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#harrison #liver #liverfunctiontests #medicine
Serum biochemical tests, also commonly referred to as “liver function tests,” can be used to (1) detect the presence of liver disease, (2) distinguish among different types of liver disorders, (3) gauge the extent of known liver damage, and (4) follow the response to treatment. However, serum biochemical tests have shortcomings. They lack sensi- tivity and specificity; they can be normal in patients with serious liver disease and abnormal in patients with diseases that do not affect the liver. Liver tests rarely suggest a specific diagnosis; rather, they suggest a general category of liver disease, such as hepatocellular or cholestatic, which then further directs the evaluation.
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#harrison #liver #liverfunctiontests #medicine
many tests, such as the aminotransferases and alkaline phosphatase, do not measure liver function at all. Rather, they detect liver cell damage or interference with bile flow.
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serum bilirubin
#harrison #liver #liverfunctiontests #medicine
Bilirubin, a breakdown product of the porphyrin ring of heme-containing proteins, is found in the blood in two fractions—conjugated and unconjugated. The uncon- jugated fraction, also termed the indirect fraction, is insoluble in water and is bound to albumin in the blood. The conjugated (direct) bilirubin fraction is water-soluble and can therefore be excreted by the kidney. Normal values of total serum bilirubin are reported between 1 and 1.5 mg/dL with 95% of a normal population falling between 0.2 and 0.9 mg/dL. If the direct-acting fraction is <5% of the total, the biliru- bin can be considered to all be indirect. The most frequently reported upper limit of normal for conjugated bilirubin is 0.3 mg/dL. Elevation of the unconjugated fraction of bilirubin is rarely due to liver disease. An isolated elevation of unconjugated bilirubin is seen primarily in hemolytic disorders and in a number of genetic conditions such as Crigler-Najjar and Gilbert’s syndromes (Chap. 45). Isolated unconjugated hyperbilirubinemia (bilirubin elevated but <5% direct) should prompt a workup for hemolysis (Fig. 330-1). In the absence of hemolysis, an isolated, unconjugated hyperbilirubinemia in an other- wise healthy patient can be attributed to Gilbert’s syndrome, and no further evaluation is required. In contrast, conjugated hyperbilirubinemia almost always implies liver or biliary tract disease. The rate-limiting step in bilirubin metab- olism is not conjugation of bilirubin, but rather the transport of conju- gated bilirubin into the bile canaliculi. Thus, elevation of the conjugated fraction may be seen in any type of liver disease including fulminant liver failure. In most liver diseases, both conjugated and unconjugated fractions of the bilirubin tend to be elevated. Except in the presence of a purely unconjugated hyperbilirubinemia, fractionation of the bilirubin is rarely helpful in determining the cause of jaundice. Although the degree of elevation of the serum bilirubin has not been critically assessed as a prognostic marker, it is important in a number of conditions. In viral hepatitis, the higher the serum bilirubin, the greater is the hepatocellular damage. Total serum bilirubin correlates with poor outcomes in alcoholic hepatitis. It is also a critical compo- nent of the Model for End-Stage Liver Disease (MELD) score, a tool used to estimate survival of patients with end-stage liver disease and assess operative risk of patients with cirrhosis. An elevated total serum bilirubin in patients with drug-induced liver disease indicates more severe injury. Unconjugated bilirubin always binds to albumin in the serum and is not filtered by the kidney. Therefore, any bilirubin found in the urine is conjugated bilirubin; the presence of bilirubinuria implies the presence of liver disease. A urine dipstick test can theoretically give the same information as fractionation of the serum bilirubin. This test is almost 100% accurate. Phenothiazines may give a false-positive reading with the Ictotest tablet. In patients recovering from jaundice, the urine biliru- bin clears prior to the serum bilirubin.
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#harrison #liver #liverfunctiontests #medicine
Serum enzyme tests can be grouped into two categories: (1) enzymes whose elevation in serum reflects damage to hepatocytes and (2) enzymes whose elevation in serum reflects cholestasis
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#harrison #medicine
The aminotransfer- ases (transaminases) are sensitive indicators of liver cell injury and are most helpful in recognizing acute hepatocellular diseases such as hepatitis. They include aspartate aminotransferase (AST) and alanine aminotransferase (ALT). AST is found in the liver, cardiac muscle, skeletal muscle, kidneys, brain, pancreas, lungs, leukocytes, and ery- throcytes in decreasing order of concentration. ALT is found primarily in the liver and is therefore a more specific indicator of liver injury. The aminotransferases are normally present in the serum in low concentra- tions. These enzymes are released into the blood in greater amounts when there is damage to the liver cell membrane resulting in increased permeability. Liver cell necrosis is not required for the release of the aminotransferases, and there is a poor correlation between the degree of liver cell damage and the level of the aminotransferases. Thus, the absolute elevation of the aminotransferases is of no prognostic signifi- cance in acute hepatocellular disorders. The normal range for aminotransferases varies widely among labo- ratories, but generally ranges from 10 to 40 IU/L.
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#harrison #medicine
The aminotransfer- ases (transaminases) are sensitive indicators of liver cell injury and are most helpful in recognizing acute hepatocellular diseases such as hepatitis. They include aspartate aminotransferase (AST) and alanine aminotransferase (ALT). AST is found in the liver, cardiac muscle, skeletal muscle, kidneys, brain, pancreas, lungs, leukocytes, and ery- throcytes in decreasing order of concentration. ALT is found primarily in the liver and is therefore a more specific indicator of liver injury. The aminotransferases are normally present in the serum in low concentra- tions. These enzymes are released into the blood in greater amounts when there is damage to the liver cell membrane resulting in increased permeability. Liver cell necrosis is not required for the release of the aminotransferases, and there is a poor correlation between the degree of liver cell damage and the level of the aminotransferases. Thus, the absolute elevation of the aminotransferases is of no prognostic signifi- cance in acute hepatocellular disorders. The normal range for aminotransferases varies widely among labo- ratories, but generally ranges from 10 to 40 IU/L.
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Transaminases 1
#harrison #liver #liverfunctiontests #medicine
The aminotransfer- ases (transaminases) are sensitive indicators of liver cell injury and are most helpful in recognizing acute hepatocellular diseases such as hepatitis. They include aspartate aminotransferase (AST) and alanine aminotransferase (ALT). AST is found in the liver, cardiac muscle, skeletal muscle, kidneys, brain, pancreas, lungs, leukocytes, and ery- throcytes in decreasing order of concentration. ALT is found primarily in the liver and is therefore a more specific indicator of liver injury. The aminotransferases are normally present in the serum in low concentra- tions. These enzymes are released into the blood in greater amounts when there is damage to the liver cell membrane resulting in increased permeability. Liver cell necrosis is not required for the release of the aminotransferases, and there is a poor correlation between the degree of liver cell damage and the level of the aminotransferases. Thus, the absolute elevation of the aminotransferases is of no prognostic signifi- cance in acute hepatocellular disorders. The normal range for aminotransferases varies widely among labo- ratories, but generally ranges from 10 to 40 IU/L.
