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Hyperglycemic Emergencies

Hyperglycemic Emergencies. Thomas Repas D.O. Diabetes, Endocrinology and Nutrition Center, Affinity Medical Group, Neenah, Wisconsin Member, Inpatient Diabetes Management Committee, St. Elizabeth’s Hospital, Appleton, WI

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Hyperglycemic Emergencies

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  1. Hyperglycemic Emergencies Thomas Repas D.O. Diabetes, Endocrinology and Nutrition Center, Affinity Medical Group, Neenah, Wisconsin Member, Inpatient Diabetes Management Committee, St. Elizabeth’s Hospital, Appleton, WI Member, Diabetes Advisory Group, Wisconsin Diabetes Prevention and Control Program Website: www.endocrinology-online.com

  2. U.S. Total Costs of Diabetes, 2002 Diabetes Care 26(3):917-932, 2003

  3. Acute Complications of Diabetes • Acute • Poor wound healing • Infections • Vascular insufficiency • Other • Hyperglycemic Emergencies • Diabetic Ketoacidosis (DKA) • Hyperosmolar Hyperglycemic Syndrome (HHS)

  4. Consequences of Poor Hospital Glycemic Control • Several studies show diabetes increases morbidity and mortality for myocardial infarction, coronary bypass surgery, and stroke. More specifically, when glucoses are elevated there may be: • Fluid and electrolyte abnormalities secondary to osmotic diuresis • Decreased WBC function • Delayed gastric emptying • Increased surgical complications including: • Relative risk for "serious" postoperative nosocomial infections increased by a factor of 5.7 when glucose >220 mg/dl • Relative odds of wound infection increased to 1.17 with glucoses were 207-227 and 1.78-1.86 when glucoses were >253. • Delayed hospital discharge • Double the mortality risk in patients admitted with a stroke

  5. Intervention Studies: Evidence That Improving Glucose Control Improves Outcome • Improved WBC function • Perioperative insulin infusion improves neutrophil phagocytic activity to 75% of baseline activity compared to only 47% in a control group • Decreased postoperative mortality • Diabetes team followed patients and controlled glucoses using perioperative IV insulin infusion and algorithm based SQ premeal insulin. Mortality of diabetic patients undergoing CABG in 1993-1996 was reduced to level of nondiabetics. Nationally, diabetic patients had 50% higher mortality • Decreased infections • Perioperative intravenous insulin infusion designed to keep glucoses <200 mg/dl reduces the risk of wound infection in diabetics after open heart operations. Incidence of Deep Wound Infections decreased from 2.4 to 1.5% • Decreased length of stay • Use of an inpatient diabetes consultation service decreased length of stay by 56%

  6. Importance of Excellent Glycemic Control • In a surgical ICU, 1548 patients were randomized to intensive vs. conventional therapy • Intensive = IV insulin to maintain BG 80 – 110 mg/dl • Conventional = begin IV insulin if BG > 215 with goal of 180 – 200 • Risk reduction in ICU mortality was 42% • Overall in hospital mortality reduced 34% • Greatest benefits were seen in patients with multiorgan failure and sepsis • Also reduced duration of mechanical ventilation, acute renal failure, and need for transfusion Van de Berghe G, et al. Intensive Insulin Therapy in Critically ill Patients. N Engl J Med. 2001;345:1359-1367.

  7. Standard treatment Cardiovascular RiskMortality After MI Reduced by Insulin Therapy in the DIGAMI Study IV Insulin 48 hours, then 4 injections daily .7 .7 All Subjects Low-risk and Not Previously on Insulin (N = 272) (N = 620) .6 .6 Risk reduction (51%) Risk reduction (28%) .5 .5 P = .011 P = .0004 .4 .4 .3 .3 .2 .2 .1 .1 0 0 0 1 2 3 4 5 0 1 2 3 4 5 Years of Follow-up Years of Follow-up Malmberg, et al. BMJ. 1997;314:1512-1515. 6-11

