Cases reported "Diabetes Mellitus, Type 1"

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1/52. Use of computed tomography and plantar pressure measurement for management of neuropathic ulcers in patients with diabetes.

    BACKGROUND AND PURPOSE: Total contact casting is effective at healing neuropathic ulcers, but patients have a high rate (30%-57%) of ulcer recurrence when they resume walking without the cast. The purposes of this case report are to describe how data from plantar pressure measurement and spiral x-ray computed tomography (SXCT) were used to help manage a patient with recurrent plantar ulcers and to discuss potential future benefits of this technology. CASE DESCRIPTION: The patient was a 62-year-old man with type 1 diabetes mellitus (DM) of 34 years' duration, peripheral neuropathy, and a recurrent plantar ulcer. Although total contact casting or relieving weight bearing with crutches apparently allowed the ulcer to heal, the ulcer recurred 3 times in an 18-month period. Spiral x-ray computed tomography and simultaneous pressure measurement were conducted to better understand the mechanism of his ulceration. OUTCOMES: The patient had a severe bony deformity that coincided with the location of highest plantar pressures (886 kPa). The results of the SXCT and pressure measurement convinced the patient to wear his prescribed footwear always, even when getting up in the middle of the night. The ulcer healed in 6 weeks, and the patient resumed his work, which required standing and walking for 8 to 10 hours a day. DISCUSSION: Following intervention, the patient's recurrent ulcer healed and remained healed for several months. Future benefits of these methods may include the ability to define how structural changes of the foot relate to increased plantar pressures and to help design and fabricate optimal orthoses.
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2/52. Normal pressure hydrocephalus in diabetic patients with recurrent episodes of hypoglycemic coma.

    The pathophysiology of brain damage induced by severe hypoglycemia is still unknown. We experienced a case with type 1 diabetes and recurrent severe hypoglycemic coma who showed a central brain atrophy and an abnormal cerebrospinal fluid flow, suggesting normal pressure hydrocephalus. Following this case, the CSF flow was studied using 111In-DTPA cisternography in six consecutive diabetic patients admitted for repeated episodes of hypoglycemic coma. All the patients showed the central brain atrophy on computed tomography and four of them (67%) had the ventricular reflux, with delayed clearance of 111In-DTPA. Two patients with abnormal CSF flow showed cognitive dysfunction by WAIS or WAIS-R. In contrast, none of five randomly selected diabetic patients, without hypoglycemic coma showed abnormal CSF flow. Our results suggest the presence of normal pressure hydrocephalus in diabetic patients with recurrent hypoglycemic coma. It may associate with the cognitive dysfunction.
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3/52. Effects of a tendo-Achilles lengthening procedure on muscle function and gait characteristics in a patient with diabetes mellitus.

    STUDY DESIGN: Case report with repeated measures. OBJECTIVES: To describe the effects of a tendo-Achilles lengthening (TAL) and total contact casting (TCC) on wound healing, motion, plantar pressure, and function in a patient with diabetes mellitus, peripheral neuropathy, neuropathic ulcer, and limited dorsiflexion range of motion (DFROM). BACKGROUND: Limited DFROM has been associated with increased forefoot pressures and skin breakdown. A TAL was expected to increase DFROM and reduce forefoot pressures during walking, but the influence on muscle performance and function was unknown. methods AND MEASURES: The patient was a 42-year-old man with a 20-year history of type 1 diabetes (NIDDM) and a recurrent neuropathic plantar ulcer. Outcome measures were DFROM, isokinetic plantar flexor muscle peak torque, in-shoe and barefoot peak plantar pressure, physical performance test (PPT) score, and peak ankle and hip moments during walking obtained from an automated gait analysis. All tests were completed pre-TAL, 8 weeks post-TAL (after immobilization in a TCC), and 7 months post-TAL. RESULTS: The wound healed in 40 days. The TAL resulted in a sustained increase in DFROM (0 to 18 degrees). Plantar flexor peak torque was reduced by 21% 8 weeks after the TAL compared with the torque before surgery but recovered fully at 7 months. Seven months following TAL, in-shoe forefoot peak plantar pressure was reduced by 55%, barefoot pressure decreased by 14%, PPT score increased by 24%, peak ankle plantar flexor moment remained decreased by 30%, and the peak hip flexor moment increased by 41% during walking. CONCLUSION: For this patient, a TAL resulted in short-term deficits in peak plantar flexor torque, but a 7-month follow-up showed improvements in ankle DFROM, walking ability, and a decrease in forefoot in-shoe peak plantar pressure.
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4/52. 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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5/52. Prevention of intraocular pressure elevations during hemodialysis.

