Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Malassezia furfur sepsis developed in a woman with hyperemesis gravidarum while she was receiving total parenteral nutrition supplemented with lipids. Fever, chills, dyspnea, pleuritic chest pain, and multiple bilateral pulmonary nodular infiltrates were the primary clinical manifestations. Lysis-centrifugation fungal blood cultures supplemented with olive oil grew M furfur. Treatment included removal of the central venous catheter line, discontinuation of the lipid emulsion, and antifungal chemotherapy. Malassezia furfur sepsis complicating total parenteral nutrition may be more common in adults than once suspected. A high index of suspicion is required to diagnose this infection, and the addition of olive oil to the fungal culture medium will provide the necessary growth factors to isolate this fungus.
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PMID:Systemic Malassezia furfur infection in an adult receiving total parenteral nutrition. 761 9

We present the case of a patient with acute onset of dyspnoea after a long-distance flight. Pulmonary embolism was suspected, but could be excluded by perfusion scintigraphy. The electrocardiogram and chest X-ray were compatible with acute myocardial infarction and pulmonary oedema, but the slightness of the elevation of pulmonary capillary wedge pressure allowed cardiogenic pulmonary oedema to be excluded. The clinical picture was then interpreted as pneumonia with sepsis and hypotension. The rapid and full clinical recovery within 48 h, together with the close temporal relationship of ingestion of hydrochlorothiazide and the onset of symptoms, allowed the diagnosis of drug-induced pulmonary oedema and anaphylactoid hypotension.
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PMID:Pulmonary oedema and hypotension induced by hydrochlorothiazide. 800 Apr 16

Since 1983 we have been involved in the diagnostic work-up and emergency treatment of a female patient now 48 years old who has a mitochondrial myopathy resembling Luft's disease. The syndrome was first described in 1959, and in more detail in 1962, by Luft and et al., who reported a picture of hypermetabolism with high temperature, extreme sweating, tachycardia, dyspnoea at rest, polydipsia, polyphagia and irritability but normal thyroid function. In 1971 and 1976 Haydar and Di Mauro presented a second case and proposed treatment with chloramphenicol. Our patient has the third case of the syndrome reported so far: her case was initially published in 1987. CASE REPORT. Since her 17th year of life the patient had suffered from episodes of fever, tachycardia and sweating. At the age of 32 these attacks worsened, leading to unconsciousness and apnoea. The patient then had to be intubated, ventilated and sometimes resuscitated. The diagnosis of MH susceptibility and Luft's disease was made on biochemical grounds after the first muscle biopsy in 1983. Therapy with chloramphenicol failed. Therapy with beta blockers, vitamin C and K or E, coenzyme Q10 and a high-caloric diet was started in 1985. The patient was registered with an emergency service, which flew her to our ICU whenever she had a severe crisis. For milder episodes she was supplied with an oxygen breathing mask at home. Myalgia increased with the episodes starting in 1988, and the patient needed dantrolene infusions and analgesics at home. To facilitate venepuncture a Port-A-Cath system was implanted in 1987, which had to be removed four times due to infection and sepsis. A muscle biopsy was taken in Rotterdam, which revealed differences in mitochondrial function from the biochemical findings recorded in 1983 and not in keeping with Luft's disease. Unfortunately, the patient was not able to undergo further metabolic investigations or therapeutic trials. ANAESTHESIA. The patient received three local and six general anaesthetics in our clinic. The muscle biopsies, two in 1983 and one in 1985, were performed under local infiltration with procaine and were uneventful. The general anaesthetics were carried out without MH trigger substances following pretreatment with dantrolene for the following surgical procedures: the repair of an extensive arterio-venous fistula between the brachiocephalicus trunk and the right jugular and subclavian vein, revision of the sternum cerclage, implantations and explanations of infectious Port-A-Cath systems. We used etomidate, propofol and fentanyl or alfentanil with nitrous oxide and oxygen for induction and maintenance of anaesthesia. Muscle relaxation was induced with vecuronium or atracurium. All cardiovascular, respiratory, metabolic and temperature measurements stayed in normal ranges. After the extensive vascular repair (av fistula) the patient had to be mechanically ventilated for some hours until normal body temperature was restored. At the end of all other periods of anaesthesia she was extubated in the operating theatre. In five cases the postoperative period was uneventful. Only once she developed a crisis with hyperthermia, tachycardia, sweating and dyspnoea. INTENSIVE CARE. From 1985 to 1992 the patient was treated in our ICU 21 times. On 11 occasions she was already intubated and being ventilated by the emergency service on arrival. Extubation was usually possible within 2-20 h. During the crisis, heart rate was about 160-190 per minute and temperature above 40 degrees C. Serum values of CK, glucose, BUN, electrolytes, lactate and thyroid hormones were always in the normal ranges. Blood gas controls showed a constant respiratory alkalosis, arterial pCO2 values decreasing to 20 mm Hg or less. In addition to mechanical ventilation, treatment consisted in dantrolene infusions and droperidol injections, supplemented from 1989 onward with piritramide injections because of the increased severity of myalgia. In 1991 we gave propofol by
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PMID:[Anesthesia and intensive therapy for a patient with mitochondrial myopathy]. 825 Feb 6

