Problems of management Medical Assignment Help

HYPOTENSION. This may lead to renal shutdown.
Plasma expanders (or whole blood) are therefore given if the systolic blood pressure is below 80 mmHg. A central venous pressure line is useful in this situation. A bladder catheter is inserted if no urine is produced within 2 hours, but routine catheterization is unnecessary.
COMA. The usual principles apply. It is essential to pass a nasogastric tube to prevent aspiration since gastric stasis is common and the rare, but fatal, complication of acute gastric dilatation may result.
CEREBRAL OEDEMA. This rare, but feared, complication has mostly been reported in children or young adults. Excessive rehydration and use of hypertonic fluids such as 8.4% bicarbonate may sometimes be responsible. The mortality is high.
HYPOTHERMIA. Severe hypothermia with a core temperature below 33°C may occur and may be overlooked unless a rectal temperature is taken with a lowreading thermometer.
LATE COMPLICATIONS. These include stasis pneumonia and deep-vein thrombosis, and occur especially in the comatose or elderly patient.
COMPLICATIONS OF THERAPY. These include hypoglycaemia and hypokalaemia. Overenthusiastic fluid replacement may precipitate pulmonary oedema in older patients. Hyperchloraemic acidosis may develop in the course of treatment since patients have lost a large variety of negatively charged electrolytes, which are replaced with chloride. The kidneys usually correct this spontaneously within a few days.

Diagnosis

Hyperglycaemia-measure blood glucose Ketonaemia-test plasma with KetostixlAcetest Acidosis-measure blood gases.

Investigations 

Blood glucose
Urea and electrolytes
Osmolality
Full blood count
Blood gases
Blood and urine culture
Chest X-ray
ECG

Subsequent management

Intravenous fluids and insulin are continued until the patient feels able to eat and keep food down. The drip is then taken down and a similar amount of insulin is given as three or four soluble subcutaneous doses per day until a maintenance regimen can be restarted. Sliding-scale regimens are often unnecessary and may even delay the establishment of stable blood glucose levels.
The treatment of diabetic ketoacidosis is incomplete without a careful enquiry into the causes of the episode and advice as to how to avoid its recurrence.

Non-ketotic hyperosmolar state

This condition, in which severe hyperglycaemia develops without significant ketosis, is the metabolic emergency characteristic of uncontrolled NIDDM. Patients present in middle or later life, often with previously undiagnosed diabetes. Common precipitating factors include consumption of glucose-rich fluids (e.g. Lucozade), concurrent medication such as thiazide diuretics or steroids, and intercurrent illness.
Non-ketotic coma and ketoacidosis represent two ends of a spectrum rather than two distinct disorders. The biochemical differences.May partly be explained as follows:
AGE. The extreme dehydration characteristic of nonketotic coma may be related to age. Old people experience thirst less acutely, and more readily become dehydrated. In addition, the mild renal impairment associated with age results in increased urinary losses of fluid and electrolytes.
THE DEGREE OF INSULIN DEFICIENCY is less severe in non-ketotic coma. Endogenous insulin levels are sufficient to inhibit hepatic ketogenesis, whereas glucose production is unrestrained.

Electrolyte changes in diabetic ketoacidosis and non-ketotic hyperosmolar state.

Electrolyte changes in diabetic
ketoacidosis and non-ketotic hyperosmolar state.

CLINICAL PRESENTATION

The characteristic clinical features are dehydration and stupor or coma. Impairment of consciousness is directly related to the degree of hyperosmolality. Evidence of underlying illness such as pneumonia or pyelonephritis may be present, and the hyperosmolar state may predispose to stroke, myocardial infarction or arterial insufficiency in the lower limbs.

INVESTIGATION AND TREATMENT

These are according to the guidelines for ketoacidosis with some exceptions. Many patients are extremely sensitive to insulin and the glucose concentration may plummet The resultant change in osmolality may cause cerebral damage. It is sometimes useful to infuse insulin at a rate of 3 U hour-I for the first 2-3 hours, increasing to 6 U hour-I if glucose is falling too slowly. Normal saline is the standard fluid for replacement. Avoid halfnormal saline (0.45%) except in exceptional circumstances, since rapid dilution of the blood may cause more cerebral damage than a few hours of exposure to hypernatraemia.

PROGNOSIS

The reported mortality is around 20-30%, mainly because of the advanced age of the patients and the frequency of intercurrent illness. Unlike ketoacidosis, nonketotic hyperglycaemia is not an absolute indication for subsequent insulin therapy, and survivors may do well on diet and oral agents.

Lactic acidosis

Lactic acidosis may occur in diabetic patients on biguanide therapy. Phenformin, the agent responsible in the great majority of reported cases, has now been withdrawn in the UK. The risk in patients taking metformin is extremely low provided that the therapeutic dose is not exceeded and the drug is withheld in patients with advanced hepatic or renal dysfunction.
Patients present with a severe metabolic acidosis, usually without significant hyperglycaemia or ketosis, and treatment is by rehydration and infusion of isotonic 1.26% bicarbonate. The mortality is in excess of 50%.

COMPLICATIONS OF DIABETES

When insulin was introduced it was assumed that it would provide complete and adequate replacement therapy, just as thyroxine does in hypothyroidism. Time proved that insulin-treated patients still have a considerably reduced life expectancy. Those diagnosed before the age of 20 years have only a 60-70% chance of living past the age of 45 years, although there are recent indications of improved survival. The excess deaths are mainly due to diabetic nephropathy, but there is also a considerable excess cardiovascular mortality. Heart diseaseperipheral vascular disease and stroke are the major causes of death in patients over the age of 50 years.

Macrovascular complications

Diabetes is a risk factor in the development of atherosclerosis. This risk is related to that of the background population. For example, Japanese diabetics are much less likely to develop atherosclerosis than patients in Europe but are much more likely to develop it than non-diabetic Japanese. The excess risk to diabetics compared with the general population increases as one moves down the body:

STROKE is twice as likely.
MYOCARDIAL INFARCTION is three to five times as likely and women with diabetes lose their prerneno pausal protection from coronary artery disease.
AMPUTA TION OF A FOOT for gangrene is 50 times as likely.
Diabetes is additive with other risk factors for large-vessel disease. In other words, the diabetic who smokes or is obese, hypertensive or hyperlipidaemic adds the risks conferred by these conditions to that of diabetes itself.

Duration of diabetes

Age

Systolic hypertension

Hyperinsulinaemia due to insulin resistance associated with obesity and syndrome X Hyperlipidaemia, particularly hypertriglyceridaemia Proteinuria (including microalbuminuria) Other factors are the same as for the general population.

Insulin resistance

Hyperinsulinaemia due to insulin resistance associated with obesity is sometimes known as ‘syndrome X. Confusingly the same term is used by cardiologists for a rare variant of angina. Syndrome X includes glucose intolerance, hypertension, central obesity and dyslipoproteinaemia (increased very low density lipoprotein and reduced high-density lipoprotein). It is found in patients with NIDDM and carries a high risk of coronary artery disease.

Microvascular complications

In contrast to macrovascular disease, which is prevalent in Western populations as a whole, microvascular disease is specific to diabetes. Small blood vessels throughout the body are affected but the disease process is of particular danger in three sites:
• Retina
• Renal glomerulus
• Nerve sheath
Diabetic retinopathy, nephropathy and neuropathy tend to manifest 10-20 years after diagnosis in young patients. They present earlier in older patients, probably because these have had unrecognized diabetes for months or even years prior to diagnosis.

Posted by: brianna

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