Cases reported "Diabetic Neuropathies"

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1/21. An unusual manifestation of diabetes mellitus.

    MEDICAL history: Type 2 diabetes mellitus for five years; unexplained 35-lb weight loss three years ago; Bell's palsy on right side many years ago. MEDICATIONS: glipizide, 10 mg/day. family history: Father died of leukemia at age 65; mother has kidney stones; no diabetes or neuromuscular disease. SOCIAL history: insurance salesman; heterosexual, promiscuous, uses condoms; smokes (25 pack years); does not drink. physical examination: Well-nourished, well developed, not in acute distress; had difficulty rising from a sitting position because of right lower extremity weakness. blood pressure, 154/74; pulse, 88; temperature, 36.6 degrees C; respiratory rate, 16. Head, eyes, ears, nose, and throat: normal. neck: normal. Heart: S4. Lungs: clear. abdomen: mildly obese. extremities: no cyanosis, clubbing, or edema; atrophy and weakness of right thigh and both calves; wide-based gait; able to walk on toes but not heels. Neurologic responses: cranial nerves intact; deep tendon reflexes, 1 symmetrically; plantar reflexes, flexor bilaterally. skin: macular rash in sun-exposed areas. LABORATORY FINDINGS: Hemoglobin, 13.2 gm/dL; mean corpuscular volume, 80 micron 3; white blood cell count, 7,200/mm3 (normal differential); platelet count, 137,000/mm3. serum: electrolytes, normal; blood urea nitrogen, 18 mg/dL; creatinine, 0.8 mg/dL; glucose, 308 mg/dL; total protein, albumin, liver enzymes, and creatine kinase, normal. urine: 1 glucose. Venereal disease test: nonreactive; hiv test: negative. DIFFERENTIAL diagnosis: dermatomyositis; heavy-metal poisoning; diabetic amyotrophy. HOSPITAL COURSE: The patient was given 50 mg/day of oral amitriptyline to alleviate the painful paresthesias and was switched to 20 U/day of subcutaneously injected neutral protamine Hagedorn (NPH) insulin to normalize the blood glucose level. Histologic studies of skin and muscle showed sun damage and neuropathic changes, respectively. There was no evidence of vasculitis. Screening for heavy-metal toxins produced negative results.
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2/21. Clinico-pathological features of postural hypotension in diabetic autonomic neuropathy.

    We report the clinico-pathological features and management of a 49-year-old male with a 30-year history of Type 1 diabetes mellitus who had nephropathy (proteinuria 1.81 g/24 h, creatinine 136 micromol/l), proliferative retinopathy and severe somatic and autonomic neuropathy. A sural nerve biopsy demonstrated marked myelinated fibre loss with unmyelinated fibre degeneration and regeneration combined with extensive endoneurial microangiopathy. The management of the patient's blood pressure problems (supine hypertension) and symptomatic postural hypotension is discussed.
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3/21. smoking--a renal risk factor.

    One of the most important tasks of clinical and experimental nephrology is to identify the risk factors of progression of renal failure. A major renal risk factor which has not been sufficiently acknowledged despite increasing evidence is cigarette smoking. Diabetologists were the first to recognize the adverse effects of smoking on the kidney: both in type 1 and in type 2 diabetes smoking (i) increases the risk of development of nephropathy and (ii) nearly doubles the rate of progression to end-stage renal failure. Until recently it was not known whether smoking also increases the risk to progress to end-stage renal failure in patients with primary renal disease. A retrospective multicenter European case-control study showed that smoking is an independent risk factor for end-stage renal failure in patients with inflammatory and noninflammatory renal disease, i.e. IgA glomerulonephritis and polycystic kidney disease. The pathogenesis of the smoking-related renal damage is largely unknown. The intermittent increase in blood pressure during smoking seems to play a major role in causing renal damage, but further potential pathomechanisms are presumably also operative. smoking as a renal risk factor is of great interest to diabetologists as well as nephrologists, but unfortunately so far this information has had little impact on patient management. The present article reviews the current knowledge about the renal risks of smoking and discusses the potential mechanisms of smoking-mediated renal injury.
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4/21. One pair must last a lifetime. Case studies of foot care in diabetes.

    Neuropathy is the second most important of the four major 'traffic light' warnings for future foot problems (vascular, neuropathy, structural, self care). Peripheral neuropathy is a significant clinical problem in 20% of patients with diabetes. Painful neuropathy can disrupt patients lives but simple effective interventions are available. Painless neuropathy is often not perceived to be a problem by the patient or their doctor but puts the foot at risk from trauma (physical, chemical and thermal). patients with neuropathy need systematic reassessment of self and professional diabetes care, and education about footwear and foot care. A podiatrist can be invaluable in prescribing appropriate footwear and orthotics to distribute foot pressure and in educating patients about self care. patients with the 'double whammy' of neuropathy and vascular disease are at extreme risk of limb threatening problems and should have a regular monitoring program by themselves (or their carers) and their professionals as well as an 'action plan' to detect and deal with problems early.
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5/21. diabetes mellitus and its chronic complications.

    diabetes mellitus is a major cause of morbidity and mortality, and it is a major risk factor for early onset of coronary heart disease. Complications of diabetes are retinopathy, nephropathy, and peripheral neuropathy. Currently, treatment involves diet modification, weight reduction, exercise, oral medications, and insulin. In recent years, important advances have been made into the pathogenesis of diabetes that affect the cardiovascular, renal, and nervous systems; vision; and the lower extremities, especially the feet. The progression of diabetic retinopathy and nephropathy can be slowed or prevented with tight glucose and blood pressure control. Neuropathy remains a major problem causing significant impairment. Ongoing clinical trials and testing of various medications to determine their effectiveness in treating the complications of diabetes have met with some success, but there still is much to learn about this disease.
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6/21. Intravitreal triamcinolone acetonide for the management of diabetic papillopathy.

