Diabetic hyperosmolar coma
Diabetic
ketoacidosis
Causes
- 20% cases initial presentation
of DM
- failure to take insulin (Type I DM)
- infection
- sterile inflammation eg MI
- excessive physical activity
Clinical features
Symptoms
- when history available varies from a few weeks to a few days
- osmotic symptoms
- anorexia
- vomiting +/- diarrhoea. Vomiting particularly useful as a warning in known
diabetic
- abdo pain (uncommon): dull persistent discomfort often affecting whole abdomen
but usually centred on the umbilicus
Signs
3 cardinal signs:
- dehydration
- overbreathing
- ketones on breath
Others:
- confusion/coma
- +/- shock
- signs of DM and complications
- +/- signs of precipitating factor
Differential diagnosis
- hypoglycaemic coma
- hyperosmolar coma
- lactic acidosis
- CVA
Investigations
- hyperglycaemia
- metabolic acidosis. Initially high anion gap but as ketones excreted becomes
normal anion gap acidosis
- hyperkalaemia usual, but hypokalaemia possible
- features of dehydration
- glycosuria and ketonuria while urine flow adequate
- ECG
- CXR
- cultures
- FBC
Treatment
General
- CVP line
- NG tube - wide bore as contents may be viscous
- urinary catheter
- SC heparin unless clearly contra-indicated
Fluids
- NB patients with rapid onset of DKA are not necessarily severely dehydrated
unlike patients who have gone out of control slowly.
- urine output most useful indicator of hydration. If urine output is good
patient is not severely dehydrated.
- circulatory collapse should be treated with plasma expanders and blood not
crystalloids
- start replacement with 1L N/saline over 1 hour and then decrease to 100 ml/hr
but titrate against urine flow
- when plasma glucose has decreased to 10 mmol/l start giving IV glucose.
Hyperglycaemia is more rapidly corrected than acidosis
- if K+ <3.5 mmol/l start KCl infusion immediately. Do not give insulin until
K+ >3.5 mmol/l
- accompany all infusions of insulin with an infusion of K+ at ³ 2 mmol/hr.
Monitor K+ hourly then 2 hrly.
Acidosis
- use of bicarbonate controversial. No evidence that administration improves
outcome.
- pH < 7.0: 100 mmol bicarbonate and 13 mmol KCl over 20-40 min. Repeat
after 60-90 min if pH still <7.0
Insulin
- initially 10 U/hr. Titrate against glucose
- aim to lower plasma glucose by 5 mmol/hr. Excessively rapid correction of
hyperosmolality associated with the development of cerebral oedema
Miscellaneous
- no evidence that routine administration of phosphate of any benefit
- likewise magnesium only indicated if arrhythmias occur
Complications
Cerebral oedema
>95% of cases occur in patients < 20 yrs with 1/3 in those <5yrs
more common in newly diagnosed diabetics
subclinical brain swelling appears to be common during the treatment of DKA
and may be present even before IV rehydration is started
presentation varies: may be a gradual worsening of coma from admission or
more commonly a gradual improvement followed by a sudden deterioration with
LOC, fixed dilated pupils or respiratory arrest. Only 1/2 have a period of
neurological deterioration during which intervention may be effective before
respiratory arrest
most cases occur 4-12 h after start of treatment
aetiology is unknown. Possible factors include cerebral anoxia from reduced
blood volume and haemoconcentration, high initial glucose concentration,
excessive rates of IV fluid infusion, fall in plasma Na concentration and
tissue hypoxia due to rapid infusion of bicarbonate (left shift of Hb
dissociation curve). Animal studies suggest that insulin itself is required
for the development of cerebral oedema
management: exclude hypoglycaemia, 0.5 g/kg of mannitol over 5-10 mins, ICP
monitoring and hyperventilation (both improve outcome), CT.
Epidemiology
- 10/100 000/yr
- 6 times less common than DKA
- 30% previously undiagnosed diabetics
Clinical features
- more common in elderly
- onset insidious
- infection, intercurrent cardiovascular disease, steroids, diuretics and intake
of glucose rich fluids are precipitant causes
- dehydration
- +/- hyperventilation due to cerebral dehydration
- +/- focal neurological signs due to dehydration or thrombosis
Investigation
- marked hyperglycaemia. Often >50 mmol/L
- no detectable ketonuria or acidosis
- hypernatraemia (may be hypo-)
- uraemia
- +/- respiratory alkalosis
- increased osmolality
Differential diagnosis
- ketoacidosis
- hypoglycaemia
- CVA (NB may be concurrent)
- lactic acidosis
Treatment
- fluid replacement with isotonic saline
- insulin infusion
- K+ - less required than in ketocacidosis
- consider anti-coagulation
Further reading
Edge JA. Management of diabetic ketoacidosis in childhood. Br
J Hosp Med, 1996; 55:508-12
© Charles Gomersall December 1999
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