::IMVA :: Internacional Medical Veritas Association ::
Diabetes is disabling, deadly and
on the rise and in certain places has reached fifty
percent of local populations.
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Diabetic Neuropathy
Diabetic
neuropathy, a complication of both type one and type two
diabetes, is probably the most common complication of the
disease.[i]Studies
suggest that up to 50% of people with diabetes are
affected to some degree. Diabetic neuropathy is a nerve
disorder caused by diabetes. The two main classifications
of neuropathy are peripheral neuropathy, affecting the
extremities, arms, legs, hands and feet, and autonomic
neuropathy, affecting the organ systems, mainly affecting
the nerves of the digestive, cardiovascular systems,
urinary tract and sexual organs.
Symptoms of
peripheral nerve damage (neuropathy) are basically
weakness, usually in the arms and hands or legs and feet,
often with pain burning, tingling, or other abnormal
sensations. Numbness or decreased sensation, difficulty
walking and difficulty using the arms and hands or legs
and feet are all common. Peripheral sensory neuropathy can
initiate physiologic events that lead to distal extremity
ulceration and eventual amputation.
Nerve damage caused
by diabetes can also lead to problems with internal organs
such as the digestive tract, heart, and sexual organs,
causing indigestion, diarrhea or constipation, dizziness,
bladder infections, and impotence.[ii]
Diabetic neuropathy is a major cause of impotence in
diabetic men.[iii]
Autonomic neuropathies are believed to be implicated in
“silent heart attacks” of diabetes, where the full
symptoms of myocardial infarction are not felt by the
person.
In some cases,
neuropathy can flare up suddenly, causing weakness and
weight loss. Neuropathy may cause both pain and
insensitivity to pain in the same person. Often, symptoms
are slight at first, and since most nerve damage occurs
over a period of years, mild cases may go unnoticed for a
long time. In some people, mainly those afflicted by focal
neuropathy, the onset of pain may be sudden and severe.
A major risk
factor of this condition is the
level and duration of elevated blood glucose.
Scientists do not
know ‘exactly’ what causes diabetic neuropathy, but
several factors are likely to contribute to the disorder.
High blood glucose, a condition associated with diabetes,
causes chemical changes in nerves. These changes impair
the nerve’s ability to transmit signals. High blood
glucose also damages blood vessels that carry oxygen and
nutrients to the nerves. Keeping blood sugar levels as
close to the normal range as possible slows the onset and
progression of nerve disease caused by diabetes.[iv]
An increase in oxidative stress also may result in
neuropathy. Hyperglycemia can increase intracellular
sorbitol and fructose levels within neuronal tissue, which
may lead to the production of harmful free radicals and an
alteration of neuronal function.
It is possible
to reduce amputation
rates by between 49% and 85%.[v]
Recently, researchers have
focused on the effects of excessive glucose metabolism on
the amount of nitric oxide in nerves. Nitric oxide dilates
blood vessels. In a person with diabetes, low levels of
nitric oxide may lead to constriction of blood vessels
supplying the nerve, contributing to nerve damage.
Scientists also know that high glucose levels affect many
metabolic pathways in the nerves.
While the
medical and the research industry is focused on the fact
that hyperglycemia is the primary cause of peripheral
neuropathy, little attention is paid to the effects of
hypoglycemia,[vi]
or low blood sugars. This seems to be a far too ignored
piece of the puzzle of diabetes, worsening as diabetics
are pushed to achieve lower and lower blood sugars, and
with faster acting synthetic insulin. Research shows us
that too rapid lowering of blood sugars from a
longstanding hyperglycemic state,[vii]and that episodes of sustained hypoglycemia can and do
cause neuropathy.[viii]
From 1993 to
1995, about 67,000 amputations were performed each
year among people with diabetes. In 2002, about 82,000
non-traumatic
lower-limb amputations were performed in people with
diabetes.[ix]
The direct cost of an amputation associated with diabetes
is estimated to be between US$30,000 and US$60,000. The
estimated cost for three years of subsequent care ranges
from US$43,000 to US$63,000 – mainly due to the increased
need for
home care and social services.