Between March 1982 and June 1992, 17 patients (age: 21-76 years) were diagnosed with pseudoaneurysm of the thoracic aorta (PTA). Four PTAs developed post-trauma while 13 developed after aortic or cardiac surgery. Unusual presentations included: dyspnea, hoarseness, dysphagia, massive hemoptysis (2 degrees to aortobronchial fistula), massive hematemesis (2 degrees to aorto-esophageal fistula), superior vena cava syndrome, paralyzed right hemidiaphragm, and herald bleeding from the sternotomy. The interval between initial operation and recognition of PTA varied from three months to eight years while the four posttraumatic PTAs presented 5 to 26 years postinjury. The sites of postoperative PTA were: the aortotomy (3), proximal vein graft anastomosis (4), aortic cannulation site (2), and distal anastomosis of ascending aortic graft replacement (4). Aortography was very sensitive, outlining the false aneurysm in 13/13. Five patients had transesophageal echo-cardiography with one false negative. Seven patients died (41%), three from postoperative PTAs from massive hemorrhage intraoperatively and four from sepsis and multiorgan failure following repair. We conclude that patients who have previously had aortic or cardiac surgery or a history of blunt chest trauma presenting with unusual cardiorespiratory symptoms should be aggressively evaluated for PTA. Due to the magnitude of the operative problems encountered, repair of PTA is associated with a significantly high rate of mortality.
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PMID:Pseudoaneurysms of the aorta after cardiac surgery or chest trauma. 825 35

Adult respiratory distress syndrome (ARDS) is a rare but important complication of blood transfusion because it has a mortality rate of 50-60%. ARDS is characterised by noncardiogenic pulmonary oedema and is often associated with major trauma and/or sepsis. Clinical features include dyspnoea, tachypnoea, chills and extensive crepitations. The pathogenesis has not been elucidated completely and a number of hypotheses have been proposed. Factors which have been implicated include neutrophil sequestration and complement activation, macrophages, metabolites of the arachidonic acid cascade and cytokines, all of which contribute to the amplification of the inflammatory process. In particular, leucoagglutinins have been implicated with blood transfusions. Treatment is generally supportive as specific therapeutic strategies remain largely unproven.
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PMID:Blood transfusion related adult respiratory distress syndrome. 844 6

A 29-year-old woman, with a slightly elevated temperature for 3 weeks, increasing dyspnoea at rest, markedly reduced general condition and in heart failure, was found to have a leucocytosis of 100,000/microliters, anaemia (haemoglobin 6.3 g/dl) and thrombocytopenia (41,000/microliters). There were 62% plasma cells in the blood smear. Immunoelectrophoresis of serum and urine revealed kappa-light chains and immunocytology demonstrated IgG-kappa. There was no radiological evidence of osteolysis, while ultrasound examination showed multiple abdominal lymphomas and marked hepatosplenomegaly. Bone marrow smear showed a 90% infiltration of plasma cells. High-dosage melphalan treatment (single intravenous injection of 140 mg/m2) resulted in complete remission after myelodepression over several weeks. Two extramedullary recurrences 5 and 12 months after the diagnosis had been made were successfully treated with high-dosage melphalan, but it was associated with severe and long-lasting myelodepression. Septicaemia with renal and hepatic failure developed and the patient died 6 weeks after the third course of high-dosage melphalan, 14 months after the diagnosis.
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PMID:[Acute plasma cell leukemia. Clinical course during high-dose melphalan therapy]. 846 34

