Acute diabetic complication dr. mohamed ibrahim (1) (1)
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Acute diabetic complication dr. mohamed ibrahim (1) (1)
- 1. Dr. Mohamed Ibrahim Youssef Family Medicine Specialist Albassam Diabetic Center
- 2. Diabetic ketoacidosis (DKA). Hyperosmolar hyperglycemic State. Hypoglycemia.
- 3. Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS)are two of the most serious acute complications of diabetes. DKA=hyperglycemia ,ketosis , acidosis. HHS= hyperosmolarity , hyperglycemia ,altered mental status.
- 5. DKA = 3 letters= triad of D K A Diabetic glucose >250 mg/dL Keto ketones – both in urine and in serum acetoacetate, acetone, betahydroxybutyrate fruity smell. If the Ketone level is below 0.6 mmol/L is normal. The person with a reading above 1.5 mmol/L indicate a greater risk for developing Ketoacidosis (DKA). Acidosis Increased anion gap AG=[(Na)-(Hco3+CL)],metabolic acidosis; HCO3- <15, pH<7.30 The normal blood pH is tightly regulated between 7.35 and 7.45.
- 6. Traditional teaching # reality Traditional DKA seen in type1,<65 year old. HHS seen in type2,>65 year old. Reality Most patients with DKA or HHS have type 2 DM , and many patients with DKA are >65 years old
- 7. Hyperglycemia ↑Insulin ↑Glucose uptake↓Glucose production ↓Gluconeogenesis ↓Glycogenolysis Normoglycemia
- 8. Hyperglycemia ↑Insulin ↓Glucose uptake↑Glucose production ↑ Gluconeogenesis ↑ Glycogenolysis Hyperglycemia
- 10. Infection i.e. (Pneumonia, sepsis,UTI) Inadequate insulin Inadequate water intake Infarction (myocardial) Intoxication(cocaine)Recurrent DKA Ischaemic(Stroke) injury Insult (Emotional) Infant(Pregnancy) New onset type 1 (20 to 25 %) Drugs. I
- 11. DKA HHS
- 12. DKA evolves rapidly, over 24-hour period. Hhs develop more insidiously (days). Polyuria, polydipsia, and weight loss. Fatigue ,dyspnea , vomiting, preceding febrile illness ,and polyphagia . Dehydration( tachycardia, poor skin turgor, dry mucous membranes, and orthostatic hypotension) . Neurologic symptoms(hemiparesis, hemianopsia or seizures) are most common in hhs. Hyperventilation and abdominal pain with dka.
- 13. • Abdominal pain It is more common in children, unusual in HHS It is multifactorial Metabolic acidosis. Not hyperglycamiea.?pancreatitis Delayed gastric emptying. Ileus from electrolyte disturbances It sometimes mimicks acute abdomen.
- 14. Insulin Deficiency Glucose uptake Proteolysis Lipolysis Amino Acids Glycerol Free Fatty Acids Gluconeogenesis Glycogenolysis Hyperglycemia Ketogenesis Acidosis Osmotic diuresis Polyuria Polydipsia Dehydration Dry tongue ,Tachycardia ,Hypotension Fruity breath (acetone smel) nail polish remover Kussmaul breathing (acidotic) Mental status changes Electrolyte imbalance Clinical manifestations
- 16. DD of acidotic breathing ◦ Renal failure. ◦ Amonia increase in HCF. ◦ Hysterical . DD of diabetic coma ◦ Lactic acidosis ◦ Hyperosmolar non-ketotic coma. ◦ Hypoglycemia . DD of coma in general. DD of acute abdomen.
