therapeutic or pro- phylactic interest (penicillin G, amoxicillin, injectable 3GCs, rifampicin, and ciprofloxacin) [108]. In 2015 all strains assessed at the national reference center (n = 322) were susceptible to 3GCs, rifampicin, and ciprofloxacin. However, just like in 2006, 30% of these strains showed reduced susceptibility to penicillin G and amoxicillin
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Meningocoque
#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
The empirical treatment with a 3GC is therefore highly likely to be effective when administered at the high dosage usually rec- ommended in this indication. However, the use of amoxicillin at high dosage is probably ineffective against strains with reduced susceptibility to penicillin G and amoxicillin (Table 6)
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
H. influenzae. The susceptibility profiles of H. influenzae strains have not substantially changed since 2005. Eighteen per cent (84/470) of all strains assessed at the Haemophilus national reference center in 2013 (vs 19% in 2005) were resistant to amoxicillin (MICs > 2 mg/l) through penicillinase secretion, and 18% (85/470) (vs 19% in 2005) had a modified PLP3 with amoxicillin MICs between 2 and 16 mg/l and cefotaxime MICs between 0.064 and 1 mg/l.
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Haemophilus
#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
PLP3 modification (preferred target of cephalosporins) is associated with reduced cross susceptibility to all beta-lactams, although at variable rates depending on the position and number of mutations, and type of beta-lactam. Resistance to amoxicillin is often moderate, with MICs ranging from 1 to 16 mg/l (modal MIC at 2 mg/l). Clavulanic acid does not restore susceptibility to amoxicillin. The activity of first-generation and second-generation cephalosporins is reduced, just like that of carbapenems. 3GCs remain the most active cephalosporins, with MICs rarely exceeding 0.125 mg/l
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Nineteen per cent (29/156) of invasive strains assessed at the Haemophilus national reference center in 2013 were resistant to amoxicillin (MIC > 2 mg/l), including only two strains with a modified PLP3. No strain was resistant to injectable 3GCs (MIC ≤ 0.125 mg/l) [109]. Only one strain (0.6%) was resistant to fluoroquinolones, and all were susceptible to rifampicin
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
However, H. influenzae strains with higher resistance level have been isolated in France since 2013 from patients presenting with pulmonary tract infections, and in 2016 from a patient presenting with meningitis. These strains are resistant to oral cephalosporins (cefpodoxime and cefixime) but also to cefotaxime (MICs ranging from 0.25 to 1 mg/l). They show intermediate susceptibility to meropenem (MIC ≥ 0.5 mg/l), and most of them remain susceptible to ceftriaxone (O. Gaillot, national reference center for Haemophilus infections, private data).
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Regarding aminoglycosides, the prognostic analysis of patients enrolled in the MONALISA cohort and presenting with Liste- ria bacteremia and/or neurolisteriosis highlights the association between a better prognosis in terms of case fatality at 3 months and aminoglycoside prescription [110].
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
As for the susceptibility of other bacteria to antibiotics, it should be reminded that L. monocytogenes is naturally resistant to cephalosporins
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Adding aminoglyco- sides to amoxicillin in case of Listeria meningitis suspicion is always recommended, even more so when microbiological documentation is available
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Susceptibility of E. coli strains isolated from meningitis patients is not specific. Resistance to aminopenicillins is high (48% to 60% of strains), but resistance to 3GCs and to gentam- icin reported for all invasive strains reached almost 10% in 2013 [111]
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
The second objective of bacterial meningitis treatment is to avoid sequelae. Sequelae are less common if CSF sterilization is rapidly obtained [85,86]
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
The proportion of sterilized CSF 12 or 24 hours after treatment initiation depends on the bacterium [115]: pneumococcal meningitis is associated with longer time to CSF sterilization [116]. “Early” sterilization takes approxi- mately the same time for all administered antibiotics, provided the bacterium is susceptible to the antibiotic [115]
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Flashcard 7089278029068

Tags
#DAG #causality #has-images #statistics
[unknown IMAGE 7089278553356]
[unknown IMAGE 7089275145484]

statusnot learnedmeasured difficulty37% [default]last interval [days]               
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Flashcard 7089283534092

Tags
#DAG #causality #has-images #statistics
[unknown IMAGE 7089284058380]
[unknown IMAGE 7089282223372]

statusnot learnedmeasured difficulty37% [default]last interval [days]               
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Flashcard 7089289039116

Tags
#DAG #causality #has-images #statistics
[unknown IMAGE 7089289563404]
[unknown IMAGE 7089287728396]

statusnot learnedmeasured difficulty37% [default]last interval [days]               
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Flashcard 7089292971276

Tags
#DAG #causality #has-images #statistics
[unknown IMAGE 7089293495564]
[unknown IMAGE 7089287728396]

statusnot learnedmeasured difficulty37% [default]last interval [days]               
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Flashcard 7089298476300

Tags
#DAG #causality #has-images #statistics
[unknown IMAGE 7089299000588]
[unknown IMAGE 7089297165580]

statusnot learnedmeasured difficulty37% [default]last interval [days]               
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Flashcard 7089303981324

Tags
#DAG #causality #has-images #statistics
[unknown IMAGE 7089304505612]
[unknown IMAGE 7089302670604]

statusnot learnedmeasured difficulty37% [default]last interval [days]               
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Flashcard 7089307913484

Tags
#DAG #causality #has-images #statistics
[unknown IMAGE 7089308437772]
[unknown IMAGE 7089302670604]

statusnot learnedmeasured difficulty37% [default]last interval [days]               
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Flashcard 7089311321356

Tags
#DAG #causality #has-images #statistics
[unknown IMAGE 7089311845644]
[unknown IMAGE 7089302670604]

statusnot learnedmeasured difficulty37% [default]last interval [days]               
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Flashcard 7089316302092

Tags
#DAG #causality #has-images #statistics
[unknown IMAGE 7089317088524]
[unknown IMAGE 7089314991372]

