Diagnosis and Management of Hyperglycemic Crises Diabetic Ketoacidosis Hyperglycemic Hyperosmolar State DR GOZASHTI 1
OVERVIEW 2
DKA and HHS Are Life-Threatening Emergencies Diabetic Ketoacidosis (DKA) Hyperglycemic Hyperosmolar State (HHS) Plasma glucose >250 mg/d. L Plasma glucose >600 mg/d. L Arterial p. H <7. 3 Arterial p. H >7. 3 Bicarbonate <15 m. Eq/L Bicarbonate >15 m. Eq/L Moderate ketonuria or ketonemia Minimal ketonuria and ketonemia Anion gap >12 m. Eq/L Serum osmolality >320 mosm/L 3
Characteristics of DKA and HHS Diabetic Ketoacidosis (DKA) Hyperglycemic Hyperosmolar State (HHS) Absolute (or near-absolute) insulin deficiency, resulting in • Severe hyperglycemia • Ketone body production • Systemic acidosis Severe relative insulin deficiency, resulting in • Profound hyperglycemia and hyperosmolality (from urinary free water losses) • No significant ketone production or acidosis Develops over hours to 1 -2 days Develops over days to weeks Most common in type 1 diabetes, but increasingly seen in type 2 diabetes Typically presents in type 2 or previously unrecognized diabetes Higher mortality rate 4
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Definition of Diabetic Ketoacidosis* Acidosis * Ketosis Hyperglycemia Adapted from Kitabchi AE, Fisher JN. Diabetes Mellitus. In: Glew RA, Peters SP, ed. Clinical Studies in Medical Biochemistry. New York, NY: Oxford University Press; 1987: 105. 6
• euglycemic DKA has been reported in patients with type 1 diabetes who were: • vomiting • fasting • had been treated with insulin prior to presentation, • Pregnancy • treated with sodium–glucose cotransporter 2 (SGLT 2) inhibitors 7
Ketosis-Prone Type 2 Diabetes • studies have indicated that about half of previously undiagnosed adult African Americans (AAs) and Hispanic subjects with unprovoked DKA have type 2 diabetes 8
• The evidence for type 2 diabetes in these patients include: • obesity • family history of diabetes • relatively preserved insulin secretion • low prevalence of beta cell autoimmunity • the ability to discontinue insulin therapy during the period of near-normoglycemia 9
• Predictors of remission include : absence of autoimmunity with preserved beta cell function as determined by a fasting Cpeptide level of >1. 0 ng/dl (0. 33 nmol/l) or a glucagon-stimulated C-peptide of >1. 5 ng/dl (0. 5 nmol/l) 10
• Recurrence of ketosis occurs within 12– 24 months in nearly 60% of patients who are treated with lifestyle modification alone. • Small dose sulfonylureas such as glyburide 1. 25 to 2. 5 mg/day) and glipizide 2. 5 mg/day and the thiazolidinedione pioglitazone 30 mg/day have been shown to prolong remission and prevent recurrence of DKA. 11
PATHOGENESIS AND PATHOPHYSIOLOGY 12
Diabetic Ketoacidosis: Pathophysiology Unchecked gluconeogenesis Hyperglycemia Osmotic diuresis Dehydration Unchecked ketogenesis Ketosis Dissociation of ketone bodies into hydrogen ion and anions Anion-gap metabolic acidosis • Often a precipitating event is identified (infection, lack of insulin administration) 13
Insulin Deficiency Hyperglycemia Hyperosmolality Glycosuria Δ MS Dehydration Renal Failure Shock Electrolyte Losses CV Collapse 14
Insulin Deficiency Lipolysis FFAs Ketones Acidosis CV Collapse 15
Insulin Deficiency Hyperglycemia Hyperosmolality Glycosuria Δ MS Lipolysis FFAs Ketones Dehydration Renal Failure Shock Electrolyte Losses Acidosis CV Collapse 16
Hyperosmolar Hyperglycemic State: Pathophysiology Unchecked gluconeogenesis Hyperglycemia Osmotic diuresis Dehydration • Presents commonly with renal failure • Insufficient insulin for prevention of hyperglycemia but sufficient insulin for suppression of lipolysis and ketogenesis • Absence of significant acidosis • Often identifiable precipitating event (infection, MI) 17
