Diabetic Emergencies

(CLINICAL PHARMACY-II)
DIABETIC EMERGENCIES
Hypoglycaemia and extreme hyperglycaemia, causing diabetic ketoacidosis or hyperosmolar hyperglycaemic
state, constitute the three acute emergencies associated with diabetes.
1. Hypoglycaemia
2. Diabetic ketoacidosis
3. Hyperosmolar hyperglycaemic state
1. Hypoglycaemia:
• Hypoglycaemia can occur both with insulin treatment and in those taking some oral agents, especially the
longer-acting sulphonylureas, for example, chlorpropamide and glibenclamide.
• However, symptoms caused by the release of counter-regulatory hormones predominantly adrenaline
(epinephrine), Nor-adrenaline (norepinephrine) and glucagon tend to occur when the venous serum
glucose drops below 3.0 mmol/L in healthy individuals.
• If the serum glucose is allowed to drop to around 2 mmol/L, there are acute changes in cerebral function
which lead initially to confusion. This is followed by coma, seizures and death if the glucose drops below
about 0.5 mmol/L. Any cerebral malfunction is termed neuroglycopaenia.
Causes:
• Decrease Carbohydrate Consumption, Increase Carbohydrate utilization.
Symptoms:
• Symptoms simply may not occur because of autonomic neuropathy, drugs which suppress autonomic
symptoms, such as β-blockers, and alcohol intoxication.
• Symptoms are
Autonomic Neuroglycopaenic Other

• Sweating • Faintness • Hunger
• Trembling • Loss of concentration • Headache
• Tachycardia • Drowsiness • Perioral
• Palpitations • Visual disturbances tingling/numbness
• Pallor • Abnormal behaviour
(agitation, aggressiveness)
• Confusion
• Coma
Treatment of hypoglycaemia:
• If the patient is able to swallow safely without the risk of aspiration, then glucose should be taken orally.
However, if unable to swallow or if there is a risk of aspiration because, for example, of a decreased level
of consciousness, parenteral treatment should be given, either intravenous glucose or intramuscular
glucagon.
• The most effective oral treatments are pure sources of glucose, for example, five glucose tablets or glucose
drinks such as 150 mL of Lucozade®. In an emergency, hot drinks should be avoided as they might burn
and drinks containing milk are not suitable as the fat in milk slows down sugar absorption.
pg. 1 Muhammad Hammad 116 (2019-24)

• Blood glucose levels should be measured about 10–15 min after treating hypoglycaemia. If below 3.5
mmol/L, more glucose should be consumed. If above 3.5 mmol/L and the next meal will be over 1 h, then
a long-acting carbohydrate is also required, for example, bread or biscuits.
• However, if the person is taking an α-glucosidase inhibitor such as acarbose, then monosaccharide
carbohydrates must be given because disaccharides and polysaccharides will not be absorbed due to
inhibition of the enzymes cleaving carbohydrate into absorbable monosaccharide units.
• Parenteral treatment should be required, 25 g of intravenous glucose or 1 mg of intramuscular glucagon is
recommended.
• Glucagon takes approximately 15–20 min to work, but if the person has liver disease (cirrhosis) or is
malnourished, then glucagon may not work because glucagon acts by mobilizing glucose stores from the
liver. In such cases, intravenous glucose must be given.
• A number of serious extravasation injuries, some necessitating amputation of the affected limb, have been
caused by 50% glucose. As a consequence, many hospitals now use 20% glucose.
2. Diabetic ketoacidosis:
• Absence of insulin causes extreme hyperglycaemia, which leads to diabetic ketoacidosis. Diabetic
ketoacidosis is normally associated with type 1 diabetes.
• Precipitating factors for diabetic ketoacidosis in type 1 disease are usually omission of insulin dose, acute
infection, trauma or myocardial infarction.
• It occurs because absence of insulin causes extreme hyperglycaemia. At the same time, the normal
restraining effect of insulin on lipolysis is removed.
• Non-esterified fatty acids are released into the circulation and taken up by the liver, which produces acetyl
coenzyme A (acetyl CoA). The capacity of the tricarboxylic acid cycle to metabolise acetyl CoA is rapidly
exceeded.
• Ketone bodies, acetoacetate and hydroxybutyrate are formed in increased amounts and released into the
circulation.
• Further, osmotic diuresis, caused by hyperglycaemia, lowers serum volume, causing dizziness and
weakness due to postural hypotension.
• Weakness is increased by potassium loss, caused by urinary excretion and vomiting due to stimulation of
the vomiting centre by ketones, and catabolism of muscle protein.
• When the blood gets acidic, there are many positively
charged hydrogen ions present in the blood. Cells will
exchange these extracellular protons with intracellular
potassium, so initially there will be hyperkalemia. In
addition to helping glucose enter cells, insulin also
stimulates the sodium-potassium ATPases that help
potassium get into cells; without insulin, more potassium
stays in the extracellular fluid. Since this extracellular
potassium is quickly excreted, even though the blood
potassium levels remain high, total body potassium is
depleted.
• Ketoacidosis exacerbates the dehydration and hyperosmolarity by producing anorexia, nausea and
vomiting.
• As serum osmolarity rises, impaired consciousness ensues with coma developing in approximately 10%
of cases.
• Metabolic acidosis causes stimulation of the medullary respiratory centre, giving rise to Kussmaul
respiration (deep and rapid breathing) in an attempt to correct the acidosis. The patient's breath may have
the fruity odour of acetone (ketones) commonly described as smelling like pear drops or nail varnish
remover.

