Pathology
The pathophysiologic basis of neuropathy in diabetes appear to be two-fold;metabolic as described in section 5.0 invoking the effects of hyperglycemia via sorbitol and AGE etc., and secondly the effect of ischemia on peripheral nerves.
Diabetes MeUitusClinical Types of Neuropathy
1) Polyneuropathy
Predominantly sensory, or sensori-motor distal polyneuropathy is the most common type of neuropathy in diabetes. Here, the patient experiences paresthesias, numbness, feeling of heaviness, burning in the feet, made much worse at night. There may or may not be evidence of objective evidence of nerve involvement in terms of demonstrable loss of sensation, or loss of reflexes.The dreaded complications of this are foot ulcerations and Charcots joint. While foot ulcerations are common the Charcot joint, or neuropathic arthropathy is rarer. This occurs in the metatarso-phalangeal and metatarso-tarsal joints, and is due to impaired proprioception deep pain sensation and autonomic insensitivity.Recurrent trauma may cause pathologic fractures of the metatarsal bones. The joint appears swollen, and warm but is painless. It can be confused clinically with osteomyelitis. The X-ray picture shows extensive new bone formation and disorganization of the joint mimicking osteomyelitis.
2) Proximal motor neuropathy (diabetic amyotrophy)
This is a particularly painful neuropathy in which there is acute or subacute onset of severe thigh pain, which is worse at night. It usually affects elderly males, who lose weight, may become depressed, and report moderate to severe pain which may be more one side than on the other. There is objective weakness and wasting of ilio-psoas, quadriceps and often hamstring muscles. The knee jerk is usually lost. Sensory symptoms are usually absent or minimal.There may be doubt about the possibility of lumbar disc disease or neoplastic nerve compression causing the symptoms. Diabetic proximal neuropathy can be differentiated clinically from compressive disc disease by normal straight-leg raising, normal spine flexion, lack of back pain, prominent nocturnal symptoms,and absence of relief with bedrest. However, when there is doubt about the diagnosis imaging of the lumbar spine (MRI) may be needed.The patient gets partial or complete relief from medications listed below; after 6 to 8 months the pain slowly recedes and drugs may be tapered off. A great deal of support and reassurance is needed to get patients through this very painful episode.
Diabetic Mononeuropathy
Paresis of single nerves anywhere in the body can occur suddenly, and are believed to be due to occlusion of the vasa nervorum supplying the nerve. They could also be involved mechanically as in entrapment the best example is carpal tunnel involvement. The clinical symptom would depend on whether it is a sensory, motor, or mixed nerve, and the anatomic function.Extra-ocular nerve involvement has been mentioned above, and is one of the commonest to be involved. The 7'h cranial nerve is also known to be commonly involved. Ischemia of the optic nerve head is also thought to be due to diabetes and is a cause of visual loss.
Intercostal and abdominal wall nerves are also rarely involved giving rise to severe chest and abdominal pain, often mimicking myocardial pain or intra-abdominal pathology, and results in many diagnostic searches. The pain is usually unilateral and can be distributed over more than one dermatomal segment. There may be weight loss, but after a few months symptoms of pain do resolve.Management of Diabetic Neuropathy Management of neuropathy whether painless or painful begins with good control of hyperglyceinia.
Pain control is best achieved with the use of tricyclic anti-depressants in low doses.Arnitryptiline 25 mgs at bedtime usually brings considerable relief in a few days, but in some cases doses upto 75 or 100 ings may be needed. Those patients with ischemic heart disease should not receive these drugs for fear of inducing arrhythmias.Carbamezepine in doses of lOOnlgs at bedtime stepped up to about 200 mgs twice a day is useful both as an add-on to those who do not find relief with anlitryptiline alone, or as a single agent in those in whom it is contraindicated.Gabapentin is another drug which is used as an anticonvulsant has been found to be useful in those patients who do not find sufficient relief with a combillation of the above medications.
Other Remedies
Many other agents are available in the market as useful for diabetic neuropathy, but there are little scientific evidence, and in clinical usage ase not effective in comparison to the above drugs. These agents are chromium compounds, GLA(gamma linoleic acid), and methyl cobalamine.
