Cases reported "Respiratory Insufficiency"

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1/178. zidovudine-associated type B lactic acidosis and hepatic steatosis in an hiv-infected patient.

    A 34-year-old obese woman with human immunodeficiency virus (hiv) infection diagnosed a year earlier was seen because of nausea, vomiting, and intermittent diarrhea for 3 weeks. Her current medications included zidovudine. physical examination revealed tachypnea and tender hepatomegaly. Computed tomography of the abdomen showed hepatomegaly with fatty infiltration. liver enzymes were within normal range except for elevated lactate dehydrogenase (LDH). The serum bicarbonate value was low, with a lactate level three times normal. The tachypnea and dyspnea worsened as lactate concentrations rapidly increased to 15 times normal. Although her Po2 and cardiac index were initially adequate, the patient had acute respiratory failure. She died with multiorgan dysfunction, including hepatic failure, severe lactic acidemia, disseminated intravascular coagulation, and renal failure. autopsy revealed hepatomegaly and massive steatosis. physicians should consider lactic acidosis in patients taking zidovudine and having unexplained tachypnea, dyspnea, and low serum bicarbonate concentrations.
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2/178. Pulmonary manifestations of poems syndrome: case report and literature review.

    phrenic nerve paresis is an unusual complication of POEMS (polyneuropathy, organomegaly, endocrinopathy, M-protein spike and skin changes) syndrome. In this report, we describe a case of poems syndrome in which a 56-year-old woman presented with dyspnea and ventilatory failure due to bilateral phrenic nerve paralysis. To our knowledge, only one other case of phrenic neuropathy in poems syndrome has been reported.
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3/178. Syndrome of inappropriate secretion of antidiuretic hormone associated with amyotrophic lateral sclerosis in respiratory failure.

    A 65-year-old man who had muscle weakness and dysarthria was admitted for investigation of motor neuron disease. He had lost 12 kg of weight in 6 months. Neurological findings disclosed upper and lower motor neuron disturbances with normal sensory nerve function, and needle electromyography showed a neurogenic pattern. Laboratory findings on admission demonstrated dilutional hyponatraemia due to an excessive secretion of antidiuretic hormone (ADH). Based on these findings, the patient was diagnosed as having the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with amyotrophic lateral sclerosis (ALS). During the night of first hospital day, the patient complained of severe dyspnoea, and mechanical ventilation was commenced. Following the mechanical ventilation, plasma ADH levels and serum sodium concentration were normalized. We propose that respiratory failure secondary to the atrophy of respiratory muscle might be responsible for the development of SIADH.
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4/178. Proximal diabetic neuropathy presenting with respiratory weakness.

    A patient is described with proximal diabetic neuropathy presenting with respiratory weakness. A 50 year old man developed progressive shortness of breath over 2 months. He also had weakness of hip flexion. phrenic nerve responses were absent, and spontaneous activity was seen in the intercostal and lumbar paraspinal muscles with long duration neurogenic MUPs and reduced recruitment in the diaphragm. Without treatment, the patient began to improve with resolution of his proximal leg weakness and breathing difficulties. Proximal diabetic neuropathy is another cause of neuromuscular respiratory weakness.
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5/178. A case of serious organophosphate poisoning treated by percutaneus cardiopulmonary support.

    We report a case of respiratory arrest, refractory circulatory collapse, and severe hypothermia following ingestion of an organophosphate insecticide. In addition to conventional management, including mechanical ventilation, administration of vasopressors, enteral lavage, charcoal hemoperfusion and administration of antidotes, extracorporeal cardiopulmonary support in the form of percutaneous cardiopulmonary support was successfully employed. Percutaneous cardiopulmonary support may be used for severe but potentially reversible pulmonary or cardiovascular toxicity induced by organophosphates as well as complicated severe hypothermia.
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6/178. Respiratory failure as a complication of pharyngitis: Lemierre's syndrome.

