The Diagnosis and Management of Diabetic Coma

Topics: Diabetes mellitus, Insulin, Blood sugar Pages: 7 (1680 words) Published: September 19, 2005
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))


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...

References: EMANCIPATOR K (1999) Laboratory diagnosis and Monitoring of Diabetes Mellitus, American Journal of Pathology, 112(5) PP665-674
EVERS IM, TER BRAAK EW, DE VALK HW, VAN DER SCHOOT B, JANSSEN N, VISSER GH (2002) Risk indicators Predictive For Severe Hypoglycemia During The First Trimester of Type 1 Diabetic Pregnancy, Diabetes Care, 25 (3) Pp554-559
Previous course notes, BIOM2003
MARTIN ELIZABETH A (2002) Concise Medical DictionarySixth Edition, Oxford, Oxford University Press, Pp148, 190-191, 374, 665-666, 717
MAYNE Philip D. (2001) Clinical Chemistry Sixth Edition, London, Arnold, Pp209-210
MOHSENI S (2001) Hypoglycemic Neuropathy, Acta Neuropathology, 102 (5) Pp 413-421
PITTELOUD N, PHILIPPE J (2000) Characteristics of Caucasian Type 2 Diabetic Patients During Ketoacidosis and Follow-up, Schweiz Med Wochenschr , 130, Pp576 - 582
TORTORA Gerard J, GRABOWSKI Sandra Reynolds (2000) Principles of Anatomy and Physiology Ninth Edition, New York, John Wiley & Sons Ltd., Pp 41, 964, 966, c-0, c-1
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