Autonoinic Neuropathy
The autonomic nerves are coillmonly iilvolved by diabetes and are an ilnporti.int cause of morbidity and death. A wide variety of signs and syinptoms are caused and me outlined below:
Cardiovascular System
The vagal input to the heart is coinmonly involved initially, so the unapposed syinpathetic input cruses resting tachycardia. Later complete autonornic deilervation results in a fixed heart rate. Sudden cardiac standstill especially during anesthesia and surgery is a possibility.Postural hypotensioil due to loss of syinpathetic neural input is common, A fall of 30 inin Hg systolic pressure in assuming the upright posture is diagnostic. It is a coin~non cause of dizziness blackouts and falls it is especially common and of gseat clinical significance in elderly diabetics in whom age- related postural hypotension exacerbates the problcm.Postural hypotension can be managed in mild cases with supportive bandages to the legs to prevent pooling in the legs; high salt diet, if there is no hypertension or heart failure; and sleeping with head end raised. In severe cases fludrocortisone can be used.
Urogenital Syndomc
Parasympathetic neives supply the urinary bladder muscle (detrusor). When the nerves are involved by diabetes, the bladder is unable to contract forcefully enough resulting in increasingly large residue post voiding. Ultimately the bladder may become totally non-contractile leading to retention. When the intravesical pressure exceeds the pressure of the internal sphincter, ovelllow incontinence occurs. This situation of retention and subsequent ovefflow can be confused with obstructive uropathy due to BPH (Benign Prostatic Hyperlrophy). A useful point to note that in diabetic cystopathy, the person has painless retention of urine as bladder sensation is lost. However to confuse the picture and individual patient may have both conditions contributing to the retention and incontinence.
The management of such patients needs specialist referral. The urologist will assess the urine flow rate, post-void residue, and possible cystourethrogram to assess which component is causative. Intermittent self catheterization is a technique which is now recognized to be a useful and safe alternative to continuous bladder drainage.
Erectile Dysfunction
This is a frequent and disturbing symptom in men and may be the earliest evidence of autonomic involvement. The loss of parasympathetic input results in inability of the vessels of the corpora cavernosa to dilate and cause pknile rigidity. Since this is a non-reversible condition, the treatments in the past included mechanical devices such as penile prosthesis and injection of papaverine into the penis. Currently, the most effective treatment is sildanefil. This agent activates nitric oxide which is involved in endothelial relaxation and causes dilatation of corpora caveinosa vessels. Sildanefil 25 to 50 mgs., an hour before coitus is quite effective. It is absolutely contraindicated in patients who are being treated with nitrates.
Gastrointestinal
The gast~ic motility is impaired. This results in vomiting, belching early satiety, and loss of appetite. Because of erratic gastric emptying the blood sugar control becomes difficult to regulate. Treatment starts with prokinetic agents such as doinperidome and mosapride, and metoclopramide (dopamine antagonists). Small frequent meals may be advised.
Diarrhoea
Diabetic diarrhoea manifests as profuse watery nocturnal diarrhoea which lasts for days at times alternating with periods of constipation. Fecal incontinence due to reduced anal sphincter tone, and reduced rectal sensation is a disabling symptom.Diarrhoea pathogenesis involves reduced gut motility and bacterial overgrowth and abnormal bile salt metabolism.
Treatment entails antibiotics (doxycycline) for reduction of bacterial overgrowth.Clonidine (alpha agonist) has been used because of evidence that reduced alpha two receptor mediated reduces fluid absorption and is a cause of diarrhoea.
Sweatilzg Abnormalities
Gustatory Sweating: This refers to abnormal excessive sweating after meals.Focal Loss of Sweating: This occurs mainly on the trunk in localized areas. It is also seen in diabetic feet.
Hypoglycemia Unawnreness: Hypoglycemia causes sympathetic nerve mediated symptoms such as sweating, hunger, tachycardia. These sy~nptoms are absent or blunted ion those with autonomic neuropathy.
