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Diabetic Coma: Causes, Precipitating Factors, Clinical Presentations And Diagnosis

Updated on February 18, 2014

What Leads To Diabetic Coma?


Clinical Manifestations

All diabetics are predisposed to ketoacidosis, especially those with IDDM. In a few cases, the diagnosis of diabetes may be made for the first time when the patient presents in coma.

Precipitating factors

  1. Withdrawal or reduction in insulin dosage.
  2. Infections
  3. Trauma or surgery
  4. Medical emergencies like acute myocardial infarction and cerebrovascular accidents
  5. Large carbohydrate intake
  6. Drugs which aggravate the diabetic state, e.g corticosteroids
  7. Pyschological stress

In the majority of cases, the condition is precipitated by sudden withdrawal of insulin in the presence of an offending factor.

Clinical Features

Since the metabolic derangement takes time to develop, the onset of ketosis is gradual over a few days, but in some young symptoms are those of uncontrolled diabetes such as extreme fatigue, polyuria, vomiting and insomnia. Drowsiness and altered behaviou should draw attention to the possibility of ketoacidosis. The clinical state steadily deteriorates. Some cases present with abdominal symptoms like severe pain and distention which may be mistaken for surgical emergencies.

The fully established case is characteristic. The patient is dehydrated, drowsy or deeply comatose. The respiration is deep and sighing, this condition is known as “Kussmaul’s respiration”. A fruity smell of acetone may be detectable in the breath. Eyeball tension is low and blood pressure is low. The limbs are flaccid and deep reflexes are sluggish. Plantar response is upgoing. The abdomen may be distended due to gastric dilatation or paralytic ileus which result from autonomic neuropathy. Initially, the pupils are normal, but they may dilate, when the coma becomes deep. In some cases, fundal examination may reveal lipemia retinalis (milky plasma in the retinal vessels).

Diagnosis Of Diabetic Coma



Any deterioration of the general condition, loss of control of the diabetic state, bizarre symptoms, fatigue, vomiting and altered behaviour occurring in a diabetic should be investigated for ketoacidosis.

The diagnosis should be established by urine examination and blood biochemistry. Urine shows sugar and acetone. Acetoacetic acid and acetone can be detected by Rothera’s test or Acetest tablets of Ketostix. The tests can be semi-quantified by noting the speed of development and depth of colour and also testing the urine in progressive dilutions. Acetone disappears on boiling and acetoacetic acid also decomposes on boiling. Plasma ketones can be detected by Kotestix or chemical methods. Acetoacetic acid can also be tested by the Gerhardt’s test (Ferric chloride test). Blood sugar is considerably elevated in most cases, but in some, the elevation may be only moderate. Serum triglycerides are elevated.

Clinical and biochemical data to assess the severity of diabetic ketoacidosis

Increasing polyuria, thirst, weakness, tiredness
Severe polyuria, polydipsia, over-breathing, smell of acetone in breath, weakness, somnolence, vomiting
Symptoms of moderate ketosis with drowsiness progressing to stupor and coma
Flushed face and skin, tachycardia, tachypnea, slight smell of acetone in breath
Kussmaul’s breathing, loss of skin turgor, soft eyeballs, small pulse volume, heavy adour of acetone in breath, drowsiness and weakness
Severe dehydration, hypotension, extreme tachycardia, air hunger, coma.
Above 2%
Above 2%
+++ in 1:4 dilution
+++ in 1:8 dilution
Positive in undiluted serum (3- 6 mmol/liter)
Positive 2- 3 fold dilution (6- 12 mmol/liter)
Positive in 1:4 dilution above (12 mmol/liter)
Above 18 mEq/liter
10- 18 mEq/liter
Below 10 mEq/liter
Often elevated
Usually elevated
7.1 or less
Appropriate water deficit
1 to 2 Liters
2 to 4 liters
5 to 8 Liters
Appropriate Sodium Deficit
Less than 100 mEq
100- 250 mEq
250- 480 mEq

Distinguishing Diabetic Comas From Others


Differential Diagnosis

The diagnosis is easily suspected if coma occurs in a known case of diabetes, but the previous history may not be forthcoming always. So also the diabetic may develop other disorders leading to coma, eg. Cerebrovascular accident. Diabetic coma has to be differentiated from hypoglycemic coma, cerebrovascular accidents, other causes of metabolic coma, head injuries, poisoning and intracranial infections like meningitis and encephalitis. In cerebrovascular accidents, the onset is rapid and localizing neurological signs are present. When a diabetic develops a cerebrovascular accident, diabetic ketosis may also co-exist. Another point to be remembered is that, in cerebral hemorrhage and subarachnoid hemorrhage, temporary glycosuria may develop even in nondiabetics, but this passes off when the acute stage is over. Moreover, this is not usually associated with ketonuria and acidosis. Other common causes of ketoacidosis are starvation and severe vomiting. In this glycosuria does not occur and blood glucose levels are low. Other causes of metabolic acidosis levels are low. Other cases of metabolic acidosis such as renal failure, lactic acidosis, poisoning (acids, salicylates) and circulatory shock have to be excluded.

Hyperosmolar nonketotic coma is rare in comparison to diabetic coma. The former is characterized by dehydration, hypotension and disturbances of higher functions, ending in coma. This is more frequent in subjects with NIDDM. In this condition, the blood glucose is very high and ketonuria and metabolic acidosis are absent.

© 2014 Funom Theophilus Makama


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