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Diabetic ketoacidosis and the hyperosmolar hyperglycaemic state share impaired insulin action,
but differ in the relative contributions of ketogenesis, dehydration and hyperosmolality.
Diabetic ketoacidosis arises from absolute insulin deficiency.
The body behaves as if starving, lipolysis releases fatty acids,
and the liver converts them into ketoacids.
The hyperosmolar hyperglycaemic state arises when a little insulin remains.
That remnant cannot control glucose, but it suppresses lipolysis and ketogenesis,
so acidosis is absent.
Glucose instead climbs above 33 mmol/L, osmotic diuresis becomes torrential,
and the effective osmolality exceeds 320 mOsm/kg.
Ketoacidosis is defined by a pH below 7.3,
a bicarbonate below 18 mmol/L and strongly positive ketones.
It is typical of type 1 disease,
although type 2 patients under severe stress
or on SGLT2 inhibitors are not immune.
The acid-base picture is a high anion gap metabolic acidosis with respiratory compensation.
Ketoacids consume bicarbonate,
and Kussmaul breathing lowers carbon dioxide to defend the pH.
The expected carbon dioxide follows Winter's formula,
1.5 times the bicarbonate plus 8.
A value above prediction signals a tiring patient and a mixed disorder.
Two electrolytes deceive.
Measured sodium is diluted as glucose draws water from cells,
so it must be corrected upward before dehydration is judged.
Potassium is shifted out of cells by insulin deficiency and acidosis,
so the serum value is normal or high
while the total body store is depleted.
Diabetic ketoacidosis and the hyperosmolar hyperglycaemic state share impaired insulin action,
but differ in the relative contributions of ketogenesis, dehydration and hyperosmolality.
Treatment therefore follows a fixed sequence: fluid, potassium, then insulin.
Isotonic saline restores perfusion, one litre in the first hour.
Potassium is read before insulin is started.
Below 3.3 mmol/L, insulin is withheld until potassium is replaced.
Between 3.3 and 5.2 mmol/L,
20 to 30 mmol is added to each litre.
Above 5.2 mmol/L, none is given yet.
A fixed-rate intravenous infusion of 0.1 units per kilogram per hour
then follows.
Oral hypoglycaemic agents have no place.
Once glucose falls below about 14 mmol/L,
10 per cent dextrose is added,
and the insulin continues until ketones are below 0.6 mmol/L,
pH exceeds 7.3 and the anion gap has closed.
Basal insulin is given before the infusion stops.
Bicarbonate is not routine.
It is considered only when the pH is below 6.9,
because earlier use deepens hypokalaemia,
shifts the oxygen dissociation curve leftward and may paradoxically acidify the brain.
Cerebral oedema is the feared complication in children and young adults.
Headache,
a falling heart rate with rising blood pressure
and a declining conscious level demand immediate treatment.
Glucose should fall by roughly 3 mmol/L per hour, never faster.
Prevention is the sick-day rule.
Basal insulin is never omitted,
glucose is checked every two to four hours,
and ketones are measured whenever glucose exceeds 15 mmol/L or vomiting begins.
Ketones above 1.5 mmol/L
or an inability to keep fluids down mean hospital,
not waiting.
Hypoglycaemia sits at the other end of the same axis.
A conscious patient takes fifteen grams of glucose
and rechecks after fifteen minutes;
an unconscious patient receives intravenous dextrose or intramuscular glucagon,
the counter-regulatory hormone from alpha cells.
Diabetic ketoacidosis and the hyperosmolar hyperglycaemic state share impaired insulin action,
but differ in the relative contributions of ketogenesis, dehydration and hyperosmolality.