Diabetic Coma

Coma may be due to a variety of causes not directly related to diabetes.

Certain causes directly related to diabetes require differentiation:

(1) Hypoglycemic coma resulting from excessive doses of insulin or oral hypoglycemic agents.

(2) Hyperglycemic coma associated with either severe insulin deficiency (diabetic ketoacidosis) or mild to moderate insulin deficiency (hyperglycemic hyperosmolar state).

(3) Lactic acidosis is associated with diabetes, particularly in diabetics stricken with severe infections or with cardiovascular collapse.

Diabetic Ketoacidosis

Diabetic ketoacidosis may be the initial manifestation of type 1 diabetes or may result from increased insulin requirements in type 1 diabetes patients during infection, trauma, myocardial infarction, or surgery.

It is a life-threatening medical emergency with a mortality rate of just under 5% in individuals under 40 years of age, but with a more serious prognosis in the elderly, who have mortality rates over 20%.

Ketoacidosis may develop in patients with type 2 diabetes when severe stress such as sepsis or trauma is present.

Diabetic ketoacidosis is one of the more common serious complications of insulin pump therapy.

Clinical Findings

The appearance of diabetic ketoacidosis coma is usually preceded by a day or more of polyuria (excessive or an abnormally large production or passage of urine) and polydipsia (excessive thirst or excess drinking) associated with marked fatigue, nausea and vomiting, and, finally, mental stupor that can progress to coma.

Drowsiness is fairly common but frank coma only occurs in about 10% of patients.

On physical examination, evidence of dehydration in a stuporous (a serious mental state where people don’t respond to normal conversation, instead, they respond only to physical stimulation, such as pain).

A patient with rapid deep breathing and a “fruity” breath odor of acetone would strongly suggest the diagnosis of diabetic coma.

Hypotension with tachycardia indicates profound fluid and electrolyte depletion, and mild hypothermia is usually present.

Abdominal pain and even tenderness may be present in the absence of abdominal disease.

Conversely, cholecystitis or pancreatitis may occur with minimal symptoms and signs.

Laboratory Findings

Acidosis may be severe (pH ranging from 6.9 to 7.2 There can be hyperventilation. Fluid depletion is marked.

Patients with mild diabetic ketoacidosis are alert and have pH levels between 7.25 and 7.30.

Those with moderate ketoacidosis have pH levels between 7.0 and 7.24 and are either alert or a little drowsy.

Those with severe ketoacidosis are stuporous and have a pH of less than 7.0.

Those with mild ketoacidosis can be treated in the emergency department, but those with moderate or severe ketoacidosis require admission to the ICU.

Therapeutic goals are to restore plasma volume and tissue perfusion, reduce blood glucose and osmolality toward normal, correct acidosis, replenish electrolyte losses, and identify and treat precipitating factors.

Gastric intubation is recommended in the comatose patient to prevent vomiting and aspiration that may occur as a result of gastric atony (failure of the stomach to contract normally, causing a delay in the movement of food out of the stomach), a common complication of diabetic ketoacidosis.

An indwelling catheter may also be necessary.

In patients with preexisting cardiac or renal failure or those in severe cardiovascular collapse, a central venous pressure catheter should be inserted to evaluate the degree of hypovolemia and to monitor subsequent fluid administration.

A comprehensive flowsheet that includes vital signs, serial laboratory data, and therapeutic interventions (e.g., fluids, insulin) should be meticulously maintained by the clinician responsible for the patient’s care.

Plasma glucose should be recorded hourly and electrolytes and pH at least every 2–3 hours during the initial treatment period.

Bedside glucose meters should be used to titrate insulin therapy. The patient should not receive sedatives or opioids.

Fluid Replacement

In most patients, the fluid deficit is 4–5 L. Initially, 0.9% saline solution is the solution of choice to help reexpand the contracted vascular volume and should be started in the emergency department as soon as the diagnosis is established.

Failure to give enough volume replacement (at least 3–4 L in 8 hours) to restore normal perfusion is one of the most serious therapeutic shortcomings adversely influencing satisfactory recovery.

Insulin replacement

Immediately after initiation of fluid replacement, regular insulin should be given intravenously.

Replacement of insulin deficiency helps correct the acidosis by reducing the flux of fatty acids to the liver, reducing ketone production by the liver, and also improving the removal of ketones from the blood.

Insulin treatment reduces hyperosmolality by reducing hyperglycemia.

It accomplishes this by increasing the removal of glucose through peripheral utilization as well as by decreasing the production of glucose by the liver.

Potassium

Total body potassium loss from polyuria and vomiting may be high, serum potassium is usually normal to slightly elevated before the institution of treatment.

As the acidosis is corrected, potassium flows back into the cells, and hypokalemia can develop if potassium replacement is not instituted.

Sodium Bicarbonate

The use of sodium bicarbonate in the management of diabetic ketoacidosis is recommended for diabetic patients in ketoacidosis if the arterial blood pH is 7.0 or less, with careful monitoring to prevent overcorrection.

Phosphate

Phosphate replacement is seldom required in treating diabetic ketoacidosis.

Treatment of Associated Infection

Antibiotics are prescribed as indicated.

Cholecystitis and pyelonephritis may be particularly severe in these patients.

Prognosis

Low-dose insulin infusion and fluid and electrolyte replacement combined with careful monitoring of patients’ clinical and laboratory responses to therapy has dramatically reduced the mortality rates of diabetic ketoacidosis.

After recovery and stabilization, patients should be instructed on how to recognize the early symptoms and signs of ketoacidosis.

The patient should be instructed to contact the clinician if ketonuria persists, especially if there is vomiting and an inability to keep down fluids.

Recurrent episodes of severe ketoacidosis often indicate poor compliance with the insulin regimen, and these patients will require intensive counseling