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Transaminases 2
#harrison #liver #liverfunctiontests #medicine
Any type of liver cell injury can cause modest elevations in the serum aminotransferases. Levels of up to 300 IU/L are nonspecific and may be found in any type of liver disorder. Minimal ALT ele- vations in asymptomatic blood donors rarely indicate severe liver disease; studies have shown that fatty liver disease is the most likely explanation. Striking elevations—that is, aminotransferases >1000 IU/L—occur almost exclusively in disorders associated with exten- sive hepatocellular injury such as (1) viral hepatitis, (2) ischemic liver injury (prolonged hypotension or acute heart failure), or (3) toxin- or drug-induced liver injury. The pattern of the aminotransferase elevation can be helpful diag- nostically. In most acute hepatocellular disorders, the ALT is higher than or equal to the AST. Whereas the AST:ALT ratio is typically <1 in="" patients="" with="" chronic="" viral="" hepatitis="" and="" nonalcoholic="" fatty="" liver="" disease,="" a="" number="" of="" groups="" have="" noted="" that="" as="" cirrhosis="" develops,="" this="" ratio="" rises="" to="">1. An AST:ALT ratio >2:1 is suggestive, whereas a ratio >3:1 is highly suggestive, of alcoholic liver disease. The AST in alcoholic liver disease is rarely >300 IU/L, and the ALT is often normal. A low level of ALT in the serum is due to an alcohol-induced deficiency of pyridoxal phosphate.
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Transaminases 3
#harrison #liver #liverfunctiontests #medicine
The aminotransferases are usually not greatly elevated in obstruc- tive jaundice. One notable exception occurs during the acute phase of biliary obstruction caused by the passage of a gallstone into the com- mon bile duct. In this setting, the aminotransferases can briefly be in the 1000–2000 IU/L range. However, aminotransferase levels decrease quickly, and the biochemical tests rapidly evolve into those typical of cholestasis.
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enzymes that reflect cholestasis
#harrison #liver #liverfunctiontests #medicine
The activities of three enzymes— alkaline phosphatase, 5′-nucleotidase, and γ-glutamyl transpeptidase (GGT)—are usually elevated in cholestasis. Alkaline phosphatase and 5′-nucleotidase are found in or near the bile canalicular membrane of hepatocytes, whereas GGT is located in the endoplasmic reticulum and in bile duct epithelial cells. Reflecting its more diffuse localization in the liver, GGT elevation in serum is less specific for cholestasis than are elevations of alkaline phosphatase or 5′-nucleotidase.
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enzymes that reflect cholestasis 2
#harrison #liver #liverfunctiontests #medicine
Elevation of liver-derived alkaline phosphatase is not totally specific for cholestasis, and a less than threefold elevation can be seen in almost any type of liver disease. Alkaline phosphatase elevations greater than four times normal occur primarily in patients with cholestatic liver disorders, infiltrative liver diseases such as cancer and amyloidosis, and bone conditions characterized by rapid bone turnover (e.g., Paget’s disease). In bone diseases, the elevation is due to increased amounts of the bone isoenzymes. In liver diseases, the elevation is almost always due to increased amounts of the liver isoenzyme. If an elevated serum alkaline phosphatase is the only abnormal finding in an apparently healthy person, or if the degree of elevation is higher than expected in the clinical setting, identification of the source of elevated isoenzymes is helpful (Fig. 330-1). This problem can be approached in two ways. First, and most precise, is the fractionation of the alkaline phosphatase by electrophoresis. The second, best sub- stantiated, and most available approach involves the measurement of serum 5′-nucleotidase or GGT. These enzymes are rarely elevated in conditions other than liver disease.
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enzymes that reflect cholestasis 3
#harrison #liver #liverfunctiontests #medicine
In the absence of jaundice or elevated aminotransferases, an elevated alkaline phosphatase of liver origin often, but not always, suggests early cholestasis and, less often, hepatic infiltration by tumor or gran- ulomata. Other conditions that cause isolated elevations of the alkaline phosphatase include Hodgkin’s disease, diabetes, hyperthyroidism, congestive heart failure, amyloidosis, and inflammatory bowel disease. The level of serum alkaline phosphatase elevation is not helpful in distinguishing between intrahepatic and extrahepatic cholestasis. There is essentially no difference among the values found in obstruc- tive jaundice due to cancer, common duct stone, sclerosing cholangitis, or bile duct stricture. Values are similarly increased in patients with intrahepatic cholestasis due to drug-induced hepatitis, primary biliary cirrhosis, rejection of transplanted livers, and, rarely, alcohol-induced steatohepatitis. Values are also greatly elevated in hepatobiliary dis- orders seen in patients with AIDS (e.g., AIDS cholangiopathy due to cytomegalovirus or cryptosporidial infection and tuberculosis with hepatic involvement).
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serum albumin in liver disease
#harrison #liverfunctiontests #medicine
Hypoalbuminemia is more common in chronic liver disorders such as cirrhosis and usually reflects severe liver damage and decreased albumin synthesis. One exception is the patient with ascites in whom synthesis may be normal or even increased, but levels are low because of the increased volume of distribution. However, hypoalbuminemia is not specific for liver disease and may occur in protein malnutrition of any cause, as well as protein-losing enterop- athies, nephrotic syndrome, and chronic infections that are associated with prolonged increases in levels of serum interleukin 1 and/or tumor necrosis factor, cytokines that inhibit albumin synthesis. Serum albumin should not be measured for screening in patients in whom there is no suspicion of liver disease.
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#fracture #orthopedics
A fracture is a break in the continuity of a bone. It can be classified on the basis of aetiology, the relationship of the fracture with the external environment, the displacement of the fracture, and the pattern of the fracture.
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traumatic fracture
#fracture #orthopedics
A fracture sustained due to trauma is called a traumatic fracture*. Normal bone can withstand considerable force, and breaks only when subjected to excessive force. Most fractures seen in day-to-day practice fall into this category e.g., fractures caused by a fall, road traffic accident, fight etc.
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Pathological fracture
#fracture #orthopedics
A fracture through a bone which has been made weak by some underlying disease is called a pathological fracture. A trivial or no force may be required to cause such a fracture e.g., a fracture through a bone weakened by metastasis. Although, traumatic fractures have a predictable and generally successful outcome, pathological fractures often go into non-union.
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stress fracture
#fracture #orthopedics
This is a special type of fracture sustained due to chronic repetitive injury (stress) causing a break in bony trabeculae. These often present as only pain and may not be visible on X-rays.
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displaced fracture
#fracture #orthopedics
A fracture may be displaced. The factors responsible for displacement are: (i) the fracturing force; (ii) the muscle pull on the fracture fragments; and (iii) the gravity. While describing the displacements of a fracture, conventionally, it is the displacement of the distal fragment in relation to the proximal fragment which is mentioned. The displacement can be in the form of shift, angulation or rotation
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Flashcard 6985465072908