- 17. HHSDKA More in elderlyMore in childrenAge More in type IIMore in type IDM type > 600> 250Glucose + or -+++++Ketonuria/emia >7.3<7.3pH >15<15HCO3 HyperosmolarityVariableS osmolarity Sensitive to small doseVariableSensitivity to insulin
- 18. HypoglycemiaDKA Insulin overdose or hyperinsulinemia Insulin deficiency or increased counter-reg hormones Etiology AcuteGradualOnset -S of Brain glucopenia - S of sympathetic overactivity S of hyperglycemia S of dehydration S of acidosis Symptoms and signs hypoglycemiahyperglycemiaRBS NoYesKetonuria NoYesKetonemia Rapidly recover if earlyNo effectIV glucose Golden rule Any diabetic patient with DKA versus hypoglycemia, give glucose even before glucose measuring
- 19. Diagnosis Triad for diagnosis Hyperglycemia > 300 mg/dl Ketonemia and ketonuria(Direct assay of beta- hydroxybutyrate levels is preferred) Blood gas metabolic acidosis pH < 7.3 High anion gap =(Na ) – (Cl + HCO3) > 10 may reach 20 and Bicarbonate <15 mEq/L
- 20. Direct measure oxidation May be absent in mild cases
- 21. For diagnosis Other findings ◦ Electrolyte serum level Hyperkalemia (rarely Hypokalemia), Hyponatremia (rarely Hypernatremia ) ◦ Investigation for the cause such as Urine Analysis, AMI panel and ECG, Chest x-ray ◦ Hyperosmolarity Normal = 285-295 (mOsmol/kg)
- 22. For monitoring RBS :every 1 hour till RBS reaches 200 mg/dl or less, then every 6 hours Venous ph (for DKA) every two to four hours. Direct measurement of beta- hydroxybutyrate(not urine ketones) Electrolytes serum level every 4 hours till correction
- 23. Treatment of predisposing factors. Initial hospital management ◦ Care of comatosed patients(Airway, breathing, and circulation (ABC) status ◦I.V fluids ◦Electrolytes replacement. ◦Insulin . ◦ Treatment of complications if happen. Once resolved ◦ Convert to home insulin regimen. ◦ Prevent recurrence.
- 24. Fluid deficit 3-6 liters for DKA and 8-10liters in HHS. Over 24 hours. Patients with hypovolemic shock. Isotonic saline as quickly as possible. Patients without shock (and without heart failure), isotonic saline 15 to 20 ml/kg for the first 2 hours.
- 25. Then according to state of hydration, serum electrolyte levels, and the urine output. Measure “corrected” sodium . Add dextrose to the saline solution when the serum glucose reaches 200 mg/dl (11.1 mmol/L) in DKA or 250 to 300 mg/dl (13.9 to 16.7 mmol/L) in HHS
- 26. ◦ If Hyperkalemia (> 5.3 meq/L) initially present. No treatment as it resolves quickly with insulin. ◦ If normal level (3.3-5.3 meq/L) Add (20-30) mEq for each Liter of infused fluid. ◦ If Hypokalemia (<3.3meq/L) Add 40 mEq for each Liter of infused fluid.
- 27. Not recommend for routine use . considered if severe hypophosphatemia occurs..what symptoms . When needed, potassium or sodium phosphate 20 to 30 meq can be added to 1 litter of IV fluids.
- 28. Bicarbonate given if the arterial PH is less than 6.90. We give 100 meq of sodium bicarbonate in 400 ml sterile water with 20 meq of potassium chloride, if the serum potassium is less than 5.3 meq/L, administered over two hours.
- 29. • IV bolus of 0.1 units/kg regular insulin. • Infusion insulin at 0.1 units/kg/hr • (Check BG every 1hour. • ( goal of reduction is 50-80 mg/dl/hr) When reaches ◦ 200 mg/dL in DKA or 250 to 300 mg/dL in HHS, the IV saline solution is switched to dextrose in saline, and decrease the insulin infusion rate to 0.02 to 0.05 U/kg per hour.
- 32. DKADKA
- 33. HHSHHS
- 34. Infection ◦ Precipitates DKA ◦ Leukocytosis can be secondary to acidosis Shock ◦ If not improving with fluids r/o MI Vascular thrombosis Pulmonary Edema ◦ Result of aggressive fluid resuscitation Cerebral Edema ◦ First 24 hours due to aggressive correction of hyperglycemia or administration of hypotonic solution ◦ c/p: Mental status changes ◦ Tx: Mannitol ◦ May require intubation with hyperventilation
- 35. Never omit insulin. Prevent dehydration and hypoglycemia. Monitor blood sugars frequently. Monitor for ketosis. Provide supplemental fast acting insulin. Treat underlying triggers. Maintain contact with medical team.
