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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

UTHSCSA Pediatric Resident Curriculum for the PICU

Hyperglycemia syndromes

Diabetic Ketoacidosis

Ketoacidosis-Hypersomolar Coma

spectrum of dka and hyperosmolar coma
Spectrum of DKA and Hyperosmolar Coma







Pure Ketoacidosis

Rapid Onset

Marked Insulin



Slow Onset

Mild Insulin


diabetic ketoacidosis
Diabetic Ketoacidosis
  • Hyperglycemia
  • Ketonemia
  • Metabolic Acidosis
  • Insulin Deficiency is the primary defect in patients with DKA













Pyruvate, CO2


Normal Insulin Activity

insulin deficiency
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
  • 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.
persistent catabolism
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
hyperosmolar state
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
hyperosmolar state1
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
electrolyte loss
Electrolyte Loss







Intracellular exchange

of potassium with

hydrogen ions



Ketoacids draw out intravascular cations

of Sodium and Potassium



Phosphorous is also depleted in the osmotic diuresis

fluid balance in diabetic hyperosmolarity
Fluid Balance in DiabeticHyperosmolarity

ECF = 14 L

ICF = 28 L




ECF hyperosmolar from ICF autotransfusion

Osmotic Diuresis


ECF and ICF both hyperosmolar

Osmotic Diuresis

clinical findings in dka
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%.
clinical findings of hyperosmolarity
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.
precipitating factors for hyperosmolarity
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)
laboratory findings in dka hyperosmolarity
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.
calculation of osmolarity
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


effective osmolarity
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.
approach to therapy
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

  • 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.
  • 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
  • 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.
insulin replacement
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.
insulin replacement1
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.
  • 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.
  • 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.
cerebral edema
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.
  • 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.
cerebral edema clinical signs
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.
cerebral edema therapy
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.
evaluation of therapy
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.
  • Infection esp. urinary tract infection.
  • Pancreatitis
  • Disseminated intravascular coagulation.
  • Arterial and venous thrombosis.
  • Hypoglycemia with seizure.
  • Hypokalemia with dysrhythmias.
thromboembolism in diabetes
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).
  • 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
dka in type 2 diabetics
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.
dka in type 2 diabetes
DKA in Type 2 Diabetes
  • Hyperosmolarity, obesity, lethargy, and a relative hypercoagulopathy increase the propensity for EMBOLISM and THROMBOSIS in Type 2 diabetics.