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Management of Diabetic ketoacidosis

Diabetic ketoacidosis (DKA) :- Is a life-threatening acute complication of diabetes mellitus. It occurs when insulin therapy is absent, or becomes inadequate for the current physiological state, usually as a result of intercurrent illness. It is normally seen in type 1 diabetics and may be a presenting feature of undiagnosed type 1 diabetes, particularly in children. However, it is not unheard of in type 2 diabetics.

Clinical manifestation (1) Symptoms Nausea / vomiting. Thirst / polyuria. Abdominal pain. Shortness of breath.

Clinical manifestation (2) physical findings Tachycardia. Dehydration / hypotension. Tachypnea / kussmaul respirations / respiratory distress. Abdominal tenderness ( may resemble acute pancreatitis or surgical abdomen) Lethargy / obtundation / cerebral edema / possibly coma.

Clinical manifestation (3) precipitating events Inadequate insulin administration. Infection (pneumonia/UTI/gastroenteritis/sepsis) infraction (cerebral,coronary,mesenteric,peripheral) Drugs (cocaine) Pregnancy.

pathphysiology Inadequate insulin secretion hyperglycemia cellular starvation Induce secretion of glucagon, catecholamine, cortical, & GH. Stress response encourage proteolysis & lipolysis FFA convert to ketoacid, Acetoacetate, β-hydroxybutyrate & aceton metabolic acidosis Encourage glycogenolysis, gluconeogenesis further glucose huge osmotic diuresis and gross dehydration Dehydration tissue perfusion lactic acidosis

Management of diabetic ketoacidosis Confirm diagnosis. Admit to hospital. Assess serum electrolytes & acid-base status . Replace fluids. Administer short acting insulin. Assess patient : what precipitate the episode Replace K+. Continue above until patient is stable. Administer intermediate or long acting insulin as soon as patient is eating.

Management of diabetic ketoacidosis 1- Confirm diagnosis (plasma glucose, positive serum ketones, metabolic acidosis). 2- Admit to hospital: intensive-care setting may be necessary for frequent monitoring or if ph <7.00 or unconscious.

3- Assess: serum electrolytes (K+ , Na+ , Mg+2 , Cl-, bicarbonate , phosphate) acid-base status-pH, HCO3-, Pco2, β-hydroxybutyrate 4- Replace fluids: 2 -3 L of 0.9% saline over first 1-3 h (10-15 ml/kg per hour); subsequently, 0.45% saline at 150-300 ml/h; change to 5% glucose and 0.45% saline at 100-200 ml/h when plasma glucose reaches 250 mg/dL (14 mmol/L).

5- Administer short-acting insulin: IV (0.1 units/kg) or IM (0.3 units/kg), then 0.1 units/kg per hour by continuous IV infusion; increase 2-to3-fold if no response by 2-4 h. If initial serum potassium is corrected to >3.3 mmol/L (3.3.meq/L).

6- Assess patient: What precipitated the episode (noncompliance, infection, trauma, infraction, cocaine)? Initiate appropriate workup for precipitating event(cultures,CXR,ECG). 7- Measure capillary glucose every 1-2 h; measure electrolytes (especially K+, bicarbonate, phosphate) and anion gap every 4 h for first 24 h.

8- Monitor blood pressure, pulse, respirations, mental status, fluid intake and output every 1-4 h. 9- Replace K+: 10 meq/h when plasma K+<5.5 meq/L, ECG normal, urine flow and normal creatinine documented; administer 40-80 meq/h when plasma K+<3.5 meq/L or if bicarbonate is given.

Very rarely k+ replacement may need to be given before insulin if the patient profoudly hypokalaemic to begin with e.g. k+ < 3.5 mmol/L If the patient is hyperkalaemic do not give K+ therapy-recheck after 30 minute.

10- Continue above until patient is stable, glucose goal is 150-250 mg/dL, and acidosis is resolved. Insulin infusion may be decreased to 0.05-0.1 units/kg per hour. 11- Administer intermediate or long-acting insulin as soon as patient is eating. Allow for overlap in insulin infusion and subcutaneous insulin injection.

Mild diabetic ketosis If the patient is fully conscious & there has been no nausea or vomitting for at least 12 h intravenous therapy is unnecessary it is reasonable to give small doses of insulin s.c 4-6 hourly & fluids by mouth .

Complications Cerebral oedema – commoner in children/adolescents where it affects around 1% of cases of DKA. Mortality is significant and estimated at 20-90%. Presents in first 24 hours with headache, behavioural changes and urinary incontinence progressing to abrupt neurological deterioration and coma. Pulmonary oedema due to overzealous fluid replacement or as a spontaneous phenomenon. Iatrogenic hypoglycaemia or hypokalaemia. Cardiac dysrhythmia due to electrolyte disturbance(particularly K+)or metabolic asidosis.

Complications Myocardial suppression due to metabolic acidosis. Venous thromboembolism. Myocardial infraction(may be a cause of, or complication of DKA). Diabetic retinopathic changes may be seen prior to or after therapy for DKA . Hypophosphataemia- rarely has significant clinical effects. Adult respiratory distress syndrome. Death still occurs.

Prognosis Prognosis is excellent in cases that are appropriately managed and which present before progression to coma. Prognosis worsens with age and the severity of the underlying precipitating pathology (particularly MI, sepsis and pneumonia). The presence of coma at presentation, hypothermia or persistent oliguria are poor prognostic indicators.

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