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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.

Diabetic hyperosmolal non-ketotic coma

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

 

©Charles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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