statusnot learnedmeasured difficulty37% [default]last interval [days]               
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#GAN #data #sequential #synthetic
Generating synthetic time-series and sequential data is more challenging than tabular data where normally all the information regarding one individual is stored in a single row. In sequential data, information can be spread through many rows, like credit card transactions, and preservation of correlations between rows — the events — and columns — the variables is key. Furthermore, the length of the sequences is variable; some cases may comprise just a few transactions while others may have thousands.
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#GAN #data #sequential #synthetic
we describe and apply an extended version of a recent powerful method to generate synthetic sequential data — DoppelGANger. It is a framework based on Generative Adversarial Networks (GANs) with some innovations that make possible the generation of synthetic versions of complex sequential datasets.
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Considering the bacterial concentrations initially observed after the first lumbar puncture (approximately 5 log/ml for S. pneumoniae and Haemophilus, and 4 log/ml for meningococci) [117] and the need for early CSF sterilization, the operational treatment objective is to reach an in vivo bactericidal level of 0.5 log CFU/ml/h. This data can only be assessed with an analysis of experimental model results
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Pharmacodynamic parameters more often focus on the mini- mum bactericidal concentration (MBC) than on the MIC, while efficacy parameters depend on the antibiotic class.
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A strong correlation is observed between the three main parameters: concentration ratio in CSF/MBC (CCSF/MBC), area under the curve of CSF concentration (AUCCSF) and MBC ratio, and concentration time fraction in CSF/MBC (TCSF/MBC). On the basis of experimental works, CCSF/MBC ratio ≥ 5 is associated with early sterilization [119,122,123]
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For the use of 3GCs in the treatment of experimental pneumococcal menin- gitis “resistant” to 3GCs, it has been demonstrated that the TCSF/MBC ratio had to be at least equal to 95% of time to obtain sterilization [123]; this may also be expressed by the need for a minimum concentration (in CSF) always higher than the MBC. Beta-lactam prescription therefore requires immediately efficient CSF concentrations
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Lipophilic antibiotics (quinolones, rifampicin, and to a lesser extent linezolide), antibiotics with low molecular weight (quinolone, rifampicin, fosfomycin), and those with low protein binding are associated with a more rapid and more important diffusion.
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Other factors play a role in antibiotic penetration such as inflammation of the meninges, which facilitates the diffusion of beta-lactams in the meninges [119]
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Some antibiotic molecules may also be administered via con- tinuous infusion following a loading dose to obtain optimal and rapid diffusion [125]. Continuous infusion helps optimize the probability of antibiotic therapy success in case of systemic infections [127] and increases the meningeal and cerebro- meningeal penetration of antibiotics. Continuous infusion is particularly useful with beta-lactams with a relatively short half- life and with glycopeptides such as vancomycin. However, the benefit of the continuous infusion in case of bacterial meningitis has not been clinically proven
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Cefotaxime and ceftriaxone are most frequently used because of their bactericidal properties and their good diffusion in CFS [128] . Ceftriaxone has a slightly better in vitro activity profile against S. pneumoniae than cefotaxime [129]. However, cefo- taxime may be administered at very high doses without inducing adverse events. Ceftriaxone has high protein binding rate, which may theoretically limit its diffusion in CSF [130]
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Vancomycin is only used in combination, either via contin- uous infusion following a loading dose or through clustered injections to optimize CSF concentrations. A proportional relation may be observed between serum and meningeal con- centrations [131,132]. Using continuous infusion and even with corticosteroid addition, sufficient CSF levels of vancomycin are obtained when vancomycin blood levels are at least 25–30 mg/l [132]. Tolerability of S. pneumoniae to vancomycin seems rare although more frequent in case of resistance to beta-lactams. It is also associated with poorer treatment response and relapses [133–138]. These findings are also observed in experimental models [135]. No pneumococcal strain tolerant to vancomycin has been observed in France so far
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Many clinical and experimental studies demonstrated the limitations of vancomycin in the management of community- acquired pneumococcal meningitis: • ineffectiveness of vancomycin alone in obtaining a cure following pneumococcal meningitis, leading to the con- traindication of vancomycin alone [139]; • no potentialization of 3GC bactericidia in experimental models of pneumococcal meningitis [140,141]; • benefits of vancomycin in experimental models, when adding a 3GC, only if the pneumococcus is resistant to the 3GC (MIC > 2 mg/l); very rare in France (no strain reported in 2014); • reduced penetration of vancomycin in the CSF in case of co-administration of dexamethasone [122] (currently highly recommended). Reduced penetration has been associated with delayed sterilization in experimental meningitis with resistant strain to 3GCs and concomitant administration of corticosteroids [142]; • the risk of nephrotoxicity of vancomycin is higher in adults when administered at high doses [143]. Adding vancomycin should therefore not be suggested in the absence of benefits and in case of toxic risks. This data is not available in children
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The authors of a mouse study reported that rifampicin reduced lipoteichoic and teichoic acid concentrations as well as early mortality [144]
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Clinical prospective studies are required. However, the authors of a clinical retrospective study reported that adding rifampicin to a 3GC was not associated with better prognosis in the multivariate analysis [6]
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Except for the last case patient reported, cephalosporin failure observed in this study was either due to very high MICs (> 2 mg/l) — no longer observed nowadays — or to an insufficient dose.
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Goldwater [150] (2005) thus assessed the rate of 3GCs in the CSF of 14 children treated with ceftriaxone 100 mg/kg/day or with cefo- taxime 200 mg/kg/day who had undergone a second lumbar puncture. The lowest rate was 0.58 mg/l and the highest rate was 35 mg/l, with a median rate of approximately 3 mg/l. No failure was observed as strains had low MICs of approximately 0.01 mg/l. The same diversity of rates was observed in a study of 19 patients who received 300 mg/kg/day of cefotaxime asso- ciated with vancomycin, without dexamethasone injection. The median CSF rate of cefotaxime was 4.4 mg/l (1.9–10.7 mg/l)
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Compared with studies assessing lower doses of cefo- taxime (200 mg/kg/day), increasing the dose of cefotaxime to 300 mg/kg/day in children does not seem to be associated with a significant increase in CSF concentrations [151].
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The CSF levels observed in this study were not high enough to reach the optimal inhibitory quotient for strains with cefotaxime MICs ≥ 0.5 mg/l. Required values for the inhibitory quotient are also not reached for strains with MICs of 1 mg/l. No clinical study is available to assess the potential impact of insufficient concentrations on clinical outcome.
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Therefore, the systematic addition of vancomycin is no longer required. It should be restricted to cases where injectable 3GC MICs are > 0.5 mg/l. Obtaining 3GC CSF concentrations five times higher than the MIC is in that case not guaranteed. An early switch with IV amoxicillin (200 mg/kg/day, four times a day) is recommended if the strain is susceptible to the molecule (amoxicillin MIC ≤ 0.5 mg/l).
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GPIP also suggested favoring cefotaxime (instead of ceftri- axone) at the initial dosing of 300 mg/kg/day divided into four intravenous infusions because of the very long half-life of ceftri- axone and of its high digestive concentrations. These properties may favor the emergence of Enterobacteriaceae strains resistant to 3GCs through ESBL production [152]. However, the theoret- ical risk in terms of ecological impact should be assessed and compared with the benefit/risk ratio of such choice
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
On the basis of currently available data and especially epidemiological data, when the optimal dose of 3GC is admin- istered for the treatment of pneumococcal meningitis, the systematic addition of vancomycin is not justified in adults and children
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Guidelines for the first-line antibiotic therapy depend on the positivity of the direct examination or PCR tests (Table 8). Cor- ticosteroids may be administered before antibiotics
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Patients presenting with meningitis and turbid CSF should be prescribed an empirical antibiotic therapy as soon as the physician per- forming the lumbar puncture notices the turbid CSF
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Physicians should NOT wait for the results of the direct examination and the CSF biochemical analysis to initiate antibiotics; while wait- ing for Gram staining results, the choice of empirical antibiotic therapy should comply with treatment guidelines for meningi- tis with a negative direct examination
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S. pneumoniae suspicion. A monotherapy with cefo- taxime 300 mg/kg/day is recommended. The administration is performed intravenously either with a continuous infusion or a discontinuous infusion with a minimum of four infusions (75 mg/kg/6 h). The daily dose for the continuous infusion is initiated immediately after the administration of a loading dose of 50 mg/kg over one hour.
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Ceftriaxone may be administered at a dosage of 100 mg/kg/day as one or two intravenous infusions. A pharmacokinetic modeling study reported the benefit of cef- triaxone administration as two infusions daily in patients with normal renal function (glomerular filtration rate > 30 ml/min)
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Although cefotaxime has better parmacokinetic param- eters (higher protein binding for ceftriaxone) and ceftriaxone shows better microbiological data (MIC usually one dilution lower than cefotaxime), there is no clinical study available to recommend one molecule over the other.
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There is no consensus on the maximum dose in adults: some studies report doses of 24 g/day of cefotaxime [146]. Children (< 15 years of age) may receive cefotaxime at the max- imum daily dose of 12 g (4 g maximum for ceftriaxone).
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Doses should be adjusted to the renal function. Measuring residual plasma concentrations after 48 hours of treatment may be indi- cated when administering a daily dose > 10 g/day, or in patients aged > 70 years or with a creatinine clearance < 30 ml/min
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N. meningitidis suspicion. A monotherapy with cefo- taxime 200 mg/kg/day is recommended. The administration is performed intravenously either with a continuous infusion or a discontinuous infusion with a minimum of four infusions (50 mg/kg/6 h). The daily dose for the continuous infusion is administered concomitantly with the loading dose of 50 mg/kg over one hour. Ceftriaxone may be administered at a dose of 75 mg/kg/day as one or two intravenous infusions.
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Listeriosis suspicion. A two-drug combination therapy is recommended with intravenous amoxicillin 200 mg/kg/day divided into 4 to 6 infusions and intra- venous gentamicin 5–6 mg/kg/day as a single daily dose over 30 minutes.
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H. influenzae suspicion. A monotherapy with cefo- taxime 200 mg/kg/day is recommended. The administration is performed intravenously either with a continuous infusion or a discontinuous infusion with a minimum of four infusions (50 mg/kg/6 h). The daily dose for the continuous infusion is administered concomitantly with the loading dose of 50 mg/kg over one hour. Ceftriaxone may be administered at a dose of 75 mg/kg/day as one or two intravenous infusions
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E. coli suspicion. A monotherapy with cefotaxime 200 mg/kg/day is recommended. The administration is per- formed intravenously either with a continuous infusion or a discontinuous infusion with a minimum of four infusions (50 mg/kg/6 h). The daily dose for the continuous infusion is administered concomitantly with the loading dose of 50 mg/kg over one hour. Ceftriaxone may be administered at a dose of 75 mg/kg/day as one or two intravenous infu- sions.
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When ESBL-producing E. coli meningitis is highly suspected (ESBL colonization or positive specimen from another site), cefotaxime or ceftriaxone should be replaced by meropenem 40 mg/kg three times daily as a slow IV infusion (expert advice required)
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Negative direct examination and negative PCR tests The distribution of microorganisms is in that case different, as detailed in Table 9 using the results of the COMBAT cohort of adult patients presenting with bacterial meningitis. As the sensitivity of the direct examination is lower in case of Listeria meningitis, the respective proportion of this microorganism is more important in patients presenting with meningitis with a negative direct examination (Table 9)
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Evidence for listeriosis: age > 70 years, comorbidities, immunodeficiency, progressive onset of symptoms, rhomben- cephalitis (cranial nerve involvement and/or cerebellar syn- drome)
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[unknown IMAGE 7089399401740]
[MENINGO-ENCEPHALITE] - Méningites SPILF 2019
#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation #has-images
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ED neg PCR neg
#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
12.8.2.2. Evidence for listeriosis. A triple therapy with cephalosporin, amoxicillin, and aminoglycoside is recom- mended. Cefotaxime is administered at the dose of 300 mg/kg/day. The administration is performed intravenously either with a contin- uous infusion or a discontinuous infusion with a minimum of four infusions (75 mg/kg/6 h). The daily dose for the continuous infusion is initiated immediately after the administration of a loading dose of 50 mg/kg. Ceftriaxone may be administered at a dose of 100 mg/kg/day as one or two intravenous infusions. Amoxicillin is administered at the dose of 200 mg/kg/day intravenously, divided into 4 to 6 infusions. Gentamicin is administered at the dose of 5 mg/kg/day intra- venously as a single daily dose over 30 minutes in adults and at the dose of 5–8 mg/kg in children
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[unknown IMAGE 7089404382476]
[MENINGO-ENCEPHALITE] - Méningites SPILF 2019
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ED neg PCR neg
#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
12.8.2.3. Beta-lactam allergy. Severe allergy to beta-lactams is defined as a history of immediate anaphylactic hypersensitivity, including anaphylactic shock. Except for these extremely rare cases, the use of cefotaxime or ceftriaxone is recommended. One should bear in mind that the CSF diffusion of aztreonam is poor. Meropenem could be used because of the associated low risk of cross allergy [154]. However, no data is available to draft guidelines in this rare situation. The infectious disease specialist’s advice should be sought, and the first 24 hours of treatment may be monitored in the continuous monitoring unit (even if the patient’s state does not require it) (Table 10)
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As cefotaxime is mainly renally excreted (including 60% as unchanged form and 20% as active metabolites), the dosing regimen should be adjusted to the renal function. As the suscep- tibility of the causative agent is initially unknown, we suggest using high antibiotic doses the first 24 hours and then reducing them by 25% to 75% according to the renal function impairment (25% reduction for a glomerular filtration rate [GFR] between 30 and 60 ml/min, 50% reduction for a GFR between 15 and 30 ml/min, 75% reduction for a GFR below 15 ml/min). High antibiotic doses should not be adjusted in patients receiving continuous hemofiltration
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The ceftriaxone dose should also be adjusted as it is equally excreted from the hepato-biliary and renal routes. A full dose may also be administered the first 24 hours (2 injections/24 h). A 50% reduction of the dose may be suggested when the creatinine clearance is < 30 ml/min (single administration) [153]. Plasma (to avoid excessive dosing) and CSF concentrations should be measured in all these situations to check if CSF antibiotic concentrations are at least 10 times higher than the MIC
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Dexamethasone is the only adjuvant to the bacterial meningi- tis treatment to have been extensively assessed in clinical studies.
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Dexamethasone reduces the inflammation of the subarach- noid spaces and the vasogenic edema induced by meningitis, which are associated with potentially deleterious effects
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This anti-inflammatory activity was highest in animal models when dexamethasone was administered before or at the same time as the first dose of antibiotic
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[unknown IMAGE 7089418800396]
[MENINGO-ENCEPHALITE] - Méningites SPILF 2019
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A meta-analysis of randomized studies concluded to the benefit of dexamethasone in children as it helped reduce the frequency of severe hearing loss when the causative agent was H. influenzae or S. pneumoniae and when the first injection was administered before or at the same time as the first dose of antibiotics [155]
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The most recent Cochrane meta-analysis (2015) included 25 randomized trials (1517 adults and 2511 children) for a total of 4121 bacterial meningitis cases [155]. Irrespective of the microorganism, findings from this meta-analysis revealed that corticosteroids were not associated with reduced case fatality but with morbidity improvement in terms of neurological sequelae reduction and hearing loss reduction. Taking into consideration the type of microorganisms or the country’s socio-economic sta- tus, the subgroup analyses revealed that corticosteroids were associated with reduced case fatality for microbiologically con- firmed pneumococcal meningitis only and in industrialized countries only
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In the randomized, double-blind, and placebo-controlled European study of 301 adult patients presenting with bacte- rial meningitis included in this meta-analysis, patients were followed up for an average of 13 years. The impact of corti- costeroids on the reduction of case fatality, observed during the initial follow-up, was sustained up to 20 years after the initial episode [156]
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Conversely, the prospective French study MONALISA reported that dexamethasone prescription was an independent risk factor for increased mortality, thus contraindicating its use when listeriosis is confirmed [110]
