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Department
of Podiatry - Vascular Assessment
Diabetes
Mellitus
Diabetes
Mellitus is a chronic disorder of carbohydrate, fat and protein metabolism
(Cotran, 1999). A defective or deficient insulin secretory response, which
translates into impaired carbohydrate (glucose) metabolism, is a characteristic
feature of diabetes mellitus, as is the resultant hyperglycemia –
about 3% of the world population suffer from diabetes mellitus, approximately
100 million people, making it one of the most common non-communicable
diseases (Cotran, 1999).
CLASSIFICATION: Diabetes mellitus commonly occurs in two forms,
Type 1 and Type 2. The two common variants share chronic hyperglycemia
as a common link, the two forms differing in patterns of inheritance,
insulin responses, and origins.
Type 1 Diabetes: previously known as Insulin Dependant Diabetes
Mellitus (IDDM) and juvenile onset, accounts for about 10% of all cases
of primary diabetes (Cotran, 1999). This form of diabetes usually develops
in childhood, manifesting itself and becoming severe at puberty. Due to
the destruction of beta-cell mass within the pancreas, the patient is
left with an near absolute lack of insulin. Without insulin they are at
risk of developing metabolic complications such acute ketoacidosis and
coma (Cotran, 1999).
Three interlocking mechanisms are thought to be responsible for the islet
cell destruction: genetic susceptibility, autoimmunity and environmental
insult.
Type 2 Diabetes: previously known as Non Insulin Dependant Diabetes
Mellitus (NIDDM), type 2 accounts for about 85 – 90% of all cases
of primary diabetes. Type 2 is more common in populations that enjoy a
more affluent, sedentary lifestyle, the condition may be present sub-clinically
for many years before its diagnosis, the condition most commonly diagnosed
in the 4th and 5th decades of life (Tollafeild, 1999). The two metabolic
factors that characterize type 2 are a derangement in beta-cell secretion
of insulin and a decreased response of peripheral tissues to respond to
insulin (insulin resistance) (Cotran, 1999).
While there have been many recent advances in our understanding of type
2, the exact pathogenesis remains elusive. It is believed that genetic
predisposition and environmental influences converge to cause hyperglycemia
– the is no evidence to support autoimmune involvement (Cotran, 1999).
While an understanding of the types, patterns of inheritance, insulin
responses and pathogenic mechanisms is important, it must be remembered
that the long standing complications in blood vessels, kidneys, eyes and
nerves are the same and are the major causes of morbidity and mortality
from diabetes.
COMPLICATIONS OF DIABETES: The complications of diabetes can be considered
under two categories: the acute and the chronic complications.
Acute Complications:
Hypoglycaemia: is described as a less than normal amount of glucose in
the blood, symptoms usually occurring when the blood glucose levels fall
below 3mmol/L (Payne, 2001). The symptoms are usually caused by administration
of too much insulin, excessive secretion of insulin by the islet cells
of the pancreas or dietary deficiency, missed meals and extremely vigorous
exercise. (Mosby, 1999). The condition may cause weakness, headache, hunger,
visual disturbances, ataxia, anxiety, and personality changes and if left
untreated, delirium, coma and death (Mosby, 1999). Treatment is aimed
at administration of glucose orally if the patient is conscious and intravenously
if the patient is unconscious.
It is important to remember that some of those with diabetes have few
warning symptoms of hypoglycaemia, especially if the diabetes has been
long standing, autonomic neuropathy is present or the patient is taking
beta-blockers – a condition known as hypoglycaemic unawareness (Payne,
2001).
Ketoacidosis: is a life threatening condition and has up to 10-15% mortality
(Payne, 2001). It is defined as acidosis accompanied by an accumulation
of ketones in the body, resulting from extensive breakdown of fats because
of faulty carbohydrate metabolism – insulin deficiency (Mosby, 1999).
It is characterized by a fruity odor of acetone on the breath, mental
confusion, dyspnea, nausea, vomiting, dehydration, weight loss and if
untreated coma and death. Emergency treatment includes the administration
of insulin and intravenous fluids and the evaluation and correction of
electrolyte imbalances (Mosby, 2001).
Chronic Complications: the morbidity associated with long-standing
diabetes results from a number of serious complications namely microangiopathy,
retinopathy, nephropathy and neuropathy. As those with diabetes are now
living longer, there is an ever-increasing incidence of these chronic
complications and as a result, podiatric involvement (Payne, 2001).