- 36. Plasma glucose is usually high but not always. ◦ DKA can be present with RBS < 300 due to Impaired gluconeogenesis Liver disease Acute alcohol ingestion Prolonged fasting. Pregnancy. Ketone (acetoacetic acid by nitroprusside tablets (Acetest)or reagent sticks (Ketostix) in urine may be –ve in DKA, but always +ve in blood(betahydroxybuteric acid which is the predominant ketone)
- 38. High WBC may be present without infection.>>>Bandaemia High creatinine may be present without true renal function(it may cross react with ketone bodies). Blood urea may be elevated with prerenal azotemia secondary to dehydration. Serum amylase is often raised even in the absence of pancreatitis. Creatine kinase and troponin levels mildly increase in the absence of myocardial damage
- 39. Definition: ◦ In diabetic patients if low plasma glucose concentration≤70 mg/dl. (With or without symptoms) Clinical classification: ◦ Severe hypoglycemia. ◦ Documented symptomatic hypoglycemia . ◦ Asymptomatic hypoglycemia. ◦ Probable symptomatic hypoglycemia ◦ Pseudohypoglycemia
- 40. Symptoms. Risk factor assessment: ◦ Ask about hypoglycemia at every visit. ◦ Review the self-monitoring of blood glucose (SMBG) Prevention: ◦ consider more modest goals for A1C values. ◦ Education.
- 41. Treatment For asymptomatic or symptomatic hypoglycemia ,ingest carbohydrates. 15 to 20 grams of oral glucose is typically sufficient. Glucose may be ingested in the form of tablets, juice, milk, glucagon(0.5 to 1.0) mg given as a subcutaneous or intramuscular injection. If difficult IV access .(or at home) EDUCATION . IV dextrose (25 g of 50 percent glucose [dextrose]) can be administered to treat hypoglycemia in patients with impaired consciousness and established IV access (typically in hospital).
- 42. الشكر مع
Editor's Notes
- PRECIPITATING FACTORS — A precipitating event can usually be identified in patients with diabetic ketoacidosis (DKA) or hyperosmolar hyperglycemic state (HHS) (table 2) [1-3]. The most common events are infection (often pneumonia or urinary tract infection) and discontinuation of or inadequate insulin therapy. Compromised water intake due to underlying medical conditions, particularly in older patients, can promote the development of severe dehydration and HHS [3-5]. Other conditions and factors associated with DKA and HHS include: ●Acute major illnesses such as myocardial infarction, cerebrovascular accident, sepsis, or pancreatitis. ●New onset type 1 diabetes, in which DKA is a common presentation. ●In established type 1 diabetes, omission of insulin in setting of gastroenteritis when patient mistakenly stops insulin because of reduced oral intake. ●Drugs that affect carbohydrate metabolism, including glucocorticoids, higher-dose thiazide diuretics, sympathomimetic agents (eg, dobutamine andterbutaline) [6], and second-generation “atypical” antipsychotic agents [7]. ●Cocaine use, which has been associated with recurrent DKA [8,9]. ●Psychological problems associated with eating disorders and purposeful insulin omission, particularly in young patients with type 1 diabetes [10]. Factors that may lead to insulin omission in younger patients include fear of weight gain, fear of hypoglycemia, rebellion from authority, and the stress of chronic disease. ●Poor compliance with the insulin regimen. ●Malfunction of continuous subcutaneous insulin infusion devices (CSII), which was initially reported in the early 1980s [11]. Pump malfunction is now uncommon, but system failure due to blockage or leakage in the syringe or the infusion set or connectors, causing an interruption of infusion flow infusion set, can lead to DKA. The frequency of DKA with pump therapy, however, appears to be no different from that with multiple daily injections of insulin [12].
