General Overview Of The Complications Of Diabetes Mellitus, Diabetic Ketoacidosis And Come
A General Overview
At present, the management of uncomplicated diabetes is very satisfactory, but complications develop in the diabetic with the passage of time. Though, the acute complications can be prevented or effectively treated, the chronic complications are not entirely preventable even with the best of metabolic control. But proper control of blood sugar throughout the day and night does reduce the rate and progress of these complications considerably.
- Metabolic complications: Diabetic ketoacidosis and coma, Nonketotic hyperosmolar coma and lactic acidosis.
- Infective episodes: systemic infections, pneumonia and bronchopneumonia, urinary tract infections, skin infections.
- Surgical complications: Boils, carbuncles, diabetic gangrene.
Long term complications:
- Cardiovascular system: Early onset of atheroma, ischemic heart disease, cerebrovascular disorders especially thrombosis, occlusion of major vessels leading to peripheral gangrene and ischemia.
- Nervous system: Peripheral neuropathy, mononeuritis multiplex, autonomic neuropathy, cerebrovascular occlusions, diabetic amyotrophy.
- Excretory system- Kidneys: Recurrent urinary tract infection, chronic pyelonephritis, papilitis necroticans, diabetic glomerulosclerosis, renal failure.
- Eyes: Cataract, retinopathy, iridocyclitis, glaucoma, changes in refraction during the initial phases of drug therapy (insulin presbyopia).
- Respiratory system: Pulmonary tuberculosis.
- Alimentary system: Stomatitis, xerostomia, dental sepsis, halitosis, loosening of teeth, gastric distension, paralytic ileus, nocturnal diarrhea, hepatic enlargement.
- Bones and Joints: Osteoporosis, neuropathic joints.
- Skin: Monilial infection of the genitalia, pruritis vulvae, necrobiosis lipoidica diabeticorum, trophic ulcers of the feet.
- Complications during pregnancy and delivery.
- Complications due to therapy: Hypoglycemia, drug toxicity.
Acute metabolic complications are the major short term complications of Diabetes mellitus. Diabetic ketoacidosis, lactic acidosis and hyperosmolar coma may present as medical emergencies.
Diabetic Ketoacidosis And Coma
Diabetic ketoacidosis (DKA) is caused by the gross derangement of carbohydrate and fat metabolism brought on by severe deficiency of insulin and this is characterized by hyperglycemia, presence of excess ketone bodies in blood and urine and metabolic acidosis. In the early stages, the ketosis may be mild and easily correctable, but later, it becomes clinically pronounced and resistant to therapy. Diabetic ketoacidosis is a common medical emergency encountered in the medical casualties of all major hospitals in the developing countries.
Pathogenesis: Insulin deficiency may be absolute or it may be a conditioned deficiency brought on by the precipitating factors. Severe insulin deficiency results in hyperglycemia. Hyperglycemia leads to hyperosmolarity or the plasma which causes a shift of intracellular fluid to the extracellular compartment with consequent cellular dehydration. Osmotic dieresis leads to loss of water and sodium from the extracellular compartment. Severe loss of water and electrolytes results in the shrinkage of extracellular fluid volume and hypotension. Reduction of renal blood flow impairs renal function.
In the presence of insulin deficiency, fat cells undergo lipolysis. This releases excess of fatty acids which reach the liver but they are only incompletely metabolized. Due to this, large amounts of ketone bodies, viz, acetoacetic acid, beta-hydroxyl-butyric acid, and acetone are formed.
Apart from insulin deficiency, other concomitant metabolic derangements also contribute to the severity of ketosis, Growth hormone and glucocorticoids which antagonize the action of insulin are produced in excess. These enhance gluconeogenesis, lipolysis and ketogenesis in the liver. All the ketone bodies are excreted in urine. Acetone being volatile, is present in the expired air and this imparts a fruity smell to the breath. Acidosis gives rise to peripheral vasodilation which aggravates hypotension and leads to shock. The plasma bicarbonate level is reduced progressively as ketosis worsens.
Another serious metabolic consequence is the abnormal shift of potassium. Potassium moves out of the cells into the extracellular compartment leading to hyperkalemia. Potassium is lost in urine, resulting in the net loss of potassium for the body even in the presence of hyperkalemia. When the metabolic abnormality gets corrected under treatment with insulin, fluids and electrolytes, the glucose and potassium re-enter the cells. This leads to severe hypokalemia which may be fatal, if undetected and treated promptly.
Serum magnesium concentration falls. Total body phosphorus is also lowered. The erythrocyte 2,3-diphosphoglycerate levels are also lowered and as a consequence, the oxygen dissociation curve is shifted to the left. This leads to tissue anoxia. Once ketosis develops, if left untreated, it proceeds to diabetic coma.
© 2014 Funom Theophilus Makama