The pathophysiologic basis of neuropathy in diabetes appear to be two-fold;metabolic as described in section 5.0 invoking the effects of hyperglycemia via sorbitol and AGE etc., and secondly the effect of ischemia on peripheral nerves.
Diabetes MeUitusClinical Types of Neuropathy
1) Polyneuropathy
Predominantly sensory, or sensori-motor distal polyneuropathy is the most common type of neuropathy in diabetes. Here, the patient experiences paresthesias, numbness, feeling of heaviness, burning in the feet, made much worse at night. There may or may not be evidence of objective evidence of nerve involvement in terms of demonstrable loss of sensation, or loss of reflexes.The dreaded complications of this are foot ulcerations and Charcots joint. While foot ulcerations are common the Charcot joint, or neuropathic arthropathy is rarer. This occurs in the metatarso-phalangeal and metatarso-tarsal joints, and is due to impaired proprioception deep pain sensation and autonomic insensitivity.Recurrent trauma may cause pathologic fractures of the metatarsal bones. The joint appears swollen, and warm but is painless. It can be confused clinically with osteomyelitis. The X-ray picture shows extensive new bone formation and disorganization of the joint mimicking osteomyelitis.
2) Proximal motor neuropathy (diabetic amyotrophy)
This is a particularly painful neuropathy in which there is acute or subacute onset of severe thigh pain, which is worse at night. It usually affects elderly males, who lose weight, may become depressed, and report moderate to severe pain which may be more one side than on the other. There is objective weakness and wasting of ilio-psoas, quadriceps and often hamstring muscles. The knee jerk is usually lost. Sensory symptoms are usually absent or minimal.There may be doubt about the possibility of lumbar disc disease or neoplastic nerve compression causing the symptoms. Diabetic proximal neuropathy can be differentiated clinically from compressive disc disease by normal straight-leg raising, normal spine flexion, lack of back pain, prominent nocturnal symptoms,and absence of relief with bedrest. However, when there is doubt about the diagnosis imaging of the lumbar spine (MRI) may be needed.The patient gets partial or complete relief from medications listed below; after 6 to 8 months the pain slowly recedes and drugs may be tapered off. A great deal of support and reassurance is needed to get patients through this very painful episode.
Diabetic Mononeuropathy
Paresis of single nerves anywhere in the body can occur suddenly, and are believed to be due to occlusion of the vasa nervorum supplying the nerve. They could also be involved mechanically as in entrapment the best example is carpal tunnel involvement. The clinical symptom would depend on whether it is a sensory, motor, or mixed nerve, and the anatomic function.Extra-ocular nerve involvement has been mentioned above, and is one of the commonest to be involved. The 7'h cranial nerve is also known to be commonly involved. Ischemia of the optic nerve head is also thought to be due to diabetes and is a cause of visual loss.
Intercostal and abdominal wall nerves are also rarely involved giving rise to severe chest and abdominal pain, often mimicking myocardial pain or intra-abdominal pathology, and results in many diagnostic searches. The pain is usually unilateral and can be distributed over more than one dermatomal segment. There may be weight loss, but after a few months symptoms of pain do resolve.Management of Diabetic Neuropathy Management of neuropathy whether painless or painful begins with good control of hyperglyceinia.
Pain control is best achieved with the use of tricyclic anti-depressants in low doses.Arnitryptiline 25 mgs at bedtime usually brings considerable relief in a few days, but in some cases doses upto 75 or 100 ings may be needed. Those patients with ischemic heart disease should not receive these drugs for fear of inducing arrhythmias.Carbamezepine in doses of lOOnlgs at bedtime stepped up to about 200 mgs twice a day is useful both as an add-on to those who do not find relief with anlitryptiline alone, or as a single agent in those in whom it is contraindicated.Gabapentin is another drug which is used as an anticonvulsant has been found to be useful in those patients who do not find sufficient relief with a combillation of the above medications.
Other Remedies
Many other agents are available in the market as useful for diabetic neuropathy, but there are little scientific evidence, and in clinical usage ase not effective in comparison to the above drugs. These agents are chromium compounds, GLA(gamma linoleic acid), and methyl cobalamine.
