What is a diabetic coma?
It is a medical emergency and an acute life-threatening event that occurs in people with Diabetes Mellitus.
What causes a diabetic coma to occur?
- diabetes that is undiagnosed
- failure to take insulin as prescribed
- treatment that is not adequate
What happens with a diabetic coma?
There is not adequate insulin to metabolize glucose so fats are used for energy. When these fats are broken down it causes ketone waste to build up causing metabolic acidosis. The body attempts to react to counteract the state of acidosis. What happens is that the alkali reserve is depleted causing water, potassium and sodium chloride to be lost. The respiratory rate increases, in a process called kussmaul breathing, as the body attempts to blow off excess carbon dioxide that will eventually cause hypoxia. Urinary excretion is also increased leading to dehydration.
What are the warning signs and symptoms of a diabetic coma?
- headache that is dull
- epigastric pain
- facial flushing
- lips are parched
- eyes sunken
- increased body temp to begin with then decreased
- drop in systolic blood pressure
- circulatory collapse
The treatment for a diabetic coma includes the immediate administration of short-acting insulin and replacing electrolytes and fluids to counteract the acidosis and dehydration.
There are five types of diabetic coma a person with diabetes must be aware of
1. Diabetic Ketoacidosis (DKA; Diabetic Coma)
Diabetic Ketoacidosis occurs when there is a severe increase in blood sugar associated with poorly controlled diabetes. As a result there is an increase in the metabolism of fat and protein for energy sources. When fats are metabolized this results in the production of fatty acids that are converted into ketone bodies. An increase in the number of circulating ketone bodies leads to acidosis. This occurs mainly with type 1 diabetics. The onset can be rapid or over several days. This can be caused from stress, surgery, infection, or lack of insulin control.
With DKA (diabetic ketoacidosis) there is severe hyperglycemia 300 to 1500 mg/dl. DKA is often caused due to infection, emotional stress, fever, increased food intake, pregnancy or inadequate insulin dose. Hyperkalemia (increased potassium), metabolic acidosis, weakness, thirst, urine ketones and sugar are increased, nausea, vomiting, diarrhea, fruity breath, kussmaul respirations, abdominal pain, level of consciousness decreases, confusion increasing to coma, skin will be warm dry and flushed. Kussmaul respirations are very deep respirations that occur as the body attempts to blow off carbon dioxide.
Heart rate will be increased. Urine output is increased. Due to the dehydration there will be an increased body temp, polyuria, polydispia, weight loss, dry skin, sunken eyes. Large amounts of ketones will be in urine and serum Ph will be below 7.25 (acidotic). Hematocrit will be high due to dehydration. BUN and creatinine will be elevated due to dehydration. DKA occurs in all age groups with primarily type 1 diabetes but can occur with severe distress with type 2 diabetics. If left untreated DKA leads to coma and death.
2. HHNC – Hyperosmolar Hyperglycemia Non Ketotic Coma
This is a condition where there is enough insulin produced to prevent the breakdown of fat but severe hyperglycemia occurs. HHNC can be caused by infection, diarrhea, vomiting, failure to comply with dietary and medication regimen, stress, prolonged exposure to drugs that induce hyperglycemia such as steroids or poor fluid intake. In the absence of the acidotic state there is a severe dehydration and electrolyte imbalance. With HHNC hyperglycemia ranges from 700 to 2000 mg/100dL. This is seen mostly with geriatric type 2 diabetics. Because the body is able to maintain a very low level of insulin production this keeps the fat from being broken down resulting in ketone bodies and acidosis.
What does happen is osmotic diuresis because of the hyperglycemia causing the patient to become dehydrated quickly. HHNC will present with skin that is warm and flushed, lethargy, decreased LOC ( Level of Consciousness), weakness, thirst, increased body temp due dehydration, hematocrit will be high due to dehydration, increased heart rate, hypertension ( increased blood pressure), hyperglycemia, increased urine output, and glycosuria. BUN (Blood, Urea, Nitrogen) and creatinine levels will be increased. HHNC occurs often in elderly people that are undiagnosed type 2 diabetics. Elderly are also at a greater risk for dehydration due to their altered thirst perception.
As the patient becomes acidotic potassium moves out of the cell leaving the cell depleted of potassium, serum potassium remains normal due to the excessive excretion. With the hyperglycemia/hyperosmolar state osmotic diuresis is the result causing the serum potassium to be excreted. With dehydration the serum potassium becomes concentrated and does not show the loss of cellular potassium. When the acidosis and osmolarity are corrected and insulin is given the potassium will shift back into the cells causing hypokalemia (decreased potassium) to occur.
3. Exogenously induced hypoglycemia (insulin coma)
This occurs when the blood glucose level falls below 60 mg/dl. This can be a side effect of insulin therapy or hypoglycemic medications taken by mouth. It can occur when a meal is skipped, diabetic patient takes too much insulin, vomits a meal, or is over exercising. The signs and symptoms that are seen are a result of the sympathetic nervous system being stimulated or due to the reduced supply of glucose to the brain. What will be felt by the patient is muscle weakness, diplopia, feeling faint, tingling and numbness of the fingers lips and tongue. What will we be able to see? Diaphoresis, shaking, increased heat rate, and confusion. The patient should be given glucose orally if alert. Glucagon may be given intravenously to stimulate glycogenolysis. Patient maybe given 50% dextrose via IV if necessary.
4. Endogenously induced Hypoglycemia (Reactive Hypoglycemia)
Blood glucose falls below 60 mg/dl. This is caused by an overproduction of insulin or an insulin-like substance. This maybe caused by a tumor with the ability to produce insulin, or an autoimmune disease. This can be brought on by the under production of glucose due the hormonal deficiency including ACTH, glucagon and catecholamine’s. This can be the result of liver disease or brought on by drugs such as alcohol, propranolol and salicylate’s.
Depending on the cause the patient may need surgery to remove the insulin producing tumor, diazoxide therapy to suppress insulin production or hormone replacement to correct deficiencies. Patient should discontinue drugs that cause hypoglycemia. If possible correction of liver disease will also mitigate this condition. Patients should eat a low carbohydrate diet with high protein and avoid simple sugars and fasting.
5. Reactive (functional) Hypoglycemia
Reactive Hypoglycemia is due to rapid gastric emptying and often occurs after gastric surgery. This rapid gastric emptying stimulates the production of excessive amounts of insulin resulting in a low blood sugar. The patient will feel anxious, irritable, weak, fatigued. You will be able to observe hypoglycemia, pallor, and diaphoresis. Rapidly absorbed sugars should be avoided. Frequent meals are helpful. Patients who experience reactive hypoglycemia should increase protein, complex carbohydrates and fiber due to their ability to slow gastric emptying and slow glucose absorption.
A diabetic coma is a life threatening condition that needs to be dealt with quickly. Knowing the signs and symptoms is the first step to preventing this deadly occurrence.