  8. Common Errors in Inpatient Diabetes Management • Admission orders • Overly high glycemic targets • Lack of therapeutic adjustment • Overutilization of “sliding scales” • Underutilization of IV insulin

  9. Hyperglycemic Emergencies

  10. Hyperglycemic Emergencies • Diabetic Ketoacidosis (DKA) • Occurs in type 1’s • May or may not occur with other illness • Typically younger patients • Mortality <5 % under optimal management • Hyperosmolar Hyperglycemic Syndrome (HHS) • Occurs in type 2’s • Often occurs with other concurrent illness • Typically older patients • Mortality ~ 15%

  11. Precipitating Factors • Infection (Pneumonia and UTI most common) • Previously undiagnosed diabetes • Inadequate insulin treatment • Noncompliance with therapy • Unknown or other causes

  12. Symptoms and Clinical Findings • Diabetic Ketoacidosis: can present rapidly (<24hrs) • nausea & vomiting (most common symptom) • fruity (acetone) breath odor • abdominal pain (but always rule out other pathology also) • Kussmaul breathing (rapid and deep inspiration) • HHS: often more insidious in presentation (develops over several days) • May have polyuria, polydipsia, and weight loss for days before diagnosis. • More likely to have mental status changes or even coma, and/or seizures or other focal neurologic findings. • Both DKA & HHS can have evidence of dehydration such as poor skin turgor, dry oral mucosa, hypotension

  13. Diagnostic Criteria DKA HHS Plasma Glucose >250 >600 Arterial pH <7.3 >7.3 Serum Bicarb <15 >15 Ketones Positive None or small Serum Osmolality Varies >320 Anion Gap >10 <12 Mental Status Varies Stupor/coma

  14. Anion Gap A.G.=(Na+) - (Cl- + HCO3-) Normal= 7 to 9 mEq/l

  15. Serum osmolality2[measured Na] + glucose/18Normal=285+5

  16. Corrected Sodium For each 100 mg/dl glucose >100 mg/dl, add 1.6 mEq to sodium value for corrected serum sodium value

  17. Other Causes of Metabolic Acidosis • Alcoholic Ketoacidosis • Starvation Ketoacidosis • Lactic Acidosis • Chronic Renal Failure • Drug induced • Salicylate, Methanol, Ethylene Glycol, Paraldehyde

  18. Therapeutic Goals • Improving circulatory volume and tissue perfusion • Decreasing serum glucose and plasma osmolality towards normal • Clearing of urine and serum of ketones at a steady rate • Correcting electrolyte imbalances • Identifying and treating precipitating factors

  19. Patient Outcomes: Neurologic status • Hyperosmolarity can be associated with mental status changes, stupor or coma • The presence of such mental status changes without hyperosmolarity requires consideration of other causes • Cerebral edema is a rare, but serious complication with high mortality (>70%). • Consider cerebral edema when: • Lethargy with deterioration of mental status • Decrease in arousal • Headache • Seizures • Other: Incontinence, pupillary changes, bradycardia, respiratory arrest

  20. Patient Outcomes: Fluid & electrolyte balance • During therapy for DKA or HHS, blood should be drawn every 2–4 h for determination of serum electrolytes, blood urea nitrogen, creatinine, osmolality, and venous pH (for DKA). • Frequently, repeat arterial blood gases are unnecessary; venous pH (which is usually 0.03 units lower than arterial pH) and/or anion gap can be followed to monitor resolution of acidosis.