Diabetic Hyperglycemic Crises Diabetic Ketoacidosis (DKA) Hyperglycemic Hyperosmolar State (HHS) Younger, type 1 diabetes Older, type 2 diabetes No hyperosmolality Hyperosmolality Volume depletion Electrolyte disturbances Acidosis No acidosis 18
Predictors of Future Near-Normoglycemic Remission in Adults With DKA • • • African-American, Hispanic, other minorities Newly diagnosed diabetes Obesity Family history of type 2 diabetes Negative islet autoantibodies Fasting C-peptide levels – >0. 33 nmol/L within 1 week or – >0. 5 nmol/L during follow-up Umpierrez GE, et al. Ann Intern Med. 2006; 144: 350 -357. 19
FOCUS ON ACIDOSIS 20
Anion Gap Metabolic Acidosis • The normal anion gap in m. Eq/L is calculated as: [Na] - [Cl + HCO 3] • The normal gap is <12 m. Eq/L • Causes of anion gap acidosis (unmeasured anions) include: – – Ketoacidosis (diabetic, alcoholic) Lactic acidosis (lactate [underperfusion, sepsis]) Uremia (phosphates, sulfates) Poisonings/overdoses (methanol, ethylene glycol, aspirin, paraldehyde) • In ketoacidosis, the “delta” of the anion gap above 10 -12 m. Eq/L is composed of anions derived from keto-acids 21
Hyperchloremic Metabolic Acidosis (Non-anion Gap) • Hyperchloremic acidosis (ie, expansion acidosis) is common during recovery from DKA due to – Fluid replacement with saline (Na. Cl) – Renal loss of HCO 3 • Following successful treatment of DKA, a nonanion–gap acidosis may persist after the ketoacidosis has cleared (ie, after closing of the anion gap) • Closing of the anion gap is a better sign of recovery from DKA than is correction of metabolic acidosis 22
Ketone Bodies in DKA O O CH 3 – CH 2 – C O- Acetoacetate OH O CH 3 – CH 2 – C H O CH 3 – CH 3 O- -Hydroxybutyrate Acetone • Unless -hydroxybutyrate ( -OH B) is specifically ordered, the ketone bodies are estimated by the nitroprusside reaction in the lab, which measures only acetone and acetoacetate (Ac. Ac) • Acetone is not an acid 23
Ketone Body Equilibrium in DKA Ac. Ac NADH + H+ -OH B NAD+ • In DKA, the dominant ketoacid is -hydroxybutyric acid ( -OH B), especially in cases of poor tissue perfusion/lactic acidosis • During recovery, the balance shifts to acetoacetic acid (Ac. Ac) 24
Significance of Ketone Measurements • -hydroxybutyrate can only be measured using specialized equipment not available in most in-house laboratories • During recovery, results from the nitroprusside test might wrongly indicate that the ketone concentration is not improving or is even getting worse • The best biochemical indicator of resolution of ketoacid excess is simply the anion gap • There is no rationale for follow-up ketone measurements after the initial measurement has returned high 25
Coexisting Conditions (Altered Redox States) Drive Balance Toward NADH and β-OH B Lactic Acidosis Alcoholic Ketoacidosis Fulop M, et al. Arch Intern Med. 1976; 136: 987 -990; Marliss EB, et al. N Engl J Med. 1970; 283: 978 -980; Levy LJ, et al. Ann Intern Med. 1973; 79: 213 -219; Wrenn KD, et al. Am J Med. 1991; 91: 119 -128. 26
Molar Ratio of -OH B to Ac. Ac Normal health 2 to 1 DKA 3 -4 to 1 DKA with high redox state 7. 7 -7. 8 to 1 • Significance: Increase of measured ketones may be misleadingly small in DKA with coexisting lactic acidosis and/or alcoholism Marliss EB, et al. N Engl J Med. 1970; 283: 978 -980. 27
PATIENT PRESENTATION 28
Clinical Presentation of Diabetic Ketoacidosis History • • • Thirst Polyuria Abdominal pain Nausea and/or vomiting Profound weakness Physical Exam • • • Kussmaul respirations Fruity breath Relative hypothermia Tachycardia Supine hypotension, orthostatic drop of blood pressure • Dry mucous membranes • Poor skin turgor 29
