Rory Hafford searches the literature for some of the many ‘red flags’ for diabetes and examines the treatment options available for patients
Before the discovery of insulin, more than half of diabetes patients died as a result of ketoacidosis. Today, this figure is much less dramatic, coming in at around 2 per cent, provided, of course, the condition is managed properly.
Broadly speaking, in diabetic ketoacidosis, the body goes to its store of fat as opposed to the normal route of using carbohydrates for fuel. This, in turn, sets off a cascade of blood sugars because insulin is unavailable to transport sugar into cells for future use.
As the bubbling sea of blood sugar rises, alarm bells go off in the kidneys, resulting in a urine dump. There is a heavy price to pay for this development: urine output is increased markedly and dehydration begins to take hold.
Clinical features
It is a delicate balancing act; any form of stress can precipitate severe ketoacidosis in someone with even a mild form of diabetes. The signs are classic: intense thirst and polyuria will invariably be present. So too the twin terrors of constipation and cramp. In children, this can ramp up a notch to acute abdominal pain, with or without vomiting.
The level of consciousness has always been a factor in the differential diagnosis. However, this is a variable sign. A patient with dangerous ketosis and requiring urgent treatment ‘may actually walk into hospital’, according to Macleod et al (1). To add to the symptom picture, consider dry tongue, sighing respirations and the smell of acetone on the breath.
Treatment options
When it comes to managing the condition, speed is of the essence. You need to overcome ketosis, by means of insulin to permit glucose utilisation; shock, acidosis and water and electrolyte depletion, by means of appropriate intravenous fluids; infection, if present, by means of antibiotics.
Fluid replacement and insulin administration, intravenously, are the crucial first steps. Intravenous therapy is required since even when the patient is able to swallow, fluids given by mouth may be poorly absorbed. Cerebral oedema is an ever-present danger, lurking in the long grass if an excessive rate of fluids is administered.
Potassium
Potassium is typically added to arrest body depletion; but, again, caution is advised due to the fact that every patient in diabetic ketoacidosis is potassium depleted and nearly all will require intravenous potassium to prevent the development of dangerous hypokalaemia during the course of treatment.
Once blood glucose levels have fallen below 300mg/dl, glucose may be co-administered with ongoing insulin administration to avoid the development of hypoglycaemia. Patients with mild acidosis, with modest fluid and electrolyte loss and who can drink fluid and follow medical instructions, can be sent home after treatment.
Diabetes and infection
Infection tends to occur with greater frequency and severity in diabetic patients than in non-diabetic patients. This, in itself, perpetuates a vicious cycle in which infection results in uncontrolled hyperglycaemia which, in turn, causes further aggravation of infections. According to Dr Bharat Trivedi, (2) there is a typical association of infection with diabetes, as sugar is a good medium for rapid and abundant growth of organisms and, at the same time, infection itself disturbs the blood sugar levels and may precipitate ketoacidosis.
There are a number of reasons why people with diabetes are more prone to infection; so much so that the World Health Organization has included diabetes in its classification of secondary immunodeficiency diseases. This could be due to, or determined by, alterations involving polymorphonuclear granulocytes and/or lymphocytic subset activity, according to Dr Trivedi’s research.
Polymorphonuclear granulocytes represent the host’s first defence barrier against bacterial agents. Alteration in chemotaxis, phagocytosis, immunoglobulin production and complementary functions do occur in diabetic patients.
Diabetic patients appear to have skin infections more often than their non-diabetic counterparts. Sensory neuropathy, atherosclerotic vascular disease and hyperglycaemia all predispose diabetic patients to skin and soft-tissue infections.
Blood glucose levels >250mg/dl significantly increase a patient’s risk for soft-tissue infection, according to research by Dr John Deasy of the San Mateo General Hospital. The predominant organisms are Group A streptococcus and Staphylococcus aureus.
Great concern
Of great concern to the general public but especially to people with chronic diseases such as diabetes, Dr Deasy remarked, is the increase in community-associated methicillin-resistant S. aureus. A recent report, presented in the Royal College of Physicians in Dublin, found that Ireland is particularly affected by this scourge.
Dr Edmond Smyth, Consultant Microbiologist in Beaumont Hospital, said: “There is good evidence that the burden of MRSA infection in Ireland is greater than in most other European countries and while there are some positive indications that infection rates are declining, MRSA infection is still a major issue resulting in illness and, in some cases, death.”
According to Macleod et al, poor control of diabetes is associated with a lowered resistance to infection. Alternatively, latent diabetes may be unmasked by a severe infection such as a carbuncle or pneumonia. Glucose tolerance may return to normal, at least temporarily, when the infection is controlled by appropriate antimicrobial therapy.
l Pulmonary tuberculo-sis. If a diabetic shows unexplained weight loss, increase in insulin requirements, or symptoms of pulmonary disease, clinical and radiological examination of the lungs should be undertaken;
l Urinary tract infection. The presence of glucose in the urine provides a favourable medium for the growth of bacteria.
l Candidosis. In the majority, abolition of glycosuria brings rapid relief.
Diabetic neuropathies
About 60-70 per cent of people with diabetes have some form of neuropathy. Risk rises with age and duration. The highest rates, therefore, are among people who have been battling the disease for more than 25 years.
The nerve damage is likely due to a combination of factors:
l Metabolic factors, such as high blood glucose, duration, blood fat level complications;
l Neurovascular factors, leading to damaged blood vessels;
l Autoimmune factors leading to inflammation;
l Mechanical injury to the nerves;
l Genetics;
l Smoking.
The main symptoms can include: numbness and tingling; muscle atrophy; digestive problems; dizziness or fainting; urination problems; ED; general weakness.
With regard to treatment options, the first step is to attempt to normalise blood glucose levels. Monitoring, meal planning, lifestyle and exercises advice, insulin and/or other medication.
Medications used to treat diabetic nerve pain include: tricyclic antidepressants; anticonvulsants; and opioids.
References
Davidson’s Principles & Practice of Medicine. John Macleod, et al. Churchill Livingstone,
2 Dr Bharat Trivedi. Prof and Head of Department of Endocrinology. Municipal Medical College, Ahmedabad
About Greg Baxter
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