DIABETIC METABOLIC EMERGENCIES

Diabetic ketoacidosis

Diabetic ketoacidosis (DKA) results from insulin deficiency and is seen in the following circumstances:

■ Previously undiagnosed diabetes

■ Interruption of insulin therapy

■ The stress of intercurrent illness (e.g. infection or surgery).

Most cases of diabetic ketoacidosis are preventable. The most common error is for insulin to be reduced or stopped because the patient is not eating or is vomiting. Insulin should never be stopped and most patients need a larger dose when ill.

Pathogenesis

Ketoacidosis is a state of uncontrolled catabolism associated with insulin deficiency. In the absence of insulin there is an unrestrained increase in hepatic gluconeogenesis. High circulating glucose levels result in an osmotic diuresis by the kidneys and consequent dehydration. In addition, peripheral lipolysis leads to an increase in circulating free fatty acids, which are con-verted within the liver to acidic ketones, leading to a metabolic acidosis. These processes are accelerated by the ‘stress hormones' - catecholamines, glucagon and cortisol - which are secreted in response to dehydration and intercurrent illness.

Clinical features

There is profound dehydration secondary to water and electrolyte loss from the kidney and exacerbated by vomiting. The eyes are sunken, tissue turgor is reduced, the tongue is dry and, in severe cases, the blood pressure is low. Kussmaul's respiration (deep rapid breathing) may be present, as a sign of respiratory compensation for metabolic acidosis, and the breath smells of ketones (similar to acetone). Some disturbance of consciousness is common, but only 5% present in coma. Body temperature is often subnormal despite intercurrent infection. A few patients have abdominal pain and rarely this may cause confusion with a surgical acute abdomen.

Investigations

The diagnosis is based on the demonstration of hyperglycaemia in combina-tion with acidosis and ketosis:

■ Hyperglycaemia- blood glucose > 11 mmol/L

■ Ketonaemia- blood ketones > 3.0 mmol/L. Blood ketones are best measured using a finger prick sample and near-patient meter which

measures β-hydroxybutyrate, the major ketone in DKA. If not available, plasma ketones can be semi-quantitatively measured in the supernatant of a centrifuged blood sample using a dipstick that measures ketones

■ Acidosis - blood pH < 7.3 and/or bicarbonate (HCO3) < 15 mmol/L. Venous blood gives similar pH and HCO3 to arterial. Acidosis is high anion gap (p. 349)

■ Urine Stix testing shows heavy glycosuria and ketonuria

■ Serum urea and electrolytes. Urea and creatinine are often raised as a result of dehydration. The total body potassium is low as a result of osmotic diuresis, but the serum potassium concentration is often raised because of the absence of the action of insulin, which allows potassium to shift out of cells

■ Full blood count may show an elevated white cell count even in the absence of infection

■ Further investigations are directed towards identifying a precipitating cause: blood cultures, chest radiograph and urine microscopy and culture to look for evidence of infection, and an ECG and cardiac proteins to look for evidence of myocardial infarction.

Management

Immediate emergency management (ABC) is necessary in all patients. Admis-sion to the intensive care unit is recommended in the seriously ill. The aims of treatment are to replace fluid and electrolyte loss (Table 15.4), replace insulin, and restore acid-base balance over a period of about 24 hours (Emergency Box 15.1). Therapy of diabetic ketoacidosis shifts potassium into cells, resulting in profound hypokalaemia and death if not treated prospec-tively. Cerebral oedema (presents with headache, irritability, reduced con-scious level) may complicate therapy and results from rapid lowering of blood glucose and osmolality. When the patient has recovered, it is necessary to determine the cause of the episode and advice and information provided to prevent recurrence.

Hyperosmolar hyperglycaemic state

This is a life-threatening emergency characterized by marked hypergly-caemia, hyperosmolality and mild or no ketosis. It is the metabolic emergency