Autonoinic Neuropathy
The autonomic nerves are coillmonly iilvolved by diabetes and are an ilnporti.int cause of morbidity and death. A wide variety of signs and syinptoms are caused and me outlined below:
Cardiovascular System
The vagal input to the heart is coinmonly involved initially, so the unapposed syinpathetic input cruses resting tachycardia. Later complete autonornic deilervation results in a fixed heart rate. Sudden cardiac standstill especially during anesthesia and surgery is a possibility.Postural hypotensioil due to loss of syinpathetic neural input is common, A fall of 30 inin Hg systolic pressure in assuming the upright posture is diagnostic. It is a coin~non cause of dizziness blackouts and falls it is especially common and of gseat clinical significance in elderly diabetics in whom age- related postural hypotension exacerbates the problcm.Postural hypotension can be managed in mild cases with supportive bandages to the legs to prevent pooling in the legs; high salt diet, if there is no hypertension or heart failure; and sleeping with head end raised. In severe cases fludrocortisone can be used.
Urogenital Syndomc
Parasympathetic neives supply the urinary bladder muscle (detrusor). When the nerves are involved by diabetes, the bladder is unable to contract forcefully enough resulting in increasingly large residue post voiding. Ultimately the bladder may become totally non-contractile leading to retention. When the intravesical pressure exceeds the pressure of the internal sphincter, ovelllow incontinence occurs. This situation of retention and subsequent ovefflow can be confused with obstructive uropathy due to BPH (Benign Prostatic Hyperlrophy). A useful point to note that in diabetic cystopathy, the person has painless retention of urine as bladder sensation is lost. However to confuse the picture and individual patient may have both conditions contributing to the retention and incontinence.
The management of such patients needs specialist referral. The urologist will assess the urine flow rate, post-void residue, and possible cystourethrogram to assess which component is causative. Intermittent self catheterization is a technique which is now recognized to be a useful and safe alternative to continuous bladder drainage.
Erectile Dysfunction
This is a frequent and disturbing symptom in men and may be the earliest evidence of autonomic involvement. The loss of parasympathetic input results in inability of the vessels of the corpora cavernosa to dilate and cause pknile rigidity. Since this is a non-reversible condition, the treatments in the past included mechanical devices such as penile prosthesis and injection of papaverine into the penis. Currently, the most effective treatment is sildanefil. This agent activates nitric oxide which is involved in endothelial relaxation and causes dilatation of corpora caveinosa vessels. Sildanefil 25 to 50 mgs., an hour before coitus is quite effective. It is absolutely contraindicated in patients who are being treated with nitrates.
Gastrointestinal
The gast~ic motility is impaired. This results in vomiting, belching early satiety, and loss of appetite. Because of erratic gastric emptying the blood sugar control becomes difficult to regulate. Treatment starts with prokinetic agents such as doinperidome and mosapride, and metoclopramide (dopamine antagonists). Small frequent meals may be advised.
Diarrhoea
Diabetic diarrhoea manifests as profuse watery nocturnal diarrhoea which lasts for days at times alternating with periods of constipation. Fecal incontinence due to reduced anal sphincter tone, and reduced rectal sensation is a disabling symptom.Diarrhoea pathogenesis involves reduced gut motility and bacterial overgrowth and abnormal bile salt metabolism.
Treatment entails antibiotics (doxycycline) for reduction of bacterial overgrowth.Clonidine (alpha agonist) has been used because of evidence that reduced alpha two receptor mediated reduces fluid absorption and is a cause of diarrhoea.
Sweatilzg Abnormalities
Gustatory Sweating: This refers to abnormal excessive sweating after meals.Focal Loss of Sweating: This occurs mainly on the trunk in localized areas. It is also seen in diabetic feet.
Hypoglycemia Unawnreness: Hypoglycemia causes sympathetic nerve mediated symptoms such as sweating, hunger, tachycardia. These sy~nptoms are absent or blunted ion those with autonomic neuropathy.
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