Tags
#fracture #orthopedics
Question
what is a closed fracture?
Answer
A fracture not communicating with the external environment, i.e., the overlying skin and other soft tissues are intact, is called a closed fracture.

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Flashcard 6985467432204

Tags
#fracture #orthopedics
Question
Open fracture
Answer
A fractur e with break in the overlying skin and soft tissues, leading to the fracture communicating with the external environment, is called an open fracture.

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Flashcard 6985469267212

Tags
#fracture #orthopedics
Question
Internally open
Answer
The sharp fractur e end pierces the skin fr om within, resulting in an open fracture.

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Flashcard 6985471626508

Tags
#fracture #orthopedics
Question
The object causing the fracture lacerates the skin and soft tissues over the bone, as it breaks the bone, resulting in an open fracture.
Answer
The object causing the fracture lacerates the skin and soft tissues over the bone, as it breaks the bone, resulting in an open fractur e.

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Flashcard 6985473985804

Tags
#fracture #orthopedics
Question
Simple fracture:
Answer
A fracture in two pieces, usually easy to treat, is called simple fractur e, e.g. a transverse fracture of humer us

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Flashcard 6985476345100

Tags
#fracture #orthopedics
Question
Complex fracture
Answer
A fracture in multiple pieces, usually difficult to tr eat, is called complex fracture, e.g. a communited fracture of tibia

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Flashcard 6985479752972

Tags
#anemia #harrison #hematology #irondefeciencyanemia #medicine
Question
signs of advanced tissue iron deficiency.
Answer
Cheilosis (fissures at the corners of the mouth) and koilonychia (spooning of the fingernails)

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nemia in addition to the usual signs of anemia—fatigue, pallor, and reduced exercise capacity. Cheilosis (fissures at the corners of the mouth) and koilonychia (spooning of the fingernails) are <span>signs of advanced tissue iron deficiency. The diagnosis of iron deficiency is typically based on laboratory results. <span>

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Flashcard 6985481325836

Tags
#anemia #harrison #hematology #irondefeciencyanemia #medicine
Question
usual signs of anemia
Answer
fatigue, pallor, and reduced exercise capacity

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male or post-menopausal female means gastrointestinal blood loss until proven otherwise. Signs related to iron deficiency depend on the severity and chronicity of the anemia in addition to the <span>usual signs of anemia—fatigue, pallor, and reduced exercise capacity. Cheilosis (fissures at the corners of the mouth) and koilonychia (spooning of the fingernails) are signs of advanced tissue iron deficien

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Flashcard 6985485782284

Tags
#orthopedics
Question
A joint is subluxated
Answer
A joint is subluxated when its articular surfaces are partially displaced but r etain some contact between them

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Flashcard 6985487355148

Tags
#orthopedics
Question
A joint is dislocated when
Answer
A joint is dislocated when its articular surfaces are so much displaced that all contact between them is lost.