- CLINICAL PRESENTATION — Diabetic ketoacidosis (DKA) usually evolves rapidly, over a 24-hour period. In contrast, symptoms of hyperosmolar hyperglycemic state (HHS) develop more insidiously with polyuria, polydipsia, and weight loss, often persisting for several days before hospital admission. The earliest symptoms of marked hyperglycemia are polyuria, polydipsia, and weight loss. As the degree or duration of hyperglycemia progresses, neurologic symptoms, including lethargy, focal signs, and obtundation, can develop. This can progress to coma in later stages. Neurologic symptoms are most common in HHS, while hyperventilation and abdominal pain are primarily limited to patients with DKA. Neurologic symptoms — Neurologic deterioration primarily occurs in patients with an effective plasma osmolality above 320 to 330 mosmol/kg [1,13-15] (see 'Plasma osmolality' below). Mental obtundation and coma are more frequent in HHS than DKA because of the usually greater degree of hyperosmolality in HHS (table 1) [16]. In addition, some patients with HHS have focal neurologic signs (hemiparesis or hemianopsia)and/or seizures [16-20]. Mental obtundation may occur in patients with DKA, who have lesser degrees of hyperosmolality, when severe acidosis exists [21]. However, stupor or coma in diabetic patients with an effective plasma osmolality lower than 320 mosmol/kg demands immediate consideration of other causes of the mental status change. Abdominal pain in DKA — Patients with DKA may present with nausea, vomiting, and abdominal pain; although more common in children, these symptoms can be seen in adults [22]. Abdominal pain is unusual in HHS. In a review of 189 consecutive episodes of DKA and 11 episodes of HHS, abdominal pain was reported in 46 percent of patients with DKA compared with none of the patients with HHS [23]. Abdominal pain was associated with the severity of the metabolic acidosis (occurring in 86 percent of those with a serum bicarbonate ≤5 but only 13 percent of those with a serum bicarbonate ≥15 mEq/L) but did not correlate with the severity of hyperglycemia or dehydration. Possible causes of abdominal pain include delayed gastric emptying and ileus induced by the metabolic acidosis and associated electrolyte abnormalities [1]. Other causes for abdominal pain, such as pancreatitis, should be sought when they occur in the absence of severe metabolic acidosis and when they persist after the resolution of ketoacidosis. Physical examination — Signs of volume depletion are common in both DKA and HHS and include decreased skin turgor, dry axillae and oral mucosa, low jugular venous pressure, tachycardia, and, if severe, hypotension. Neurologic findings, noted above, also may be seen, particularly in patients with HHS. (See'Neurologic symptoms' above and "Etiology, clinical manifestations, and diagnosis of volume depletion in adults".) Patients with DKA may have a fruity odor (due to exhaled acetone; this is similar to the scent of nail polish remover) and deep respirations reflecting the compensatory hyperventilation (called Kussmaul respirations).
- Abdominal pain in DKA — Patients with DKA may present with nausea, vomiting, and abdominal pain; although more common in children, these symptoms can be seen in adults [22]. Abdominal pain is unusual in HHS. In a review of 189 consecutive episodes of DKA and 11 episodes of HHS, abdominal pain was reported in 46 percent of patients with DKA compared with none of the patients with HHS [23]. Abdominal pain was associated with the severity of the metabolic acidosis (occurring in 86 percent of those with a serum bicarbonate ≤5 but only 13 percent of those with a serum bicarbonate ≥15 mEq/L) but did not correlate with the severity of hyperglycemia or dehydration. Possible causes of abdominal pain include delayed gastric emptying and ileus induced by the metabolic acidosis and associated electrolyte abnormalities [1]. Other causes for abdominal pain, such as pancreatitis, should be sought when they occur in the absence of severe metabolic acidosis and when they persist after the resolution of ketoacidosis.
- Physical examination — Signs of volume depletion are common in both DKA and HHS and include decreased skin turgor, dry axillae and oral mucosa, low jugular venous pressure, tachycardia, and, if severe, hypotension. Neurologic findings, noted above, also may be seen, particularly in patients with HHS. (See 'Neurologic symptoms' above and "Etiology, clinical manifestations, and diagnosis of volume depletion in adults".) Patients with DKA may have a fruity odor (due to exhaled acetone; this is similar to the scent of nail polish remover) and deep respirations reflecting the compensatory hyperventilation (called Kussmaul respirations). Kussmaul breathing is a deep and labored breathing pattern often associated with severe metabolic acidosis, particularlydiabetic ketoacidosis (DKA) but also renal failure. It is a form of hyperventilation, which is any breathing pattern that reduces carbon dioxide in the blood due to increased rate or depth of respiration. In metabolic acidosis, breathing is first rapid and shallow[1] but as acidosis worsens, breathing gradually becomes deep, labored and gasping. It is this latter type of breathing pattern that is referred to as Kussmaul breathing.
