The Laboratory Diagnosis and Management of Diabetic Coma

The Laboratory Diagnosis and management of Diabetic Coma

Diabetes is any disorder of the metabolism which causes excessive thirst and the production of large volumes of urine. A coma is a state of unrousable unconsciousness. (Martin (2002)) There are two types of diabetes:

Diabetes Insipidus (DI) is a rare metabolic disorder, the symptoms of which are the production of large quantities of dilute urine and an increased thirst. It is caused by a deficiency of the pituitary hormone Anti-diuretic hormone (ADH / vasopressin) which regulates water reabsorption in the kidneys. (Martin (2002))

Diabetes Mellitus (DM) has symptoms of polyuria, wasting and glycosuria (mellitus means 'sweet urine') as well as the following tests to give a laboratory diagnosis of DM:

Venous plasma glucose >11.1 mmol / L or

Fasting venous plasma glucose > 7.0 mmol / L or

Plasma venous glucose concentration > 11.1 mmol / L two hours after taking 75 g glucose in an oral glucose tolerance test (OGTT).

There are two types of DM; insulin dependent DM (IDDM or type 1) and non-insulin dependent DM (NIDDM or type 2)

Type 1 is caused by the destruction of pancreatic b cell destruction, which can be predicted by the detection of the presence of antibodies (Abs) to islet cells, (Pitteloud, Philippe (2000)) insulin and glutamic acid dehydrogenase (GAD) (a neurotransmitter) and a decrease in b cell insulin secretion. This destruction causes a decrease in insulin production, the hormone which stimulates glucose to be stored in the muscle and liver as glycogen.

Type 1 causes an abrupt onset of severe symptoms, including a tendency to ketosis and a dependence on exogenous insulin.

Type 2 is caused by a diet high in saturated fats, a lack of exercise and obesity. This is because the constantly high glucose levels cause insulin to be produced at constantly high levels, and so the body becomes desensitized to its effect as cells in target tissues posses fewer insulin receptors. Characteristics of NIDDM are that insulin is present, symptoms are moderate (tiredness and thirst), there is no tendency to ketosis and patients are not dependent on exogenous insulin. High blood glucose is controlled by diet, possibly with diabetic drugs.

Complications of DM are:

Cataract, as excessive blood glucose binds to lens proteins.

Retinopathy (micro-angiopathy) caused by hemorrhage, etc..

Neuropathy, both peripheral and CNS, affecting the furthest points of longest nerves first, e.g. diabetic foot.

Peripheral vascular disease, causing impotence and ulcerated foot.

Diabetic nephropathy, with albuminaemia, renal failure and cardiovascular disease, and

psychological aspects.

In DM ketosis is caused because of the use of fat as an alternate energy source to glucose, which leads to disturbances of acid-base balance, accumulation of ketones (ketosis) and leads to diabetic coma. (Martin (2002))

Body

There are four main causes of diabetic coma:

Diabetic ketoacidosis,

Hyperosmolar non-ketotic coma (precoma),

Hypoglycemia, and

Cerebrovasculature accidents.

In diabetic ketoacidosis (DKA) a lack of insulin causes too much glucose to be present in the blood (hyperglycemia), causing plasma hyperosmolarity and glycosuria. Glycosuria causes an increase in urine production, dehydrating the patient causing a reduction in glomerular filtration rate (GFR) (Mayne (2001)) and uraemia (high concentrations of urea and other urine excretion products in the blood). (Martin (2002)) Ketones from ketosis, in particular beta hydroxybutyrate, induce nausea and vomiting that consequently aggravate fluid and electrolyte loss already existing in DKA; this causes further water and electrolyte loss. This causes cellular dehydration and loss of water from cerebral cells, which is thought to be the cause of the confusion and coma which results.

Symptoms are extreme thirst, lethargy, frequent urination (due to high blood glucose levels), nausea, vomiting, abdominal pain, progressive drowsiness, deep, rapid breathing and a fruity or acetone smell on the breath may also be present.

This cause of diabetic coma is treated by the administration of insulin. Gluconeogenesis is inhibited, glucose enters the cells, and sodium-free water follows by osmosis, rehydrating the cells. But this causes a rise in plasma sodium levels, which if too rapid can cause the patient to remain confused or comatosed until these levels fall. This effect can also occur if isomolar or stronger saline is accidentally given.

Diabetic ketoacidosis only occurs in type 2 patients when under extreme stress.

Hyperosmolar non-ketotic coma is a condition in which there is noticeable hyperglycemia but without detectable ketoacidosis. Symptoms are decreased consciousness, extreme dehydration and extremely high glucose. The mechanism of this is less clear, but thought that the levels of insulin are high enough to suppress lipolysis, and so no ketones are produced; but insufficient to suppress gluconeogenesis or stimulate glucose uptake into cells, and so hyperglycemia occurs. Therefore dehydration and coma occur by the same mechanism as by ketoacidosis, and insulin can be used to treat the patient, with the same risk from high plasma sodium levels.

Hypoglycemia occurs when a patient accidentally administers too much insulin or sulphonylurea (Mayne (2001)) (a hypoglycemic drug for type 2 DM, which stimulate pancreatic b cells to produce insulin) (Martin (2002)) causing too much insulin to be present in the blood; does not eat 'normally' or takes excessive exercise after a usual insulin or hypoglycemic drug