    intraocular pressure (IOP) may rise during hemodialysis sessions in predisposed patients because of a rapid drop in osmolality at the blood compartment. A patient with diabetes had painful ocular episodes during hemodialysis that were associated with an IOP increase. We modified the dialysis parameters to prevent a rapid decrease in osmolality by creating conductivity and ultrafiltration profiles and adding a colloid solution at the beginning of the procedure. After instituting these changes, the patient became asymptomatic and did not have variations in IOP during the dialysis sessions.
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6/52. review and case report of idiopathic lower extremity compartment syndrome and its treatment in diabetic patients.

    Diabetic muscle infarction is a rare complication of diabetes mellitus. However, idiopathic compartment syndrome in the diabetic patient is even a rarer disease, which has been reported only in three cases up to date. The disease seems to occur in patients affected by type 1 diabetes mellitus with a history of poorly controlled glucose levels. MRI aids in the diagnosis by delineating the edema of the muscle. However, definitive diagnosis is made using the Stryker needle unit. Treatment is accomplished by immediate two-incision fasciotomy. We present a case where a 34 yr-old female with a long standing history of poorly controlled Type 1 diabetes mellitus presented with a painful right lower extremity and was diagnosed with compartment syndrome. In our patient, a single incision fasciotomy to release the pressure was sufficient and might be considered as an alternative and less morbid procedure in the diabetic patient with already poorly healing tissues. We conclude that the muscle infarction in these patients is from diffuse microangiopathic disease leading to muscular infarction and fluid accumulation in the cells causing a decrease in the space in the compartment in question causing compartment syndrome.
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7/52. pulmonary edema associated with hyperbaric oxygen therapy.

    We report three cases of pulmonary edema associated with hyperbaric oxygen therapy, including one fatality. All three patients had cardiac disease and reduced left ventricular (LV) ejection fractions (EFs). Two patients had diabetes, and one patient had severe aortic stenosis. Hyperbaric oxygen therapy may contribute to pulmonary edema by increasing LV afterload, increasing LV filling pressures, increasing oxidative myocardial stress, decreasing LV compliance by oxygen radical-mediated reduction in nitric oxide, altering cardiac output between the right and left hearts, inducing bradycardia with concomitant LV dysfunction, increasing pulmonary capillary permeability, or by causing pulmonary oxygen toxicity. We advise caution in the use of hyperbaric oxygen therapy in patients with heart failure or in patients with reduced cardiac EFs.
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8/52. peroneal nerve palsy: a complication of umbilical artery catheterization in the full-term newborn of a mother with diabetes.

