There is no evidence that diabetic patients with good glycaemic control are more prone to infection than normal subjects. However, poorly controlled diabetes entails increased susceptibility to the following infections:
(a) Staphylococcal infections (boils, abscesses, carbuncles)
(b) Mucocutaneous candidiasis
2 Urinary tract
(a) Urinary tract infections (in women)
(c) Perinephric abscess
(a) Staphylococcal and pneumococcal pneumonia
(b) Gram-negative bacterial pneumonia
One reason why poor control lends to infection is that chemotaxis and phagocytosis by polymorphonuclear leucocytes is impaired at high blood glucose concentrations. Conversely, infections may lead to loss of glycaemic control, and are a common cause of ketoacidosis. Insulintreated patients need to increase their dose by up to 25% in the face of infection, and non-insulin-treated patients may need insulin cover while the infection lasts. Patients should be told never to omit their insulin dose, even if they are nauseated and unable to eat; instead they should test their blood glucose frequently and seek urgent medical advice.
Skin and joints
Joint contractures in the hands are a common consequence of childhood diabetes. The sign may be demonstrated by asking the patient to join the hands as if in prayer; the metacarpophalangeal and interphalangeal joints cannot be apposed. Thickened, waxy skin can be noted on the backs of the fingers. These features may be due to glycosylation of collagen and are not progressive. The condition is sometimes referred to as diabetic cheiroarthropathy.
Osteopenia in the extremities is also described III IDDM but rarely leads to clinical consequences.
Smooth control of diabetes minimizes the risk of infection and balances the catabolic response to anaesthesia and surgery. The procedure for insulin-treated patients is simple:
1 Long acting and/or intermediate insulin should be stopped the day before surgery with soluble insulin substituted.
2 Whenever possible, diabetic patients should be first on the morning theatre list.
3 An infusion of glucose, insulin and potassium is given during surgery. The insulin can be injected into the glucose solution or administered by syringe pump. A standard combination is 16 U of soluble insulin with 10 mmol KCl in 500 ml of 10% dextrose, infused at 100 rnl hour-I.
4 Postoperatively, the infusion is maintained until the patient is able to eat. Other fluids needed in the perioperative period must be given through a separate intravenous line and must not interrupt the glucose/insulin/potassium infusion. Glucose levels are checked every 2-4 hours and potassium levels are monitored. The amount of insulin and potassium in each infusion bag is adjusted either upwards or downwards according to the results of regular monitoring of the blood glucose and serum potassium concentrations. The same approach is used in the emergency situation, with the exception that a separate variable rate insulin infusion may be needed to bring blood glucose under control before surgery.
Non-insulin-treated patients should stop medication 2 days before the operation. Patients with mild hyperglycaemia (fasting blood glucose below 8 mmol litre””) can be treated as non-diabetic. Those with higher levels are treated with soluble insulin prior to surgery, and with glucose, insulin and potassium during and after the procedure, as for insulin-treated patients.
Pregnancy and diabetes
Modern management has transformed the outcome of pregnancy in women with diabetes. Thirty years ago one pregnancy in three ended with the death of the fetus or neonate. Today, the results in specialized centres approach those of non-diabetic pregnancy. This improvement is due to meticulous glycaemic control and careful medical and obstetric management. When the pregnancy is planned, optimal glycaemic control is sought prior to conception.
Glycaemic control in pregnancy
The patient should perform daily home blood glucose profiles; the renal threshold falls in pregnancy and urinetests are therefore of little or no value. Insulin requirements rise, and intensified insulin regimens may become necessary. The aim is to maintain blood glucose and Hb Ale or fructosamine levels within the normal range.
General management The patient is seen at intervals of 2 weeks or less at a clinic managed jointly by obstetrician and physician. Circumstances permitting, the aim should be outpatient management with a spontaneous vaginal delivery at term. Retinopathy and nephropathy may deteriorate during pregnancy. Expert fundoscopy and urine testing for protein should be undertaken at booking, 28 weeks and before delivery.
Obstetric problems associated with diabetes
Poorly controlled diabetes is associated with macrosomia, hydrarnnios, pre-eclampsia and intrauterine death. Ketoacidosis in pregnancy carries a 50% fetal mortality,but maternal hypoglycaemia is relatively well tolerated. Neonatal problems Maternal diabetes, especially when poorly controlled, is associated with fetal macrosomia. The infant of a diabetic mother is more susceptible to hyaline membrane disease than non-diabetic infants of similar maturity. In addition, neonatal hypoglycaemia may occur. The mechanism is as follows: maternal glucose crosses the placenta, but insulin does not; the fetal islets hypersecrete to combat maternal hyperglycaemia, and a rebound to hypoglycaemic levels occurs when the umbilical cord is severed. These complications are due to hyperglycaemia in the third trimester. Poor glycaemic control in the first trimester carries an increased risk of congenital malformations, particularly of the cardiovascular and central nervous systems.