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#Diabetes #Diabète #Gestion #Hopital #Hospital #Management #Type2
If a patient was previously eating but is unable to eat after the evening meal in preparation for a procedure the next morning, oral antihyperglycemic drugs should be omitted on the day of a procedure (surgical or diagnostic). If procedures are arranged as early in the day as possible, antihyperglycemic therapy and food intake can simply then be shifted to later in the day
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(or similar brands) are on the hospital formulary. Of note, GLP-1 receptor agonists are expensive and often not on hospital formularies; their use in the hospital setting is therefore uncommon. <span>If a patient was previously eating but is unable to eat after the evening meal in preparation for a procedure the next morning, oral antihyperglycemic drugs should be omitted on the day of a procedure (surgical or diagnostic). If procedures are arranged as early in the day as possible, antihyperglycemic therapy and food intake can simply then be shifted to later in the day. If the illness requiring admission is more severe (eg, an infection requiring hospitalization), hyperglycemia is more likely, even when there is decreased food intake, and most acutely




#Diabetes #Diabète #Gestion #Hopital #Hospital #Management #Type2
Overt hyperglycemia (≥180 mg/dL [10.0 mmol/L]) in patients previously treated with oral agents who are not eating can be treated briefly with intermittent, subcutaneous doses of regular (every six hours) or rapid-acting (every four to six hours) insulin, provided the blood glucose is not severely elevated, responds well to the insulin, and the problem lasts only a day or two at most (see 'Correction insulin' above). If eating, rapid-acting insulin is preferred, administered before meals. However, a more formal and comprehensive insulin regimen, including some form of basal insulin, is usually preferred when hyperglycemia persists (algorithm 1 and algorithm 2).
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g hospitalization), hyperglycemia is more likely, even when there is decreased food intake, and most acutely ill patients will need insulin. In this setting, oral agents should be discontinued. <span>Overt hyperglycemia (≥180 mg/dL [10.0 mmol/L]) in patients previously treated with oral agents who are not eating can be treated briefly with intermittent, subcutaneous doses of regular (every six hours) or rapid-acting (every four to six hours) insulin, provided the blood glucose is not severely elevated, responds well to the insulin, and the problem lasts only a day or two at most (see 'Correction insulin' above). If eating, rapid-acting insulin is preferred, administered before meals. However, a more formal and comprehensive insulin regimen, including some form of basal insulin, is usually preferred when hyperglycemia persists (algorithm 1 and algorithm 2). Oral agents should never be administered to patients who are not eating. In addition, many oral agents have specific contraindications that may occur in hospitalized patients: ●Metformi




#Diabetes #Diabète #Gestion #Hopital #Hospital #Management #Type2
Oral agents should never be administered to patients who are not eating. In addition, many oral agents have specific contraindications that may occur in hospitalized patients
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red before meals. However, a more formal and comprehensive insulin regimen, including some form of basal insulin, is usually preferred when hyperglycemia persists (algorithm 1 and algorithm 2). <span>Oral agents should never be administered to patients who are not eating. In addition, many oral agents have specific contraindications that may occur in hospitalized patients: ●Metformin – Metformin is contraindicated in situations in which renal function and/or hemodynamic status is either impaired or threatened, due to the increased risk of lactic acidosis




#Diabetes #Diabète #Gestion #Hopital #Hospital #Management #Type2
Metformin is contraindicated in situations in which renal function and/or hemodynamic status is either impaired or threatened, due to the increased risk of lactic acidosis. Examples would include patients with acute cardiac or pulmonary decompensation, acute renal failure, dehydration, sepsis, urinary obstruction, or in those undergoing surgery or radiocontrast studies.
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2). Oral agents should never be administered to patients who are not eating. In addition, many oral agents have specific contraindications that may occur in hospitalized patients: ●Metformin – <span>Metformin is contraindicated in situations in which renal function and/or hemodynamic status is either impaired or threatened, due to the increased risk of lactic acidosis. Examples would include patients with acute cardiac or pulmonary decompensation, acute renal failure, dehydration, sepsis, urinary obstruction, or in those undergoing surgery or radiocontrast studies. Given the typical case mix in most acute care hospitals, in more cases than not, metformin should probably be discontinued at least temporarily. (See "Metformin in the treatment of adul




#Diabetes #Diabète #Gestion #Hopital #Hospital #Management #Type2
Sulfonylureas (eg, glyburide, glipizide, glimepiride) are associated with hypoglycemia that can be severe and prolonged. Although they may be continued during the hospitalization in stable patients who are expected to eat regularly, unexpected alterations in meal intake will increase the risk for hypoglycemia
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e reduction in the setting of impaired renal function. (See "Dipeptidyl peptidase 4 (DPP-4) inhibitors for the treatment of type 2 diabetes mellitus", section on 'Candidates'.) ●Sulfonylureas – <span>Sulfonylureas (eg, glyburide, glipizide, glimepiride) are associated with hypoglycemia that can be severe and prolonged. Although they may be continued during the hospitalization in stable patients who are expected to eat regularly, unexpected alterations in meal intake will increase the risk for hypoglycemia. On balance, sulfonylureas should usually be discontinued, at least temporarily, in the hospitalized patient. In particular, sulfonylureas should be discontinued in the patient with acu




#Diabetes #Diabète #Gestion #Hopital #Hospital #Management #Type2
On balance, sulfonylureas should usually be discontinued, at least temporarily, in the hospitalized patient. In particular, sulfonylureas should be discontinued in the patient with acute myocardial infarction (MI) because there is some concern that they may adversely affect ischemic preconditioning
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d. Although they may be continued during the hospitalization in stable patients who are expected to eat regularly, unexpected alterations in meal intake will increase the risk for hypoglycemia. <span>On balance, sulfonylureas should usually be discontinued, at least temporarily, in the hospitalized patient. In particular, sulfonylureas should be discontinued in the patient with acute myocardial infarction (MI) because there is some concern that they may adversely affect ischemic preconditioning. (See "Glycemic control for acute myocardial infarction in patients with and without diabetes mellitus" and "Sulfonylureas and meglitinides in the treatment of type 2 diabetes mellitus"