Diagnosis of Diabetic Ketoacidosis:

• Diagnosis requires demonstration of hyperglycaemia and metabolic acidosis with the presence of ketones.
• The biochemical diagnosis of ketoacidosis is usually made at the bedside and confirmed in the laboratory.
• Urinalysis will show marked glycosuria and ketonuria.
• A blood glucose test strip usually shows a blood glucose level of more than 22 mmol/L.
Treatment of diabetic ketoacidosis:

• Treatment comprises fluid volume expansion (initially with 0.9% sodium chloride), correction of
hyperglycaemia and the presence of ketones (by infusion of insulin), prevention of hypokalaemia, and
identification and treatment of any associated infection (if any).
3. Hyperosmolar Hyperglycaemic State:

• HHS is associated with type 2 disease and has a higher mortality rate (15%) than diabetic ketoacidosis.
• HHS usually occurs in middle-aged or elderly people, about 25% of whom have previously undiagnosed
type 2 diabetes.
• In HHS, unlike diabetic ketoacidosis, there is no significant ketone production and therefore no severe
acidosis.
• Hyperglycaemia occurs gradually over a sustained period of time, leading to dehydration due to osmotic
diuresis which, if severe, results in hyperosmolarity.
• Hyperosmolarity may increase blood viscosity and the risk of thromboembolism.
• Factors precipitating HHS are infection, myocardial infarction, poor adherence with medication regimens
or medicines which cause diuresis or impair glucose tolerance, for example, glucocorticoids.
Diagnosis of HHS:
• The diagnostic features of HHS are hyperglycaemia (often in the region of 55 mmol/L, which is generally
much higher than for diabetic ketoacidosis), dehydration and hyperosmolarity.
• There may be a mild metabolic acidosis but without marked ketone production.
• Conscious levels on presentation range from slight confusion to coma. In some cases, seizures occur.
• Serum sodium and potassium levels are usually normal, but creatinine is high.

• The average fluid deficit is 10 L, so circulatory collapse is common.
Treatment of HHS:
• Treatment requires fluid replacement to stabilise blood pressure and improve circulation and urine output.
• Sodium chloride 0.9% or 0.45% (if serum sodium is greater than 150 mmol/L) is given and monitoring of
blood pressure and cardiovascular status undertaken.
• Potassium may be added if required. Insulin treatment is started via intravenous infusion but is not
aggressive, since fluid replacement also lowers serum glucose levels.
• Prophylaxis or treatment for thromboembolism may also be required.

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(CLINICAL PHARMACY-II)

Autonomic Neuroglycopaenic Other

pg. 1 Muhammad Hammad 116 (2019-24)

pg. 2 Muhammad Hammad 116 (2019-24)

Diagnosis of Diabetic Ketoacidosis:

Treatment of diabetic ketoacidosis:

3. Hyperosmolar Hyperglycaemic State:

pg. 3 Muhammad Hammad 116 (2019-24)

• The average fluid deficit is 10 L, so circulatory collapse is common.

pg. 4 Muhammad Hammad 116 (2019-24)

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