Abnormally high blood sugar (or hyperglycemia) can be a life-threatening condition and warrants prompt recognition treatment. For a person with diabetes, this can be caused by missed diabetes medication such as insulin or oral hypoglycemic tablets, intake of too much food or by illness and stress.

There are two types of hyperglycemic emergencies. Hyperosmolar hyperglycemic syndrome (known before as hyperosmolar nonketotic coma or HONKC) is associated with severe dehydration, and diabetic ketoacidosis (DKA) in which low insulin levels create an accumulation of ketone acids (by-products of fat breakdown making the blood acidic).

The signs and symptoms of these emergencies can overlap, and resemble stroke or intoxication from alcohol, drugs or chemicals. Hence, in a patient who is unconscious, determining the cause of the coma can be very difficult and would usually require intensive care unit admissions.

Hyperosmolar Hyperglycemic Syndrome (HHS)

This occurs more commonly in middle-aged or elderly type 2 diabetics, presenting with very high blood glucose but no excess production of ketones. This is responsible for one in 1,000 hospital admissions and manifests more severely in the elderly. It is characterized by weakness, drowsiness and confusion preceding the actual coma. The onset of this condition can be insidious, and the patient may experience polyuria (excessive urination), polydipsia (excessive thirst) and lassitude (weakness) for several days to weeks. Inability to have adequate fluid intake due to altered sensorium and too much fluid lost in the urine can lead to severe dehydration consequently triggering imbalance in electrolytes, glucose level and water. HHS can be precipitated by infection, heart attack, stroke or intake of medications such as steroids and phenytoin.

Very crucial in the management of HHS is fluid replacement. Adequate hydration can alleviate the hyperglycemia to manageable range and is a life-saving measure. Concomitant correction of electrolytes, such as sodium and potassium is also essential. Fluid administration should be individualized, for in elderly patients, overaggressive hydration might lead to fluid overload manifesting as congestion (fluid in the lungs) or cerebral edema (brain swelling). Insulin helps stabilize blood glucose levels in order to halt the vicious cycle of electrolyte and glucose disparity.

Diabetic Ketoacidosis (DKA)
This condition is characterized by severe insulin deficiency for which the body cannot utilize glucose as fuel, and turns to fat cells for energy to save the cells from starvation. Breakdown of fat cells lead to ketone formation creating chaos in the body’s healthy state. Studies have shown that two to eight percent of hospital admissions among diabetics are due to DKA. Unfortunately, many cases of DKA occur as recurrent episodes attributed to treatment failure. Deliberate insulin omission was cited as one of the common causes that spark off ketoacidosis. Before the advent of insulin use, all diabetic patients with DKA usually died, but during the last three decades, with intensive insulin therapy, mortality rate for DKA has dropped to two to 10 percent.

DKA often presents as the first symptom for type 1 diabetes commonly caused by increased insulin requirements during stressful situations such as severe or untreated infection. It can also present in type 2 diabetes but less commonly. DKA usually presents with polyuria, polydipsia associated with unusual fatigue, nausea, vomiting and epigastric discomfort. A fruity odor of the breath due to acetone is characteristic for DKA. Acidosis which is the hallmark of DKA stimulates the respiratory center in the brain and causes rapid and deep respiration (Kussmaul breathing). Other signs included are loss of skin turgor, dry mucous membranes, tachycardia (fast heart beat) and lowering of blood pressure.

Treatment of DKA requires fluid replacement, insulin administration and correction of electrolyte abnormality especially potassium which usually drops precipitously with intensive insulinization.

The precipitating cause such as infections should also be traced and treated accordingly.

The “Crises”

The basic underlying mechanism for both DKA and HHS is a reduction in the net production of circulating insulin coupled with a concomitant elevation of the counterregulatory or “stress” hormones (i.e., glucagon, cortisol, catecholamines and growth hormone). This seeming hormonal mix increases glucose production by the liver and prevents glucose utilization in the peripheral circulation.

Treatment in general for these diabetic emergencies include respiratory support, fluid replacement, insulin administration to correct hyperglycemia, replacement of electrolytes, correction of acidosis in DKA, prevention of complications and patient support and education.

Patient and family education is the cornerstone for preventing hyperglycemic emergencies. Many cases of DKA and HHS occur after incorrect reduction or omission of insulin treatment. Drug-to-drug interaction and mechanism of action of each oral hypoglycemic must be known to the patient. Home glucose monitoring also counts a lot in determining the pattern of glucose control at home in order to adjust medications. All diabetic patients and families need to learn “sick day management,” adjustments to the usual diabetic control regimen for illness. Among the sick day rules are more frequent glucose monitoring, high fluid intake and early consultation with the health care provider.

Hyperosmolar hyperglycemic syndrome and diabetic ketoacidosis may be life-threatening and can result in devastating complications but can be successfully treated recognized early and pro intervened. More so, primary prevention of these diabetic crises is possible with proper patient education, unconditional family support and vigilant primary care physicians.

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