Lab Findings in DKA • • • Severe hyperglycemia Increased blood and urine ketones Low bicarbonate High anion gap Low arterial p. H Low PCO 2 (respiratory compensation) 30
• In severely ill patients, hypotension, shock and altered consciousness may be present. 31
• Mental status can vary from full alertness to profound lethargy or coma. • The pathogenesis of altered sensorium in DKA is not known with certainty, while some studies suggest: • hyperosmolarity • acidosis 32
• in a retrospective analysis of over 200 cases of DKA we determined that acidosis was the prime • determinant of altered sensorium, but hyperosmolarity played a synergistic role in patients with severe acidosis to precipitate depressed sensorium. 33
• Combination of severe acidosis and hyperosmolarity predicted altered onsciousness with 61% sensitivity and 87% specificity 34
• Abdominal pain, which usually correlates with the severity of acidosis and may be confused with acute abdomen in 50– 75% of cases. • In the absence of acidosis, another etiology for abdominal pain should be pursued. • Hematemesis could occur in up to 25% of patients, due to gastritis 35
• Patients with DKA could have leukocytosis, which may be proportional to the severity of acidosis, hypercortisolemia and elevation of catecholamines. • Leukocytosis greater than 25, 000/μL may suggest a concurrent infection which warrants further evaluation 36
• The admission serum sodium is usually low because of the efflux of water from the intracellular to the extracellular space in the presence of hyperglycemia. • An increase in serum sodium concentration in the presence of hyperglycemia indicates a rather profound degree of water loss. 37
• The measured value can be corrected by • adding 1. 6 mmol/l (1. 6 m. Eq/L) of sodium for every 5. 6 mmol/l (100 mg/dl) of glucose above 5. 6 mmol/l (100 mg/dl). • Measured serum sodium and glucose concentrations may be falsely lowered by severe hypertriglyceridemia 38
• Unless the plasma is cleared of chylomicrons, pseudonormoglycemia and seudohyponatremia can occur. 39
Potassium Balance in DKA • Potassium is dominantly intracellular • Urinary losses occur during evolution of DKA (due to glycosuria) • Total body potassium stores are greatly reduced in any patient with DKA • Potassium moves from inside the cell to the extracellular space (plasma) – – – During insulin deficiency In presence of high blood glucose As cells buffer hydrogen ions • Blood levels of potassium prior to treatment are usually high but may drop precipitously during therapy 40
• Measured serum creatinine may be falsely elevated due to dehydration or interference with the assay by elevated acetoacetate. • Serum creatinine should be monitored during hydration and resolution of acidosis. 41
• Drugs that have sulfhydryl groups can interact with the reagent in the nitroprusside reaction, thus giving a false positive result such as captopril 42
• Clinical judgment and other biochemical considerations may be relevant in interpreting the value of positive nitroprusside reaction in patients taking captopril who are suspected to have DKA. 43
Differential Diagnosis • in alcoholic ketoacidosis (AKA), total ketone bodies are much greater than in DKA with a higher BOHB to acetoacetate ratio of 7: 1 versus a ratio of 3: 1 in DKA. • Patients with AKA seldomly present with hyperglycemia. 44
starvation ketosis • Patients with poor oral intake could present with mild ketoacidosis, (starvation ketosis), but this may not occur in individuals on prolonged Fasting. • patients with starvation ketosis rarely present with serum bicarbonate concentration less than 18 m. Eq/L, and do not exhibit hyperglycemia 45