  21. Fluid replacement should correct estimated deficits within the first 24 h. The induced change in serum osmolality should not exceed 3 mOsm · kg–1 H2O · h–1 In patients with renal or cardiac compromise, monitoring of serum osmolality and frequent assessment of cardiac, renal, and mental status must be performed during fluid resuscitation to avoid iatrogenic fluid overload. Patient Outcomes: Fluid & electrolyte balance

  22. Calculating Fluid Deficit BWD (L) = 0.6 (weight kg) ([measured Na] – 140) 140

  23. Patient Outcomes: Blood Glucose • Blood Glucose must be monitored every 1 to 2 hours during treatment • Goal is to decrease plasma glucose concentration at a rate of 50–75 mg · dl–1 · h–1

  24. Patient Outcomes: Ketones • Ketonemia typically takes longer to clear than hyperglycemia. • Direct measurement of ß-OHB in the blood is the preferred method for monitoring DKA. The nitroprusside method only measures acetoacetic acid and acetone. • However, ß-OHB, the strongest and most prevalent acid in DKA, is not measured by the nitroprusside method. • During therapy, ß-OHB is converted to acetoacetic acid, which may lead the clinician to believe that ketosis has worsened. • Therefore, assessments of urinary or serum ketone levels by the nitroprusside method should not be used as an indicator of response to therapy.

  25. Patient Outcomes: Hemodynamic status • Successful progress with fluid replacement is judged by hemodynamic monitoring (improvement in blood pressure), measurement of fluid input/output, and clinical examination.

  26. Patient Outcomes: Identifying and treating precipitating factors • It is essential to identify and treat precipitating factors • Chest x-rays, urinalysis, blood cultures and other studies should be obtained where appropriate

  27. Therapeutic Interventions • Replacement of Fluids and electrolytes • Insulin Therapy • Potassium • Phosphate • Bicarbonate

  28. Replacement of Fluids and electrolytes • Initial fluid therapy is directed toward expansion of the intravascular and extravascular volume and restoration of renal perfusion. • In the absence of cardiac compromise, isotonic saline (0.9% NaCl) is infused at a rate of 15–20 ml · kg–1 body wt · h–1 or greater during the 1st hour ( 1–1.5 l in the average adult). • Subsequent choice for fluid replacement depends on the state of hydration, serum electrolyte levels, and urinary output. • In general, 0.45% NaCl infused at 4–14 ml · kg–1 · h–1 is appropriate if the corrected serum sodium is normal or elevated; 0.9% NaCl at a similar rate is appropriate if corrected serum sodium is low.

  29. Insulin Therapy • Unless the episode of DKA is mild, regular insulin by continuous intravenous infusion is the treatment of choice. • In adult patients an intravenous bolus of regular insulin at 0.15 units/kg body wt, followed by a continuous infusion of regular insulin at a dose of 0.1 unit · kg–1 · h–1 (5–7 units/h in adults), should be administered. • An initial insulin bolus is not recommended in pediatric patients; a continuous insulin infusion of regular insulin at a dose of 0.1 unit · kg–1 · h–1 may be started in these patients.

  30. Insulin Therapy • If plasma glucose does not fall by 50 mg/dl from the initial value in the 1st hour, check hydration status; if acceptable, the insulin infusion may be doubled every hour until a steady glucose decline between 50 and 75 mg/h is achieved. • When the plasma glucose reaches 250 mg/dl in DKA or 300 mg/dl in HHS, it may be possible to decrease the insulin infusion rate to 0.05–0.1 unit · kg–1 · h–1 (3–6 units/h), and dextrose (5–10%) may be added to the intravenous fluids. • Thereafter, the rate of insulin administration or the concentration of dextrose may need to be adjusted to maintain the above glucose values until acidosis in DKA or mental obtundation and hyperosmolarity in HHS are resolved.

  31. Potassium • Despite total-body potassium depletion, mild to moderate hyperkalemia is not uncommon in patients with hyperglycemic crises. • To prevent hypokalemia, potassium replacement is initiated after serum levels fall below 5.5 mEq/l, assuming the presence of adequate urine output. • Generally, 20–30 mEq potassium (2/3 KCl and 1/3 KPO4) in each liter of infusion fluid is sufficient to maintain a serum potassium concentration within the normal range of 4–5 mEq/l. • Rarely, DKA patients may present with hypokalemia. In such cases, potassium replacement should begin with fluid therapy, and insulin treatment should be delayed until potassium concentration is restored to >3.3 mEq/l to avoid arrhythmias or cardiac arrest and respiratory muscle weakness.