It has been
forced upon me that diabetic
gangrene is not heaven sent, but earth born.
E.P. Joslin,
1934
Early in the last
century, soon after the discovery of insulin, Joslin
made the important observation noted above: he stated that
it was not inevitable that a certain proportion of the
diabetic population would develop foot ulceration or
gangrene. He concluded that it was something to do with
the way that we as health care professionals look after
our patients, or the way that patients look after
themselves, which results in conditions collectively
referred to as ‘the diabetic foot.’[x]
The medical establishment likes to think that great steps
have been taken in diabetes management[xi]but in
the area of the diabetic foot little impact has been made
in the depressing statistics for rates of amputations and
foot ulcers. Foot ulcers develop in approximately 15
percent of patients with diabetes, and foot disorders are
a leading cause of hospitalization among such patients.
Eighty-five percent of lower-limb amputations in patients
with diabetes are preceded by foot ulceration, suggesting
that prevention and appropriate management of foot lesions
are of paramount importance.[xii]
Diabetic foot ulcer. Ulceration is caused by several
factors acting together, but particularly by neuropathy.
Every 30
seconds a leg is still lost because
of diabetes somewhere in the world.[xiii]
It is very painful to look at
these pictures and imagine ourselves or a loved one with
foot ulcers, gangrene, and eventual foot amputation. One
can get indignant knowing that just a little bit of
applied medical intelligence could avoid
much of this.
[i]
Mary L. Johnson, RN, CDE, International Diabetes
Center, Minneapolis, Minnesota, and colleagues[12]
evaluated 206 persons for the microvascular
complications of peripheral neuropathy, retinopathy,
and nephropathy. On average, subjects had diabetes for
approximately 10 years and demonstrated good glucose
control (hemoglobin A1C 7.3% ±1.4%). Forty-eight
percent of study subjects had microvascular
complications, even though they had generally good
glycemic control and a relatively short duration of
diabetes. Diabetic nephropathy was identified in 20%
of the study population; retinopathy was identified in
11%; and symptoms of diabetic peripheral neuropathy
were identified in 63%. Diagnosis with a 10-g
Semmes-Weinstein monofilament only identified 16% of
patients with neuropathy. However, over 30% of the
subjects exhibited sensory deficits after clinical
examination.
www.medscape.com/ viewarticle/508218
[ii]Additional
symptoms that may be associated with this disease:
Swallowing difficulty
Speech impairment
Loss of function or feeling in the muscles
Muscle contractions
Muscle atrophy
Uncoordinated movement
Dysfunctional movement
Joint pain
Hoarseness or changing voice
Fatigue
Facial paralysis
Eyelid drooping
Bowel or bladder dysfunction
Breathing difficulty
From the National Institutes of Health (NIH) National
Library of Medicine (NLM) MEDLINEplus Medical
Encyclopedia.
[iii] WHO, 2002;
http://www.who.int/mediacentre/factsheets/fs138/en/print.html
[iv]
A 10-year clinical study that involved 1,441
volunteers with insulin-dependent diabetes (IDDM) was
recently completed by the National Institute of
Diabetes and Digestive and Kidney Diseases. The study
proved that keeping blood sugar levels as close to the
normal range as possible slows the onset and
progression of nerve disease caused by diabetes. The
Diabetes
Control and Complications Trial (DCCT)
studied two groups of volunteers: those who followed a
standard diabetes management routine and those who
intensively managed their diabetes. Persons in the
intensive management group took multiple injections of
insulin daily or used an insulin pump and monitored
their blood glucose at least four times a day to try
to lower their blood glucose levels to the normal
range. After 5 years, tests of neurological function
showed that the risk of nerve damage was reduced by 60
percent in the intensively managed group. People in
the standard treatment group, whose average blood
glucose levels were higher, had higher rates of
neuropathy. Although the DCCT included only patients
with IDDM, researchers believe that people with
noninsulin-dependent diabetes would also benefit from
maintaining lower levels of blood glucose.