Table 15.4 Average loss of fluid and electrolytes in an adult with ketoacidosis

Water

5-7 L

Sodium

500 mmol

Potassium

350 mmol

Emergency Box 15.1

Management of diabetic ketoacidosis

Phase I management
• Fluid replacement: 0.9% sodium chloride with 20 mmol KCI per L. An average regimen would be 1 L in 30 minutes, then 1 L in 1 hour, then 1 L in 2 hours, then 1 L in 4 hours, then 1 L in 6 hours
• Insulin: soluble insulin 6 units/h by intravenous infusion, or 20 units i.m. stat. followed by 6 units i.m. hourly. Aim for fall in blood glucose of approx. 5 mmol/h. Adjust infusion rate by 50% to achieve this
• Adjust KCI concentration depending on results of 2 hours’ blood K measurement. Temporarily delay if serum potassium >5.0 mmol/L
Increase to 30–40 mmol/L if serum potassium is low, e.g. <3.5 mmol/L.
IF:
• Blood pressure below 80 mmHg, give plasma expander (colloid, p. 326)
• pH below 7.0 give 500 mL of sodium bicarbonate 1.26% plus 10 mmol KCI over 1 hour. Repeat if necessary to bring pH up to 7.0.
Phase 2 management
• When blood glucose falls to 10–12 mmol/L change infusion fluid to 1 L 5% dextrose plus 20 mmol KCl 6-hourly. Continue insulin (necessary to switch off ketogenesis) with dose adjusted according to hourly blood glucose test results (e.g. i.v. 3 units/h glucose 15 mmol/L; 2 units/h
when glucose 10 mmol/L).
Phase 3 management
• Once stable and able to eat and drink normally, transfer patient to four-times-daily subcutaneous insulin regimen (based on previous 24 hours insulin consumption, and trend in consumption). Overlap s/c insulin with insulin infusion by 30 minutes.
Special measures
• Broad-spectrum antibiotic if infection likely
• Bladder catheter if no urine passed in 2 hours
• Nasogastric tube if drowsy or protracted vomiting
• Consider CVP pressure monitoring if shocked or if previous cardiac or renal impairment
• Consider s.c. prophylactic heparin in comatose, elderly or obese patients.
Monitoring
• Vital signs, volume of fluid given and urine output hourly
• Finger prick glucose hourly for 8 hours
• Laboratory glucose and electrolytes 2-hourly for 8 hours, then 4–6 hourly, adjust K replacement according to results.
Note: The regimen of fluid replacement set out above is a guide for patients with severe ketoacidosis. Excessive fluid can precipitate pulmonary and cerebral oedema; adequate replacement must therefore be tailored to the individual and monitored carefully throughout treatment.

characteristic of uncontrolled type 2 diabetes mellitus (often previously undiagnosed). Infection is the most common precipitating cause, particularly pneumonia.

Clinical features

Endogenous insulin levels are reduced but are still sufficient to inhibit hepatic ketogenesis, whereas glucose production is unrestrained. Patients present with profound dehydration (secondary to an osmotic diuresis) and a decreased level of consciousness, which is directly related to the elevation of plasma osmolality. The main biochemical differences between ketoacidosis and the hyperosmolar hyperglycaemic state are illustrated in Table 15.5.

Management

Investigations and treatment are the same as for ketoacidosis with the excep-tion that a lower rate of insulin infusion (3 U/h) is often sufficient, as these patients are extremely sensitive to insulin. The rate may be doubled after 2-3 h if glucose is falling too slowly. The hyperosmolar state predisposes to stroke, myocardial infarction, or arterial thrombosis, and prophylactic sub-cutaneous heparin is given.

Prognosis

Mortality rate is around 20-30%, mainly because of the advanced age of the patients and the frequency of inter-current illness. Unlike ketoacidosis, the hyperosmolar hyperglycaemic state is not an absolute indication for subse-quent insulin therapy, and survivors may do well on diet and oral agents.

Table 15.5 Typical biochemistry in diabetic ketoacidosis and the hyperosmolar hyperglycaemic state illustrating the main differences

Examples of blood values

Severe ketoacidosis

Hyperosmolar hyperglycaemic State

Na+ (mmol/L)

140

155

K+ (mmol/L)

5

5

Cl- (mmol/L)

100

110

HCO3- (mmol/L)

15

25

Urea (mmol/L)

8

15

Glucose (mmol/L)

30

50

Serum osmolality (mOsm/kg)*

328

385

Arterial pH

7.0

7.35

*See page 324 for definition and discussion of plasma osmolarity

Lactic acidosis

This is a rare complication in patients taking metformin; the mortaility is high. Patients present with severe metabolic acidosis without significant hyper-glycaemia or ketosis. Treatment is by rehydration and infusion of isotonic 1.26% bicarbonate.

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Liver, biliary tract and pancreatic disease
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