    Umbilical artery catheters are an essential aid in the treatment of newborn infants who have cardiopulmonary disease. However, it is well-known that umbilical artery catheterization is associated with complications. The most frequent visible problem in an umbilical line is blanching or cyanosis of part or all of a distal extremity or the buttock area resulting from either vasospasm or a thrombotic or embolic incidence. Ischemic necrosis of the gluteal region is a rare complication of umbilical artery catheterization. We report the case of a full-term infant of an insulin-dependent diabetic mother with poor blood glucose control who developed a left peroneal nerve palsy after ischemic necrosis of the gluteal region after umbilical artery catheterization. The infant was born weighing 5050 g. The mother of the infant had preexisting diabetes mellitus that was treated with insulin from the age of 14 years. The metabolic control of the mother had been unstable both before and during the pregnancy. The neonate developed respiratory distress syndrome soon after birth and was immediately transferred to the neonatal intensive care unit. Mechanical ventilation via endotracheal tube was quickly considered necessary after rapid pulmonary deterioration. Her blood glucose levels were 13 mg/dL. A 3.5-gauge umbilical catheter was inserted into the left umbilical artery for blood sampling without difficulty when the infant required 100% oxygen to maintain satisfactory arterial oxygen pressure. Femoral pulses and circulation in the lower limbs were normal immediately before and after catheterization. A radiograph, which was taken immediately, showed the tip of the catheter to be at a level between the fourth and fifth sacral vertebrae. The catheter was removed immediately. Circulation and femoral pulses were normal and no blanching of the skin was observed. Another catheter was repositioned and the tip was confirmed radiologically to be in the thoracic aorta between the sixth and seventh thoracic vertebrae. The catheter was continuously flushed with heparinized solution. Three days after umbilical arterial catheterization, bruising was observed over the left gluteal region. The catheter was immediately removed despite its correct position. Over the next few days, the bruised skin and underlying tissues became necrotic. The area affected was 3 x 4 cm in diameter, with central necrosis surrounded by a rim of dark, red skin, which, in turn, was sharply demarcated from normal skin by a narrow, pale zone. Surgical excision of the gluteal necrosis was performed, but a deep ulcer 3 cm in diameter was left. The gluteal ulcer required 1 month to heal completely with extensive scar tissue formation. Throughout this period, the infant showed active movements in all of her limbs. At 4 weeks of age deterioration of all movement below the left knee with a dropping foot was observed. Severe peroneal nerve palsy was confirmed through nerve conduction studies, and there was electromyographic evidence of degeneration of the muscles supplied by the peroneal branch of the sciatic nerve. A Doppler study, which was also conducted, revealed no vascular damage. Treatment with physiotherapy and night-splinting of the left ankle was instituted. Repeated examination and nerve conduction tests at 3 months showed slow improvement with the left peroneal nerve remaining nonexcitable. At the time of this writing, the infant is 6 months old, and muscular strength below the left knee is still weak and atrophic changes in the form of muscle-wasting are already present. The rest of her motor development is normal. In our case, gangrene of the buttocks and sciatic nerve palsy followed displacement of the tip of the catheter into the inferior gluteal artery, a main branch of the internal iliac artery supplying the gluteus maximus, the overlying skin, and the sciatic nerve. The gangrenous changes were probably caused by vascular occlusion resulting from catheter-induced vasospasm of the inferior gluteal artery. sciatic nerve palsy associated with umbilical artery catheterization has been postulated to be caused by vascular occlusion of the inferior gluteal artery. Infants of diabetic mothers may exhibit changes in coagulation factors and be at increased risk of thrombotic complications in utero and postnatally. In addition, maternal diabetes mellitus is associated with an increased incidence of congenital abnormalities, the incidence of which is 3 to 5 times higher than that among nondiabetic mothers. Although no particular or specific abnormalities have been associated with maternal disabilities, abnormalities of the cardiovascular system, including the development of umbilical vessels, frequently occur. This complication of umbilical artery catheterization has not been widely reported. We describe the first case that refers to gluteal gangrene and peroneal nerve palsy after umbilical artery catheterization of a newborn infant of a diabetic mother with poor blood glucose control. It should be noted that there were no contributing factors except that of the displacement of the catheter into the inferior gluteal artery. We speculate that the displacement of the tip of the catheter, with no difficulty in the present case, was associated with the maldevelopment of normal branching patterns of arteries after exposure of the fetus to hyperglycemia. In conclusion, umbilical artery catheterization is possibly associated with vascular occlusion, particularly in infants of diabetic mothers. Frequent inspection after the procedure has been performed is of the utmost importance especially in these neonates who often suffer from cardiopulmonary disease and require catheterization of their umbilical artery.
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9/52. Prehospital cardiac arrest in diabetic ketoacidemia: why brain swelling may lead to death before treatment.

    An adolescent is reported with type 1 diabetes mellitus and diabetic ketoacidemia (DKA) who died from brain herniation prior to treatment with intravenous fluids and intravenous insulin. The pathophysiology of raised intracranial pressure (ICP) and water intoxication is discussed. As DKA evolves, water and electrolyte losses are replaced by very hypotonic fluids taken orally, leading to a physiologic excess of free water that would cause brain swelling prior to treatment. central nervous system acidosis may interfere with normal compensatory mechanisms that help prevent small increases in ICP. The pathophysiology of pre-treatment brain swelling has important implications for rehydration with intravenous fluids and treatment with insulin. Prevention of DKA is paramount as well as complete postmortem evaluation of patients who die from this disease.
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10/52. 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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