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Hyperglycemia syndromes

UTHSCSA Pediatric Resident Curriculum for the PICU. Hyperglycemia syndromes. Diabetic Ketoacidosis Ketoacidosis-Hypersomolar Coma. Spectrum of DKA and Hyperosmolar Coma. Ketoacidosis- Hyperosmolar Coma. Pure Hyperosmolar Coma. Pure Ketoacidosis. Rapid Onset Marked Insulin Lack.

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Hyperglycemia syndromes

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  1. UTHSCSA Pediatric Resident Curriculum for the PICU Hyperglycemia syndromes Diabetic Ketoacidosis Ketoacidosis-Hypersomolar Coma

  2. Spectrum of DKA and Hyperosmolar Coma Ketoacidosis- Hyperosmolar Coma Pure Hyperosmolar Coma Pure Ketoacidosis Rapid Onset Marked Insulin Lack Intermediate Slow Onset Mild Insulin Lack

  3. Diabetic Ketoacidosis • Hyperglycemia • Ketonemia • Metabolic Acidosis

  4. Pathophysiology • Insulin Deficiency is the primary defect in patients with DKA Adipose Muscle Hepatocyte Glycogen Glucose Glucose Glucose-P Free fatty acids Amino Acids Pyruvate, CO2 Ketoacids Normal Insulin Activity

  5. Insulin Deficiency • Breakdown of storage forms of energy to meet energy needs. (Catabolism) • Glycogenolysis • Lipolysis • Gluconeogenesis (from amino acids, lipids) • Glucagon unopposed by Insulin stimulates this catabolic reaction

  6. Pathophysiology • Skeletal and cardiac tissues are able to use free fatty acids and ketone bodies as an energy source. • Glucose can not be used by these tissues in the absence of insulin. • The brain is an insulin-independent tissue and continues to use available glucose.

  7. Persistent Catabolism • Hyperglycemia is worsened by further intake of glucose. • Excess Ketone bodies from Lipolysis • Acetone • -hydroxybutyrate (BHB) • Acetoacetate (AA) • Ratio of BHB/AA normally 3:1 is driven to 15:1 in severe DKA • Ketone test measures only acetoacetate

  8. Hyperosmolar State • Hyperglycemia acts as an osmotic diuretic with obligatory loss of water and electrolytes. • Osmolality = 2(Na) + Glucose/18 + BUN/2.8 (normal  293 ) • Ketosis/hyperglycemia stimulate vomiting with aggravation of dehydration

  9. Hyperosmolar State • Hypovolemia secondary to dehydration can promote decreased tissue perfusion with anaerobic metabolism and elevated lactate production • Total fluid deficit in severe DKA usually averages around 10% of the total body weight

  10. Electrolyte Loss K I D N E Y Intracellular exchange of potassium with hydrogen ions K+ H+ Ketoacids draw out intravascular cations of Sodium and Potassium Glucose Ketoacids Phosphorous is also depleted in the osmotic diuresis

  11. Fluid Balance in DiabeticHyperosmolarity ECF = 14 L ICF = 28 L ICF ECF H2O ECF hyperosmolar from ICF autotransfusion Osmotic Diuresis H2O ECF and ICF both hyperosmolar Osmotic Diuresis

  12. Clinical Findings in DKA • Polyuria, Polydipsia, Polyphagia • Dehydration + orthostasis • Vomiting (50-80%) • Küssmaul respiration if pH < 7.2 • Temperature usually normal orlow, if elevated think infection! • Abdominal pain present in at least 30%.

  13. Clinical Findings of Hyperosmolarity • Lethargy, delirium • Hyperosmolar coma is the first sign of diabetes in 50-60 % of adult patients. • Hyperglycemia usually > 700-800mg/dl • Osmolarity above 340 mOsm/L is required for coma to be present.

  14. Precipitating Factors for Hyperosmolarity • Too little insulin • Infection, even minor. • Severe stress. • Hypokalemia (Required by insulin). • Inadequate fluid intake • Infancy (can not ask for fluids) • Incapacitation (can not get to fluids/ask)

  15. Laboratory Findings in DKA-Hyperosmolarity • Glucose > 700mg/dl • Total body sodium low, level high, normal or low. • Potassium high, normal or low. • Large urine ketones • Bicarbonate < 15 mEq/L, pH < 7.2 • Leukocytosis 15,000-40,000 even without infection. High temp = infection.

  16. Calculation of Osmolarity Effective Osmolarity(mOsm/L) 2(Na = K) + Glucose (mg/dl)/20 = 280 - 295 mOsm/L A calculated osmolarity less than 340 mOsm/L is unlikely to cause coma. Other processes must be considered (stroke, infection, toxin). DKA does not cause coma in the absence of hyperosmolarity.

  17. Effective Osmolarity • The effective osmolarity calculation uses only those biologically effective molecules which are able to draw water out of the cell. • Urea and other molecules measured in the lab (alcohol) move freely between the intra and extravascular spaces and don’t draw water out of the cell.

