medicnotes.org.uk :: Diabetic ketoacidosis

Diabetic ketoacidosis (DKA)

DKA is the hallmark of IDDM. Its main causes can be grouped as follows:

Previously undiagnosed DM
Interruption of insulin therapy
Stress of intercurrent illness

The most common cause is omission of insulin because the patient feels unable to eat owing to nausea/vomiting. Insulin should never be stopped.

Pathogenesis:

DKA is a state of uncontrolled catabolism associated with insulin deficiency
Insulin deficiency is a necessary precondition since only a modest elevation in insulin levels is sufficient to inhibit hepatic ketogenesis
Stable patients do not readily develop DKA when insulin is withdrawn

In the absence of insulin:

Hepatic glucose production accelerates
Peripheral glucose uptake is reduced
Rising glucose levels lead to an osmotic diuresis, loss of fluid and electrolytes and dehydration.
Plasma osmolality rises
Renal perfusion falls

In parallel, rapid lipolysis occurs, leading to:

Elevated circulating free-fatty acids (FFAs)
The FFAs are broken down to fatty acyl-CoA within the liver cells
This, in turn, is converted to ketone bodies within the mitochondria

Accumulation of ketone bodies:

Produces a metabolic acidosis
Typically associated with nausea/vomiting, leading to further loss of fluid and electrolytes
The excess ketones are excreted in the urine but also appear on the breath, producing a distinctive smell similar to that of acetone
Respiratory compensation for the metabolic acidosis leads to hyperventilation (described as ‘air hunger’)

Untreated, severe DKA is invariably fatal.

Clinical features:

Acidosis
Hyperventilation (Kussmaul respiration). This becomes less marked in severe acidosis owing to respiratory depression
Nausea
Vomiting
Abdominal pain (can be so severe as to be confused with an acute abdomen)
Severe dehydration
Most patients are confused and in a stupor
5% present in a coma

Management:

Replace fluid losses with normal saline
Replace electrolyte losses. Potassium levels need to be monitored with great care. Patients have a total body potassium deficit although initial plasma levels may not be low. Insulin therapy leads to uptake of potassium by the cells with a consequent fall in plasma levels. Potassium is, therefore, given as soon as insulin therapy is started.
Restore the acid-base balance. A patient with healthy kidneys will rapidly compensate for the metabolic acidosis once the circulating volume is restored. Only consider bicarbonate if the pH is < 7
Administer insulin. Soluble insulin is given as an IV infusion where facilities for adequate supervision exist, otherwise as hourly IM injections. Do not give subcutaneously as the peripheral blood flow is reduced in a shocked patient
Monitor blood glucose closely
Replace the energy losses
Seek the underlying cause (especially infection)

Problems of management:

Hypotension. This may lead to renal failure. Give plasma expanders or whole blood if systolic BP < 80mmHg
Coma. It is essential to pass a NG tube to prevent a drowsy patient aspirating when vomiting
Cerebral oedema. Rare and believed to be due to excessive rehydration. High mortality
Hypothermia. Monitor patient’s temperature rectally to avoid this
Late complications (e.g. stasis pneumonia and DVT)


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	Diabetic ketoacidosis (DKA) DKA is the hallmark of IDDM. Its main causes can be grouped as follows: Previously undiagnosed DM Interruption of insulin therapy Stress of intercurrent illness The most common cause is omission of insulin because the patient feels unable to eat owing to nausea/vomiting. Insulin should never be stopped. Pathogenesis: DKA is a state of uncontrolled catabolism associated with insulin deficiency Insulin deficiency is a necessary precondition since only a modest elevation in insulin levels is sufficient to inhibit hepatic ketogenesis Stable patients do not readily develop DKA when insulin is withdrawn In the absence of insulin: Hepatic glucose production accelerates Peripheral glucose uptake is reduced Rising glucose levels lead to an osmotic diuresis, loss of fluid and electrolytes and dehydration. Plasma osmolality rises Renal perfusion falls In parallel, rapid lipolysis occurs, leading to: Elevated circulating free-fatty acids (FFAs) The FFAs are broken down to fatty acyl-CoA within the liver cells This, in turn, is converted to ketone bodies within the mitochondria Accumulation of ketone bodies: Produces a metabolic acidosis Typically associated with nausea/vomiting, leading to further loss of fluid and electrolytes The excess ketones are excreted in the urine but also appear on the breath, producing a distinctive smell similar to that of acetone Respiratory compensation for the metabolic acidosis leads to hyperventilation (described as ‘air hunger’) Untreated, severe DKA is invariably fatal. Clinical features: Acidosis Hyperventilation (Kussmaul respiration). This becomes less marked in severe acidosis owing to respiratory depression Nausea Vomiting Abdominal pain (can be so severe as to be confused with an acute abdomen) Severe dehydration Most patients are confused and in a stupor 5% present in a coma Management: Replace fluid losses with normal saline Replace electrolyte losses. Potassium levels need to be monitored with great care. Patients have a total body potassium deficit although initial plasma levels may not be low. Insulin therapy leads to uptake of potassium by the cells with a consequent fall in plasma levels. Potassium is, therefore, given as soon as insulin therapy is started. Restore the acid-base balance. A patient with healthy kidneys will rapidly compensate for the metabolic acidosis once the circulating volume is restored. Only consider bicarbonate if the pH is < 7 Administer insulin. Soluble insulin is given as an IV infusion where facilities for adequate supervision exist, otherwise as hourly IM injections. Do not give subcutaneously as the peripheral blood flow is reduced in a shocked patient Monitor blood glucose closely Replace the energy losses Seek the underlying cause (especially infection) Problems of management: Hypotension. This may lead to renal failure. Give plasma expanders or whole blood if systolic BP < 80mmHg Coma. It is essential to pass a NG tube to prevent a drowsy patient aspirating when vomiting Cerebral oedema. Rare and believed to be due to excessive rehydration. High mortality Hypothermia. Monitor patient’s temperature rectally to avoid this Late complications (e.g. stasis pneumonia and DVT)
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