Handbook of Diabetes, 4th Edition, Excerpt #11: Diabetic Ketoacidosis, Hyperglycaemic Hyperosmolar State and Lactic Acidosis

Hyperglycaemia causes an osmotic diuresis that leads to dehydration and loss of electrolytes. Sodium depletion is worsened because of diminished renal sodium reabsorption due to insulin deficiency. Metabolic acidosis leads to the loss of intracellular potassium in exchange for hydrogen ions, and insulin deficiency also results in potassium loss from cells. These processes can result in high circulating plasma potassium.

The symptoms of DKA include increasing polyuria and thirst, weight loss, weakness, drowsiness and eventually coma (in about 10% of cases) (Box 12.2). Abdominal pain can occur, particularly in the young, and should resolve within 24 hours. If not, alternative causes should be looked for. Physical signs include dehydration, hypotension, tachycardia and hypothermia. Acidosis stimulates the respiratory centre, which results in deep and rapid (Kussmaul) respirations. The smell of acetone on the patient’s breath (similar to nail-varnish remover) may be obvious to some, but many people are unable to detect it.

Box 12.2 Clinical features of diabetic ketacidosis • Polyuria and nocturia; thirst • Weight loss • Weakness • Blurred vision • Acidotic (Kussmaul) respiration • Abdominal pain, especially in children • Leg cramps • Nausea and vomiting • Confusion and drowsiness • Coma (10% of cases)

The mechanism by which DKA induces coma is obscure, but impaired consciousness generally correlates with plasma glucose concentration and osmolality; coma at presentation is associated with a worse prognosis. This is because the unconscious brain stops utilising circulating ketone bodies which therefore accumulate more rapidly and result in a worsening metabolic acidosis. Co-existing causes of coma, such as stroke, head injury, meningitis and drug overdose, should always be considered and excluded if clinical signs suggest one of these diagnoses. Cerebral oedema should be suspected when the conscious level declines during treatment (see below).

Treatment

Diabetic ketoacidosis is a medical emergency. A rapid history, physical examination and bedside blood and urine tests should allow a provisional diagnosis in the emergency department and avoid treatment delays (Figure 12.3). Immediate bedside investigations should include blood glucose concentration and a test for the presence of urine or blood ketones with reagent strips, followed by laboratory measurements of blood glucose, urea, Na + , K + , Cl − , bicarbonate (for calculation of the anion gap), arterial blood pH and gas tensions, blood count, and blood and urine cultures. Venous pH could suffice if an arterial sample is difficult to obtain.

Initial treatment involves rehydration, usually with isotonic saline (0.9%) with appropriate supplements. Although initial serum potassium levels may be normal or even high, there will be an overall deficiency, and replacement should commence more or less immediately at 20 mmol/L unless there is significant renal failure or hyperkalaemia > 5.2 mmol/L. Serum potassium will fall with treatment as a result of correction of acidosis and insulin administration, both of which increase cellular uptake. Careful and regular monitoring of serum potassium is essential as treatment-induced hypokalaemia is a significant cause of cardiac dysrhythmia and even death (Table 12.3 ).

 

CASE HISTORY A 32-year-old woman with type 1 diabetes was 30 weeks pregnant. She had been unwell with dysuria and vague abdominal pain, and felt nauseous. She presented to the obstetric day unit where she was found to be slightly breathless and mildly febrile (37.9 ° C), and urinalysis showed 3+ ketones, trace proteinuria and glycosuria 55 mmol/L (990 mg/dL). Her capillary blood glucose was 11.9 mmol/L (21 4 mg/dL). A diagnosis of urinary tract infection was made, she was commenced on oral cefalexin and discharged. Twelve hours later she was brought to the accident and emergency department severely breathless and vomiting with severe abdominal pain. She was tachycardic (pulse 120/min, regular), hypotensive (BP 90/50 mmHg lying, 70/40 mmHg sitting), dehydrated and unwell. Laboratory plasma glucose was 35.6 mmol/L (641 mg/dL), blood 3-hydroxybutyrate was 8.1 mmol/L. Arterial pH was 7.0. She was commenced on IV saline and insulin. She made a rapid recovery over the next 24 hours. Her abdominal pain settled, fetal ultrasound was normal. She was delivered by elective caesarean section at 36 weeks gestation. Comment: Pregnancy is considered to be a proketotic state. Serum bicarbonate routinely falls in normal pregnancy; the normal range is 16 – 19 mmol/L. This means that DKA can occur at a relatively low blood glucose; case of normoglycaemic DKA have been described.The clues were the heavy ketonuria and her breathlessness. After this case, new guidelines were drawn up that mandated serum electrolyte samples and whole-blood ketone tests in all diabetic women presenting with ketonuria to the obstetric unit irrespective of the blood glucose result. Urinary tract infection rarely occurs without either positive urinary nitrite or leucocytes; proteinuria alone is not diagnostic.