- Emergent DKA management in adults: rapid overview Clinical featuresDKA usually evolves rapidly over a 24-hour period.Common, early signs of ketoacidosis include nausea, vomiting, abdominal pain, and hyperventilation. The earliest symptoms of marked hyperglycemia are polyuria, polydipsia, and weight loss.As hyperglycemia worsens, neurologic symptoms appear, and may progress to include lethargy, focal deficits, obtundation, seizure, and coma.Common causes of DKA include: infection; noncompliance, inappropriate adjustment, or cessation of insulin; new onset diabetes mellitus; and myocardial ischemia.Evaluation and laboratory findingsAssess vital signs, cardiorespiratory status, and mental status.Assess volume status: vital signs, skin turgor, mucosa, urine output.Obtain the following studies: serum glucose, urinalysis and urine ketones, serum electrolytes, BUN and creatinine, plasma osmolality, mixed venous blood gas, electrocardiogram; add serum ketones if urine ketones present.Diabetic ketoacidosis (DKA) is characterized by hyperglycemia, an elevated anion gap metabolic acidosis, and ketonemia. Dehydration and potassium deficits are often severe.Serum glucose is usually greater than 250 mg/dL (13.9 mmol/L) and less than 800 mg/dL (44.4 mmol/L). In certain instances (eg, insulin given prior to ED arrival), the glucose may be only mildly elevated.Additional testing is obtained based on clinical circumstances and may include: blood or urine cultures, lipase, chest x-ray.ManagementStabilize the patient's airway, breathing, and circulation.Obtain large bore IV (≥16 gauge) access; monitor using a cardiac monitor, capnography, and pulse oximetry.Monitor serum glucose hourly, and basic electrolytes, plasma osmolality, and venous pH every two to four hours until the patient is stable.Determine and treat any underlying cause of DKA (eg, pneumonia or urinary infection, myocardial ischemia).Replete fluid deficits:• Give several liters of isotonic (0.9 percent) saline as rapidly as possible to patients with signs of shock.• Give isotonic saline at 15 to 20 mL/kg per hour, in the absence of cardiac compromise, for the first few hours to hypovolemic patients without shock.• After intravascular volume is restored, give one-half isotonic (0.45 percent) saline at 4 to 14 mL/kg per hour if the corrected serum sodium is normal or elevated; isotonic saline is continued if the corrected serum sodium is reduced.• Add dextrose to the saline solution when the serum glucose reaches 200 mg/dL (11.1 mmol/L).Replete potassium (K+) deficits:• Regardless of the initial measured serum potassium, patients with DKA have a large total body potassium deficit.• If initial serum K+ is below 3.3 mEq/L, hold insulin and give K+ 20 to 30 mEq/hour IV until K+ concentration is above 3.3 mEq/L.• If initial serum K+ is between 3.3 and 5.3 mEq/L, give K+ 20 to 30 mEq per liter IV fluid; maintain K+ between 4 to 5 mEq/L.• If initial serum K+ is above 5.3 mEq/L do not give K+; check K+ every 2 hours.Give insulin:• Do not give insulin if initial serum K+ is below 3.3 mEq/L; replete K+ first.• Give all patients without a serum K+ below 3.3 mEq/L regular insulin. Either of two regimens can be used: 0.1 units/kg IV bolus, then start a continuous IV infusion 0.1 units/kg per hour; OR do not give bolus and start a continuous IV infusion at a rate of 0.14 units/kg per hour.• Continue insulin infusion until ketoacidosis is resolved, serum glucose is below 200 mg/dL (11.1 mmol/L), and subcutaneous insulin is begun.Give sodium bicarbonate to patients with pH below 7.00:• If the arterial pH is between 6.90 and 7.00, give 50 meq of sodium bicarbonate plus 10 meq of potassium chloride in 200 mL of sterile water over two hours.• If the arterial pH is below 6.90, give 100 meq of sodium bicarbonate plus 20 meq of potassium chloride in 400 mL sterile water over two hours.