Microangiopathy: one of the most common morphologic features of diabetes
is diffuse thickening of the basement membrane, the thickening being most
evident in the capillaries of the skin, skeletal muscle, retina, renal
glomeruli and renal medulla (Kumar, 1999). Despite this increased thickness
of basement membranes, the capillaries are more permeable than normal
to plasma proteins. This microangiopathy underlies the development of
diabetic nephropathy and some forms of neuropathy (Cotran, 1999).
Nephropathy: is a common cause of end stage renal failure and is associated
with considerably higher levels of mortality, especially from cardiovascular
disease – it is the most common cause of premature death in those
with diabetes (Payne, 2001). Nephropathy is a manifestation of the microvascular
changes associated with diabetes, abnormal renal haemodynamics are identifiable
early in the course of diabetic nephropathy, in type 1’s the glomerular
filtration rate is raised at diagnosis (Payne, 2001).
Retinopathy: Visual impairment is one of the more feared complications
of long-standing diabetes, two basic physiological changes are apparent
in diabetic retinopathy. Increased capillary permeability and closure
of retinal capillaries leading to vascular leakage and retinal oedema,
accumulation of lipid seen as hard exudate in the retina and retinal ischaemia
(Payne, 2001). Diabetic retinopathy progresses from backround changes
of micro-aneurysms, small hemorrhages and scattered hard exudates to more
advanced lesions including cotton wool spots, focal venous dilations,
dark red blot hemorrhages and dilated, tortuous small vessels with the
final development of new vessel (Payne, 2001).
Neuropathy:
is a descriptive term meaning a demonstrable disorder, either clinically
evident or subclinical, that occurs in the setting of diabetes mellitus
without other causes for peripheral neuropathy. The neuropathic disorder
includes manifestations in the somatic and/or autonomic parts of the peripheral
nervous system (Consensus Statement: Diabetic Neuropathy, Diabetes Care
19, 1996). Diabetic neuropathy when established is characterized by loss
of nerve fibers due to axonal degeneration. The speed of conduction is
reduced and the function of the nerve impaired. The clinical picture of
diabetic neuropathy is one that is predominantly sensory and symmetrical.
It follows a stocking in glove distribution, first appearing in the most
distal apices of the limbs. The patient will complain of pain, which is
sharp, stabbing or burning, particurlarly on the plantar aspect of the
foot and anterior aspect of the legs (Payne, 2001). The skin may be tender
(hyperaesthesia) or numb (parasthesia) – the most useful early clinical
signs are decreased vibration sensation and absent ankle jerks.
Macrovascular: the development of atherosclerosis is accelerated in
diabetes mellitus, leading to increased morbidity and mortality as a result
of the associated complications of atherosclerosis (Bowker, 2001). Virtually
all of the large vessels are involved in this process, clinical manifestations
are apparent as a result of atherosclerotic narrowing and thrombosis of
coronary, cerebral and leg vasculature (Bowker, 2001). In type 1 diabetes,
the macrovascular complications start sometime after the onset of the
diabetes, but in type 2 diabetes, the clock starts ticking well before
the clinical onset of diabetes (Payne, 2001). Those in the pre diabetic
state are characterized with the presence of insulin resistance, which
is associated with coronary artery disease, hypertension and diabetes
(Payne, 2001). Those who are insulin resistant have a more atherogenic
lipid profile – small dense LDL lipoproteins, low HDL cholesterol
and elevated triglycerides (Payne, 2001).
Pathogenesis of Complications: Most of the available experimental
and clinical evidence suggests that the complications are a consequence
of the metabolic derangements, mainly hyperglycaemia ( see ‘United
Kingdom Prospective Diabetes Study’ and ‘Diabetes Control and
Complications Trial’) (Cotran, 1999). The two metabolic events that
appear to be involved in the genesis of these complications are 1) non-enzymatic
glycosylation and 2) intracellular hyperglycaemia with disturbances in
pylol pathways (Cotran, 1999).
THE
‘AT RISK’ FOOT:
As a result of the metabolic complications of hyperglycaemia as outlined
above, the extremities of those patients with diabetes are at an increased
risk of trauma resulting in tissue breakdown, ulceration, gangrene and
amputation. To compound the situation, once an injury has been sustained,
the time taken to heal the wound is prolonged and the likelihood of infection
dramatically increases. In light of this, the role of the podiatrist within
the multi-disciplinary diabetic management team is three-fold and encompasses
wound prevention, wound management and patient education.
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