• DKA should be distinguished from • high anion gap acidosis including lactic acidosis, advanced chronic renal failure as well as ingestion of drugs such as salicylate, methanol and ethylene glycol. 46
• Isopropyl alcohol which is commonly available as rubbing alcohol can cause considerable ketosis and high osmolar gap without metabolic Acidosis. • however, it has a tendency to cause hypoglycemia rather than hyperglycemia. 47
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Clinical Presentation of Hyperglycemic Hyperosmolar State • Compared to DKA, in HHS there is greater severity of: – – Dehydration Hyperglycemia Hypernatremia Hyperosmolality • Because some insulin typically persists in HHS, ketogenesis is absent to minimal and is insufficient to produce significant acidosis 49
Clinical Presentation of Hyperglycemic Hyperosmolar State Patient Profile • • • Older More comorbidities History of type 2 diabetes, which may have been unrecognized Disease Characteristics • More insidious development than DKA (weeks vs hours/days) • Greater osmolality and mental status changes than DKA • Dehydration presenting with a shock-like state 50
Electrolyte and Fluid Deficits in DKA and HHS Parameter DKA* HHS* Water, m. L/kg 100 (7 L) 100 -200 (10. 5 L) Sodium, mmol/kg 7 -10 (490 -700) 5 -13 (350 -910) Potassium, mmol/kg 3 -5 (210 -300) 5 -15 (350 -1050) Chloride, mmol/kg 3 -5 (210 -350) 3 -7 (210 -490) Phosphate, mmol/kg 1 -1. 5 (70 -105) 1 -2 (70 -140) Magnesium, mmol/kg 1 -2 (70 -140) Calcium, mmol/kg 1 -2 (70 -140) * Values (in parentheses) are in mmol unless stated otherwise and refer to the total body deficit for a 70 kg patient. Chaisson JL, et al. CMAJ. 2003; 168: 859 -866. 51
Initial Laboratory Evaluation of Hyperglycemic Emergencies • • • Comprehensive metabolic profile Serum osmolality Serum and urine ketones Arterial blood gases Lactate (? ) CBC Urinalysis ECG Blood cultures (? ) 52
Laboratory Diagnostic Criteria of DKA and HHS Parameter Normal range DKA HHS 76 -115 ≥ 250 ≥ 600 7. 35 -7. 45 ≤ 7. 30 >7. 30 22 -28 ≤ 15 >15 275 -295 ≤ 320 >320 <12 >12 Variable Serum ketones Negative Moderate to high None or trace Urine ketones Negative Moderate to high None or trace Plasma glucose, mg/d. L Arterial p. H* Serum bicarbonate, mmol/L Effective serum osmolality, mmol/kg Anion gap, † mmol/L * If venous p. H is used, a correction of 0. 03 must be made. † Calculation: Na+ - (Cl- + HCO 3 -). Chaisson JL, et al. CMAJ. 2003; 168: 859 -866. 53
![Formulas for Estimating Serum Osmolality and Effective Osmolality 2 x [Na+ m. Eq/L] +](https://present5.com/presentation/6fc0010e6e70505a01a33961eaa5e0cc/image-54.jpg "Formulas for Estimating Serum Osmolality and Effective Osmolality 2 x [Na+ m. Eq/L] +")
Formulas for Estimating Serum Osmolality and Effective Osmolality 2 x [Na+ m. Eq/L] + [glucose mg/d. L] / 18 + [BUN mg/d. L] / 2. 8 = Sosm (mosm/Kg H 2 O) 54
TREATMENT RECOMMENDATIONS 55
Treatment With IV Fluids and Dextrose • For severe hypovolemia, during the first 1 -2 hours (in absence of cardiac compromise), give 1 -1. 5 L 0. 9% Na. Cl • (15– 20 ml/kg body weight per hour) • The subsequent choice for fluid replacement depends on the state of hydration, serum electrolyte levels, and urinary output. • In general, 0. 45% Na. Cl infused at 4– 14 ml/kg/h is appropriate if the corrected serum sodium is normal or elevated; 0. 9% Na. Cl at a similar rate is appropriate if corrected serum sodium is low. 56
• Adequate fluid replacement is assessed by hemodynamic monitoring (improvement in blood pressure and pulse), measurement of fluid input and output, blood chemistry and clinical examination 57