  32. Phosphate • Despite whole-body phosphate deficits in DKA, serum phosphate is often normal or increased at presentation. • Phosphate concentration decreases with insulin therapy. • Studies have failed to show any beneficial effect of phosphate replacement on the outcome in DKA and overzealous phosphate therapy can cause severe hypocalcemia. • However, to avoid complications, careful phosphate replacement may sometimes be indicated in patients with cardiac dysfunction, anemia, or respiratory depression and in those with serum phosphate concentration <1.0 mg/dl. • When needed, 20–30 mEq/l potassium phosphate can be added to replacement fluids.

  33. Bicarbonate • Bicarbonate use in DKA remains controversial • At a pH >7.0, reestablishing insulin activity blocks lipolysis and resolves ketoacidosis without any added bicarbonate. • Studies have failed to show either beneficial or deleterious changes in morbidity or mortality with bicarbonate therapy in DKA patients with pH between 6.9 and 7.1 • No studies concerning the use of bicarbonate in DKA with pH values <6.9 have been reported.

  34. Bicarbonate • Because severe acidosis may cause adverse vascular complications, it is a consensus for adult patients with a pH <6.9, 100 mmol sodium bicarbonate be added to 400 ml sterile water and given at a rate of 200 ml/h. • In patients with a pH of 6.9–7.0, 50 mmol sodium bicarbonate is diluted in 200 ml sterile water and infused at a rate of 200 ml/h. • Thereafter, pH should be assessed every 2 h until the pH rises to 7.0, and treatment should be repeated every 2 h if necessary. • No bicarbonate is necessary if pH is >7.0.

  35. Bicarbonate • In the pediatric patient, there are no well designed studies in patients with pH <6.9. • If the pH remains <7.0 after the initial hour of hydration, it seems prudent to administer 1–2 mEq/kg sodium bicarbonate over the course of 1 h. • No bicarbonate therapy is required if pH is 7.0

  36. Complications of Therapy • Hypoglycemia • Hypokalemia • Cerebral Edema • Acute Respiratory Distress Syndrome • Hyperchloremic metabolic acidosis

  37. Hypoglycemia • Before of the advent or low dose insulin protocols, this occurred in as many as 25% of patients • Close monitoring of BG’s, decreasing IV insulin rate when BG improves and adding dextrose to IV fluids when BG < 250 all can reduce risks of hypoglycemia

  38. Hypokalemia • Insulin therapy, correction of acidosis, and volume expansion decrease serum potassium concentration. • Labs should be ordered every 2 to 4 hours to closely monitor this. • To prevent hypokalemia, potassium replacement is initiated after serum levels fall below 5.5 mEq/l,

  39. Cerebral Edema • Cerebral edema is a rare, but serious complication with high mortality (>70%). • It is more common in children, especially those with newly diagnosed diabetes • Consider cerebral edema when: • Lethargy with deterioration of mental status • Decrease in arousal • Headache • Seizures • Other: Incontinence, pupillary changes, bradycardia, respiratory arrest • Prevention measures include: • gradual replacement of sodium and water deficits in patients who are hyperosmolar • addition of dextrose to the hydrating solution once blood glucose reaches 250 mg/dl.

  40. Prevention of DKA & HHS • Hyperglycemic emergencies are often preventable through better access to medical care, proper education, and effective communication • Sick day management should be reviewed with all patients periodically, including: • When to call health care provider • BG goals and when/how to use additional short acting insulin • Means to address fever & treat infection • Initiating easily digestible liquid diet with carbs and electrolytes • Advise to never stop insulin • Instruction for family members and caregivers • Consultation by a dedicated diabetic education team prior to discharge from hospital are useful for instruction of self management skills

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