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Time to corticosteroid initiation was assessed in 22 trials included in the 2015 Cochrane meta-analysis [155]. Corti- costeroids were administered before or at the same time as antibiotics in 13 trials (3143 patients) and after antibiotics in nine trials (797 patients). No significant difference was observed in terms of dexamethasone benefit between both administration modalities based on the analysis of the various endpoints
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
However, corticosteroids should be administered as soon as possible after antibiotic therapy initia- tion when they cannot be administered before or at the same time as antibiotics. No study assessing the maximum time to corti- costeroid administration following antibiotic therapy initiation is available. On the basis of experts’ advice, the 2016 Euro- pean guidelines recommend a maximum time to corticosteroid administration of 4 hours [56]. The 2016 British guidelines rec- ommend a maximum time of 12 hours [55].
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Dexamethasone injection is recommended, just before or at the same time as the first injection of antibiotics in case of: • a suspicion of bacterial meningitis without microbiological confirmation, but with an empirical antibiotic treatment deci- sion taken. This scenario is observed when: ◦ the indication for brain imaging delays the lumbar puncture (neurological contraindications to the lumbar puncture) (Question 1), ◦ the lumbar puncture is contraindicated for non- neurological reasons (Question 1), ◦ turbid or even purulent CSF is observed at lumbar puncture, ◦ a negative direct examination of CSF is observed at lum- bar puncture, but other CSF and blood biological findings confirm the bacterial meningitis diagnosis; • initial microbiological diagnosis indicative of: ◦ pneumococcal bacterial meningitis (Binax positive and/or Gram-positive cocci at CSF direct examination), ◦ meningococcal bacterial meningitis (Gram-negative cocci at CSF direct examination). Several experts do not recom- mend dexamethasone in this scenario.
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
The initial dose of dexamethasone in adults is 10 mg every 6 hours, for 4 days. This treatment is not recommended in immunocompromised patients and in patients presenting with neuroinvasive listeriosis [12].
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
When the corticosteroid therapy cannot be administered just before or at the same time as the first injection of antibiotics, it should be administered as soon as possible up to 12 hours following antibiotic initiation.
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Following definitive identification of the microorganism, dexamethasone should be continued for a total duration of four days in case of documented pneumococcal and Haemophilus meningitis. Whether or not to continue dexamethasone for four days in case of meningococcal meningitis is left to the physician’s choice. There is no indication for continuing dexam- ethasone in case of meningitis caused by other microorganisms
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Onset of thrombosis with cerebral ischemia several days or several weeks later, following an initially favorable outcome, is observed in 1% of patients [158]. Most of these patients present with pneumococcal meningitis and have received dexametha- sone. Most experts believe that dexamethasone should therefore be reintroduced when this rebound effect occurs without failure of the antibiotic therapy
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Children or infants Dexamethasone injection is recommended, just before or at the same time as the first injection of antibiotics in case of: • a suspicion of bacterial meningitis without microbiological confirmation, but with an empirical antibiotic therapy deci- sion taken in infants aged between 3 and 12 months. This scenario is observed when: ◦ the indication for brain imaging delays the lumbar puncture (neurological contraindications to the lumbar puncture) (Question 1), ◦ the lumbar puncture is contraindicated for non- neurological reasons (Question 1), ◦ turbid or even purulent CSF is observed at lumbar puncture, ◦ a negative direct examination of CSF is observed at lum- bar puncture, but other CSF and blood biological findings confirm the bacterial meningitis diagnosis; • an initial microbiological diagnosis indicative of: ◦ pneumococcal bacterial meningitis (Binax positive and/or Gram-positive cocci at CSF direct examination), ◦ H. influenzae bacterial meningitis (Gram-negative bacilli at CSF direct examination). The initial dose of dexamethasone in children is 0.15 mg/kg every 6 hours, for 4 days. The benefit of a corticosteroid therapy initiated after the antibiotic therapy is not confirmed in children
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Patients are then admitted to health facilities with variable means. Yet, the short-term outcome cannot be entirely predicted even when the patient’s initial status is reassuring. The subse- quent health facility should therefore be carefully chosen.
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No objective criteria have been established to define a min- imum qualitative standard as no study has ever compared prognoses depending on the hospitalization ward. However, admission criteria to the ICU have been suggested for children [3,4] and adults [7,13,15]: • extensive purpura; • Glasgow score ≤ 8; • focal neurological signs; • signs of brainstem involvement, usually indicative of intracra- nial hypertension: bradycardia, tachycardia, respiratory rate abnormalities; • status epilepticus; • hemodynamic instability
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Consultation with the ICU team is recommended for all patients, even in the absence of such criteria and irrespective of the patient’s initial clinical status.
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In case of non-admission to the ICU, patients should be admitted to a ward where close mon- itoring of consciousness and hemodynamic parameters (every hour) can be implemented the first 24 hours minimum
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Seizures are observed in 6–13% of adults and 20–30% of children at the initial phase of bacterial meningitis, most often within a few hours of admission. Unlike seizures observed sev- eral days after treatment initiation, early seizures in children are not indicative of unfavorable outcome when short and gener- alized [159] . Prolonged seizures may cause ischemic necrosis lesions and destruction of cortical neurons especially in the temporal lobe
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Seizure treatment — and consequently the (secondary) prevention of recurrences — should rely on conventional antiepileptic drugs (diphenylhydantoin or phenobarbital). The benefit of antiepileptic drugs administered for primary pre- vention has never been proven and such treatment cannot be recommended considering available data.
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Symptomatic ICH is common in patients presenting with meningitis and is associated with a higher risk of unfavorable outcome and death [160,161].
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Correction of low blood pressure initially relies on fluid replacement. Antihypotensive or inotropic agents are recom- mended in case of fluid replacement failure.
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Other studies are required to conclude on the benefit of such treatment. The use of glycerol is not recommended
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
No human clinical data is available on the benefit of man- nitol in the management of bacterial meningitis. A single bolus could nevertheless be suggested in case of immediately life-threatening ICH. The benefit of hypertonic saline solu- tion, suggested in some experimental studies, has never been assessed in a randomized study and therefore cannot be recom- mended
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Severe ICH may also be treated as follows: rising the patient’s head at 20–30 ◦ , sedation, mechanical ventilation [164]
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
A meta-analysis [166] including the three studies assessing fluid restriction versus normal hydration demonstrated that fluid restriction was not associated with any benefit but with a higher risk of neurological sequelae at three months (RR 0.42; 95% CI 0.20–0.89). Conventional sodium and water intake combined with daily monitoring of natremia and diure- sis are recommended to detect and to treat truly inappropriate antidiuresis.
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Temperature of patients presenting with meningitis and severe intracranial hypertension should be lowered as well as when fever is not well tolerated, but physicians should not necessarily try to bring it back to normal. Moderate hypothermia (34–36 ◦ C) in adults pre- senting with meningitis and coma is not recommended because it may worsen the patient’s prognosis, as demonstrated in a randomized study [167].
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Elevated glycemia (> 1.5 g/l or 8.3 mmol/l) is observed in more than one in two adult patients presenting with bacterial meningitis [12]. Yet, hyperglycemia in patients presenting with sepsis has deleterious effects on immunity and increases the risk of thrombosis [168] . Several scientific societies recommend using intravenous insulin therapy to lower the glycemia below 1.8 g/l following hemodynamic stabilization in adult patients presenting with sepsis [169]. It seems reasonable to comply with this recommendation in case of bacterial meningitis and sepsis in adults
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
The initial treatment should be reevaluated daily based on clinical outcome and as soon as the causative agent has been identified; MICs for amoxicillin, ceftriaxone, and cefo- taxime should be kept in mind
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
The microbiology laboratory should immediately inform the medical team of the CSF culture positivity and MICs as soon as they have been deter- mined
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Pneumocoque
#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
When the clinical outcome is favorable, the choice of the antibiotic therapy depends on the pneumococcal MICs for 3GCs and amoxicillin (Table 11): • 3GC MICs ≤ 0.5 mg/l: ◦ when the amoxicillin MICs are ≤ 0.5 mg/l, the 3GC should ideally be replaced by amoxicillin 200 mg/kg divided into 4 to 6 infusions/day or as a continuous administration. Oth- erwise, the 3GC may be continued but dosage should be adjusted to the 3GC MICs, ◦ the 3GC should be continued if the amoxicillin MICs are > 0.5 mg/l. The 3GC dose may be reduced (cefotaxime to 200 mg/kg/day or ceftriaxone to 75 mg/kg/day); • 3GC MICs > 0.5 mg/l (1.5% of pneumococcal strains isolated from invasive infections in France in 2014). It is here recommended to: • always perform a control lumbar puncture with CSF culture, antibiotic concentration measurement in CSF and blood, and dosing adjustment based on concentration results. Several experts recommend always adding vancomycin for children and infants while waiting for the CSF culture results following control lumbar puncture; • ask for the advice of an infectious disease specialist and a microbiologist when the culture is positive.
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Pneumocoque
#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
When the clinical outcome is unfavorable after 48–72 hours of treatment (no improvement of consciousness disorders and/or signs of sepsis), systematic brain imaging is recommended (ide- ally an MRI) to detect an empyema or intracranial complications that could require surgery. Control lumbar puncture and CSF culture are recommended in the absence of imaging abnormal- ities explaining the unfavorable outcome. An additional CSF sample should be collected to measure the 3GC concentration
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
The antibiotic therapy should be optimized following advice from the multidisciplinary team (infectious disease specialist and microbiologist): • checking whether the administered 3GC doses are optimal (recommended dose and administration modalities, concen- tration/MIC ratio); • choosing the 3GC with the lowest MIC; • discussing whether a second antibiotic should be added: rifampicin (10 mg/kg every 12 hours in adults, or 20 mg/kg every 12 hours in children) or vancomycin (loading dose of 30 mg/kg over one hour, and then daily dose of 40–60 mg/kg/day to be adjusted to obtain residual plasma concentrations between 15 and 20 mg/l) or combination of vancomycin and rifampicin (no resistance to rifampicin and vancomycin among pneumococcal strains isolated in France in 2014)
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Analyzing the cause of microbiological failures documented with the non-sterilization of the CSF culture after 48 hours of treatment for pneumococcal meningitis is recommended. The analysis should for instance check the compliance with guidelines (time to treatment initiation, adequate doses and administration modalities for the prescribed 3GC), look for undrained infectious sites (empyema, ventriculitis, suppurative otitis media, sinusitis), and measure the 3GC concentration in CSF and put it into perspective with the isolated pneumococcal MIC
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Guidelines on antibiotic therapy duration for pneumococcal meningitis are mainly based on treatment habits and experts’ advice because randomized studies are lacking. Treatment should be discontinued after 10 to 14 days: after 10 days in case of rapidly favorable outcome (within the first 48 hours) and in case of beta-lactam-susceptible pneumococcal meningitis (3GC MIC ≤ 0.5 mg/l); after 14 days when both of these criteria are missing
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[unknown IMAGE 7089477258508]
[MENINGO-ENCEPHALITE] - Méningites SPILF 2019
#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation #has-images
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Documented meningococcal meningitis When the clinical outcome is favorable, 3GC doses should not exceed 200 mg/kg/day for cefotaxime and 75 mg/kg/day for cef- triaxone (Table 11). When the amoxicillin MIC is ≤ 0.125 mg/l, the 3GC may be replaced by amoxicillin 200 mg/kg divided into 4 to 6 infusions/day or as a continuous administration. However, the short treatment duration of meningococcal meningitis does not require antibiotic de-escalation in this specific case. Treatment should be discontinued after 4 to 7 days (4 days in case of rapidly favorable outcome with apyrexia within 48 hours). No additional treatment for pharyngeal decontamination is indicated when patients have received at least 24 hours of 3GC treatment (i.e., all patients if initial recommendations have been followed).
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Documented L. monocytogenes meningitis The antibiotic therapy relies on the combination of amoxi- cillin 200 mg/kg divided into 4 to 6 infusions/day or as a contin- uous administration for a total duration of 21 days (reduced to 14 days in case of favorable outcome), and gentamicin 5 mg/kg/day as a single 30-minute infusion the first five days (Table 11)
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Management strategies in the absence of microbiological documentation (sterile CSF and blood cultures at 48–72 hours; negative direct examination) Several scenarios may be considered. In case of favorable clinical outcome within the first 48 hours of the antibiotic therapy and if the initial CSF has been col- lected while the patient had already received prior antibiotic therapy, the diagnosis may be a partially treated bacterial menin- gitis. When the bacterial meningitis diagnosis is still considered (absence of alternative diagnosis; suggestive initial symptoms), the initial antibiotic therapy is continued for 14 days
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In case of unfavorable clinical outcome after 48–72 hours of treatment (no improvement of consciousness disorders and/or signs of sepsis), brain imaging should always be performed. In the absence of contraindication, a control lumbar puncture is recommended. If the second CSF analysis is still indicative of bacterial meningitis, one should rule out listeriosis or tubercu- losis as 3GCs are not active against these bacteria and as they are difficult to identify
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Considering the diagnostic progress made over the past years, the absence of microbiological documentation should lead physicians to reconsider bacterial meningitis and to consider the main differential diagnoses: viral meningitis (enterovirus, her- pes virus, HIV), drug-induced meningitis (NSAIDs, antibiotics, IV immunoglobulins, etc.), inflammatory meningitis (lupus, sar- coidosis, Behc¸et’s disease, Kawasaki disease), cerebral venous sinus thrombosis, infectious site next to the meninges (epiduri- tis, spondylodiscitis, brain abscesses, empyema)
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Spirochaeta meningitis (Lyme disease, syphilis, leptospirosis) should be looked for by serological tests (± PCR) in case of a suspected source of contamination. Advice from a specialist (infectious disease specialist, neurologist, internal medicine specialist) is always welcome
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The main objective of CSF control testing is to check whether it is sterile (Table 12). Sterilization is rapidly obtained with N. meningitidis: less than two hours are required according to a study including patients treated with a 3GC [116]. As for other bacteria, CSF culture is usually sterile after 24 hours of an adequate antibiotic treatment [170]. A significant modification of CSF cytological and biochemical parameters is also observed after 48 hours of treatment [171], but no data is available to conclude on treatment modifications
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In case of favorable clinical outcome, routine CSF con- trol should only be performed in patients presenting with pneumococcal meningitis with MICs for the prescribed cephalosporin > 0.5 mg/l. CSF control may be performed after 48–72 hours of treatment for meningitis caused by unusual bac- teria (other than S. pneumoniae, N. meningitidis, Haemophilus, and Listeria).
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In case of unfavorable clinical outcome after 48–72 hours of treatment (no improvement of consciousness disorders and/or signs of sepsis), systematic brain imaging is recommended to detect an empyema or intracranial complications. A control lum- bar puncture is recommended in the absence of abnormalities explaining the unfavorable outcome at brain MRI. An addi- tional CSF sample should be collected to measure the 3GC concentration
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Clinical worsening should lead physicians to perform a lum- bar puncture after brain imaging and to discuss the potential need for additional CSF investigations, jointly with the microbiology laboratory.
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Brain imaging during treatment helps diagnose peri- or intra- parenchymatous complications and potential bone and dura mater abnormalities that may increase the risk of recurrence ( Table 13). This imaging test may also lead to changing the initial diagnosis if doubts remain
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
The main complications of bacterial meningitis observed at brain imaging are directly linked to the bacterial infection (intraparenchymal abscess, subdural empyema, bone or inner ear bacterial infection) or are a consequence of it (stroke asso- ciated with vasculitis, insudation/ischemia associated with vein thrombosis, ventricular dilatation and dilatation of subarachnoid spaces). Few articles systematically and prospectively assessed the incidence and time to onset of these complications, their clinical signs, and the outcome
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A prospective study of 86 adults presenting with pneumococcal meningitis reported arte- rial involvement (assessed by CT scan) in 22% of cases and vein thrombosis in 10% of cases. Cerebral edema was observed in 29% of cases, hemorrhage in 9% of cases, and hydrocephalus in 16% of cases [172]. The authors of that study reported 80% of complications during the first seven days and half of them during the first three days [173]. Another observational study of 696 adult bacterial meningitis episodes reported empyema or cerebritis observed by CT scan in 3.5% of cases [12]
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The main clinical signs requiring brain imaging are:

• onset of new neurological signs: seizures, paralysis (hemi- paresis, tetraparesis, paralysis of the cranial nerves except for isolated paralysis of the sixth cranial nerve), increased severity of cephalgia, change in vision;

• unexplained persistence of fever > 38.5 ◦ C, consciousness disorders, and severe cephalgia after 48–72 hours of treatment;

• rapid increase of head circumference in newborns

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[unknown IMAGE 7089504259340]
[MENINGO-ENCEPHALITE] - Méningites SPILF 2019
#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation #has-images
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Brain imaging should always be performed in the following cases: • meningitis caused by a bacterium other than S. pneumoniae or N. meningitidis; • pneumococcal meningitis in children, especially after 2 years of age, in the absence of ENT bacterial infection or if the causative serotype was included in the vaccine administered to the child. Brain imaging here aims to look for a breach in the meninges
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Brain imaging during the early follow-up of bacterial menin- gitis helps look for acquired or congenital bone and dura mater lesions or chronic infections of the inner ear and mastoiditis to prevent recurrences. These lesions and infections should be clinically looked for in children and adults presenting with pneu- mococcal meningitis and in adults presenting with Haemophilus meningitis
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Factors associated with a bone and dura mater breach requir- ing an imaging test are severe head injury, especially if sustained in the previous months, recurrence of bacterial meningitis, his- tory of neurosurgical procedure, pituitary gland surgery or some ENT procedures, rhinorrhea, or CSF otorrhea. Breach investi- gation should always be performed during the recovery phase in those cases
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Brain or spinal imaging is required to look for congenital der- mal sinus in children presenting with bacterial meningitis caused by staphylococci, Enterobacteriaceae, or multiple bacteria.
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
ENT portals of entry, reported in 25% of cases (adults and children) [30,31], should always be looked for in case of community-acquired bacterial meningitis [77,78].
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
A prospec- tive study performed in the Netherlands between 2006 and 2014 in patients aged above 16 years reported an ENT portal of entry (otitis or sinusitis) in 34% of patients presenting with menin- gitis (386/1,125). ENT-related meningitis cases reported in this study were associated with better prognosis (P = 0.041) [71]. They include otological, nasal and sinus sites.
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
The systematic clinical examination of bacterial meningitis should look for hearing loss, otalgia, and otorrhea and requires otoscopy to confirm the purulent fluid or the perforation. The nasal cavity should also be examined to look for nasal and sinus discharge. Otological causes should be distinguished from nasal and sinus causes
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Otological causes: potential sources of infection are acute otitis media, mastoiditis (although more rarely), otitis media with cholesteatoma, osteomyelitis of the base of the skull [174]. Post-traumatic or post-surgical CSF discharge may be observed in the middle or inner ear, with abscess behind the eardrum or discharge through the ear canal if perforated [175]
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
The management of otological causes requires the advice of an ENT specialist: • in case of ENT infection site suspicion; • for acute otitis media: paracentesis is recommended as soon as possible to drain purulent fluids and to perform the bacte- riological analysis; • for acute mastoiditis: the current treatment combines antibi- otics and drainage of the middle ear with paracentesis; surgery (mastoidectomy) may be indicated in case of unfavorable out- come after 48 hours. In case of chronic otitis (cholesteatoma mainly), specialized assessment and surgery should be con- sidered at the end of the meningitis treatment; • CSF discharge may spontaneously stop. If not, the breach — diagnosed by endoscopy, CT scan, or MRI — should be closed
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
Nasal and sinus causes: bacterial sinusitis is most com- mon. Post-traumatic or post-surgical rhinorrhea is also observed, although more rarely. Sinusitis associated with bacterial meningitis is often frontal or ethmoid. It may be previously known or diagnosed during the course of bacterial meningitis
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#Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation
The CT scan confirms the presence of fluids and involvement of bone structures, mainly with sphenoidal localizations
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The MRI may be useful when cavernous sinus thrombosis is suspected. Ethmoiditis mainly presents as ocular signs (ocu- lomotor palsy, sometimes mydriasis) and the CT scan is very helpful [176].
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CSF rhinorrhea, usually unilateral, may be spontaneous or triggered by head movements or abdominal compression. The CSF analysis confirms the presence of glucose. Nasal endoscopy helps identify and localize the site of discharge. A potential breach should be looked for at MRI and/or CT scan with bone window and axial and frontal millimetric views, especially of the cribriform plate and ethmoid roof depending on cases (neu- rological advice required)
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Management of nasal and sinus causes: • drainage of sinus sites should be performed in case of fluid persistence or when the patient’s general status is worrying despite antibiotic therapy administration. Endonasal drainage should be preferred but the surgical procedure may be dis- cussed depending on the sinus localization; • when rhinorrhea does not spontaneously stop, the breach should be closed through the endonasal or external route depending on the localization or size of the breach [177,178]
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When a breach is observed, antipneumococcal vaccination is recommended as suggested in the vaccination calendar for peo- ple at high risk of invasive pneumococcal infection (i.e., initial administration of the conjugate vaccine followed by the polysac- charide vaccine two months later) [179]. There is no indication for antibiotic prophylaxis or for continuing the curative antibi- otic therapy before closing the breach. Breach closure should be performed as soon as possible. There is, however, no consensus on the optimal time to surgical procedure
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The case fatality of pneu- mococcal meningitis is 11–37% (higher among adults) and neurological sequelae are observed in 30–50% of surviving patients. The rate of sequelae is also higher in adults than in children
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Neurological, hearing, cognitive, and psychological sequelae are common: 29–70% depending on studies [180]
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Pediatric hearing loss is observed at the early stage of menin- gitis and may be temporary or definitive. Inner ear impairment with cochlear ossification may be observed in the weeks follow- ing meningitis. The rate of hearing loss ranges from 10% to 13% depending on studies — lower than in adults — and depends on the causative agent (S. pneumoniae: 33%, N. meningitidis: 5%) [184].
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Several studies suggest that some factors observed at admis- sion are associated with the onset of sequelae: patient’s characteristics (elderly or children aged below one year), causative agent (S. pneumoniae, resistance to antibiotics), clinical signs of severity especially consciousness disorders, neurological complications (focal signs, cerebral edema, paral- ysis of the cranial nerves — except for paralysis of the eighth cranial nerve), hemodynamic signs (septic shock), biological signs such as low cellular reaction, high bacterial load in CSF, positive blood cultures [172,185]
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Seizures at admission are not indicative of poor prognosis, unlike late onset of seizures, prolonged seizures, or focal seizures persisting after discharge.
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A neurological clinical examination should be performed before hospital discharge in children and adults
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An age-specific hearing test is recommended at the lat- est 15 days after treatment completion for pneumococcal or Haemophilus meningitis
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Diseases or abnormalities that may have contributed to bac- terial meningitis should be looked for, such as splenectomy or asplenia, sickle cell anemia, beta-thalassemia [76,187]. Predis- posing chronic or immune diseases are observed in 10–45% of adult or pediatric studies [188,189]
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In adults, diseases such as diabetes, chronic alcoholism, can- cer, cirrhosis, hemopathy, and HIV infection should be looked for. Electrophoresis of plasma protein should also be performed in case of pneumococcal meningitis.
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Severe infections in children should lead physicians to look for an immunodeficiency. They may start with a complete blood count to look for Jolly bodies, serum IgG, IgA, and IgM measure- ment, and vaccinal serologies. Evaluation of the complement level is essential in case of meningococcal meningitis and should be performed when the first episode is observed
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One month after hospital discharge A neurological examination is recommended, and hearing loss should be looked for. When an antiepileptic treatment has been initiated at the acute phase and if no other episode has been observed, an elec- troencephalography should be performed, and the antiepileptic treatment may be discontinued based on the advice of the neu- rologist or neuropediatrician. Head circumference should be monitored in infants
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Up to one year following meningitis onset Hearing tests should be performed every three months in children. These tests may be performed by the child’s family (whispering) and by the family physician or pediatrician. Par- ents should also inform the child’s teacher about any hearing disorder. Adaptive capacities of adults should be assessed, and qual- ity of life and depression scales should be used to distinguish hearing loss, cognitive sequelae, and depression.
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Level 1: the most common signs and symptoms of central nervous system (CNS) dysfunction are: • consciousness disorders (from clouded sensorium to coma); • behavior disorders; • seizures; • focal neurological signs. Level 1: symptoms of meningitis may be absent. Level 1: fever is very common, but may be absent because of antipyretic drug intake
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Grade A: physicians must look for any occurrence of fever in the days prior to the infection onset through the patient’s and relatives’ anamneses. Grade A: any signs or symptoms of CNS dysfunction asso- ciated with fever must lead physicians to consider infectious encephalitis in the differential diagnosis.
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Level 1: no blood laboratory result is indicative of encephali- tis, but laboratory results may guide the etiological diagnosis and are needed to establish a differential diagnosis. Level 1: HIV primary infection may present as encephalitis.
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Grade A: two pairs of blood cultures must be sampled before initiating the antibiotic therapy. Complete blood count, blood electrolytes, blood glucose level (performed at the same time as the lumbar puncture), CRP test, liver function test (ASAT, ALAT, bilirubin, alkaline phosphatase), hemostasis evaluation, and CPK measurement are required. Grade A: a combined HIV serological test (simultaneous detection of HIV1/HIV2 antibodies and p24 antigen) is compul- sory. When a primary HIV infection is suspected, a viral RNA blood test (viral load) is recommended along with the serological test
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Level 1: the amount of CSF sampled must allow for diagnos- tic investigations. Level 1: CSF cell count is abnormal when > 4 nucleated cells/mm 3 are present. Level 1: the ratio of one leukocyte per 800 red blood cells is indicative of traumatic puncture or subarachnoid hemorrhage. Level 1: low levels of CSF glucose in adults refer to a CSF glucose level < 40% of simultaneous blood glucose
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Grade A: the minimum amount of CSF sampled must be 120 drops (1 drop amounts to approximately 50 !L): 20 drops (1 mL) for biochemistry tests and 80 to 100 drops (4 to 5 mL) for microbiological and virological tests. Part of the CSF must be kept (at +4 ◦ C and then, if possible, at −80 ◦ C) for additional biological tests (including tuberculosis diagnostic test)
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Grade A: herpes simplex virus (HSV), varicella zoster virus (VZV), and enterovirus PCR tests are imperative. Grade A: Mycobacterium tuberculosis detection by culture must be performed when previous PCR test results are negative or in case of high suspicion (clinical or epidemiological)
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Level 1: when the patient’s condition allows it and when it can be performed without any delay, the diagnostic benefit of a brain MRI is far superior to that of the CT-scan.
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Grade A: the MRI must include FLAIR, diffusion, T2*, and T1 sequences with and without gadolinium as well as venous and arterial vascular sequences
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Grade A: when an emergency MRI cannot be performed, a CT-scan of the brain must immediately be performed (with and without injection)
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Grade A: when the lumbar puncture cannot be performed, guidelines related to the empirical treatment of bacterial menin- gitis AND infectious encephalitis should be applied
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Grade B: an EEG may be indicated to investigate seizures, status epilepticus, and consciousness disorder
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Level 1: encephalitis presentations vary in severity, and are associated with a high morbidity and mortality. Level 1: severity is measured in terms of neurological dam- age (coma, convulsions, status epilepticus, etc.), but also affects other organs (respiratory/renal/hemodynamic failure, etc.). The rapidity and extent of neurological deterioration within the first few hours cannot be predicted
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Grade B: the following patients must initially be hospitalized in the ICU/continuous monitoring unit: • patients with a Glasgow score (GCS) ≤ 13; or • patients who experienced more than one seizure, even more so status epilepticus; or • patients requiring intubation to ventilate or protect airways; or • patients presenting with respiratory distress syndrome (often associated with aspiration pneumonia); or • patients presenting with another organ failure (shock, renal failure, etc.); or • patients presenting with behavior disorders incompatible with hospitalization in a standard unit (severely agitated patients, etc.)
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Level 1: following lumbar puncture and when the micro- scopic examination is negative, the potential severity of the encephalitis may require the urgent administration of an empir- ical anti-infective treatment.
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Level 1: in metropolitan France, HSV, VZV, Mycobacterium tuberculosis, and Listeria monocytogenes are most frequently responsible for encephalitis in non-HIV-infected adult patients.
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Level 2: assessing the benefit/risk ratio of the high dose of acyclovir (15 mg/kg/8 hours) as an empirical treatment implies: (i) a potentially better efficacy in case of VZV encephalitis; (ii) an excessive risk of toxicity (renal and/or neurological), (iii) a time-limited risk of toxicity (≤ 48 hours) in case of non-VZV encephalitis; (iv) ratio of the number of individuals exposed to that risk (all suspicions, even minor ones) over the num- ber of “true” VZV encephalitis patients who might receive this high dose regimen. This ratio is low (5% of encephalitis cases, all causes, including encephalitis of unknown origin). At this point, the benefit/risk ratio of adding an aminoglycoside seems negative
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Grade A: in the absence of a suspected etiology (clinical signs or biological features), the initial treatment must combine acy- clovir administered at an active dose against HSV (10 mg/kg every 8 hours, grade B recommendation for this dose) and amoxicillin (200 mg/kg/day as 4 infusions minimum, or as a con- tinuous administration), provided a reevaluation is performed at 48 hours
The acyclovir dose must be increased to 15 mg/kg every 8 hours in case of skin vesicles or imaging signs of vasculopathy
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Grade A: HSV, VZV, and enterovirus PCR results must be available within 48 hours. The microbiologist must be contacted within the first 48 hours.
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Grade B: an antituberculosis treatment will only be initiated (in addition to the acyclovir + amoxicillin treatment) within the first 48 hours in the following situations:

