Diabetic Ketoacidosis (DKA) Acute Complications Of Diabetes Mellitus

ACUTE COMPLICATIONS OF DIABETES MELLITUS (DKA)

DKA is characterized by the triad of hyperglycemia, anion gap metabolic acidosis, and ketonemia. Metabolic acidosis is often the major finding. The serum glucose concentration is usually greater than 500 mg/dL (27.8 mmol/L) and less than 800 mg/dL (44.4 mmol/L)  . However, serum glucose concentrations may exceed 900 mg/dL (50 mmol/L) in patients with DKA who are comatose

Diabetic Ketoacidosis

  • · Diabetic ketoacidosis (DKA)
  • · Hyperglycemic hyperosmolar state (HHS) In both there is :
  • Absolute or relative insulin deficiency Volume depletion
  • Acid base abnormality Hyperglycemia in both
  • Both are serious complications and can end in death.

DIABETIC KETOACIDOSIS 2

DIABETIC KETOACIDOSIS (DKA)

Symptoms and signs develop in 24 hours.

  • Diabetic ketoacidosis (DKA) may be the first presen­tation of DM type 1.
  • May occur in persons with known diabetes. Nausea and vomiting are usual features. There may be acute severe abdominal pain. There is hyperglyc1mia,
  • Hyperglycemia leads to :
    • Glucosuria Volume depletion Tachycardia.
    • Hypotension may occur due to :
    • Volume depletion Peripheral vasodilation.
  • Other features:
    • Kussmauls respiration Fruity odour breath Lethargy
    • CNS depression Coma
    • Cerebral edema as complication of DKA seen in children
    • Signs of infections – as infection precipitates DKA Tissue ischemia of heart and brain precipitates DKA.

Pathophysiology

  • DKA results from insulin deficiency with excess of :
  • · Glucagon
  • · Catecholamines
  • · Cortisol
  • · Growth hormone
  • DKA occurs due to –
    • Insulin deficiency
    • Glucagon excess
  • Decreased ratio of insulin to glucagon promotes glu­coneogenesis, glycogenolysis, ketone body formation in the liver.
  • Ketosis results from a marked increase in free fatty acid release from adipocytes, and ketone body syn­thesis in liver.
  • Ketone bodies are keto acids which neutralize bicar­bonates resulting in metabolic acidosis.
  • There is acidosis due to lactic acid production also. The increased free fatty acids increases TG and VLDL production.
  • Severe hypertriglyceridemia can cause pancreatitis.

DKA is precipitated by :

  • increased insulin requirement as in infection. Forgetting insulin dose.
  • Not increasing dose when reqUired to do so Delay in insulin injection in patients using short acting insulin
  • Infections Iike:-
    • Pneumonia
    • UTI
    • Gastroenteritis
  • Sepsis
  • Inadequate insulin Drugs (cocaine) Pregnancy.

Manifestations of DKA Symptoms

  • · Nausea / Vomiting
  • · Thirst / Polyuria
  • · Abdominal pain
  • · Rapid shallow respiration.

Physical findings

  • · Tachycardia
  • · Dehydration
  • · Hypotension
  • · Tachypnea
  • · Kussmaul’s respiration
  • · Abdominal tenderness
  • · Acute abdomen
  • · Lethargy
  • ·Coma / Cerebral edema.

Lab diagnosis ·

  • Hyperglycemia
  • · Ketosis
  • · Metab acidosis
  • · Serum bicarbonate low
  • · Arterial pH low 6.8 – 7.3
  • · Serum potassium may be elevated due to acidosis
  • · Blood urea may be elevated.
  • · Leucocytosis
  • · Hypertriglyceridemia
  • · Hyperlipoproteinemia
  • · Serum amylase increases (salivary gland origin, not pancreatitic)
  • · Serum sodium decreases 1.6 mg for each 100 mg/dl rise in serum glucose
  • · Ketone bodies –
    • Betahydroxybutyrate
    • Acetoacetate
  • Betahydroxybutyrate is 3 times more than ac­etoacetate.
  • But ketone detection sticks detect acetoacetate Serum and plasma assays for B-eta hydroxybutyrate more accurately reflect the true ketone body level.

Differential diagnosis DKA

  • · Starvation KA
  • · Alcoholic KA
  • · In alcoholic KA bicarbonate> 15 meq/I.

Treatment of DKA

  • 1. Diagnosis – Increase in Blood glucose and serum ketones. There is metaolic acidosis.
  • 2. Admit in ICU
  • 3. Estimation of Serum K+, Serum Na+, Mg, Cl, Bi­carbonate, Phosphate, pH, PC02, beta hydroxybutyrate
  • Renal function:
    • a. Creatinine
    • b. Urine output
  • 4. IV fluids – 2-3 litre of 0.9% saline in 1-3 hours then 0.45% saline at lesser rate, then 5% dex­trose saline (0.45%) at lesser rate when plasma glucose reaches 250 mg/dl.
  • 5. Regular / Plain insulin IV 5U, then 5 units per hour continuous IV infusion, increase to 10 units to 50 units per hour according to response in 2­4 hours.
    • If initial serum K+ is <3.3 meq/I give insulin only after serum K+ is >3.3 meq/1.
  • 6. Treat precipitating factors for DKA evaluate and treat.
  • 7. Estimation of Blood glucose – every 1 hr Serum K, Na every 4 hrs for 24 hrs Serum HC03 – every 4 hrs
  • 8. Evalvuate BP, Pulse, Respiration, Mental status, Fluid intake/ output every 2 hrs.
  • 9. Give K+ 10-80 meq/hr
  • 10. a. Blood sugar should be reduced 150 – 250 mg/ dl. Then reduce Insulin infusion to <5 U/hour
    • b. Do not hurry to stop Insulin infusion till pa­tient is fully recovered
  • 11. When patient is taking foods orally start inter-mediate or long-acting insulin.
    • Ketosis resolves less faster than hyperglycemia. Ketone bodies seem to increase by tests which de­tect only acetoacetate as beta hydroxybutyrate is converted to acetoacetate as therapy is given.
    • If serum K+ is <3.3 meq/I do not start insulin till K+ is supplemented to increase the K to >3.3 meq/I.

Why bicarbonate replacement is avoided?

  • · Rapid reversal of acidosis causes impaired cardiac function
  • · Reduce tissue oxygen
  • · Promotes hypokalemia
  • · Increased risk of cerebral edema.

In severe acidosis – arterial pH <7, ADA (American Diabetes Association) says give HC03 50 meq/I in 200 ml of 0.45% saline. If pH is <6.9 give same for 2 hrs.

Prognosis of DKA

  • Mortality less than 5% with proper management. Death may occur due to :
  • · Cerebral edema
  • · Venous thrombosis
  • · Upper GI bleeding
  • · ARDS (Acute respiratory distress syndrome).
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