    The emergence of drug-resistant organisms has promoted increased calls for judicious use of antibiotics in cases of pediatric pharyngitis. Although these recommendations are largely justified, the case of a 16-year-old girl with pharyngitis is reported to alert readers to an unusual complication, Lemierre's syndrome. This complication of pharyngitis and its relevance to changing practice habits are discussed.
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7/178. Deficiency of lamellar bodies in alveolar type II cells associated with fatal respiratory disease in a full-term infant.

    We report a case of a full-term female infant who presented with severe respiratory distress shortly after birth and died at 23 d of age with unremitting respiratory failure. Infectious and other known causes of respiratory disease in this clinical setting were excluded. Examination of a lung biopsy showed abnormal lung parenchyma with features reminiscent of desquamative interstitial pneumonitis. Ultrastructural studies revealed that alveolar type II cells lacked cytoplasmic lamellar bodies, while other organelles appeared normal. Histochemical and immunohistochemical investigations indicated normal alveolar type II cell marker expression including surfactant proteins (SP-A, SP-B, pro-SP-B, and pro-SP-C). Mutations in the coding sequences of the SP-B gene were excluded as a cause of disease. This case appears to be a novel congenital defect affecting the pulmonary surfactant system. The cellular abnormality may involve the assembly of cytoplasmic lamellar bodies in alveolar type II cells-the principal storage site of pulmonary surfactant.
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8/178. Acute respiratory failure associated with catastrophic antiphospholipid syndrome.

    We present a case of multiple organ dysfunction syndrome with acute respiratory failure due to alveolar haemorrhage associated with antiphospholipid antibodies in a 42-year-old woman with a medical history of antinuclear antibody-negative systemic lupus erythematosus and antiphospholipid syndrome. Severe respiratory failure, circulatory shock and acute renal failure necessitated artificial ventilation, inotropic and vasopressor therapy, and continuous venovenous haemofiltration. A tentative diagnosis of haemorrhagic lupus pneumonitis or pulmonary manifestation of antiphospholipid syndrome was made. Lupus anticoagulant, IgG anticardiolipin and anti-beta2-glycoprotein I antibodies were positive. High-dose glucocorticoid, anticoagulation with heparin, plasmapheresis and cyclophosphamide improved her clinical condition. Despite this, the patient died several days later of spontaneous intracranial haemorrhage. This case illustrates the uncommon manifestation of acute respiratory failure associated with antiphospholipid syndrome.
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9/178. Progressive infantile axonal polyneuropathy.

    polyneuropathies are relatively uncommon in early infancy and the majority of affected children are found to have hypomyelinating neuropathies. Axonal sensorimotor neuropathies have been described in childhood but the majority of affected children present at or after 6 months of age, have nonprogressive courses, and achieve the ability to walk, albeit late. Here we present three infants with infantile progressive axonal polyneuropathy from two families with nonconsanguineous parents. Each child presented shortly after the neonatal period and with rapid progression to quadriplegia. Involvement of the lower cranial nerves, phrenic nerves, or both was present in each child. electrophysiology was diagnostic in each child. While the diagnosis of spinal muscular atrophy was considered in each case, clinical presentation, biopsies, and genetic testing were inconsistent with this diagnosis. Recognition of this early form of progressive axonal neuropathy is important as respiratory compromise occurred early and the condition showed familial inheritance in two of our patients.
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keywords = nerve
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10/178. Respiratory weakness in neuralgic amyotrophy: report of two cases with phrenic nerve involvement.

    An isolated affection of the phrenic nerve is a rare feature in patients with neuralgic amyotrophy. We report 1 case each of bilateral and unilateral phrenic neuropathy. The first patient presented a sudden onset of severe respiratory failure without pain. The second patient developed intense pain in the neck and in the right shoulder followed by dyspnea on mild effort and orthopnea. Chest x-rays showed elevation of the diaphragm. Needle electromyography revealed denervation restricted to the diaphragm. The phrenic nerve conduction was within the normal range. The diagnosis of neuralgic amyotrophy may be particularly difficult when the palsy of the phrenic nerve appears without brachial plexus involvement or the typical shoulder pain of acute onset. In our patients, electrophysiological evaluation combined with radiographic studies, ventilatory parameters and biochemical analyses were helpful in establishing the diagnosis.
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