#Diabetes #Diabète #Gestion #Hopital #Hospital #Management #Type2
Non-sulfonylurea secretagogues (meglitinides [eg, repaglinide, nateglinide]) work similarly to the sulfonylureas but have a shorter duration of action. As a result, these prandial-administered drugs may have a theoretical advantage in hospitalized patients but should also be used cautiously, including in those with acute ischemic heart disease events.
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farction in patients with and without diabetes mellitus" and "Sulfonylureas and meglitinides in the treatment of type 2 diabetes mellitus", section on 'Cardiovascular effects'.) ●Meglitinides – <span>Non-sulfonylurea secretagogues (meglitinides [eg, repaglinide, nateglinide]) work similarly to the sulfonylureas but have a shorter duration of action. As a result, these prandial-administered drugs may have a theoretical advantage in hospitalized patients but should also be used cautiously, including in those with acute ischemic heart disease events. (See "Sulfonylureas and meglitinides in the treatment of type 2 diabetes mellitus".) ●GLP-1 receptor agonists – GLP-1 receptor agonists (eg, exenatide, liraglutide, lixisenatide, albigl




#Diabetes #Diabète #Gestion #Hopital #Hospital #Management #Type2
GLP-1 receptor agonists (eg, exenatide, liraglutide, lixisenatide, albiglutide, dulaglutide) may result in nausea and are also mainly effective for postprandial glucose management. As a result, their use should probably be avoided in the acute setting. They are also not usually included on most hospital formularies, in part due to high cost.
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be used cautiously, including in those with acute ischemic heart disease events. (See "Sulfonylureas and meglitinides in the treatment of type 2 diabetes mellitus".) ●GLP-1 receptor agonists – <span>GLP-1 receptor agonists (eg, exenatide, liraglutide, lixisenatide, albiglutide, dulaglutide) may result in nausea and are also mainly effective for postprandial glucose management. As a result, their use should probably be avoided in the acute setting. They are also not usually included on most hospital formularies, in part due to high cost. (See "Glucagon-like peptide 1 receptor agonists for the treatment of type 2 diabetes mellitus", section on 'Exenatide twice daily'.) ●SGLT2 inhibitors – Sodium-glucose co-transporter 2




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Sodium-glucose co-transporter 2 (SGLT2) inhibitors (eg, dapagliflozin, canagliflozin, empagliflozin) promote the renal excretion of glucose. They increase calorie losses, risk of dehydration and volume contraction, and genitourinary tract infections. In addition, euglycemic diabetic ketoacidosis has been reported in patients with both type 1 (during off-label use) and type 2 diabetes who were taking SGLT2 inhibitors. These drugs should therefore generally not be used in the inpatient setting
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l formularies, in part due to high cost. (See "Glucagon-like peptide 1 receptor agonists for the treatment of type 2 diabetes mellitus", section on 'Exenatide twice daily'.) ●SGLT2 inhibitors – <span>Sodium-glucose co-transporter 2 (SGLT2) inhibitors (eg, dapagliflozin, canagliflozin, empagliflozin) promote the renal excretion of glucose. They increase calorie losses, risk of dehydration and volume contraction, and genitourinary tract infections. In addition, euglycemic diabetic ketoacidosis has been reported in patients with both type 1 (during off-label use) and type 2 diabetes who were taking SGLT2 inhibitors. These drugs should therefore generally not be used in the inpatient setting. It should be noted, however, that there is growing use of these agents by cardiologists and especially heart failure specialists with some reports now suggesting benefit even in the se




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The thiazolidinediones (eg, pioglitazone, rosiglitazone) are associated with peripheral edema and should be avoided in patients with heart failure.
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ycemia in type 2 diabetes mellitus" and "Secondary pharmacologic therapy in heart failure with reduced ejection fraction (HFrEF) in adults", section on 'SGLT2 inhibitor'.) ●Thiazolidinediones – <span>The thiazolidinediones (eg, pioglitazone, rosiglitazone) are associated with peripheral edema and should be avoided in patients with heart failure. If the question of ventricular dysfunction is raised during a hospitalization, thiazolidinediones should be held until the situation is clarified. The antihyperglycemic effect of this d




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Insulin therapy should be continued in all patients already taking it to maintain a reasonably constant basal level of circulating insulin. Failing this, severe hyperglycemia or even ketoacidosis can occur, even in patients labeled as having type 2 diabetes but who have become significantly insulin deficient over a prolonged disease course.
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effective in patients who are eating and therefore have a limited role in this setting. (See "Alpha-glucosidase inhibitors for treatment of diabetes mellitus".) Patients treated with insulin — <span>Insulin therapy should be continued in all patients already taking it to maintain a reasonably constant basal level of circulating insulin. Failing this, severe hyperglycemia or even ketoacidosis can occur, even in patients labeled as having type 2 diabetes but who have become significantly insulin deficient over a prolonged disease course. ●Basal-bolus (or basal-nutritional) regimens – In the non-acute hospital setting and when the patient is eating regularly, basal insulin (NPH or detemir twice daily or glargine, detemir




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In the non-acute hospital setting and when the patient is eating regularly, basal insulin (NPH or detemir twice daily or glargine, detemir, or degludec once daily [or nightly]) in combination with short- or rapid-acting prandial (bolus) insulin (regular, lispro, aspart, glulisine) is generally effective for patients receiving insulin at home or for patients with poorly regulated blood glucose previously managed with diet or oral agents (algorithm 1)
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can occur, even in patients labeled as having type 2 diabetes but who have become significantly insulin deficient over a prolonged disease course. ●Basal-bolus (or basal-nutritional) regimens – <span>In the non-acute hospital setting and when the patient is eating regularly, basal insulin (NPH or detemir twice daily or glargine, detemir, or degludec once daily [or nightly]) in combination with short- or rapid-acting prandial (bolus) insulin (regular, lispro, aspart, glulisine) is generally effective for patients receiving insulin at home or for patients with poorly regulated blood glucose previously managed with diet or oral agents (algorithm 1). If the glucose was well managed with the outpatient insulin regimen, we typically reduce the dose by 25 to 50 percent because, in the more controlled environment of the hospital (where




