Clinical features

The cardinal symptoms of ketoacidosis include

• rapidly increasing polyuria and polydipsia

• rapid weight loss - dehydration

• nausea and vomiting - hyperketonaemia is emetic

• generalised muscular weakness

• muscular cramps.

These are followed by serious signs of cerebral dysfunction:

• progressive drowsiness and obtundation

While a decrease in the level of consciousness is common, coma is encountered in only about 10 per cent of patients. The mechanism by which ketoacidosis induces coma remains uncertain; impairment of consciousness correlates with plasma glucose concentration and osmolarity, coma at presentation being associated with a worse prognosis. Co-existing causes of coma such as stroke, head injury or drug overdose should be considered and excluded if

Table 1.2 Causes of impaired consciousness in patients with diabetes mellitus

• Diabetic ketoacidosis

• Hyperosmolar non-ketotic hyperglycaemia

• Hypoglycaemia

• Lactic acidosis

o Stroke (more common in diabetic patients) o Post-ictal (including hypoglycaemia - generalised tonic-clonic convulsions also cause a self-correcting lactic acidosis; see Chapter 6)

o Cerebral trauma (may follow hypoglycaemia) o Ethanol intoxication (may induce or exacerbate hypoglycaemia in diabetic patients) o Drug overdose serum osmolality is less than approximately 350 mOsmol/kg (Table 1.2).

Usually symptoms usually require several hours to develop, often following symptoms of an intercurrent illness. Physical signs are usually prominent in severe diabetic ketoacidosis.

• Dehydration. Variable; approximately 5 L in an average adult.

• Hypotension. Supine hypotension, in the absence of confounding effects of anti-hypertensive drugs, denotes more than 20 per cent depletion of extracellular fluid volume. Severe hypotension in ketoacidosis carries an adverse prognosis

• Tachycardia. Reflects dehydration, acidosis and sympathetic activation; drugs with anti-muscarinic effects, e.g. tricyclic antidepressants used for treatment of symptomatic neuropathy, may exacerbate tachycardia.

Severe diabetic ketoacidosis may develop within 24 hours.

Other clinical and biochemical features include the following.

• Air hunger. Acidosis stimulates the respiratory centre within the medulla oblongata, causing deep rapid respirations (Kussmaul breathing).

• Ketotic fetor. The odour of acetone may be obvious on the breath, although the capacity to detect acetone varies between individuals.

• Hypothermia. Another consequence of acidosis, which may mask a valuable sign of infection. Rectal temperature should be taken with a low reading thermometer if hypothermia is suspected; marked hypothermia carries an adverse prognosis.

• Leukocytosis. This is common with hyperketonaemia and does not necessarily indicate infection.

• Gastroparesis. A gastric succusion splash may be evident on abdominal examination as a consequence of gastric stasis; the stomach may become distended with several litres of contents, posing a risk of aspiration in patients with an impaired level of consciousness.

• Abdominal pain. Generalised abdominal pain may occur, particularly in younger patients with severe acidosis (see Chapter 2). If abdominal pain does not resolve with resolution of the acidosis, alternative causes should be suspected. Measurement of plasma amylase is unhelpful since levels may be raised non-specifically in ketoacidosis; ultrasound imaging of the pancreas may be of assistance in diagnosing pancreatitis.

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