    PURPOSE: To present a case of severe drop in vision in both eyes caused by diabetic papillopathy that was treated with an intravitreal injection of triamcinolone acetonide. DESIGN: Interventional case report. methods: A diabetic patient with bilateral diabetic papillopathy and drop in vision received sequential intravitreal triamcinolone acetonide injections to both eyes. RESULTS: Within 2 weeks of intravitreal injection, vision improved from counting fingers at 1 m to 20/50 OS, and from counting fingers at 4 m to 20/40 OD. This improvement was accompanied by resolution of disk swelling and macular edema. Vision remained stable in both eyes at 20/40 for 8 months of follow-up. No elevation of intraocular pressure beyond 21 mm Hg was noted at any time. CONCLUSION: Diabetic papillopathy with severe drop in vision can be treated with intravitreal triamcinolone acetonide injection.
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7/21. A case of syndrome of inappropriate secretion of antidiuretic hormone associated with diabetes mellitus.

    A 46-year-old man, presenting with headache, nausea, and lassitude, was diagnosed as having diabetes mellitus and hyponatremia, and admitted to Tohoku University Hospital. insulin treatment improved the hyperglycemia but aggravated hyponatremia, which was proved to be elicited by the inappropriate secretion of antidiuretic hormone (SIADH). An acute water load failed to suppress ADH release in the supine posture but slightly increased plasma atrial natriuretic peptide (ANP). On the other hand, plasma ADH markedly increased in response to an upright posture, accompanied by a fall in blood pressure and a rise in heart rate. After treatment with droxidopa "a sympathomimetic drug", ambulatory blood pressure gradually increased and hyponatremia disappeared. However, blood pressure and ADH responses to upright posture were not improved by treatment with the drug. Moreover, plasma ADH was still not sufficiently suppressed by acute water loading in the supine position, but plasma ANP markedly increased, thereby resulting in urinary dilution and natriuresis. These results suggest that exaggerated ADH release (SIADH) was brought about by the baroreceptor reflex stimulated by the postural hypotension, and also by the impaired osmoregulation associated with diabetic neuropathy, and that droxidopa improved cardiovascular function and increased ANP release with resultant urinary dilution and natriuresis in spite of slightly increased ADH release.
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8/21. Disabling postural hypotension complicating diabetic autonomic neuropathy.

    A 35-year-old Type 1 diabetic man with severe disabling postural hypotension was studied for physiological abnormalities, precipitating factors, and effect of current treatment. A 24-h blood pressure profile indicated a diurnal variation in systolic blood pressure with the lowest values recorded between 0100 and 0600 h, during which the patient often lost consciousness on standing (mean standing systolic pressure 78 mmHg at night vs 105 mmHg in the afternoon, p less than 0.001). food induced a profound fall in systolic pressure, both while supine and while standing erect. The systolic pressure fall during euglycaemia was 49 mmHg vs 3 mmHg during hypoglycaemia. plasma noradrenaline and adrenaline levels were low during euglycaemia, but increased during hypoglycaemia. Therapeutic manoeuvres aimed at increasing heart rate (by atrial tachypacing) and reducing the peripheral pooling of blood (vasoconstricting drugs and gravity suit), together with the somatostatin analogue octreotide, proved ineffective. These observations demonstrate the phenomenon of post-prandial exacerbation of postural hypotension in a Type 1 diabetic patient, and indicate that despite failure of conventional methods of treatment, hypoglycaemia increased plasma catecholamines and was effective in abolishing the blood pressure fall on standing.
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9/21. The neuropathic foot--a management scheme: a case report.

    The purpose of this case report is to present a management approach that was effective in the healing and long-term care of a neuropathic plantar ulcer in a patient with diabetes mellitus. The report demonstrates that a successful management program must go beyond the stage of healing and include patient education and techniques for reducing plantar pressures to prevent the recurrence of plantar ulcers.
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10/21. Biomechanical treatment approach to diabetic plantar ulcers. A case report.

    The purpose of this case report is to describe a physical therapy approach designed to reduce the mechanical pressure at the site of a diabetic plantar ulcer. The patient was a 69-year-old man with diabetes mellitus for 24 years, insensitive feet, and a right plantar ulcer at the first metatarsal head for 21 months. He had a fixed equinus and rear-foot varus deformity, which seemed to place increased pressure on his forefoot. The patient was treated with total contact casting and showed progressive healing until he refused additional casting. One week later, the ulcer was considerably larger. He consented to resume casting, and the ulcer was completely healed in 85 days from the initial treatment. We provided the patient with extra-depth shoes with rigid rocker-bottom soles and a polyethylene-lined ankle-foot orthosis. The ulcer remained healed at one-week and six-month follow-up visits. The primary cause of diabetic plantar ulcers is often excessive pressure on an insensitive foot, and physical therapists should utilize biomechanical principles to reduce these excessive plantar pressures.
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