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If the glucose was well managed with the outpatient insulin regimen, we typically reduce the dose by 25 to 50 percent because, in the more controlled environment of the hospital (where the amount of food consumed may be less than at home and blood glucose levels are checked regularly), patients may need considerably less insulin than they were taking in the outpatient setting
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, aspart, glulisine) is generally effective for patients receiving insulin at home or for patients with poorly regulated blood glucose previously managed with diet or oral agents (algorithm 1). <span>If the glucose was well managed with the outpatient insulin regimen, we typically reduce the dose by 25 to 50 percent because, in the more controlled environment of the hospital (where the amount of food consumed may be less than at home and blood glucose levels are checked regularly), patients may need considerably less insulin than they were taking in the outpatient setting. Different basal-bolus regimens are similarly effective in reducing A1C concentrations when insulin doses are titrated to achieve glycemic goals. As an example, in a trial of detemir/as




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In some studies, treatment with such a basal-bolus insulin regimen was associated with better glycemic outcomes than sliding-scale insulin [23-26].
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example, in a trial of detemir/aspart versus NPH/regular in 130 hospitalized patients, there was no difference in glycemic management or frequency of hypoglycemia between the two regimens [22]. <span>In some studies, treatment with such a basal-bolus insulin regimen was associated with better glycemic outcomes than sliding-scale insulin [23-26]. As an example, in one open-label, randomized trial of insulin glargine supplemented with preprandial glulisine versus sliding-scale insulin, a greater proportion of patients treated wit




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In some [25,26], but not all [23,24], trials, better glycemic management with basal-bolus versus sliding-scale insulin was associated with more hypoglycemia (glucose <70 mg/dL [3.9 mmol/L] in 23.1 and 4.7 percent of patients, respectively, and <40 mg/dL [2.2 mmol/L] in 3.8 and 0 percent, respectively).
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of insulin was more than threefold higher in the basal-bolus-treated patients than in those assigned to sliding scale, likely reflecting a failure to titrate the doses of sliding-scale insulin. <span>In some [25,26], but not all [23,24], trials, better glycemic management with basal-bolus versus sliding-scale insulin was associated with more hypoglycemia (glucose <70 mg/dL [3.9 mmol/L] in 23.1 and 4.7 percent of patients, respectively, and <40 mg/dL [2.2 mmol/L] in 3.8 and 0 percent, respectively). ●U-500 insulin – Patients treated with U-500 regular insulin at home may continue U-500 (with a 50 percent dose reduction since glucose values often improve substantially in the hospita




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Patients treated with U-500 regular insulin at home may continue U-500 (with a 50 percent dose reduction since glucose values often improve substantially in the hospital in patients previously requiring large doses of insulin at home, due to more restrictive hospital diets), if it is available from the hospital formulary. Because the high concentration of insulin delays absorption, the pharmacologic profile of U-500 regular insulin is most similar to that of NPH [27]. Thus, if U-500 is not available, U-100 NPH insulin twice daily should be substituted (again, with a 50 percent dose reduction).
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with more hypoglycemia (glucose <70 mg/dL [3.9 mmol/L] in 23.1 and 4.7 percent of patients, respectively, and <40 mg/dL [2.2 mmol/L] in 3.8 and 0 percent, respectively). ●U-500 insulin – <span>Patients treated with U-500 regular insulin at home may continue U-500 (with a 50 percent dose reduction since glucose values often improve substantially in the hospital in patients previously requiring large doses of insulin at home, due to more restrictive hospital diets), if it is available from the hospital formulary. Because the high concentration of insulin delays absorption, the pharmacologic profile of U-500 regular insulin is most similar to that of NPH [27]. Thus, if U-500 is not available, U-100 NPH insulin twice daily should be substituted (again, with a 50 percent dose reduction). We would also caution that errors are common with U-500 administration, and clear communication among patient, clinician, nursing staff, and pharmacy is imperative to ensure proper dosi




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We would also caution that errors are common with U-500 administration, and clear communication among patient, clinician, nursing staff, and pharmacy is imperative to ensure proper dosing. Although in the past U-500 insulin was dispensed using Tuberculin or U-100 syringes, a dedicated U-500 insulin syringe is available and U-500 insulin should be dispensed with the U-500 insulin syringe, if possible [28].
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ile of U-500 regular insulin is most similar to that of NPH [27]. Thus, if U-500 is not available, U-100 NPH insulin twice daily should be substituted (again, with a 50 percent dose reduction). <span>We would also caution that errors are common with U-500 administration, and clear communication among patient, clinician, nursing staff, and pharmacy is imperative to ensure proper dosing. Although in the past U-500 insulin was dispensed using Tuberculin or U-100 syringes, a dedicated U-500 insulin syringe is available and U-500 insulin should be dispensed with the U-500 insulin syringe, if possible [28]. The syringe contains scale markings from 25 to 250 units in 5-unit increments (total volume 0.5 mL). The insulin dose should be expressed in units, rather than in volumetric terms as wa




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When food intake is diminished or stopped completely in a patient treated with insulin (eg, in preparation for surgery or other procedures), planned pre-meal rapid-acting insulin is discontinued, and the dose of intermediate- or long-acting insulin is reduced. If an episode is clearly short lived (eg, a procedure done in the early morning), subcutaneous insulin (usual dose of short acting and intermediate or long acting) and breakfast can simply be delayed until after the episode.
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the potential increased cost, remains to be demonstrated. (See "Continuous subcutaneous insulin infusion (insulin pump)", section on 'Types of insulin pumps'.) ●Reduced or absent oral intake – <span>When food intake is diminished or stopped completely in a patient treated with insulin (eg, in preparation for surgery or other procedures), planned pre-meal rapid-acting insulin is discontinued, and the dose of intermediate- or long-acting insulin is reduced. If an episode is clearly short lived (eg, a procedure done in the early morning), subcutaneous insulin (usual dose of short acting and intermediate or long acting) and breakfast can simply be delayed until after the episode. The adjustment of insulin doses in preparation for surgery or other procedures is reviewed in more detail separately. (See "Perioperative management of blood glucose in adults with diab