• An effective serum osmolality >320 m. Osm/kg indicates severe dehydration, which would require aggressive fluid replacement therapy. • In patients with hypotension, aggressive fluid repletion with isotonic saline should continue until blood pressure is stable. • The administration of insulin without fluid replacement in hypotensive patients could worsen circulatory collapse. 58
• Hydration in the first hour of therapy before insulin has the following advantages: • a) it allows opportunity to obtain serum potassium value before insulin administration. • b) it prevents potential deterioration of hypotension, which could occur with the use of insulin without adequate hydration. • c) it improves insulin action and may reduce the concentration of counter regulatory hormones and hyperglycemia 59
• Energy is required for the metabolism of ketone bodies, therefore, as soon as blood glucose falls below 200 mg/dl, the sodium chloride solution should be replaced with 5% glucose containing saline solution and the rate of insulin infusion should be reduced until acidosis and ketosis resolve. 60
• When BG reaches 200 mg/d. L (DKA) or 300 mg/d. L (HHS), change to 5% dextrose with 0. 45% Na. Cl at 150 -250 m. L/hr (ie, clamping blood glucose until anion gap has closed in DKA 61
Potassium replacement • potassium replacement should be initiated when serum levels fall below 5. 3 m. Eq/l in patients with adequate urine output (50 ml/h). • 20– 30 m. Eq potassium in each liter of infusion • DKA may present with hypokalemia, especially if they have been vomiting or had been taking diuretics 62
Bicarbonate therapy • Bicarbonate therapy in DKA is controversial • a more recent systematic review which investigated the benefits and risks of bicarbonate therapy in DKA reported increased risk of cerebral edema and prolonged hospitalization in pediatric patients but no benefit 63
• Adults with p. H <6. 9 who may deteriorate without bicarbonate therapy may be given 100 mmol sodium bicarbonate in 400 ml sterile water (an isotonic solution) with 20 m. Eq KCI administered at a rate of 200 ml/h for 2 h until the venous p. H is >7. 0. • If the p. H is still <7. 0 after infusion, we recommend repeating infusion every 2 h until p. H reaches >7. 0 64
Conventional Insulin Guidelines • Initiate the correction of hypovolemic shock with fluids, and correct hypokalemia if present, before starting insulin • When starting insulin, initially infuse 0. 1 to 0. 14 units/kg/h • If plasma glucose does not decrease by 50 -75 mg in the first hour, increase the infusion rate of insulin • Continue insulin infusion until anion gap closes • Initiate subcutaneous insulin at least 2 h before interruption of insulin infusion Kitabchi AE, et al. Diabetes Care. 2009; 32: 1335 -1343. 65
• If blood glucose does not fall by 10% in the first hour, an intravenous bolus of 0. 14 U/kg should be administered followed by continuous infusion at the previous rate 66
• When the plasma glucose reaches 200 mg/dl, the insulin infusion rate should be reduced to 0. 02– 0. 05 U/kg/h. • Also, dextrose should be added to the intravenous fluids at this point 67
• The rate of insulin administration or the concentration of dextrose may be adjusted to maintain blood glucose concentration between 150 and 200 mg/dl until resolution of DKA 68
Rationale for a Dynamic Insulin Protocol for DKA and HHS • Even with low-dose insulin therapy 1, 2 – Hypokalemia and hypoglycemia may continue to occur – Failure to reduce insulin infusion rate as the blood glucose approaches target may lead to hypoglycemia • There is a lag between the change in intravenous insulin infusion rate and the resulting effects 3 1. Umpierrez GE, et al. Arch Intern Med. 1997; 157: 669 -675. 2. Burghen GA, et al. Diabetes Care. 1980; 3: 15 -20. 3. Mudaliar S, et al. Diabetes Care. 2002; 25: 1597 -1602. 69