This term refers to glucose intolerance that develops in the course of pregnancy and remits following delivery.The condition is typically asymptomatic and is demonstrated biochemically on the basis of random testing in each trimester and by oral glucose tolerance testing if the plasma glucose concentration is 7 mmol litre ” or more.
Since the renal threshold for glucose falls during normal pregnancy and glucose tolerance deteriorates, the condition may easily be misdiagnosed.
Treatment is with diet in the first instance, but most patients require insulin cover during the pregnancy. Insulin does not cross the placenta. Oral agents are avoided because of the potential risk to the fetus as they do cross the placenta.
Gestational diabetes has been associated with a higher frequency of obstetric problems, fetal macrosomia and neonatal hypoglycaemia. It is likely to recur in subsequent pregnancies. Gestational diabetes is often the harbinger of NIDDM in later life.
Not all diabetes presenting in pregnancy is gestational. True IDDM may develop, and swift diagnosis is essential to prevent the development of ketoacidosis. Hospital admission is required if the patient is symptomatic, or has ketonuria or a markedly elevated blood glucose level.
There is no precise definition for this term, which is used to describe patients with recurrent ketoacidosis and/or recurrent hypoglycaemic coma. Of these, the largest group is made up of those who experience recurrent severe hypoglycaemia.
Recurrent severe hypoglycaemia
This affects 1-3% of insulin-dependent patients. Most are adults who have had diabetes for more than 10 years. By this stage endogenous insulin secretion is negligible in the great majority of patients. Pancreatic a cells are still present in undiminished numbers, but the glucagon response to hypoglycaemia is virtually absent. Long-term patients are thus subject to fluctuating hyperinsulinaemia due to erratic absorption of insulin from injection sites, and lack a major component of the hormonal defence against hypoglycaemia. In this situation adrenaline secretion becomes vital, but this too may become impaired in the course of diabetes. Loss of adrenaline secretion has been attributed to autonomic neuropathy, but this is unlikely to be the sole cause; central adaptation to recurrent hypoglycaemia may also be a factor.
The following factors may also predispose to recurrent hypoglycaemia:
OVERTREATMENT WITH INSULIN. Frequent biochemical hypoglycaemia lowers the glucose level at which symptoms develop. Symptoms often reappear when overall glucose control is relaxed.
AN UNRECOGNIZED LOW RENAL THRESHOLD FOR GLUCOSE. Attempts to render the urine sugar-free will inevitably produce hypo glycaemia.
EXCESSIVE INSULIN DOSES. A common error is to increase the dose when a patient needs more frequent injections to overcome a problem of timing.
ENDOCRINE CAUSES. These include pituitary insufficiency, adrenal insufficiency and premenstrual insulin sensitivity.
ALIMENTARY CAUSES. These include exocrine pancreatic failure and diabetic gastroparesis.
RENAL FAILURE. The kidneys are important sites for the clearance of insulin which tends to accumulate if renal function is lost.
PATIENT CAUSES. Patients may be unintelligent, uncooperative or may manipulate their therapy.
This usually occurs in adolescents or young adults, and the most severe form is more common in girls. Although metabolic decompensation may develop very rapidly, it is often impossible to pin-point an underlying abnormality. Many theories exist concerning the causes of this condition, but all agree that it is heterogeneous. The following categories have been suggested:
IATROGENIC. Inappropriate insulin combinations may be a cause of swinging glycaemic control. For example, a once-daily regimen may cause hypo glycaemia during the afternoon or evening and pre-breakfast hyperglycaemia due to insulin deficiency.
INTERCURRENT ILLNES. Unsuspected infections, including urinary tract infections and tuberculosis, may be present. Thyrotoxicosis can also manifest as unstable glycaemic control.
PSYCHOSOCIAL CAUSES. These certainly form the largest category. It has been suggested that neuroendocrine mechanisms such as catecholamine secretion might
mediate the metabolic disturbance. Other patients undoubtedly manipulate their illness, whether consciously or unconsciously.
UNKNOWN AETIOLOGY. The most ‘brittle’ patients of all are usually female, aged 15-25 years and often overweight, and typically suffer from amenorrhoea. The insulin requirement is variable but is often high. Sophisticated ‘cheating’ has been detected in some of these patients, but this should never be assumed without convincing proof.