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Insulin can be given either subcutaneously or intravenously. Algorithms for glycemic management of nonfasting and fasting patients with type 1 diabetes who are not critically ill are shown for subcutaneous dosing regimens (algorithm 1 and algorithm 2) [13].
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nd to fluctuate more during the course of the illness or procedure. It is important to avoid hypoglycemia, even if the consequence is a temporary modest rise in the blood glucose concentration. <span>Insulin can be given either subcutaneously or intravenously. Algorithms for glycemic management of nonfasting and fasting patients with type 1 diabetes who are not critically ill are shown for subcutaneous dosing regimens (algorithm 1 and algorithm 2) [13]. If the patient is receiving nothing by mouth, the administration of basal insulin is still required. As examples: ●Patients using an insulin pump – For a patient treated with a continuo




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For a patient treated with a continuous insulin infusion via a pump, the basal insulin can be continued at the usual rate, or the overnight basal rate may be reduced by 20 percent to minimize the risk of hypoglycemia the next morning. No boluses would be administered until the patient is able to eat.
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regimens (algorithm 1 and algorithm 2) [13]. If the patient is receiving nothing by mouth, the administration of basal insulin is still required. As examples: ●Patients using an insulin pump – <span>For a patient treated with a continuous insulin infusion via a pump, the basal insulin can be continued at the usual rate, or the overnight basal rate may be reduced by 20 percent to minimize the risk of hypoglycemia the next morning. No boluses would be administered until the patient is able to eat. Since nursing staff are not always familiar or comfortable with the use of insulin pumps, patients should be alert enough to manage their pump therapy. In addition, vigilance regarding




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Catheters may inadvertently be dislodged during transfers in the operating room or in bed, and if the patient is not alert enough to provide self-care, the health care providers should consider changing to conventional injection therapy until the patient is able to manage pump therapy again.
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lways familiar or comfortable with the use of insulin pumps, patients should be alert enough to manage their pump therapy. In addition, vigilance regarding pump catheter placement is necessary. <span>Catheters may inadvertently be dislodged during transfers in the operating room or in bed, and if the patient is not alert enough to provide self-care, the health care providers should consider changing to conventional injection therapy until the patient is able to manage pump therapy again. ●Patients treated with multiple daily insulin injections – For a patient who usually takes 20 units of glargine every evening and short-acting insulin before each meal (dose based upon




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For a patient who usually takes 20 units of glargine every evening and short-acting insulin before each meal (dose based upon prevailing blood glucose and carbohydrate content of meal), the usual dose of glargine can be continued. An alternative approach is to reduce the dose of glargine by 20 percent (eg, give 16 units) to minimize the risk of hypoglycemia that might require oral ingestion of calories and thereby delay the planned procedure. Short-acting insulin should not be given, unless significant hyperglycemia is noted, as described above.
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alth care providers should consider changing to conventional injection therapy until the patient is able to manage pump therapy again. ●Patients treated with multiple daily insulin injections – <span>For a patient who usually takes 20 units of glargine every evening and short-acting insulin before each meal (dose based upon prevailing blood glucose and carbohydrate content of meal), the usual dose of glargine can be continued. An alternative approach is to reduce the dose of glargine by 20 percent (eg, give 16 units) to minimize the risk of hypoglycemia that might require oral ingestion of calories and thereby delay the planned procedure. Short-acting insulin should not be given, unless significant hyperglycemia is noted, as described above. For a patient who usually takes 24 units of NPH and 4 units of regular insulin in the morning, one-half to two-thirds (12 to 16 units) of the usual morning dose of NPH insulin can be gi




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For a patient who usually takes 24 units of NPH and 4 units of regular insulin in the morning, one-half to two-thirds (12 to 16 units) of the usual morning dose of NPH insulin can be given (if the morning blood glucose value is not too low, ie, is at least 120 mg/dL [6.7 mmol/L]). Short- or rapid-acting insulin should not be given, except if significant hyperglycemia (>200 to 250 mg/dL [11.1 to 13.9 mmol/L]) is found in the morning. In such cases, only small doses (1 to 4 units) should be given with the goals of reducing the blood glucose level to <180 mg/dL (10 mmol/L) and avoiding hypoglycemia during the ongoing fast.
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a that might require oral ingestion of calories and thereby delay the planned procedure. Short-acting insulin should not be given, unless significant hyperglycemia is noted, as described above. <span>For a patient who usually takes 24 units of NPH and 4 units of regular insulin in the morning, one-half to two-thirds (12 to 16 units) of the usual morning dose of NPH insulin can be given (if the morning blood glucose value is not too low, ie, is at least 120 mg/dL [6.7 mmol/L]). Short- or rapid-acting insulin should not be given, except if significant hyperglycemia (>200 to 250 mg/dL [11.1 to 13.9 mmol/L]) is found in the morning. In such cases, only small doses (1 to 4 units) should be given with the goals of reducing the blood glucose level to <180 mg/dL (10 mmol/L) and avoiding hypoglycemia during the ongoing fast. In all of these cases, blood glucose is measured every two to three hours until the meal is eaten. Small amounts of short- or rapid-acting insulin can be administered every six hours to