• when acid-fast bacilli are detected on CSF microscopic exam- ination, or in case of a positive real-time PCR (please see Q3)

• when highly suggestive signs are observed: underlying conditions, anamnesis, CSF characteristics, extra-neurological localizations, imaging results

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Grade B: treatment must always be reevaluated at 48 hours based on the available results of blood cultures, CSF culture, HSV/VZV and enterovirus CSF PCR, and on imaging results: • if the HSV PCR is positive: amoxicillin must be discontinued but acyclovir 10 mg/kg every 8 hours must be continued; • if the VZV PCR is positive: amoxicillin must be discontinued but acyclovir 15 mg/kg every 8 hours must be continued; • if HSV and VZV PCRs are negative and if the culture is posi- tive for Listeria or any other bacterium (CSF or blood culture): acyclovir must be discontinued, but amoxicillin must be con- tinued and gentamicin must be added to the treatment regimen (please see Q3) if the culture yielded Listeria; a specific treat- ment will need to be initiated for other bacteria; • at this point, if all results are negative, acyclovir must be con- tinued until HSV/VZV diagnosis reevaluation (second CSF PCR sampled at least 4 days after neurological sign onset), and amoxicillin must be discontinued; • in case of antibiotic consumption before lumbar puncture or indicative signs of listeriosis, amoxicillin must be continued (please see Q4); • if the enterovirus CSF PCR is positive, acyclovir and amoxi- cillin must be discontinued
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Grade C: when clinical, paraclinical, or epidemiological data highly indicative of a specific infectious agent other than those mentioned above are observed, the biological diagnosis and potential treatment relevant to this infectious agent must imme- diately be suggested. Grade C: there is, at this point, no indication requiring the addition of a corticoid therapy, except for confirmed or highly suspected tuberculosis (please see above: indications for initiat- ing an antituberculosis treatment).
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Level 1: encephalitis is responsible for brain damage and functional disorders. Level 1: 30% of encephalitis patients present with seizures. Level 1: encephalitis may be complicated by coma and/or status epilepticus, with or without convulsions. Level 1: encephalitis may be complicated by intracranial hypertension, bleeding, necrosis, vasculopathy, and cerebral edema
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Level 4: there is no specific recommendation on the manage- ment of intracranial hypertension during encephalitis. Level 4: there is no specific recommendation on the manage- ment of seizures during acute phases of encephalitis. Level 4: no study has been conducted on the evaluation of osmotherapy (by hypertonic saline solution, mannitol, corticoid therapy, or glycerol) during encephalitis.
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Level 2: little data has been published on the benefit of targeted lower temperature management during encephalitis (except for associated status epilepticus, please see below). Level 3: in case of refractory intracranial hypertension, decompressive craniectomy has occasionally been performed with satisfactory results.
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[MENINGO-ENCEPHALITE] - Encéphalites SPILF 2017
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Grade A: in case of progressive consciousness disorders, patients must be intubated and sedated (neuroprotection, airway protection), and an EEG must urgently be performed
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Grade B: neuroprotective symptomatic treatments (or control of secondary brain damage of systemic origin [SBDSO]) must be prescribed to all encephalitis patients, especially to patients with severe presentations, just like for all acute brain injuries (Table 1). The following objectives must be reached (Table 1): • normal PaO 2 ; • normal arterial blood pressure; • temperature control (please see Table 1); • normocapnia; • no severe anemia; • normoglycemia; • normal natremia
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Grade B: sedation is indicated for intubated patients. Sedation mainly relies on sedative-hypnotic drugs with antiepileptic activity (midazolam, propofol) associated with morphine analgesics. An initial sedation with propofol (short half-life) is recommended to be able to rapidly reassess the patient’s neurological status according to the mechanisms of consciousness disorders
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Grade D: it is not recommended to initiate an antiepileptic treatment as a primary prophylaxis in encephalitis patients; it may, however, be discussed when cortical lesions are observed on brain CT-scan or better on brain MRI
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Level 1: deterioration of clinical signs and symptoms may be observed during the first 48 hours, especially neurological ones, and other organ failures may occur.
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Grade A: encephalitis patients must be regularly moni- tored: neurological parameters (consciousness, occurrence of focal signs, GCS score, pupils, seizures, etc.), and other vital signs. EEGs must be performed as part of the monitoring process. Grade B: repeated transcranial Doppler procedures may be useful to assess the impact of intracranial hypertension on blood circulation, and to adjust the neurological and intensive care management
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Level 1: HSV encephalitis is associated with a 5 to 20% case fatality and with significant neurological sequelae in some survivors. Level 1: acyclovir reduces HSV encephalitis-related case fatality and sequelae. Neurological, behavior, and cognitive sequelae remain frequent and may sometimes be severe
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Level 1: both reference studies demonstrated the superiority of acyclovir 10 mg/kg every 8 hours for 10 days (vs. vidarabine). Level 3: subsequent case reports suggested administering longer treatments (up to 21 days) to reduce the risk of relapse. Level 2: acyclovir is associated with a potential renal and neurological central toxicity, boosted by excessive doses, rapid infusion rate, high concentration of the infusion solution, com- bination with other nephrotoxic drugs, and older age. Level 3: the relation between the kinetics of CSF HSV PCR becoming negative while on treatment and prognosis has never been documented in the literature. Level 4: there is no evidence-based data supporting the rela- tion between a positive CSF HSV PCR at the end of treatment and the positive or negative outcome of encephalitis
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Grade A: the acyclovir dosage for adult patients presenting with HSV encephalitis is 10 mg/kg for 1 hour every 8 hours. Grade B: for HSV encephalitis confirmed by a positive initial PCR, it is not recommended to check the CSF HSV PCR at the end of treatment in case of positive outcome. Grade C: the recommended treatment duration is 14 days in immunocompetent adults. Grade C: a 21-day treatment is recommended for immuno- compromised patients. Grade C: treatment modalities: infusion of at least 1 hour and IV saline final concentration < 5 mg/mL; the associated use of nephrotoxic drugs should be limited; adequate rehydration is needed; doses should be adapted to the renal function.
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Grade C: in case of negative clinical outcome at the end of the 14-day treatment, a lumbar puncture with HSV PCR and autoantibodies detection in CSF must be performed. A positive HSV PCR may lead to extend the acyclovir treatment to 21 days. The decision to investigate resistance to acyclovir and phar- macokinetic parameters (acyclovir concentration measurement in blood and CSF) must be discussed with all healthcare profes- sionals concerned
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Grade A: as soon as the HSV encephalitis diagnosis is sus- pected, an acyclovir treatment must be rapidly initiated (ideally within 6 hours after hospital admission). Grade B: in case of high clinical suspicion of HSV encephali- tis, but unconfirmed with the first CSF test, the acyclovir treatment must be continued while waiting for a second CSF HSV PCR sampled at least 4 days after neurological signs onset
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Level 3: randomized prospective studies are ongoing, but there is currently no well-powered study supporting or discred- iting the use of corticoids in the treatment of HSV encephalitis
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Level 1: acyclovir concentrations obtained in CSF and in the brain after the administration of oral valaciclovir does not reach therapeutic concentrations. Level 1: the authors of a randomized study demonstrated that there was no benefit in continuing an anti-HSV treatment with valaciclovir for 3 months after the end of HSV encephalitis in adults.
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Grade A: an oral treatment with valaciclovir is not recom- mended as a follow-up treatment after the end of the IV acyclovir treatment. Grade D: an adjuvant corticoid therapy is currently not rec- ommended in the treatment of HSV encephalitis
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Level 3: VZV encephalitis is associated with a high case fatality and with significant neurological sequelae. Level 3: acyclovir reduces VZV encephalitis-related case fatality and neurological sequelae
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Level 1: in vitro, VZV is less sensitive to acyclovir than HSV. Level 3: no literature data helps in defining the optimal acy- clovir treatment duration of VZV encephalitis
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Level 3: foscarnet, ganciclovir, and cidofovir have been sug- gested in the second-line treatment of VZV encephalitis in immunocompromised patients, without any official evidence of their benefit. There is currently no data on the use of these molecules in immunocompetent adults
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Level 2: VZV encephalitis can be complicated by cerebral vasculopathy. Adjuvant corticoid therapy may here be of pathophysiologi- cal interest, but clinical studies are scarce and poorly convincing
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Grade B: the recommended dosage of acyclovir in the treat- ment of VZV encephalitis is 15 mg/kg for 1 hour every 8 hours. Grade B: the recommended treatment duration for VZV encephalitis is 14 days. Grade C: foscarnet may be used in the second-line treat- ment of VZV encephalitis (failure, intolerance, resistance to acyclovir). Grade D: it is not recommended to administer an adjuvant corticoid therapy in the treatment of VZV encephalitis
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Level 2: Listeria monocytogenes encephalitis is associated with a 30% case fatality in France. It mostly affects patients presenting with at least one comorbidity and/or aged above 65 years. However, Listeria monocytogenes encephalitis is some- times observed in patients who do not fall under these two categories
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Level 2: amoxicillin is the backbone drug of Listeria monocytogenes encephalitis treatment. There is currently no evidence-based data supporting the superior efficacy of amoxi- cillin versus other antibiotics or combinations. Levels 2 and 3: no evidence-based data supports the use of gentamicin in combination with amoxicillin
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Level 1: trimethoprim-sulfamethoxazole has an in vitro bac- tericidal activity against Listeria monocytogenes. Level 2: on the basis of observational studies and in vitro microbiological data, the combination of amoxicillin and gen- tamicin is considered the reference treatment for documented neuroinvasive listeriosis
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Grade A: the recommended amoxicillin treatment for docu- mented Listeria monocytogenes encephalitis is 200 mg/kg/day divided into 4 infusions minimum or as a continuous adminis- tration every 24 hours for 21 days. Grade C: gentamicin 5 mg/kg/day as a single daily dose for 5 days maximum is recommended as an additional antibiotic
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Grade A: in case of amoxicillin contraindication (proven severe allergy), the high dose combination of trimethoprim and sulfamethoxazole (6 to 9 vials [1 vial = 80 mg/400 mg] per day divided into three IV infusions) must be administered for 21 days
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Level 2: tuberculous encephalitis is associated with a poor prognosis. Patients at highest risk are those infected with HIV, receiving immunosuppressant drugs, aged above 75 years, pre- senting with cancer, blood diseases, and those coming from high incidence countries
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Level 2: there is no evidence-based data on antituberculosis treatment duration for tuberculous encephalitis
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Level 1: tuberculous encephalitis may be complicated by vascular impairment – especially basilar meningitis –, hydrocephalus, tuberculoma/abscess, and even spinal cord compression. The systematic addition of corticoids proved effec- tive in reducing case fatality
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Grade A: in the absence of resistance, the antitubercu- losis treatment with isoniazid (I) (5 mg/kg), rifampicin (R) (10 mg/kg), and pyrazinamide (P) (30 mg/kg without exceed- ing 2 g) is the reference treatment for a duration of 2 months, followed by a dual combination therapy with IR for a total of 12 months (please refer to the table for dosing regimens).
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Ethambutol (E) (20 mg/kg) is added to the initial treatment while waiting for the antimicrobial susceptibility testing results, because it prevents the emergence of resistance if the strain proves resistant to INH
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Grade A: the systematic addition of corticoids (dexametha- sone) is recommended in the treatment of central nervous system tuberculosis. The initial daily dose ranges from 0.3 to 0.4 mg/kg of IV dexamethasone depending on the initial severity. Gradual weaning off over 8 weeks is initiated as early as the end of the first week (Table 2)
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Level 1: if the initial HSV PCR is negative, the likelihood of HSV encephalitis is very small. Level 1: the CSF HSV PCR may be negative the first four days following onset of HSV encephalitis neurological signs. Level 1: the positive predictive value (PPV) of HSV PCR is 95% and its negative predictive value (NPV) is 98%.
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Grade A: HSV encephalitis diagnosis may be ruled out when the HSV PCR performed on the second lumbar puncture four days (minimum) after onset of neurological signs is negative. In that case, acyclovir must be continued until results of this second PCR are available
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Level 1: neurological manifestations of VZV are not always related to the presence of the virus; they may be due to an immuno-inflammatory reaction. Level 1: detection methods of VZV antibody intrathecal secretion are not standardized. They must always be performed on serum and CSF samples collected less than 24 hours apart. For VZV encephalitis, intrathecal secretion of anti-VZV antibodies may be present as early as the first week following symptom onset
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VZV
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Level 1: the PCR performed within 3 to 4 days of neurological sign onset may lead to a false negative result.
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VZV
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Level 1: cerebral vasculitis is often the pathophysiological mechanism
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Grade A: in case of clinical suspicion (vesicular rash and/or cranial nerve damage) and/or suggestive MRI, and when the initial PCR is negative, another PCR should be performed on a new sample four days after symptom onset. Acyclovir should keep on being prescribed with the same dosage while waiting for the PCR results. Grade A: a negative CSF VZV PCR must lead to the detec- tion of intrathecal secretion of anti-VZV antibodies in case of indicative symptoms (vesicular rash and/or cranial nerve dam- age) and/or MRI
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Level 1: true high-risk exposure (consumption of a known contaminated product) or very high-risk exposure is a risk factor for listeriosis. Level 1: exposure to contaminated food reinforces the likeli- hood of contracting neurolisteriosis. Level 1: immunodeficiency is a risk factor for listeriosis
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Level 1: the sensitivity of the Listeria PCR depends on the primers used. The 16s PCR performance is poor. Level 2: specific real-time PCR, which amplifies the hly gene encoding for L. monocytogenes listeriolysin O in CSF, may be used to diagnose neurolisteriosis. Level 1: the sensitivity of this PCR test is 58% and its speci- ficity is 100%
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Level 1: arguments ruling out listeriosis (very low probability when these three factors are present) include: • the absence of risk factor (immunosuppression, cancer, aged > 65 years): 4% of neurolisteriosis cases are observed in young and presumably immunocompetent adults; • negative blood and CSF cultures; • negative hly PCR
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Level 1: rhombencephalitis is not more frequent in neurolis- teriosis patients than in patients receiving presumptive treatment for neurolisteriosis but whose diagnosis is not confirmed. It should not be considered highly evocative of neurolisteriosis. Level 1: no neurological and radiological signs and symptoms are currently indicative of neurolisteriosis
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Grade A: when signs and symptoms indicative of listeriosis are observed, the amoxicillin treatment must be continued even in the absence of microbiological documentation. Grade A: in the absence of signs and symptoms indicative of listeriosis, amoxicillin may be discontinued in case of negative microbiological tests
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[MENINGO-ENCEPHALITE] - Encéphalites SPILF 2017
#Encephalites #Encephalitis #Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation #has-images
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Level 1: the epidemiological context is key to assess the risk of tuberculosis. Level 1: high CSF protein level (> 1 g/L) is indicative of a bacterial infection, the most frequent being Listeria infection followed by Mycobacterium tuberculosis infection
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Level 1: the rapid diagnostic test of tuberculosis by CSF microscopic examination is rarely positive. Level 1: real-time PCR used to diagnose tuberculosis has an 84% negative predictive value. Level 1: sensitivity and specificity of serum IGRA tests are 78% and 61%, respectively. Level 1: sensitivity and specificity of CSF IGRA tests are 77% and 88%, respectively.
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Level 1: sensitivity of Mycobacterium tuberculosis micro- biological detection (direct examination and culture) increases with the amount of CSF sampled
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Grade A: it is recommended to initiate a trial of antituberculo- sis treatment if the clinical, biological, and imaging signs are, at this point, indicative of tuberculosis, even when the microscopic examination and PCR tests are negative. Grade A: a negative real-time PCR does not rule out tuber- culosis. Grade A: real-time PCR must be performed on samples of at least 2 mL, that must be centrifugated before being tested
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Grade D: blood IGRA tests are not recommended to diagnose meningitis and tuberculous encephalitis. Grade D: CSF IGRA tests are not recommended to diagnose meningitis and tuberculous encephalitis
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Level 1: no study results currently help in validating the pre- scription of corticoids to patients presenting with encephalitis of unknown origin
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Tuberculose NM
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Grade B: a corticoid and/or immunoglobulin prescription must lead to a multidisciplinary meeting
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Level 1: intracellular bacteria account, in France, for 2% of identified etiologies of presumably infectious encephalitis cases, while Spirochaeta bacteria (Treponema, Borrelia) account for 1.5%
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Grade C: in the absence of clear features indicative of one of the four most common etiologies or in case of a suspected encephalitis caused by intracellular bacteria, a trial of doxycy- cline treatment can be discussed based on the epidemiological suspicion.
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Level 1: of all causes of encephalitis identified in France in 2007, 80% were human-to-human transmission diseases. Level 1: at-risk exposure is not synonymous with a confirmed exposure nor is it synonymous with infection.
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Grade A: additional infectious investigations must be guided by the patient’s age, underlying conditions, occupational or leisure exposure, season, travels, extra-neurological signs, and biological features
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Level 1: non-infectious causes account for 22% of indicative signs of infectious encephalitis.
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Level 1: autoimmune encephalitis patients usually present with subacute symptoms of limbic encephalitis or acute dis- seminated encephalomyelitis. Diagnosis relies on anti-synaptic or anti-cellular onconeural antibody tests for autoimmune encephalitis, and on brain and spine MRI for acute disseminated encephalomyelitis
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Level 1: systemic lupus erythematosus, Sjögren’s syndrome, and Hashimoto’s encephalopathy are the most frequent alterna- tive non-infectious diagnoses.
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Grade A: for persistent encephalitis of unknown origin, a brain biopsy must be discussed at multidisciplinary meetings. It should always include non-fixed samples (microbiology) and fixed samples (pathology). Grade A: when the decision has been taken to perform a biopsy, the microbiologist must be notified to ensure pre-analysis quality of microbiological samples
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Grade A: an MRI must be performed to diagnose acute dis- seminated encephalomyelitis. Grade A: autoimmune encephalitis diagnosis by serum and CSF onconeural antibody and systemic disease detection must be performed when confronted with limbic encephalitis or encephalitis of unknown origin
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The presence or absence of normal brain function is the important distinguishing feature between encephalitis and meningitis. Patients with meningitis may be uncomfortable, lethargic, or distracted by headache, but their cerebral function remains normal. In encephalitis, however, abnormalities in brain function are a differentiating feature, including altered mental status, motor or sensory deficits, altered behavior and personality changes, and speech or movement disorders
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UpToDate
sis" and "Acute viral encephalitis in children: Treatment and prevention" and "Acute viral encephalitis in children: Pathogenesis, epidemiology, and etiology".) MENINGITIS VERSUS ENCEPHALITIS — <span>The presence or absence of normal brain function is the important distinguishing feature between encephalitis and meningitis. Patients with meningitis may be uncomfortable, lethargic, or distracted by headache, but their cerebral function remains normal. In encephalitis, however, abnormalities in brain function are a differentiating feature, including 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 of encephalitis may




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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 of encephalitis may include hemiparesis, flaccid paralysis, and paresthesias
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UpToDate
malities in brain function are a differentiating feature, including 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 of encephalitis may include hemiparesis, flaccid paralysis, and paresthesias. However, the distinction between the two entities can be frequently blurred since some patients may have both a parenchymal and meningeal process with clinical features of both. The pa




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The importance of distinguishing between encephalitis and aseptic meningitis relates to the fact that the likely cause of each syndrome is different. Some viral agents are more likely to cause aseptic meningitis, and others are more likely to cause encephalitis. (See "Aseptic meningitis in adults".)
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UpToDate
ient 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. <span>The importance of distinguishing between encephalitis and aseptic meningitis relates to the fact that the likely cause of each syndrome is different. Some viral agents are more likely to cause aseptic meningitis, and others are more likely to cause encephalitis. (See "Aseptic meningitis in adults".) VIRAL VERSUS POSTINFECTIOUS ENCEPHALITIS — Viral encephalitis can be either primary or postinfectious (ie, it occurs after the infection has resolved) [5]. ●Primary infection is charact




#Encephalites #Encephalitis #Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation #U2D

Viral encephalitis can be either primary or postinfectious (ie, it occurs after the infection has resolved) [5].

● Primary infection is characterized by viral invasion of the central nervous system (CNS). Neuronal involvement can be identified on histologic examination, which may show inclusion bodies on light microscopy or viral particles on electron microscopy. The virus can often be cultured from brain tissue.

● In postinfectious encephalitis (also called acute disseminated encephalomyelitis, or ADEM), a virus cannot be detected or recovered, and the neurons are spared [5]. However, perivascular inflammation and demyelination are prominent in this entity. The inability to recover a virus and the type of histologic abnormalities observed suggest that postinfectious encephalitis is an immune-mediated disease [6]. (See "Acute disseminated encephalomyelitis (ADEM) in adults".)

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Some viral agents are more likely to cause aseptic meningitis, and others are more likely to cause encephalitis. (See "Aseptic meningitis in adults".) VIRAL VERSUS POSTINFECTIOUS ENCEPHALITIS — <span>Viral encephalitis can be either primary or postinfectious (ie, it occurs after the infection has resolved) [5]. ●Primary infection is characterized by viral invasion of the central nervous system (CNS). Neuronal involvement can be identified on histologic examination, which may show inclusion bodies on light microscopy or viral particles on electron microscopy. The virus can often be cultured from brain tissue. ●In postinfectious encephalitis (also called acute disseminated encephalomyelitis, or ADEM), a virus cannot be detected or recovered, and the neurons are spared [5]. However, perivascular inflammation and demyelination are prominent in this entity. The inability to recover a virus and the type of histologic abnormalities observed suggest that postinfectious encephalitis is an immune-mediated disease [6]. (See "Acute disseminated encephalomyelitis (ADEM) in adults".) Despite the differences in pathogenesis and histologic findings, the clinical significance of viral versus postinfectious encephalitis is often limited. It is also important to note tha




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Despite the differences in pathogenesis and histologic findings, the clinical significance of viral versus postinfectious encephalitis is often limited. It is also important to note that a number of viral infections, such as measles, varicella, or rubella, can produce either syndrome. (See 'Viral pathogens' below.)
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irus and the type of histologic abnormalities observed suggest that postinfectious encephalitis is an immune-mediated disease [6]. (See "Acute disseminated encephalomyelitis (ADEM) in adults".) <span>Despite the differences in pathogenesis and histologic findings, the clinical significance of viral versus postinfectious encephalitis is often limited. It is also important to note that a number of viral infections, such as measles, varicella, or rubella, can produce either syndrome. (See 'Viral pathogens' below.) VIRAL PATHOGENS — A wide variety of different viruses can infect the central nervous system (CNS). Most viruses are capable of causing either meningitis or encephalitis, although, in ge




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A wide variety of different viruses can infect the central nervous system (CNS). Most viruses are capable of causing either meningitis or encephalitis, although, in general, a given virus is more likely to cause one syndrome rather than the other.
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en limited. It is also important to note that a number of viral infections, such as measles, varicella, or rubella, can produce either syndrome. (See 'Viral pathogens' below.) VIRAL PATHOGENS — <span>A wide variety of different viruses can infect the central nervous system (CNS). Most viruses are capable of causing either meningitis or encephalitis, although, in general, a given virus is more likely to cause one syndrome rather than the other. (See 'Meningitis versus encephalitis' above.) A common cause of sporadic encephalitis is herpes simplex virus (HSV) type 1 [7]. It is important to diagnose this virus because it is trea




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A common cause of sporadic encephalitis is herpes simplex virus (HSV) type 1 [7]. It is important to diagnose this virus because it is treatable, and the success of treatment is related to how early therapy is initiated.
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pable of causing either meningitis or encephalitis, although, in general, a given virus is more likely to cause one syndrome rather than the other. (See 'Meningitis versus encephalitis' above.) <span>A common cause of sporadic encephalitis is herpes simplex virus (HSV) type 1 [7]. It is important to diagnose this virus because it is treatable, and the success of treatment is related to how early therapy is initiated. (See "Herpes simplex virus type 1 encephalitis".) Other viral pathogens may be suggested by geographic location (eg, Eastern equine encephalitis in North America and Japanese encephalit