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• • • Criteria for resolution of ketoacidosis include a blood glucose <200 mg/dl and two of the following criteria: a serum bicarbonate level ≥ 15 m. Eq/l, a venous p. H >7. 3, a calculated anion gap ≤ 12 m. Eq/l. 71
• Those previously treated with insulin may be • recommenced on their home dose if they had been well controlled. • Insulin-naïve patients should receive a multidose insulin regimen beginning at the dose of 0. 5– 0. 8 U/kg/day 72
• If the patient is unable to eat, intravenous insulin and fluid replacement may be continued. • Use of long-acting insulin analogs during the initial management of DKA may facilitate transition from intravenous to subcutaneous insulin therapy. • 73
Continuation of physician orders for DKA and HHS Initiation of insulin drip, monitoring of BG, and termination of insulin drip Initiate IV insulin infusion using selected or default column assignment. Reassignment to a higher column before 4 hours of treatment requires an MD order. If BG fails to fall each hour during hrs 1 -4, notify MD Adjust column assignment for DKA or HHS based on column change rules, and adjust drip rate based on BG level Measure BG every 1 hour ( fingerstick or capillary blood sample using point-of-care glucose monitor) If BG is within target range x 4 hrs, then measure BG q 2 h. If column reassignment occurs, measure q 1 h Record BG results, insulin drip rate changes, and column reassignments on the ICU flow sheet Obtain order for SQ insulin to be administered q 1 -2 h before discontinuing IV insulin Algorithm for order to treat patient if BG <70 mg/d. L If BG is <70 mg/d. L, administer 25 ml of D 50 by IV Adjust column assignment to next lower column and use pretreatment BG to assign row Recheck BG in 5 minutes. If BG is <70 mg/d. L, repeat administration of 25 ml of D 50 by IV Column change rules after 4 hours of treatment of DKA If BG ≥ 200 mg/d. L and not falling after 3 successive hourly tests (or for 2 h) on the same column, move to next higher column If BG <180 mg/d. L after 3 successive hourly tests (or for 2 h) on the same column during infusion of fluids containing D 5 W, or if any BG <150 mg/d. L, move to next lower column Column change rules after 4 hours of treatment of HHS If BG ≥ 300 mg/d. L and not falling after 3 successive hourly tests (or for 2 h) on the same column, move to next higher column If BG <280 mg/d. L after 3 successive hourly tests (or for 2 h) on the same column during infusion of fluids containing D 5 W, or if any BG <200 mg/d. L, move to next lower column Devi R, et al. Diabetes Manage. 2011; 1: 397 -412. 74
When to Transition From IV Insulin Infusion to SC Insulin DKA • BG <200 mg/d. L and 2 of the following – HCO 3 ≥ 15 m. Eq/L – Venous p. H >7. 3 – Anion gap ≤ 12 m. Eq/L Kitabchi AE, et al. Diabetes Care. 2009; 32: 1335 -1343. HHS • Normal osmolality and regaining of normal mental status • Allow an overlap of 1 -2 h between subcutaneous insulin and discontinuation of intravenous insulin 75
Cerebral Edema • Cerebral edema is a dreaded complication of DKA in childhood 1 • Mortality may be 24%, with significant morbidity among survivors 2 • One pediatric study found that rates of fluid administration and insulin administration were not associated with cerebral edema 3 • In another case control pediatric study, insulin dose in first 2 h was significantly associated with the risk of cerebral edema 4 1. Muir AB, et al. Diabetes Care. 2004; 27: 1541 -1546. 2. Edge JA, et al. Arch Dis Child. 2001; 85: 16 -22. 3. Glaser N, et al. N Engl J Med. 2001; 344: 264 -269. 4. Edge J, et al. Diabetologia. 2006; 49: 2002 -2009. 76
