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Chapter: Medicine and surgery: Endocrine system

Diabetic ketoacidosis (DKA) - Complications of diabetes

The hyperglycaemic and metabolic acidotic state which occurs in Type I diabetes due to excess ketone production as a result of insulin deficiency. - Definition, Incidence, Aetiology, Pathophysiology, Clinical features, Complications, Investigations, Management, Prognosis.

Diabetic ketoacidosis (DKA)




The hyperglycaemic and metabolic acidotic state which occurs in Type I diabetes due to excess ketone production as a result of insulin deficiency.




Precipitating factors include infection, trauma, surgery, burns and myocardial infarction. It is associated with poor diabetic control.




Patients may omit or reduce their insulin when ill, because they are eating less and therefore believe they require less insulin. In fact, stresses such as an intercur-rent infection increase the secretion of glucagon and other counter-regulatory hormones which oppose in-sulin, so that insulin requirements increase during illness.


The result of this is a severe catabolic state: there is un-controlled glycolysis, lipolysis and protelolysis. This causes hyperglycaemia and a rise in free fatty acids which are the substrates for ketone body formation (ketogenesis) within the liver. Normally insulin opposes ketogenesis, but in conditions of insulin deficiency, glucagon and catecholamines increase ketogenesis. The ketone bodies produced are acetoacetic acid, acetone and hydroxybutyrate which result in a metabolic acidosis.

As the production rate exceeds the body’s capacity to utilise ketone bodies, both ketone body and glucose concentrations rise, causing hyperosmolarity of the extracellular fluid. The renal threshold for glucose


reabsorption (10 mmol/L) is exceeded, and an osmotic diuresis occurs so that water and electrolytes, especially sodium and potassium, are rapidly lost. This causes a severe dehydration, hypovolaemia and this compounds the problem by reducing renal perfusion, thereby reducing glucose clearance.


Dehydration is exacerbated by vomiting, which is due to central effects of ketosis.


Death is usually due to cardiac arrest.


Clinical features


Nausea, vomiting, abdominal pain, hyperventilation, shock, coma, signs of dehydration and ketotic smelling breath. Normally this occurs in a known diabetic, but it may occur as the presenting feature, particularly in young patients.




Shock and acute renal failure, cerebral oedema may occur during rehydration, adult respiratory distress syndrome, acute gastric dilatation, aspiration, hypothermia, and coma.




The diagnosis requires the demonstration of diabetes, ketosis and a metabolic acidosis. Blood glucose should be checked on capillary bedside testing and confirmed with a laboratory sample. Ketones may be detected in the urine on urinalysis. Some bedside blood glucose monitors can also detect ketones. An arterial blood gas sample is also required to demonstrate and assess the severity of metabolic acidosis.


·        U&Es and osmolality should be sent urgently.


·        Full blood count, amylase, blood cultures, urine culture, CXR and ECG are checked to identify underlying causes and complications. Consider cardiac enzymes in older patients. Serum amylase greater than three-fold normal is suggestive of acute pancreatitis, which may be the cause of DKA in up to 10% of cases.




DKA is a medical emergency. The initial management is rehydration and correction of electrolyte imbalances.

Insulin replacement is also needed to correct the hyper-glycaemia and prevent further osmotic diuresis. Any underlying illness must be treated as appropriate. Patients require a nasogastric tube for gastric decompression and emptying as there is a high risk of aspiration. Fluid and electrolytes: Patients can be as much as 10 L fluid depleted, with a K+ and Na+deficit. Monitor fluid balance (urine output etc.) during treatment. A central venous catheter may be placed to measure central venous pressure to guide fluid management. Care must be taken not to change the osmolality too rapidly, as this can lead to cerebral oedema. The osmolality will drop as glucose levels fall, and so sodium and potassium need to be given to counter this. For this reason, normal saline is always used initially:                 

·        1st hour           1.5 L

·        2nd hour                   1.0 L

·        3rd to 4th hour         1.0 L over 2 hours

·        > 5th hour       2.0 L every 8 hours

·        Change to 5% or 10% dextrose, 1 L every 8 hours once the patient is rehydrated and blood glucose is back down to 12 mmol/L. Replacement should be faster if patients are shocked and slower if there are signs of cardiac failure, fluid overload or cerebral oedema.


There is always a depletion of total body potassium, but serum K+ may be normal, high or low. Supplementation is always needed, because potassium follows glucose into the cells. However, there is a danger of hyperkalaemia, causing cardiac arrhythmias, so if K+ levels are >5 mmol/l withhold K+ and recheck after 30 minutes.

Normal K+ 20 mmol per litre of fluid

<3.5 (hypo) 40 mmol per litre


Insulin: Soluble insulin is administered intravenously by an infusion pump – start with 10 units per hour and then titrate to response. Therapy should aim to produce a gradual reduction to a glucose level of 10–15 mmol/L over a period of several hours. Hourly blood sugar and 1–2 hourly U&E’s, plasma osmolality monitoring are required. If intravenous access is not possible then sub-cutaneous or intramuscular insulin can reverse the ketoacidosis.


Bicarbonate: The use of bicarbonate is contentious. It is unlikely to improve the acidosis and has the potential of doing harm including making cerebral oedema more likely. It therefore should not normally be used in the treatment of diabetic ketoacidosis.



Overall mortality is 10% and as high as 50% in older patients with severe intercurrent illness. It is the most common cause of death in diabetic patients under 20 years old.

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