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Other viral pathogens may be suggested by geographic location (eg, Eastern equine encephalitis in North America and Japanese encephalitis in Asia) and epidemiologic clues, such as exposure history (eg, bat exposure or dog bite and rabies), regional outbreaks (eg, enterovirus type 71 in Denver, Colorado) [8], and clinical clues, such as profound weakness and rash with West Nile. Uncommon causes include varicella zoster virus, Epstein-Barr virus, HIV, human herpes virus-6, parvovirus, and Zika virus [9-13]. (See "St. Louis encephalitis" and "Arthropod-borne encephalitides" and "Clinical manifestations and diagnosis of rabies".)
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[7]. It is important to diagnose this virus because it is treatable, and the success of treatment is related to how early therapy is initiated. (See "Herpes simplex virus type 1 encephalitis".) <span>Other viral pathogens may be suggested by geographic location (eg, Eastern equine encephalitis in North America and Japanese encephalitis in Asia) and epidemiologic clues, such as exposure history (eg, bat exposure or dog bite and rabies), regional outbreaks (eg, enterovirus type 71 in Denver, Colorado) [8], and clinical clues, such as profound weakness and rash with West Nile. Uncommon causes include varicella zoster virus, Epstein-Barr virus, HIV, human herpes virus-6, parvovirus, and Zika virus [9-13]. (See "St. Louis encephalitis" and "Arthropod-borne encephalitides" and "Clinical manifestations and diagnosis of rabies".) Historical clues — The cause of viral encephalitis is apparent in some cases because of an unusual exposure history or a characteristic clinical presentation. In the absence of these fi




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Arboviruses (eg, eastern equine, western equine, St. Louis, Venezuelan equine encephalitis, and West Nile virus) cause disease when mosquitoes are active, whereas HSV can occur at any time
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sentation. In the absence of these findings, epidemiologic information such as seasonal occurrence or exposures may be helpful in establishing a specific diagnosis (table 1). Examples include: ●<span>Arboviruses (eg, eastern equine, western equine, St. Louis, Venezuelan equine encephalitis, and West Nile virus) cause disease when mosquitoes are active, whereas HSV can occur at any time. In contrast, walking in woods or marshy areas with high tick populations might suggest tick-borne encephalitides seen in Eastern Europe, Colorado tick fever (western United States), an




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In contrast, walking in woods or marshy areas with high tick populations might suggest tick-borne encephalitides seen in Eastern Europe, Colorado tick fever (western United States), and Powassan virus encephalitis. Powassan virus is transmitted by Ixodes ticks and should be considered in regions where these ticks are found (eg, eastern Canada and the north central and northeastern United States). Other tick-borne but nonviral etiologies include Lyme disease and Rocky Mountain spotted fever.
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e: ●Arboviruses (eg, eastern equine, western equine, St. Louis, Venezuelan equine encephalitis, and West Nile virus) cause disease when mosquitoes are active, whereas HSV can occur at any time. <span>In contrast, walking in woods or marshy areas with high tick populations might suggest tick-borne encephalitides seen in Eastern Europe, Colorado tick fever (western United States), and Powassan virus encephalitis. Powassan virus is transmitted by Ixodes ticks and should be considered in regions where these ticks are found (eg, eastern Canada and the north central and northeastern United States). Other tick-borne but nonviral etiologies include Lyme disease and Rocky Mountain spotted fever. (See "Epidemiology and pathogenesis of West Nile virus infection" and "St. Louis encephalitis" and "Arthropod-borne encephalitides" and "Clinical manifestations and diagnosis of Rocky M




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West Nile virus has been by far the most common cause of proven viral encephalitis in the United States [14,15]. West Nile virus first appeared in the United States in 1999, even though it had already been established in Africa, Asia, and Europe, and then spread rapidly across the country.
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y and pathogenesis of West Nile virus infection" and "St. Louis encephalitis" and "Arthropod-borne encephalitides" and "Clinical manifestations and diagnosis of Rocky Mountain spotted fever".) ●<span>West Nile virus has been by far the most common cause of proven viral encephalitis in the United States [14,15]. West Nile virus first appeared in the United States in 1999, even though it had already been established in Africa, Asia, and Europe, and then spread rapidly across the country. The incidence of other arboviruses varies significantly based upon geographic region. As examples, in the Northeast, there has been a steady increase in Powassan over the past several y




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Nipah virus encephalitis, which appeared in Malaysia and Singapore and is now present in Bangladesh, may be associated with exposure to pigs or bats [18-20]
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tions and diagnosis in nonpregnant adults and children" and "Arthropod-borne encephalitides".) ●Both geography and animal exposure can broaden the diagnostic considerations of etiologic agents. <span>Nipah virus encephalitis, which appeared in Malaysia and Singapore and is now present in Bangladesh, may be associated with exposure to pigs or bats [18-20]. Human infection with Hendra virus, which is seen in Australia, results from direct contact with infected horses. Avian influenza infection was associated with encephalitis in two patie




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Human infection with Hendra virus, which is seen in Australia, results from direct contact with infected horses.
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considerations of etiologic agents. Nipah virus encephalitis, which appeared in Malaysia and Singapore and is now present in Bangladesh, may be associated with exposure to pigs or bats [18-20]. <span>Human infection with Hendra virus, which is seen in Australia, results from direct contact with infected horses. Avian influenza infection was associated with encephalitis in two patients from Vietnam; the source of exposure was unclear but both children swam in a canal that was frequented by duck




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Avian influenza infection was associated with encephalitis in two patients from Vietnam; the source of exposure was unclear but both children swam in a canal that was frequented by ducks [ 21].
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present in Bangladesh, may be associated with exposure to pigs or bats [18-20]. Human infection with Hendra virus, which is seen in Australia, results from direct contact with infected horses. <span>Avian influenza infection was associated with encephalitis in two patients from Vietnam; the source of exposure was unclear but both children swam in a canal that was frequented by ducks [21]. Lymphocytic choriomeningitis virus (LCMV) is a human-acquired zoonosis caused by a rodent-borne arenavirus, which can be transmitted through exposure to secretions of mice, rats, and ha




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Lymphocytic choriomeningitis virus (LCMV) is a human-acquired zoonosis caused by a rodent-borne arenavirus, which can be transmitted through exposure to secretions of mice, rats, and hamsters.
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Avian influenza infection was associated with encephalitis in two patients from Vietnam; the source of exposure was unclear but both children swam in a canal that was frequented by ducks [21]. <span>Lymphocytic choriomeningitis virus (LCMV) is a human-acquired zoonosis caused by a rodent-borne arenavirus, which can be transmitted through exposure to secretions of mice, rats, and hamsters. Encephalitis resulting from a bornavirus was reported in three German breeders of variegated squirrels; the virus was also detected in a squirrel from the breeding population of one of




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Encephalitis resulting from a bornavirus was reported in three German breeders of variegated squirrels; the virus was also detected in a squirrel from the breeding population of one of the patients [ 22].
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Lymphocytic choriomeningitis virus (LCMV) is a human-acquired zoonosis caused by a rodent-borne arenavirus, which can be transmitted through exposure to secretions of mice, rats, and hamsters. <span>Encephalitis resulting from a bornavirus was reported in three German breeders of variegated squirrels; the virus was also detected in a squirrel from the breeding population of one of the patients [22]. (See "Nipah and Hendra viral encephalitis" and "Avian influenza: Epidemiology, transmission, and pathogenesis" and "Aseptic meningitis in adults".) ●Prior history of an animal exposure




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Prior history of an animal exposure or bite may also suggest the possibility of rabies encephalitis; however the absence of such a history does not eliminate the diagnostic possibility of rabies.
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ding population of one of the patients [22]. (See "Nipah and Hendra viral encephalitis" and "Avian influenza: Epidemiology, transmission, and pathogenesis" and "Aseptic meningitis in adults".) ●<span>Prior history of an animal exposure or bite may also suggest the possibility of rabies encephalitis; however the absence of such a history does not eliminate the diagnostic possibility of rabies. (See "Clinical manifestations and diagnosis of rabies".) CLINICAL MANIFESTATIONS Signs and symptoms — Patients with encephalitis have an altered mental status ranging from subtle defici




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Patients with encephalitis have an altered mental status ranging from subtle deficits to complete unresponsiveness. Symptoms and signs of meningeal irritation (photophobia and nuchal rigidity) are usually absent with a pure encephalitis, but often accompany a meningoencephalitis
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ever the absence of such a history does not eliminate the diagnostic possibility of rabies. (See "Clinical manifestations and diagnosis of rabies".) CLINICAL MANIFESTATIONS Signs and symptoms — <span>Patients with encephalitis have an altered mental status ranging from subtle deficits to complete unresponsiveness. Symptoms and signs of meningeal irritation (photophobia and nuchal rigidity) are usually absent with a pure encephalitis, but often accompany a meningoencephalitis. Seizures are common with encephalitis, and focal neurologic abnormalities can occur, including hemiparesis, cranial nerve palsies, and exaggerated deep tendon and/or pathologic reflexe




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Seizures are common with encephalitis, and focal neurologic abnormalities can occur, including hemiparesis, cranial nerve palsies, and exaggerated deep tendon and/or pathologic reflexes. Patients may appear confused, agitated, or obtunded
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o complete unresponsiveness. Symptoms and signs of meningeal irritation (photophobia and nuchal rigidity) are usually absent with a pure encephalitis, but often accompany a meningoencephalitis. <span>Seizures are common with encephalitis, and focal neurologic abnormalities can occur, including hemiparesis, cranial nerve palsies, and exaggerated deep tendon and/or pathologic reflexes. Patients may appear confused, agitated, or obtunded. The clinical presentation of aseptic meningitis is generally nonspecific, with fever, headache, nausea, and vomiting, occasionally accompanied by photophobia and a stiff neck. Physical




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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 characteristically reveals signs of nuchal rigidity, but its absence does not rule out the diagnosis.
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al neurologic abnormalities can occur, including hemiparesis, cranial nerve palsies, and exaggerated deep tendon and/or pathologic reflexes. Patients may appear confused, agitated, or obtunded. <span>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 characteristically reveals signs of nuchal rigidity, but its absence does not rule out the diagnosis. (See "Aseptic meningitis in adults".) Clues on physical examination — Although there are usually no pathognomonic findings on the initial patient encounter, certain physical examination




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Parotitis strongly suggests the diagnosis of mumps encephalitis in an unvaccinated patient with mental status changes. (See "Mumps".)
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Clues on physical examination — Although there are usually no pathognomonic findings on the initial patient encounter, certain physical examination features may suggest a particular diagnosis: ●<span>Parotitis strongly suggests the diagnosis of mumps encephalitis in an unvaccinated patient with mental status changes. (See "Mumps".) ●Flaccid paralysis, a polio-like presentation, that evolves into an encephalitis strongly suggests the possibility of West Nile virus infection [23]. In fact, it has been misdiagnosed a




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Flaccid paralysis, a polio-like presentation, that evolves into an encephalitis strongly suggests the possibility of West Nile virus infection [23]. In fact, it has been misdiagnosed as Guillain-Barré syndrome. A maculopapular rash is also seen in approximately half of patients with this infection and is not expected in other viral encephalitides.
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examination features may suggest a particular diagnosis: ●Parotitis strongly suggests the diagnosis of mumps encephalitis in an unvaccinated patient with mental status changes. (See "Mumps".) ●<span>Flaccid paralysis, a polio-like presentation, that evolves into an encephalitis strongly suggests the possibility of West Nile virus infection [23]. In fact, it has been misdiagnosed as Guillain-Barré syndrome. A maculopapular rash is also seen in approximately half of patients with this infection and is not expected in other viral encephalitides. ●Tremors of the eyelids, tongue, lips, and extremities may suggest the possibility of St. Louis encephalitis or West Nile encephalitis in the appropriate geographic location or travel h




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Tremors of the eyelids, tongue, lips, and extremities may suggest the possibility of St. Louis encephalitis or West Nile encephalitis in the appropriate geographic location or travel history
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it has been misdiagnosed as Guillain-Barré syndrome. A maculopapular rash is also seen in approximately half of patients with this infection and is not expected in other viral encephalitides. ●<span>Tremors of the eyelids, tongue, lips, and extremities may suggest the possibility of St. Louis encephalitis or West Nile encephalitis in the appropriate geographic location or travel history. ●Findings of hydrophobia, aerophobia, pharyngeal spasms, and hyperactivity suggest encephalitic rabies. Atypical presentations of rabies include seizures, cranial nerve palsies, and my




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Findings of hydrophobia, aerophobia, pharyngeal spasms, and hyperactivity suggest encephalitic rabies. Atypical presentations of rabies include seizures, cranial nerve palsies, and myoclonus
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●Tremors of the eyelids, tongue, lips, and extremities may suggest the possibility of St. Louis encephalitis or West Nile encephalitis in the appropriate geographic location or travel history. ●<span>Findings of hydrophobia, aerophobia, pharyngeal spasms, and hyperactivity suggest encephalitic rabies. Atypical presentations of rabies include seizures, cranial nerve palsies, and myoclonus. ●Grouped vesicles in a dermatomal pattern may suggest varicella zoster virus (VZV), which can occasionally cause encephalitis; however, the absence of rash does not eliminate VZV from




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Grouped vesicles in a dermatomal pattern may suggest varicella zoster virus (VZV), which can occasionally cause encephalitis; however, the absence of rash does not eliminate VZV from consideration [24]. (See "Epidemiology, clinical manifestations, and diagnosis of herpes zoster".)
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●Findings of hydrophobia, aerophobia, pharyngeal spasms, and hyperactivity suggest encephalitic rabies. Atypical presentations of rabies include seizures, cranial nerve palsies, and myoclonus. ●<span>Grouped vesicles in a dermatomal pattern may suggest varicella zoster virus (VZV), which can occasionally cause encephalitis; however, the absence of rash does not eliminate VZV from consideration [24]. (See "Epidemiology, clinical manifestations, and diagnosis of herpes zoster".) Imaging — Results of imaging in patients with encephalitis may or may not demonstrate abnormal radiographic findings on computed tomography (CT) or magnetic resonance imaging (MRI) moda




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Temporal lobe involvement is strongly suggestive of herpes simplex virus (HSV) encephalitis, although other herpes viruses (eg, VZV, Epstein-Barr virus, human herpesvirus 6) can also produce this clinical picture [25,26].
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DEM] or possibly a relatively rapid presentation of progressive multifocal leukoencephalopathy). If present, the location of abnormal signal can sometimes be suggestive of specific etiologies: ●<span>Temporal lobe involvement is strongly suggestive of herpes simplex virus (HSV) encephalitis, although other herpes viruses (eg, VZV, Epstein-Barr virus, human herpesvirus 6) can also produce this clinical picture [25,26]. ●Involvement of the thalamus or basal ganglia may be observed in the setting of encephalitis due to respiratory viral infection, Creutzfeldt-Jakob disease, arbovirus, and tuberculosis [




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Involvement of the thalamus or basal ganglia may be observed in the setting of encephalitis due to respiratory viral infection, Creutzfeldt-Jakob disease, arbovirus, and tuberculosis [27-29].
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strongly suggestive of herpes simplex virus (HSV) encephalitis, although other herpes viruses (eg, VZV, Epstein-Barr virus, human herpesvirus 6) can also produce this clinical picture [25,26]. ●<span>Involvement of the thalamus or basal ganglia may be observed in the setting of encephalitis due to respiratory viral infection, Creutzfeldt-Jakob disease, arbovirus, and tuberculosis [27-29]. ●In a study of 17 patients with confirmed West Nile infection, MRI imaging demonstrated a variety of abnormalities in the basal ganglia, thalami, mesial temporal structures, brainstem,