- Fluid replacement — In patients with DKA or HHS, we recommend vigorous IV electrolyte and fluid replacement to correct both hypovolemia and hyperosmolality. Fluid repletion is usually initiated with isotonic saline (0.9 percent sodium chloride). The optimal rate of isotonic saline infusion is dependent upon the clinical state of the patient. Isotonic saline should be infused as quickly as possible in patients with hypovolemic shock. (See "Treatment of severe hypovolemia or hypovolemic shock in adults".) In hypovolemic patients without shock (and without heart failure), isotonic saline is infused at a rate of 15 to 20 mL/kg lean body weight per hour (about 1000 mL/hour in an average-sized person), for the first couple hours, with a maximum of <50 mL/kg in the first four hours (algorithm 1 and algorithm 2) [1]. After the second or third hour, the choice for fluid replacement depends upon the state of hydration, serum electrolyte levels, and the urine output. The most appropriate IV fluid composition is determined by the “corrected” sodium concentration. The “corrected” sodium concentration can be approximated by adding 2.0mEq/L to the plasma sodium concentration for each 100 mg/100 mL (5.5 mmol/L) increase above normal in glucose concentration (calculator 1). If the “corrected” serum sodium concentration is less than 135 mEq/L,then isotonic saline should be continued at a rate of about 250 to 500 mL/hour [1]. However, if the “corrected” sodium concentration is normal or elevated, then the IV fluid is generally switched to one-half isotonic saline at a rate of 250 to 500 mL/hour in order to provide electrolyte-free water. The timing of one-half isotonic saline therapy may also be influenced by potassium balance. Potassium repletion affects the saline solution that is given, since potassium is as osmotically active as sodium. Thus, concurrent potassium replacement may be another indication for the use of one-half isotonic saline. (See 'Potassium replacement' below.) We add dextrose to the saline solution when the serum glucose reaches 200 mg/dL (11.1 mmol/L) in DKA or 250 to 300 mg/dL (13.9 to 16.7 mmol/L) in HHS. (See 'Intravenous regular insulin' below.) Adequate rehydration with correction of the hyperosmolar state may result in a more robust response to low-dose insulin therapy [11,12]. Adequacy of fluid replacement is judged by frequent hemodynamic and laboratory monitoring (see 'Monitoring' below). In patients with abnormal renal or cardiac function, more frequent monitoring must be performed to avoid iatrogenic fluid overload [9,10,12,15-18]. The goal is to correct estimated deficits (table 2) within the first 24 hours. Osmolality should not be reduced too rapidly because of concern that this may cause development of cerebral edema.
- Potassium replacement — Potassium replacement is initiated immediately if the serum potassium is <5.3 mEq/L. ●If the initial serum potassium is below 3.3 mEq/L, IV potassium chloride (KCl 20 to 40 mEq/hour, which usually requires 20 to 40 mEq/L added to saline) should be given. The choice of replacement fluid (isotonic or one-half isotonic saline) depends upon the state of hydration, corrected sodium concentration, dose of KCl, blood pressure, and a clinical assessment of overall volume status. Potassium repletion is most urgent in patients with massive potassium deficits who are hypokalemic prior to therapy [19-21]. Such patients require aggressive potassium replacement (40 mEq/hour,with additional supplementation based upon hourly serum potassium measurements) to maintain the serum potassium concentration within the normal range of 4 to 5 mEq/L. ●If the initial serum potassium is between 3.3 and 5.3 mEq/L, IV KCl (20 to 30 mEq) is added to each liter of IV replacement fluid and continued until the serum potassium (K) concentration has increased to the 4.0 to 5.0 mEq/L range. ●If the serum potassium concentration is initially greater than 5.3 mEq/L, then potassium replacement should be delayed until its concentration has fallen below this level. When potassium salts are added to IV fluids, they have the same osmotic effect as sodium salts, and this should be considered when determining the potential effects of IV fluid infusion on changes in osmolality. As an example, 40 mEq of KCl added to 1 L of fluid generates 80 mOsmol/L of electrolyte osmolality. The addition of 40 mEq of potassium to 1 L of one-half isotonic saline creates a solution with an osmolality of 234 mOsmol/L (77 mEq sodium chloride [NaCl] and 40 mEq KCl), which is essentially three-quarters isotonic saline. (The osmolality of isotonic saline is 285 to 308 mOsmol/L). If 40 mEq of KCl is added to isotonic saline, the final osmolality will be about 388 mOsmol/L. However, KCL will not have nearly the same extracellular fluid (ECF) expansion effect because most will shift into cells very rapidly. (See "Maintenance and replacement fluid therapy in adults", section on 'Choice of replacement fluid'.) Almost all patients with DKA or HHS have a substantial potassium deficit, mainly due to urinary losses related to the glucose osmotic diuresis and to secondary hyperaldosteronism. Despite the total body potassium deficit, the serum potassium concentration is usually normal or, in about one-third of cases, elevated at presentation due primarily to insulin deficiency and hyperosmolality, both of which result in potassium movement out of the cells [22]. The change in potassium distribution is rapidly reversed with the administration of insulin, resulting in an often dramatic fall in the serum potassium concentration, despite potassium replacement [19,20]. However, caution is necessary if renal function remains depressed and/or urine output does not increase to a level >50 mL/hour. Careful monitoring of the serum potassium is essential for the management of both DKA and HHS.
