Diabetic ketoacidosis
Dr. Mohammed KhalidDiabetic ketocacidosis (DKA) is a major medical emergency and remains a serious cause for morbidity in type I diabetics. It carries mortality rate of 5-10%, which is even high in elderly. DKA is a state of uncontrolled catabolism triggered by relative or absolute deficiency in circulating insulin
The triad of DKA includes:Hyperglycaemia ( blood glucose 15mmol/L)Metabolic acidosis (pH 7.33)Hyperketonaemia The deficiency of insulin ia accompanied by reciprocal elevation of counter regulatory hormones (catechlamines, glucagon, cortisol and growth hormone) resulting in increasing production of glucose by the liver (gluconeogenesis) and catabolism of fat (lipolysis), which provides the substrate free fatty acids for uncontrolled production of ketones by the liver (hepatic ketongenesis), and this production of ketones leads to acidosis.
What causes DkA
Any disorder that alter the balance between insulin and the counter regulatory hormones can precipitate DKA. DKA can develop in 5% of patients with type I DM and rarely occur in type II DM. DKA can occur due to inadequate insulin or intercurrent illness which include:Infections (pneumonia, UTI, etc.) Trauma or surgery Severe emotional stress Acute MI Drugs (steroids, pentamidine) Hormonal changes in women (pre-ovulation)
The hyperglycaemia causes a profound osmotic diuresis leading to dehydration and electrolyte loss particularly of sodium and potassium which may be lost in urine or through vomiting. Every patient with DKA is potassium depleted but the plasma concentration of potassium gives very little indication of total body deficit. The average loss of fluid in moderate to severe DKA in adults is about 6 liters, 3 liters are extracellular loss, and 3 liters are intracellualar loss. The severity of DKA is assessed by measurement of plasma bicarbonate. If it is less than 12 mmol/L it indicates severe acidosis.
Clinical features
The main clinical features are due salt and water depletion, which include: worsening of polyuria, polydyspnia, excessive thirst sensation, nausea, vomiting and abdominal pain. Acute abdominal pain can present mainly in children. Muscle cramps, blurring of vision, change in the level of consciousness, and even coma (10%).Clinical signs include hypotension, tachycardia and small volume pulse, dehydration (sunken eyes, dry furred tongue and loss of skin turger), and Kussmal breathing (acidotic breathing, or air hunger). The breath smells for acetone (acetone breathing). The patient may be drowsy, confused and even comatose. Hypothermia may be present unless there is infection.
Investigations
Blood glucose, B. urea, S. creatinine and B gases, SK+, Na+. Ketone in urine ECG Screening for infections: (CBP, GUE, urine and blood culture, CXR)
Management
It is a medical emergency, and should be treated in hospital, preferably in the ICU. The principles of therapy include: Fluid replacement Insulin therapy Potassium therapy Antibiotic therapyFluid replacement
We need 6 liters of IV fluid; 3 liters for extracellular fluid replacement by normal saline (0.9%), and liters for intracellular replacement by dextrose (5%). Early and rapid replacement is essential. The liters should be replaced over 24 hours as follows:One liter of normal saline over 30 minOne liter of normal saline over 1 hour One liter of normal saline over 2 hoursAnd one liter over 2-4 hours of N. saline when the blood glucose reach 15 mmol/L (270mg/dl), switch to 5% dextrose water (one liter/ 8 hours)Insulin therapy
Administration of short acting soluble insulin is required. If IV infusion of soluble insulin is not possible, we should start with a loading dose of 10-20 units IM as a bolus dose, followed by 5 units/ hour. The blood sugar should fall by 3-6mmol/ L (55-110mg/dl) per hour. If this does not occur, the dose of insulin should be doubled. When the B. glucose has fallen to (10-15 mmol/L (180-270mg/dl)reduce the dose of insulin to 1-4 units/ hour. SC insulin should not be resumed until the patient can eat and drink normally.Potassium replacement
If the plasma K at the beginning is ≥ 55mmol/L, there is no need to give K, but if the s.K is -55 mmol/L, K is given at a dose of 20 mmol/L of infused fluid. If it is 3. 5 mmmol/L, give 40 mmol/L of infused fluidm.Antibiotic therapy
Infection must be carefully sought and vigoursly treated by heavy antibiotics.Bicarbonate replacement
It is only indicated in severe acidosis, when the pH is less than 7. bicarbonate is given a3 00ml of 1.26% NaHCO3 infused over 30 min. all the patients need close monitoring hourly for the first 3 hours, which include: Pulse, B. pressure and urine output B. glucose, B. urea and serum electrolytes ECG Blood gas analysis Urine ketone Then 2-4 hourly check is needed for the first 24 hoursComplications
Cerebral oedema; which is treated by manitol 20% at a dose of 1mg/kg body weight ARDS DIC AMI Acute gastric dilatation Thromboembolism Acute circulatory failure