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In a study of 17 patients with confirmed West Nile infection, MRI imaging demonstrated a variety of abnormalities in the basal ganglia, thalami, mesial temporal structures, brainstem, and cerebellum in eight patients [30]. Three patients with muscle weakness also had abnormalities noted in the spinal cord and cauda equina.
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●Involvement of the thalamus or basal ganglia may be observed in the setting of encephalitis due to respiratory viral infection, Creutzfeldt-Jakob disease, arbovirus, and tuberculosis [27-29]. ●<span>In a study of 17 patients with confirmed West Nile infection, MRI imaging demonstrated a variety of abnormalities in the basal ganglia, thalami, mesial temporal structures, brainstem, and cerebellum in eight patients [30]. Three patients with muscle weakness also had abnormalities noted in the spinal cord and cauda equina. ●The presence of hydrocephalus may suggest nonviral etiologies such as bacteria, fungal, or parasitic agents [26]. ●MRI during postinfectious encephalitis may demonstrate multifocal les




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The presence of hydrocephalus may suggest nonviral etiologies such as bacteria, fungal, or parasitic agents [26].
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ia, thalami, mesial temporal structures, brainstem, and cerebellum in eight patients [30]. Three patients with muscle weakness also had abnormalities noted in the spinal cord and cauda equina. ●<span>The presence of hydrocephalus may suggest nonviral etiologies such as bacteria, fungal, or parasitic agents [26]. ●MRI during postinfectious encephalitis may demonstrate multifocal lesions mainly involving supratentorial white matter [6]. (See 'Viral versus postinfectious encephalitis' above.) Elec




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MRI during postinfectious encephalitis may demonstrate multifocal lesions mainly involving supratentorial white matter [6]. (See 'Viral versus postinfectious encephalitis' above.)
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le weakness also had abnormalities noted in the spinal cord and cauda equina. ●The presence of hydrocephalus may suggest nonviral etiologies such as bacteria, fungal, or parasitic agents [26]. ●<span>MRI during postinfectious encephalitis may demonstrate multifocal lesions mainly involving supratentorial white matter [6]. (See 'Viral versus postinfectious encephalitis' above.) Electroencephalograph — Electroencephalography is often abnormal in acute encephalitis. Focality in the temporal lobe region is suggestive of HSV encephalitis, as noted above [31]. Cere




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Electroencephalography is often abnormal in acute encephalitis. Focality in the temporal lobe region is suggestive of HSV encephalitis, as noted above [31].
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postinfectious encephalitis may demonstrate multifocal lesions mainly involving supratentorial white matter [6]. (See 'Viral versus postinfectious encephalitis' above.) Electroencephalograph — <span>Electroencephalography is often abnormal in acute encephalitis. Focality in the temporal lobe region is suggestive of HSV encephalitis, as noted above [31]. Cerebrospinal fluid findings — Examination of the cerebrospinal fluid (CSF), although not diagnostic, will usually confirm the presence of inflammatory disease of the central nervous sy




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The findings with aseptic meningitis and encephalitis are generally indistinguishable (although, rarely, there may be few, if any, CSF abnormalities with a pure encephalitis).
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ebrospinal fluid findings — Examination of the cerebrospinal fluid (CSF), although not diagnostic, will usually confirm the presence of inflammatory disease of the central nervous system (CNS). <span>The findings with aseptic meningitis and encephalitis are generally indistinguishable (although, rarely, there may be few, if any, CSF abnormalities with a pure encephalitis). The following findings are characteristic of viral CNS infections (table 2): ●Increased white blood cell (WBC) count, but usually less than 250/mm3. The differential shows a predominanc




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The following findings are characteristic of viral CNS infections (table 2):

● Increased white blood cell (WBC) count, but usually less than 250/mm3. The differential shows a predominance of lymphocytes, although early infection may reveal a predominance of neutrophils. In the latter setting, a repeat CSF cell count eight hours later will generally show a shift from neutrophils to lymphocytes [32].

● Elevated protein concentration, but usually less than 150 mg/dL.

● Usually normal glucose concentration (>50 percent of blood value), but moderately reduced values are occasionally seen with HSV, mumps, or some enteroviruses.

● Red cells are usually absent (in a nontraumatic tap); their presence in the appropriate clinical setting suggests HSV-1 infection or other necrotizing encephalitides [33].

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ous system (CNS). The findings with aseptic meningitis and encephalitis are generally indistinguishable (although, rarely, there may be few, if any, CSF abnormalities with a pure encephalitis). <span>The following findings are characteristic of viral CNS infections (table 2): ●Increased white blood cell (WBC) count, but usually less than 250/mm3. The differential shows a predominance of lymphocytes, although early infection may reveal a predominance of neutrophils. In the latter setting, a repeat CSF cell count eight hours later will generally show a shift from neutrophils to lymphocytes [32]. ●Elevated protein concentration, but usually less than 150 mg/dL. ●Usually normal glucose concentration (>50 percent of blood value), but moderately reduced values are occasionally seen with HSV, mumps, or some enteroviruses. ●Red cells are usually absent (in a nontraumatic tap); their presence in the appropriate clinical setting suggests HSV-1 infection or other necrotizing encephalitides [33]. These findings are generally quite different from those associated with bacterial meningitis, which include a higher WBC count in the CSF (>2000/mm3) with neutrophil predominance, a




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Analysis of the cerebrospinal fluid (CSF) is required as an initial diagnostic step in patients with suspected viral encephalitis.

● The opening CSF pressure should be noted and CSF should be analyzed for cell count, glucose, and protein.

● In addition to this basic testing, the initial work-up for the etiology of a viral infection should generally include: CSF polymerase chain reaction (PCR) testing for herpes simplex virus (HSV)-1, HSV-2, VZV, and enteroviruses.

● Additional testing (eg, serology for arboviruses, HIV testing) should be considered based on geographic considerations, the clinical presentation, and the exposure history. (See 'Historical clues' above.)

● Diagnostic evaluation for nonviral infectious (eg, bacteria, fungi, and mycobacteria) and noninfectious etiologies should also be considered. (See 'Differential diagnosis' below.)

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dings, it can reduce the yield of Gram stain and culture. (See "Clinical features and diagnosis of acute bacterial meningitis in adults", section on 'If LP is delayed or deferred'.) DIAGNOSIS — <span>Analysis of the cerebrospinal fluid (CSF) is required as an initial diagnostic step in patients with suspected viral encephalitis. ●The opening CSF pressure should be noted and CSF should be analyzed for cell count, glucose, and protein. ●In addition to this basic testing, the initial work-up for the etiology of a viral infection should generally include: CSF polymerase chain reaction (PCR) testing for herpes simplex virus (HSV)-1, HSV-2, VZV, and enteroviruses. ●Additional testing (eg, serology for arboviruses, HIV testing) should be considered based on geographic considerations, the clinical presentation, and the exposure history. (See 'Historical clues' above.) ●Diagnostic evaluation for nonviral infectious (eg, bacteria, fungi, and mycobacteria) and noninfectious etiologies should also be considered. (See 'Differential diagnosis' below.) The most important viral etiology to rule out in a patient with encephalitis is HSV, since this clinical entity is usually fatal if untreated. HSV should be considered, particularly if




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The most important viral etiology to rule out in a patient with encephalitis is HSV, since this clinical entity is usually fatal if untreated. HSV should be considered, particularly if there is temporal lobe focality suggested by symptoms, signs, or imaging studies.
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ues' above.) ●Diagnostic evaluation for nonviral infectious (eg, bacteria, fungi, and mycobacteria) and noninfectious etiologies should also be considered. (See 'Differential diagnosis' below.) <span>The most important viral etiology to rule out in a patient with encephalitis is HSV, since this clinical entity is usually fatal if untreated. HSV should be considered, particularly if there is temporal lobe focality suggested by symptoms, signs, or imaging studies. Diagnosis is most readily made by detecting HSV DNA by PCR on CSF [35]. While awaiting confirmation, empiric therapy with acyclovir should be initiated. (See 'Empiric therapy' below.) E




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Diagnosis is most readily made by detecting HSV DNA by PCR on CSF [ 35]. While awaiting confirmation, empiric therapy with acyclovir should be initiated. (See 'Empiric therapy' below.)
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tis is HSV, since this clinical entity is usually fatal if untreated. HSV should be considered, particularly if there is temporal lobe focality suggested by symptoms, signs, or imaging studies. <span>Diagnosis is most readily made by detecting HSV DNA by PCR on CSF [35]. While awaiting confirmation, empiric therapy with acyclovir should be initiated. (See 'Empiric therapy' below.) Enteroviruses are more commonly associated with viral meningitis, but infrequently they may cause encephalitis as well. PCR testing on the CSF sample is the diagnostic test of choice. T




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Enteroviruses are more commonly associated with viral meningitis, but infrequently they may cause encephalitis as well. PCR testing on the CSF sample is the diagnostic test of choice. The pathogen can also be cultured from the stool and throat; however, a positive stool or throat culture is not necessarily diagnostic of disease, especially in summer months.
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studies. Diagnosis is most readily made by detecting HSV DNA by PCR on CSF [35]. While awaiting confirmation, empiric therapy with acyclovir should be initiated. (See 'Empiric therapy' below.) <span>Enteroviruses are more commonly associated with viral meningitis, but infrequently they may cause encephalitis as well. PCR testing on the CSF sample is the diagnostic test of choice. The pathogen can also be cultured from the stool and throat; however, a positive stool or throat culture is not necessarily diagnostic of disease, especially in summer months. Rabies should also be considered in any patient with an undiagnosed encephalitis even with a negative exposure history. Diagnosis of rabies requires several specimens including saliva,




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Rabies should also be considered in any patient with an undiagnosed encephalitis even with a negative exposure history. Diagnosis of rabies requires several specimens including saliva, skin biopsy, and CSF since the sensitivity of any single test is limited.
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c test of choice. The pathogen can also be cultured from the stool and throat; however, a positive stool or throat culture is not necessarily diagnostic of disease, especially in summer months. <span>Rabies should also be considered in any patient with an undiagnosed encephalitis even with a negative exposure history. Diagnosis of rabies requires several specimens including saliva, skin biopsy, and CSF since the sensitivity of any single test is limited. (See "Clinical manifestations and diagnosis of rabies".) In summary, the battery of initial diagnostic tests often includes CSF culture, PCR, and serology for the suspected pathogens. F




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Viral culture has been routinely ordered by most clinicians after obtaining CSF samples. However, one review demonstrated that viruses were recovered from only 6 percent of 22,394 viral cultures of CSF samples [36].
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ing may also be required if the patient is not improving. However, even with use of PCR testing, the etiology in many cases remains undefined [35]. (See 'Definitive diagnosis' below.) Culture — <span>Viral culture has been routinely ordered by most clinicians after obtaining CSF samples. However, one review demonstrated that viruses were recovered from only 6 percent of 22,394 viral cultures of CSF samples [36]. Furthermore, in a subset analysis by suspected etiology, 1290 CSF samples were evaluated for HSV by PCR and culture. Of these, only nine samples were positive for HSV and all were ident




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Culture may still be important when rare causes of encephalitis are being considered (eg, influenza, parainfluenza, measles, mumps) for which PCR testing is unavailable.
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culture. Of these, only nine samples were positive for HSV and all were identified only by PCR testing. In most circumstances, PCR testing has replaced viral culture in the work-up of the CSF. <span>Culture may still be important when rare causes of encephalitis are being considered (eg, influenza, parainfluenza, measles, mumps) for which PCR testing is unavailable. Polymerase chain reaction — With the advent of PCR technology, significant advances have been made in the ability to diagnose viral infections of the central nervous system (CNS) [37].




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Identification of HSV-1 in the CSF is a rapid, sensitive, and specific diagnostic test for HSV-1 encephalitis [38]. Likewise, identification of HSV-2 in CSF is a rapid diagnostic test for HSV-2 meningitis.
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, significant advances have been made in the ability to diagnose viral infections of the central nervous system (CNS) [37]. CSF PCR should be performed for HSV-1, HSV-2, VZV, and enteroviruses. <span>Identification of HSV-1 in the CSF is a rapid, sensitive, and specific diagnostic test for HSV-1 encephalitis [38]. Likewise, identification of HSV-2 in CSF is a rapid diagnostic test for HSV-2 meningitis. PCR testing for other viruses will depend on the clinical situation, epidemiology, and availability. For West Nile virus, PCR testing is not as sensitive as IgM serology (the preferred




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PCR testing for other viruses will depend on the clinical situation, epidemiology, and availability. For West Nile virus, PCR testing is not as sensitive as IgM serology (the preferred test). (See "PCR testing for the diagnosis of herpes simplex virus in patients with encephalitis or meningitis".)
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on of HSV-1 in the CSF is a rapid, sensitive, and specific diagnostic test for HSV-1 encephalitis [38]. Likewise, identification of HSV-2 in CSF is a rapid diagnostic test for HSV-2 meningitis. <span>PCR testing for other viruses will depend on the clinical situation, epidemiology, and availability. For West Nile virus, PCR testing is not as sensitive as IgM serology (the preferred test). (See "PCR testing for the diagnosis of herpes simplex virus in patients with encephalitis or meningitis".) Serology — Serologic testing is most important for patients who are not improving and who do not have a diagnosis based upon PCR. Most viral etiologies require paired sera for diagnosis




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Serology — Serologic testing is most important for patients who are not improving and who do not have a diagnosis based upon PCR. Most viral etiologies require paired sera for diagnosis; thus it is prudent to save serum in the setting of acute illness that can later be used if necessary. Convalescent serology should be obtained no sooner than three weeks after the onset of the clinical illness. As an example, the presence of IgM antibodies in a single serum provides presumptive evidence of St. Louis encephalitis; however, a significant rise or fall between appropriately timed acute convalescent or early-late convalescent sera is diagnostic.
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West Nile virus, PCR testing is not as sensitive as IgM serology (the preferred test). (See "PCR testing for the diagnosis of herpes simplex virus in patients with encephalitis or meningitis".) <span>Serology — Serologic testing is most important for patients who are not improving and who do not have a diagnosis based upon PCR. Most viral etiologies require paired sera for diagnosis; thus it is prudent to save serum in the setting of acute illness that can later be used if necessary. Convalescent serology should be obtained no sooner than three weeks after the onset of the clinical illness. As an example, the presence of IgM antibodies in a single serum provides presumptive evidence of St. Louis encephalitis; however, a significant rise or fall between appropriately timed acute convalescent or early-late convalescent sera is diagnostic. West Nile has emerged as the most common cause of viral encephalitis in the United States. A single specimen looking for IgM antibodies in the serum or CSF is sufficient for diagnosis.