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In all of these cases, blood glucose is measured every two to three hours until the meal is eaten. Small amounts of short- or rapid-acting insulin can be administered every six hours to correct hyperglycemia (ie, glucose >150 to 200 mg/dL [8.3 to 11.1 mmol/L]). Intravenous glucose (at approximately 3.75 to 5 g/hour, eg, 5 percent dextrose at 75 to 100 mL per hour) should be given to limit the metabolic changes of starvation.
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In such cases, only small doses (1 to 4 units) should be given with the goals of reducing the blood glucose level to <180 mg/dL (10 mmol/L) and avoiding hypoglycemia during the ongoing fast. <span>In all of these cases, blood glucose is measured every two to three hours until the meal is eaten. Small amounts of short- or rapid-acting insulin can be administered every six hours to correct hyperglycemia (ie, glucose >150 to 200 mg/dL [8.3 to 11.1 mmol/L]). Intravenous glucose (at approximately 3.75 to 5 g/hour, eg, 5 percent dextrose at 75 to 100 mL per hour) should be given to limit the metabolic changes of starvation. (See "Cases illustrating intensive insulin therapy in special situations".) Patients receiving enteral or parenteral feedings — Patients with diabetes who are receiving total parenteral




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For example, if the intravenous insulin infusion at steady state was set at 1 unit per hour (or 24 units per day), around 80 percent of this amount (20 units) should be added to the TPN solution by the pharmacy to be given over the course of the day. The amount of insulin can then be titrated every one to two days, based upon glucose monitoring. Since more frequent adjustments are impractical and costly, the concurrent use of rapid- or short-acting insulin as correction every six hours will help to fine-tune glycemic management.
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d goal, the total daily dose of regular insulin provided by the insulin drip is calculated; 80 percent of this amount is added to the TPN fluid as regular insulin to be delivered over 24 hours. <span>For example, if the intravenous insulin infusion at steady state was set at 1 unit per hour (or 24 units per day), around 80 percent of this amount (20 units) should be added to the TPN solution by the pharmacy to be given over the course of the day. The amount of insulin can then be titrated every one to two days, based upon glucose monitoring. Since more frequent adjustments are impractical and costly, the concurrent use of rapid- or short-acting insulin as correction every six hours will help to fine-tune glycemic management. (See 'Correction insulin' above.) If TPN is interrupted, most patients with type 2 diabetes can be followed with careful glucose monitoring. Insulin should be administered if hyperglyce




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Because of the potential for inadvertent discontinuation of insulin therapy if TPN is interrupted, some clinicians recommend giving a portion of the basal insulin as an injection (eg, 50 percent) in patients with type 1 diabetes. In the example above (patient receiving 24 units of regular insulin a day, 80 percent of this amount [19 units] added to the TPN solution), approximately 10 units of regular insulin can be added to the TPN solution and 9 units of NPH, glargine, or detemir administered as a basal injection. This approach can also be used in insulin-requiring patients with type 2 diabetes.
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ll insulin is withheld. Thus, patients with type 1 diabetes require insulin when the TPN is interrupted. The amount and type of insulin depend upon the anticipated duration of the interruption. <span>Because of the potential for inadvertent discontinuation of insulin therapy if TPN is interrupted, some clinicians recommend giving a portion of the basal insulin as an injection (eg, 50 percent) in patients with type 1 diabetes. In the example above (patient receiving 24 units of regular insulin a day, 80 percent of this amount [19 units] added to the TPN solution), approximately 10 units of regular insulin can be added to the TPN solution and 9 units of NPH, glargine, or detemir administered as a basal injection. This approach can also be used in insulin-requiring patients with type 2 diabetes. Enteral feedings — In patients receiving continuous enteral feeds, the total daily dose of insulin could be administered as basal insulin alone (once-daily glargine, detemir, or deglude




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In patients receiving continuous enteral feeds, the total daily dose of insulin could be administered as basal insulin alone (once-daily glargine, detemir, or degludec, or twice-daily detemir or NPH). However, if the enteral feeds are unexpectedly discontinued, hypoglycemia may occur. Thus, a safer approach may be to administer approximately 50 percent of the total daily insulin dose as basal insulin and 50 percent as prandial (short- or rapid-acting) insulin, which is given every four (rapid-acting insulin) to six (short-acting insulin) hours [30].
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he TPN solution and 9 units of NPH, glargine, or detemir administered as a basal injection. This approach can also be used in insulin-requiring patients with type 2 diabetes. Enteral feedings — <span>In patients receiving continuous enteral feeds, the total daily dose of insulin could be administered as basal insulin alone (once-daily glargine, detemir, or degludec, or twice-daily detemir or NPH). However, if the enteral feeds are unexpectedly discontinued, hypoglycemia may occur. Thus, a safer approach may be to administer approximately 50 percent of the total daily insulin dose as basal insulin and 50 percent as prandial (short- or rapid-acting) insulin, which is given every four (rapid-acting insulin) to six (short-acting insulin) hours [30]. A similar ratio of basal-to-prandial insulin can be used for patients receiving bolus feeds, for whom the prandial insulin would be divided equally before each bolus feed. Correction ra




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If the enteral feeds (continuous or bolus) are unexpectedly discontinued, an intravenous 10 percent dextrose solution, providing a similar number of carbohydrate calories as was being administered via the enteral feeds, should be infused in order to prevent hypoglycemia, especially if the blood glucose concentration falls below 100 mg/dL.
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egular insulin alone is chosen as the initial management strategy for patients receiving enteral feeds, the addition of basal insulin is often required to maintain adequate glycemic management. <span>If the enteral feeds (continuous or bolus) are unexpectedly discontinued, an intravenous 10 percent dextrose solution, providing a similar number of carbohydrate calories as was being administered via the enteral feeds, should be infused in order to prevent hypoglycemia, especially if the blood glucose concentration falls below 100 mg/dL. Consultation — Most of the time, the treatment of hyperglycemia in patients with diabetes in these stressful circumstances can be done by the patient's internist, generalist, or hospita