- strongly considered if severe hypophosphatemia occurs (serum phosphate concentration below 1.0 mg/dL or 0.32 mmol/L), especially if cardiac dysfunction, hemolytic anemia, and/or respiratory depression develop [45-49]. When needed, potassium or sodium phosphate 20 to 30 mEq can be added to 1 L of IV fluid.
- IV regular insulin and rapid-acting insulin analogs are equally effective in treating DKA [23]. Due to cost considerations, we prefer treatment with regular insulin, rather than rapid-acting insulin analogs. Choice of IV insulin should be based upon institutional preferences, clinician experience, and cost concerns.
- Nitroprusside testing — This chemical develops a purple color in the presence of acetoacetic acid (and to a much lesser degree, acetone). Urine dipstick testing with nitroprusside tablets (Acetest) or reagent sticks (Ketostix) is widely utilized and results are available within minutes. Serum testing is necessary to determine if serum ketone levels can explain the high anion gap acidosis. A 4+ reaction with serum diluted 1:1 is highly suggestive of ketoacidosis. A 4+ reaction in more diluted serum (ie, 1:4, 1:8, etc) provides evidence of even higher concentrations of acetoacetic acid. Although one cannot directly extrapolate from the nitroprusside result to the severity of the acidosis or the magnitude of the anion gap, this is a useful semiquantitative test for the evaluation of possible ketoacidosis. Although the nitroprusside reaction is still widely used to detect ketone bodies in urine, its use for serum testing has become uncommon. Both false-negative and false-positive results should be considered. ●False-negative nitroprusside testing – The fact that nitroprusside reacts with acetoacetate and, to a lesser degree, acetone (which is not an acid), but not with beta-hydroxybutyrate, can cause diagnostic confusion. This is important because beta-hydroxybutyrate is the predominant ketone, particularly in severe DKA. The ratio of beta-hydroxybutyrate to acetoacetate, which is about 1:1 in normal subjects, can increase to as high as 10:1 in DKA [31]. It is therefore possible, although unusual, to have a negative serum nitroprusside reaction in the presence of severe ketosis. ●False-positive nitroprusside testing – False-positive nitroprusside urine ketone results can be generated by drugs containing free sulfhydryl groups that react with nitroprusside. Captopril,penicillamine, and mesna are several drugs with this property. Direct measurement of serum beta-hydroxybutyrate — For a number of reasons, including the problems described above, the serum nitroprusside test for ketone bodies has been largely replaced by direct assays for beta-hydroxybutyrate [32]. Several beta-hydroxybutyrate assay instruments are commercially available [31,33-35]. Use of such instruments will eliminate the problems associated with nitroprusside testing. One limitation of some of these assays is that beta-hydroxybutyrate cannot be quantitated above a level of 6 mEq/L. An ideal assay for ketoacids would measure the concentrations of both acetoacetate and beta-hydroxybutyrate.
- Treatment ●For a person with drug-treated diabetes, we suggest defensive actions when self-monitoring reveals a glucose level ≤70 mg/dL (3.9 mmol/L) (Grade 2C) (see 'Definition' above). Defensive actions include repeating the measurement in the near term, avoiding critical tasks such as driving, ingesting carbohydrates, and adjusting the treatment regimen. ●Patients with asymptomatic or symptomatic hypoglycemia should ingest carbohydrates. Fifteen to 20 grams of oral glucose is typically sufficient. Glucose may be ingested in the form of tablets, juice, milk, other snacks, or a meal. (See 'Symptomatic' above.) ●For the treatment of hypoglycemia in a person with impaired consciousness and no established intravenous (IV) access, we suggest the immediate administration of glucagon, rather than waiting to establish IV access (Grade 2B). The usual dose is 0.5 to 1.0 mg given as a subcutaneous or intramuscular injection. EDUCATION AND TRAINING for clinicians, friends, and family on the recognition and treatment of severe hypoglycemia, including the use of glucagon kits, is necessary. (See 'Severe' above.) ●IV dextrose (25 g of 50 percent glucose [dextrose]) can be administered to treat hypoglycemia in patients with impaired consciousness and established IV access (typically in a hospital). (See 'Severe' above.) ●In the latter settings, a subsequent glucose infusion (or food, if patient is able to eat) is often needed, depending upon the cause of the hypoglycemia, to prevent recurrence of symptoms. ●We routinely check that the patient's blood glucose monitoring equipment is accurately calibrated, that fast-acting carbohydrate is being kept available, that the patient is staying vigilant, and that glucagon kits are not out of date.