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West Nile has emerged as the most common cause of viral encephalitis in the United States. A single specimen looking for IgM antibodies in the serum or CSF is sufficient for diagnosis. A single serum specimen can also be used to diagnose mumps. Serology may also be helpful in obtaining evidence for primary Epstein-Barr virus infection, a rare cause of meningoencephalitis.
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serum provides presumptive evidence of St. Louis encephalitis; however, a significant rise or fall between appropriately timed acute convalescent or early-late convalescent sera is diagnostic. <span>West Nile has emerged as the most common cause of viral encephalitis in the United States. A single specimen looking for IgM antibodies in the serum or CSF is sufficient for diagnosis. A single serum specimen can also be used to diagnose mumps. Serology may also be helpful in obtaining evidence for primary Epstein-Barr virus infection, a rare cause of meningoencephalitis. (See "St. Louis encephalitis" and "Clinical manifestations and diagnosis of West Nile virus infection".) Brain biopsy — As a last resort, brain biopsy can be considered in the patient i




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In a report of 432 high-risk patients who underwent brain biopsy of presumptive herpes simplex encephalitis, 45 percent had the diagnosis confirmed, 9 percent had another virus detected, and 9 percent had another treatable cause [33]. This underscores the point that the clinical diagnosis of HSV encephalitis is often incorrect and needs to be confirmed by PCR testing.
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c agent in patients with aseptic meningitis and encephalitis has been variable and depends upon the population studied and the mode of testing. The following illustrates the range of findings: ●<span>In a report of 432 high-risk patients who underwent brain biopsy of presumptive herpes simplex encephalitis, 45 percent had the diagnosis confirmed, 9 percent had another virus detected, and 9 percent had another treatable cause [33]. This underscores the point that the clinical diagnosis of HSV encephalitis is often incorrect and needs to be confirmed by PCR testing. ●Among 334 patients with a case definition of encephalitis in the California Encephalitis Project, a confirmed or probable viral cause was present in 9 percent [39]; a possible cause wa




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Among 334 patients with a case definition of encephalitis in the California Encephalitis Project, a confirmed or probable viral cause was present in 9 percent [39]; a possible cause was identified in 12 percent, a noninfectious etiology in 10 percent, and a bacterial cause in 3 percent. Despite extensive testing, 62 percent of cases were unexplained.
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etected, and 9 percent had another treatable cause [33]. This underscores the point that the clinical diagnosis of HSV encephalitis is often incorrect and needs to be confirmed by PCR testing. ●<span>Among 334 patients with a case definition of encephalitis in the California Encephalitis Project, a confirmed or probable viral cause was present in 9 percent [39]; a possible cause was identified in 12 percent, a noninfectious etiology in 10 percent, and a bacterial cause in 3 percent. Despite extensive testing, 62 percent of cases were unexplained. ●In a series from the New York State Department of Health of 106 patients with presumed viral CNS infection seen in 1997 and 1998, PCR testing revealed a viral cause in 38 (36 percent)




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In a series from the New York State Department of Health of 106 patients with presumed viral CNS infection seen in 1997 and 1998, PCR testing revealed a viral cause in 38 (36 percent) [40]. The rate of detection in earlier time periods before PCR testing was much lower (about 10 percent), employing cell culture and serologic testing.
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39]; a possible cause was identified in 12 percent, a noninfectious etiology in 10 percent, and a bacterial cause in 3 percent. Despite extensive testing, 62 percent of cases were unexplained. ●<span>In a series from the New York State Department of Health of 106 patients with presumed viral CNS infection seen in 1997 and 1998, PCR testing revealed a viral cause in 38 (36 percent) [40]. The rate of detection in earlier time periods before PCR testing was much lower (about 10 percent), employing cell culture and serologic testing. In a later, larger series of almost 3500 patients from the same laboratory, PCR identified a viral etiology in CSF or brain tissue in only 14 percent (498 patients); selection bias may




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In a later, larger series of almost 3500 patients from the same laboratory, PCR identified a viral etiology in CSF or brain tissue in only 14 percent (498 patients); selection bias may have accounted for much of the difference [41]. The most common viral causes were enterovirus (72 percent), herpes simplex (15 percent), VZV (6 percent), and West Nile virus (4 percent).
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revealed a viral cause in 38 (36 percent) [40]. The rate of detection in earlier time periods before PCR testing was much lower (about 10 percent), employing cell culture and serologic testing. <span>In a later, larger series of almost 3500 patients from the same laboratory, PCR identified a viral etiology in CSF or brain tissue in only 14 percent (498 patients); selection bias may have accounted for much of the difference [41]. The most common viral causes were enterovirus (72 percent), herpes simplex (15 percent), VZV (6 percent), and West Nile virus (4 percent). DIFFERENTIAL DIAGNOSIS — It is critical that the clinician considers a broad range of causes when evaluating patients who present with encephalitis. Only some of the causes are infectio




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It is critical that the clinician considers a broad range of causes when evaluating patients who present with encephalitis. Only some of the causes are infectious, and not all infections are viral.
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much of the difference [41]. The most common viral causes were enterovirus (72 percent), herpes simplex (15 percent), VZV (6 percent), and West Nile virus (4 percent). DIFFERENTIAL DIAGNOSIS — <span>It is critical that the clinician considers a broad range of causes when evaluating patients who present with encephalitis. Only some of the causes are infectious, and not all infections are viral. A number of noninfectious etiologies can mimic central nervous system (CNS) infections. These include primary intracranial or metastatic tumors, adverse effects of medications, and auto




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A number of noninfectious etiologies can mimic central nervous system (CNS) infections. These include primary intracranial or metastatic tumors, adverse effects of medications, and autoimmune or paraneoplastic diseases, such as those associated with vasculitis or the anti-NMDA receptor (table 3). (See "Paraneoplastic and autoimmune encephalitis".)
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s critical that the clinician considers a broad range of causes when evaluating patients who present with encephalitis. Only some of the causes are infectious, and not all infections are viral. <span>A number of noninfectious etiologies can mimic central nervous system (CNS) infections. These include primary intracranial or metastatic tumors, adverse effects of medications, and autoimmune or paraneoplastic diseases, such as those associated with vasculitis or the anti-NMDA receptor (table 3). (See "Paraneoplastic and autoimmune encephalitis".) Nonviral infectious etiologies to consider in the patient with suspected CNS infection include brain abscess, syphilis, tuberculous meningitis, and fungal meningitis (eg, coccidioides),




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Nonviral infectious etiologies to consider in the patient with suspected CNS infection include brain abscess, syphilis, tuberculous meningitis, and fungal meningitis (eg, coccidioides), which can affect the sensorium. Amoebic encephalitis, often associated with freshwater swimming, should also be an occasional consideration. (See "Pathogenesis, clinical manifestations, and diagnosis of brain abscess" and "Central nervous system tuberculosis: An overview" and "Coccidioidal meningitis" and "Neurosyphilis".)
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ects of medications, and autoimmune or paraneoplastic diseases, such as those associated with vasculitis or the anti-NMDA receptor (table 3). (See "Paraneoplastic and autoimmune encephalitis".) <span>Nonviral infectious etiologies to consider in the patient with suspected CNS infection include brain abscess, syphilis, tuberculous meningitis, and fungal meningitis (eg, coccidioides), which can affect the sensorium. Amoebic encephalitis, often associated with freshwater swimming, should also be an occasional consideration. (See "Pathogenesis, clinical manifestations, and diagnosis of brain abscess" and "Central nervous system tuberculosis: An overview" and "Coccidioidal meningitis" and "Neurosyphilis".) Knowledge of the patient's underlying immune status is also critical, since the differential diagnosis is even broader in immunocompromised hosts (eg, toxoplasmic encephalitis and crypt




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Knowledge of the patient's underlying immune status is also critical, since the differential diagnosis is even broader in immunocompromised hosts (eg, toxoplasmic encephalitis and cryptococcal meningitis). (See "Toxoplasmosis: Acute systemic disease" and "Epidemiology, clinical manifestations, and diagnosis of Cryptococcus neoformans meningoencephalitis in patients with HIV".)
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deration. (See "Pathogenesis, clinical manifestations, and diagnosis of brain abscess" and "Central nervous system tuberculosis: An overview" and "Coccidioidal meningitis" and "Neurosyphilis".) <span>Knowledge of the patient's underlying immune status is also critical, since the differential diagnosis is even broader in immunocompromised hosts (eg, toxoplasmic encephalitis and cryptococcal meningitis). (See "Toxoplasmosis: Acute systemic disease" and "Epidemiology, clinical manifestations, and diagnosis of Cryptococcus neoformans meningoencephalitis in patients with HIV".) EMPIRIC THERAPY — There are no specific therapies for most central nervous system (CNS) viral infections. However, some important exceptions apply: ●Empiric treatment for herpes simplex




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There are no specific therapies for most central nervous system (CNS) viral infections. However, some important exceptions apply:

● Empiric treatment for herpes simplex virus (HSV)-1 infection with acyclovir (10 mg/kg intravenously every eight hours) should always be initiated as soon as possible if the patient has encephalitis without apparent explanation [42]. Early therapy is vital because it is associated with a significant decrease in mortality and morbidity [1] (see "Herpes simplex virus type 1 encephalitis"). Acyclovir should also be administered if varicella zoster virus encephalitis is likely.

● Since a number of other treatable illnesses may present in a similar manner to viral CNS infections, consideration of alternative diagnoses, such as tuberculosis and drug-induced delirium, is essential (table 3) [43].

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. (See "Toxoplasmosis: Acute systemic disease" and "Epidemiology, clinical manifestations, and diagnosis of Cryptococcus neoformans meningoencephalitis in patients with HIV".) EMPIRIC THERAPY — <span>There are no specific therapies for most central nervous system (CNS) viral infections. However, some important exceptions apply: ●Empiric treatment for herpes simplex virus (HSV)-1 infection with acyclovir (10 mg/kg intravenously every eight hours) should always be initiated as soon as possible if the patient has encephalitis without apparent explanation [42]. Early therapy is vital because it is associated with a significant decrease in mortality and morbidity [1] (see "Herpes simplex virus type 1 encephalitis"). Acyclovir should also be administered if varicella zoster virus encephalitis is likely. ●Since a number of other treatable illnesses may present in a similar manner to viral CNS infections, consideration of alternative diagnoses, such as tuberculosis and drug-induced delirium, is essential (table 3) [43]. A list of the major pathogens that produce the clinical syndrome of encephalitis, along with suggested initial treatment, appears in the table (table 4) [44]. INCREASED INTRACRANIAL PRE




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A list of the major pathogens that produce the clinical syndrome of encephalitis, along with suggested initial treatment, appears in the table (table 4) [44].
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treatable illnesses may present in a similar manner to viral CNS infections, consideration of alternative diagnoses, such as tuberculosis and drug-induced delirium, is essential (table 3) [43]. <span>A list of the major pathogens that produce the clinical syndrome of encephalitis, along with suggested initial treatment, appears in the table (table 4) [44]. INCREASED INTRACRANIAL PRESSURE — Symptoms and signs of increased intracranial pressure (ICP) include headache, vomiting, and a decreased level of consciousness. Information on the inci




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Symptoms and signs of increased intracranial pressure (ICP) include headache, vomiting, and a decreased level of consciousness. Information on the incidence or management of raised cerebrospinal fluid (CSF) pressure in patients with viral encephalitis is limited.
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A list of the major pathogens that produce the clinical syndrome of encephalitis, along with suggested initial treatment, appears in the table (table 4) [44]. INCREASED INTRACRANIAL PRESSURE — <span>Symptoms and signs of increased intracranial pressure (ICP) include headache, vomiting, and a decreased level of consciousness. Information on the incidence or management of raised cerebrospinal fluid (CSF) pressure in patients with viral encephalitis is limited. All of the "standard" therapeutic interventions for lowering CSF pressure (eg, steroids, mannitol) have been used in this setting, but none have been shown to be of well-established ben




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All of the "standard" therapeutic interventions for lowering CSF pressure (eg, steroids, mannitol) have been used in this setting, but none have been shown to be of well-established benefit. Although dexamethasone has been shown to reduce brain edema and improve neurologic outcomes in patients with pneumococcal meningitis, there are only limited retrospective data on the use of steroids in viral encephalitis [45]; extrapolating these data to patients with viral encephalitis may not be valid. (See "Dexamethasone to prevent neurologic complications of bacterial meningitis in adults".)
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adache, vomiting, and a decreased level of consciousness. Information on the incidence or management of raised cerebrospinal fluid (CSF) pressure in patients with viral encephalitis is limited. <span>All of the "standard" therapeutic interventions for lowering CSF pressure (eg, steroids, mannitol) have been used in this setting, but none have been shown to be of well-established benefit. Although dexamethasone has been shown to reduce brain edema and improve neurologic outcomes in patients with pneumococcal meningitis, there are only limited retrospective data on the use of steroids in viral encephalitis [45]; extrapolating these data to patients with viral encephalitis may not be valid. (See "Dexamethasone to prevent neurologic complications of bacterial meningitis in adults".) However, serial ICP monitoring should be part of the management of a patient with encephalitis with documented elevated ICP, since this parameter has been associated with a negative pro




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However, serial ICP monitoring should be part of the management of a patient with encephalitis with documented elevated ICP, since this parameter has been associated with a negative prognosis [46]. Relieving elevated ICP may decrease secondary brain injury while the patient is responding to anti-infective therapy [47]. Whether any of these interventions may have a positive impact on outcome has not been determined in prospective clinical trials.

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al encephalitis [45]; extrapolating these data to patients with viral encephalitis may not be valid. (See "Dexamethasone to prevent neurologic complications of bacterial meningitis in adults".) <span>However, serial ICP monitoring should be part of the management of a patient with encephalitis with documented elevated ICP, since this parameter has been associated with a negative prognosis [46]. Relieving elevated ICP may decrease secondary brain injury while the patient is responding to anti-infective therapy [47]. Whether any of these interventions may have a positive impact on outcome has not been determined in prospective clinical trials. Various strategies to reduce intracranial pressure are discussed elsewhere. (See "Evaluation and management of elevated intracranial pressure in adults", section on 'General management'




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Most studies of viral encephalitis are focused on short-term outcomes. As an example, one prospective study in France examined 167 surviving patients with a history of encephalitis three years after enrollment [48]. Sixty-one percent survived without sequelae, while 18 percent were mildly impaired, 14 percent were severely impaired, and 1 percent remained in a vegetative state.
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s strategies to reduce intracranial pressure are discussed elsewhere. (See "Evaluation and management of elevated intracranial pressure in adults", section on 'General management'.) PROGNOSIS — <span>Most studies of viral encephalitis are focused on short-term outcomes. As an example, one prospective study in France examined 167 surviving patients with a history of encephalitis three years after enrollment [48]. Sixty-one percent survived without sequelae, while 18 percent were mildly impaired, 14 percent were severely impaired, and 1 percent remained in a vegetative state. The most frequent sequelae included difficulties in concentration, behavioral and speech disorders, and memory loss. One-quarter of those who were previously employed had not returned t




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The most frequent sequelae included difficulties in concentration, behavioral and speech disorders, and memory loss. One-quarter of those who were previously employed had not returned to work.
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years after enrollment [48]. Sixty-one percent survived without sequelae, while 18 percent were mildly impaired, 14 percent were severely impaired, and 1 percent remained in a vegetative state. <span>The most frequent sequelae included difficulties in concentration, behavioral and speech disorders, and memory loss. One-quarter of those who were previously employed had not returned to work. In the California Encephalitis Project, more than 1500 patients with encephalitis were enrolled from 1998 through 2005 [26]. A confirmed or probable etiologic agent was identified for o




#Encephalites #Encephalitis #Meningite #Meningitis #Meningo-encephalite #Meningoencephalitis #Reco #Recommandation #U2D
In the California Encephalitis Project, more than 1500 patients with encephalitis were enrolled from 1998 through 2005 [26]. A confirmed or probable etiologic agent was identified for only 16 percent of cases.
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The most frequent sequelae included difficulties in concentration, behavioral and speech disorders, and memory loss. One-quarter of those who were previously employed had not returned to work. <span>In the California Encephalitis Project, more than 1500 patients with encephalitis were enrolled from 1998 through 2005 [26]. A confirmed or probable etiologic agent was identified for only 16 percent of cases. Although the vast majority of patients did not have an established diagnosis, those presenting with diffuse cerebral edema or intractable seizures had a poor neurologic recovery and inc