Potassium Repletion in DKA • K+ >5. 2 m. Eq/L – Do not give K+ initially, but check serum K+ with basic metabolic profile every 2 h – Establish urine output ~50 m. L/hr • K+ <3. 3 m. Eq/L – Hold insulin and give K+ 20 -30 m. Eq/hr until K+ >3. 3 m. Eq/L • K+ = 3. 3 -5. 2 m. Eq/L – Give 20 -30 m. Eq K+ in each L of IV fluid to maintain serum K+ 4 -5 m. Eq/L 77
Phosphorus Repletion in DKA • A sharp drop of serum phosphorus can also occur during insulin treatment • Treatment is usually not required – Caregiver can give some K+ as K- phos 78
Fluid and Electrolyte Management in HHS • Treatment of HHS requires more free water and greater volume replacement than needed for patients with DKA • To avoid heart failure, caution is required in the elderly with preexisting heart disease • Potassium – Usually not significantly elevated on admission (unless in renal failure) – Replacement required during treatment 79
Causes of Morbidity and Mortality in DKA • Shock • Hypokalemia during treatment • Hypoglycemia during treatment • Cerebral edema during treatment • Hypophosphatemia • Acute renal failure • Adult respiratory distress syndrome • Vascular thrombosis • Precipitating illness, including MI, stroke, sepsis, pancreatitis, pneumonia 80
DKA Management Pitfalls • Not assessing for and/or treating underlying cause of the DKA • Not watching K+ closely enough and/or not replacing K+ aggressively enough • Following serial serum ketone concentrations • Following serum bicarbonate instead of the anion gap, with misinterpretation of expansion acidosis as “persistent ketoacidosis” • Interrupting IV insulin too soon (eg, patient not yet eating, anion gap not yet closed) 81
DKA Management Pitfalls • Occurrence of rebound ketosis consequent to inadequate insulin dosing at transition (eg, failure to give SC insulin when glucose is “low” or injudicious use of sliding scale insulin) • Inappropriate extension of hospitalization to “fine -tune” an outpatient regimen • Inadequate patient education and training • Inadequate follow-up care 82
FINDING THE CAUSE AND PREVENTING RECURRENCE 83
Possible Precipitating Causes or Factors in DKA: Type 1 Diabetes • Nonadherence to insulin regimen or psychiatric issues • Insulin error or insulin pump malfunction • Poor “sick-day” management • Infection (intra-abdominal, pyelonephritis, flu) • Myocardial infarction • Pancreatitis • Other endocrinopathy (rare) • Steroid therapy, other drugs or substances 84
Possible Precipitating Causes or Factors in DKA: Type 2 Diabetes • • Nonadherence to medication regimen Poor “sick-day’ management Dehydration Renal insufficiency Infection (intra-abdominal, pyelonephritis, flu) Myocardial infarction, stroke Other endocrinopathy (rare) Steroid therapy, other drugs or substances 85
Predischarge Checklist • Diet information • Glucose monitor and strips (and associated prescription) • Medications, insulin, needles (and associated prescription) • Treatment goals • Contact phone numbers • “Medic-Alert” bracelet • “Survival Skills” training 86
Education in Type 1 Diabetes to Prevent DKA • Recognize symptoms and findings that require contact with a healthcare provider • Prevent ketoacidosis through self-management skills: – – Glucose testing Appropriate use of urine acetone testing Appropriate maintenance of insulin on sick days Use of supplemental insulin during illness • Address social factors 87
Summary • DKA and HHS are life-threatening emergencies • Management involves – – – Attention to precipitating cause Fluid and electrolyte management Insulin therapy Patient monitoring Prevention of metabolic complications during recovery Transition to long-term therapy • Patient education and discharge planning should aim at prevention of recurrence 88
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