  18. Approach to Therapy • Correcting the hyperosmolar state and dehydration is the initial aim of therapy. • Insulin therapy should be undertaken only after the patient is stable hemodynamically. Glucose and H2O H2O lost in urine Loss of ECF, vascular collapse and death

  19. Rehydration • Consider most patients with DKA to be approximately 10% dehydrated. • The difference between the patient’s weight at baseline and presentation is an accurate measure of volume loss. • Normal Saline is the replacement fluid of choice to restore hemodynamics.

  20. Rehydration • Bolus fluids until correction of circulatory failure. • Correct deficit over 36 to 48 hours. • Provide maintenance fluids (1600cc/m2/d) at the same time. • Subtract resuscitation fluids from deficit. • Avoid fluid administration > 4L/m2/d

  21. Electrolytes • Sodium content varies between 75 to 154 mEq/L. Reduce as sodium levels approach normal. • Total body potassium is reduced. When K levels reach “normal” add 20-40 mEq/L as both KCL and Kphos. • Maximum K infusion rate 0.5 mEq/kg/hr.

  22. Insulin Replacement • Insulin is essential for lowering glucose to normal and correcting acidosis. • Following initial fluid replacement, then administer 0.1U/kg IV and initiate an infusion at 0.1U/kg/hr. (Regular Insulin). • Check serum glucose hourly and avoid dropping glucose > 100mg/dl/h.

  23. Insulin Replacement • When serum glucose falls below 300 mg/dl, add 5% Dextrose to maintain stable glucose levels. • Falling glucose should be managed with increased glucose concentration. Donot decrease insulin infusion until the metabolic acidosis is corrected.

  24. Bicarbonate • Should only be used to treat symptomatic hyperkalemia. • May be used for pH less than 7.0 to provide some relief of Küssmaul respiration (1mEg/kg over 1-2 hours). • Inappropriate use may result in hypokalemia and paradoxical CNS acidosis.

  25. Intubation • Most patients requiring intubation have hypovolemia. • Avoid drugs which lower blood pressure. • Consider a small volume load first. • For patients with cerebral edema, avoid medication which raise ICP (Ketamine, Succinylcholine). • Consider Thiopental and Lidocaine. • Have Mannitol available for sudden ICP.

  26. Cerebral Edema • May be sub-clinical at start of therapy. • CSF pressure is usually normal initially. • Usually occurs unpredictably within the first 24 hours of therapy. • Classically, patient’s labs are improving. • No way to determine who will get this complication.

  27. Pathophysiology • Brain conserves water by producing osmoprotective molecules (taurine). • Osmolarity becomes disproportionately higher in the brain than other tissues. • Sudden fall in serum osmolarity moves fluid across the blood-brain barrier. • Brain becomes relatively hypervolemic.

  28. Cerebral Edema-Clinical Signs • Initial complaint of headache. • Progresses to decreasing level of consciousness, hypertension, papilledema and bradycardia. • Coma and death soon follow. • Cerebral edema is a complication of therapy, not a progression of DKA.

  29. Cerebral Edema - Therapy • The best therapy is to prevent it with careful rehydration. • Diagnosis available with CT scan. • Therapy for acute episode: • Intubation and hyperventilation • IV Mannitol 0.5 - 1.0 Gram/Kg as bolus. • IV sedation. • Slow the rate of osmolar correction.

  30. Evaluation of Therapy • Controlled reduction in serum glucose. • Correction of acidosis “closing the gap”. • Clearing of serum ketones. • Clinical improvement • fall in respiratory rate • improved perfusion • improving mental status.

  31. Complications • Infection esp. urinary tract infection. • Pancreatitis • Disseminated intravascular coagulation. • Arterial and venous thrombosis. • Hypoglycemia with seizure. • Hypokalemia with dysrhythmias.

  32. Thromboembolism in Diabetes • In several studies, thromboembolism accounted for 20 to 50% of mortality. • Virchow’s triad: stasis, endothelial damage and hypercoagulopathy. • Hypercoagulopathy: • Hyperreactivity of platelets • Hyperfibrinogenemia (Especially Type 2) • Elevated plasminogen activator (Type 2).

  33. Thromboembolism • Endothelial Damage • Elevated levels of von Willebrand factor associated with endothelial damage • Seen in decompensated diabetes esp. those with microvascular disease • Catheter placement • Promotes venous stasis • Potential endothelial damage

  34. DKA in Type 2 Diabetics • Recent study: Arch of Internal Medicine • 39% of patients had Type 2 diabetes. • Majority of patients with Type 2 diabetes were Hispanic. • 51% of patients were obese • Type 2 diabetics more likely to have slow onset of ketoacidosis and progression to hyperosmolar coma.

  35. DKA in Type 2 Diabetes • Hyperosmolarity, obesity, lethargy, and a relative hypercoagulopathy increase the propensity for EMBOLISM and THROMBOSIS in Type 2 diabetics.

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