[v]
2005 Survey Results Fact Sheet; http://www.diabetesincontrol.com/modules.php?name=News&file=article&sid=3253
[vi]Episodes of
hypoglycemia will also cause the release of
counterregulatory hormones which act to elevate the
blood sugars for the following 24-48 hours, further
complicating the issue of “good control”. Even the ADA
states recognition of the fact that it is difficult to
maintain blood glucose levels within their
recommendations, for any appreciable length of time.
Yet target levels have been lowered over the past few
years to levels that may be causing more hypoglycemia
than ever before. Studies in children show a high
rate of hypoglycemia at night for sustained periods of
time. Unnoticed by caregivers. Hypoglycemia can occur
before the diagnosis of diabetes, and during treatment
with oral antihyperglycemic drugs or insulin
injections.
[vii]
Insulin induced neuropathy has been reported
previously in people with diabetes treated with
insulin, and subsequently reported in patients with
insulinomas. However, neuropathy caused by rapid
glycaemic control in patients with poorly controlled
diabetes with chronic hyperglycaemia is not a widely
recognised entity among clinicians worldwide. It is
expected that this phenomenon of paradoxical
complication of neuropathy in the face of drastic
decreases in glycosylated haemoglobin concentrations
will assume greater importance with clinicians
achieving glycaemic targets at a faster pace than
before. Under-recognised paradox of neuropathy from
rapid glycaemic control.
Postgrad Med J.
2005 Feb;81(952):103-7.Leow
MK,
Wyckoff J.
Department of Endocrinology, Division of Medicine, Tan
Tock Seng Hospital, Singapore.
mleowsj@massmed.org
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&
[viii]
The effect of sustained insulin-induced hypoglycemia
on peripheral nerve function and structure
was examined in rats. After a period of hypoglycemia (less than 2.5 mmol/L) of at least 72 h, axonal
degeneration and reduction of the maximal
amplitude of the evoked muscle action potential
occurred, the two abnormalities being
correlated negatively (r = -0.99, 2P =
0.00097). One of five rats developed paresis of both
hindlegs as well as nerve damage and
perikaryal alterations of lower motor neurons. Peripheral
neuropathy in rats induced by insulin treatment: P
Sidenius and J Jakobsen ; Diabetes, Vol 32, Issue 4
383-386, Copyright 1983 by American Diabetes
Asssociation.
http://diabetes.diabetesjournals.org/cgi/content/abstract/32/4/383
[ix]
http://diabetes.niddk.nih.gov/dm/pubs/statistics/index.htm#11
[x]
Joslin EP. The menace of diabetic gangrene. N Engl J
Med 1934; 211: 16–20
[xi]
Although the treatment of diabetes has become
increasingly sophisticated, with over a dozen
pharmacological agents available to lower
blood glucose, a multitude of ancillary supplies and
equipment available, and a clear
recognition by health care professionals
and patients that diabetes is a serious disease,
the normalization of blood glucose for any appreciable
period of time is seldom achieved . In
addition, in well-controlled so-called "intensively"
treated patients, serious complications still occur, and the economic and personal burden
of diabetes remains.
Furthermore, microvascular disease is already present
in many individuals with undiagnosed or newly
diagnosed type 2 diabetes .
http://care.diabetesjournals.org/cgi/content/full/diacare;27/suppl_1/s47
[xii]
Andrew J.M. Boulton. Professor of Medicine, University
of Manchester, and Department of Medicine, Manchester
Royal Infirmary, Manchester, UK
www.d4pro.com/idm/ site/leading_article5.htm
[xiii]The
Ten Commandments of the Diabetic Foot BMJ:
2005;331:1497 (24 December)
doi:10.1136/bmj.331.7431.1497
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