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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 unusable 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 pyuria, 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-antipathy) 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 keto acidosis, Hyperosmolar non-keto tic coma (prema), Hypoglycemia, and Cerebrovasculature accidents. In diabetic keto acidosis (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 uremia (high concentrations of urea and other urine excretion products in the blood). (Martin (2002) ) Ketones from ketosis, in particular beta hydroxy butyrate, 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, re hydrating the cells. But this causes a rise in plasma sodium levels, which if too rapid can cause the patient to remain confused or comatose d until these levels fall. This effect can also occur if iso molar or stronger saline is accidentally given. Diabetic keto acidosis only occurs in type 2 patients when under extreme stress. Hyperosmolar non-keto tic coma is a condition in which there is noticeable hyperglycemia but without detectable keto acidosis. 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 keto acidosis, 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 administration. This causes glucose to be stored in cells and so the patients cerebral cells are glucose starved, causing loss of consciousness and coma. Here hypoglycemia causes a distal axonopathy including both degenerative and regenerative events, but motor axons seem to be more vulnerable than sensory axons. (Mohseni (2001) ) Here a glucose injection or glucagon or adrenaline injection to stimulate glucose release into the blood would provide glucose to the cells.
The risk of severe hypoglycemia is increased in type 1 diabetic pregnancy if there is a history of severe hypoglycemia before gestation, longer duration of diabetes or a higher total daily insulin dose. (Evers et Al (2002) ) Cerebrovasculature accidents cause coma due to blocking blood vessels to the vein and starving part of the brain of nutrients and oxygen. This is more likely to occur in diabetic patients due to the increased risk of vasculature disease. (Mayne (2001) ) Diagnosis If the initial symptoms of the patient, before entering a diabetic coma, are as stated in the introduction, then the following laboratory tests can be used to confirm diagnosis. The American Diabetes Association recommends that to diagnose DM the fasting plasma glucose levels are used rather than the previous oral glucose tolerance test, with a diagnostic cut off of 126 mg / d L or 7. 0 mmol/L. (Emancipator (1999) ) Diabetic keto acidosis comprises symptoms of hyperglycemia, ketosis and acidosis. The following tests are done, with the stated results being reference ranges for DKA: Test type Test Normal reference range DKA reference range Blood Glucose 70 - 110 mg / d L > 250 mg / d L pH 7. 35 - 7. 45 < 7. 3 Serum HCO 3 24 mEq/L < 15 mmol/L Ketone > 1: 4 Potassium 3. 5 - 5. 0 mEq/L High / in reference (low in cells) Sodium 136 - 148 mEq/L Low Chloride 95 - 105 mEq/L Low Phosphate 1. 7 - 2. 6 mEq/L Low Anion gap ([Na K]-[Cl HCO 3 ]) High (13 mEq/L) (Tortora, Grabowski (2000) ) In hyperosmolar nonketotic coma, test done are: serum electrolytes, which show hypo or hyper -natraemia (blood sodium), hyperglycemia and low potassium. Renal function tests show increased BUN and creatinine activity.
Ketones are normal to mildly higher, and urine shows glucosuria and ketonuria. Also: Test Normal reference range DKA reference range Glucose 70 - 110 mg / d L > 800 mg / d L serum os molarity > 320 m Osm / d L Hypoglycemia will mainly show a drastically lowered glucose concentration. Cerebrovasculature accidents would show diabetic symptoms but not at critical levels, as it simply vasculature disease which has occurred due to the higher risk due to DM. Brain scans would show up any blockages in the brain vascular system, and treatment could be assessed accordingly. Treatment Diabetic keto acidosis should have the cause of the condition treated once discovered. The elevated blood glucose should be reduced by administering insulin, and fluids and electrolytes replaced to reduce further dehydration and coma caused by high sodium concentrations, as explained previously.
re hydrating should allow ketones to be expelled from the body in the urine. Hyperosmolar non-keto tic coma should be treated in the same way. Hypoglycemia can be treated with a glucose injection or glucagon or adrenaline injection to stimulate glucose release into the blood, to provide glucose to the cells. Cerebrovasculature accidents are likely to need some sort of surgery as they are not caused by glucose levels as are the other causes of diabetic coma. When insulin is used it should be realized that a low dose regimen has the advantage of not inducing severe hypoglycaemia or hypokalaemia, and that only short-acting insulin is used for correction of hyperglycemia.
Acid-base balances should be corrected with sodium bicarbonate only if acidosis starts to threaten the patients life. With all cases the patient should be monitored and assessed to discover the cause of the coma and plan to prevent further attacks, possibly by better self-control and monitoring of the disease. An electrocardiogram could be done as signs of acute myocardial infarction could be painless in patients with autonomic nephropathy. Conclusion Diabetic comas are caused by either a decrease or increase of glucose in the blood causing dehydration or starvation of cells, including those in the brain. The treatment of this must be done carefully so as not to cause further damage by increasing electrolyte concentrations within such fragile cells, but whilst re hydrating the cells and providing sufficient glucose. Therefore laboratory diagnosis is vital to determine the correct cause and therefore the correct course of treatment for the patient.
Without the laboratory tests available treatment may be a 50: 50 chance of whether the cause is glucose concentrations being too high or too low. Many causes of diabetic coma can be treated easily with hormones and fluids. References EMANCIPATOR K (1999) Laboratory diagnosis and Monitoring of Diabetes Mellitus, American Journal of Pathology, 112 (5) PP 665 - 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) Pp 554 - 559 Previous course notes, BIOM 2003 MARTIN ELIZABETH A (2002) Concise Medical Dictionary Sixth Edition, Oxford, Oxford University Press, Pp 148, 190 - 191, 374, 665 - 666, 717 MAYNE Philip D. (2001) Clinical Chemistry Sixth Edition, London, Arnold, Pp 209 - 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, Pp 576 - 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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Research essay sample on The Laboratory Diagnosis And Management Of Diabetic Coma