Some conditions that predispose to ventilatory failure increase the work of breathing (chronic obstructive pulmonary disease [COPD], obesity, kyphoscoliosis), whereas others cause severe respiratory muscle weakness. Specific reasons for muscle weakness include critical illness (electrolyte imbalance, acidemia, shock, sepsis), chronic illness (poor nutrition, cachexia), and neuromuscular diseases. Inspiratory muscle weakness from mechanical disadvantage to the diaphragm is characteristic of asthma and COPD. The increased work of breathing combined with muscle weakness increases the pressure needed to inspire a breath and decreases maximal inspiratory pressure. When this pressure exceeds 0.4, dyspnea and inspiratory muscle fatigue ensue. One way to lower this pressure and avert fatigue is to lower the tidal volume. Ventilatory drive is high, not low, in ventilatory failure. Concomitant shortening of inspiration and breath duration cause the small tidal volume and increased respiratory rate. Gas exchange is compromised by ventilation/perfusion imbalance, and the ratio of dead space to tidal volume is also increased by rapid, shallow breathing. Reduction in tidal volume minimizes dyspnea, but the small tidal volume is inadequate for gas exchange. Acute treatment of respiratory muscle failure involves respiratory muscle rest through mechanical ventilation and removal of noxious influences (infection, metabolic disarray), whereas chronic treatment involves rebuilding the contractile apparatus by nutritional repletion and training.
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PMID:Respiratory muscles and ventilatory failure: 1993 perspective. 850 1

Topical congenital pulmonary vein stenosis is a uncommon defect, both isolated or associated to other cardiac abnormalities. Only the localization of the lesions seems to affect the survival, because 60% of survival cases has unilateral stenosis; the severity of associated cardiac lesions become the prognosis poor. We describe two cases: 1st case, a 43 days old boy presented with heart failure and convulsion and had a diagnosis of pulmonary hypertension, atrial septal defect and tricuspid regurgitation, without pulmonary abnormalities. He had recurrent pulmonary infections and a cerebral ischemia in the following months, and died at 15 months of age for sepsis. Autopsy revealed stenosis and atresia in all pulmonary veins, with venous and arterial hypertension. There was also aortic hypoplasia and aortic and tricuspid valves indifferentiation; 2nd case, a 7 days old girl had a diagnosis of aortic coarctation and atrial and ventricular septal defects. Surgical corrections, at 38 and 46 days old, firstly of the aortic coarctation and after for the septal defects, disclosed and relief a supra-valvar mitral stenosis, but she remained on heavy respiratory insufficiency. At 6 months old, she returned to the hospital with dyspnea and cianosis, heart failure and hemoptisis; a sepsis developed and she died. At autopsy, there were severe pulmonary vein stenosis on the left and in the superior right veins, with pulmonary hypertension and hemorrhage.
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PMID:[Pulmonary vein stenosis. Report of 2 cases and review of the literature]. 854 96

We evaluated the efficacy of noninvasive mechanical ventilation (NIMV) in alleviating distress and avoiding intubation in patients with de novo acute respiratory failure complicating primary medical disorders. Eleven consecutive patients with severe respiratory distress were entered. In all patients a decision to intubate on an urgent basis had been made, but NIMV could be initiated within minutes. The patients suffered from acute pulmonary edema (five), sepsis/ARDS (two), status asthmaticus (two), and severe pneumonia (two). Dyspnea score (max=10) was (+/- SD) 8.4 +.- 1.6, scale for accessory muscle use (max=5) was 4.2 +/- 0.7, and respiratory rate was 37.6 +/- 3.8 min -1. Pa CO2, pH, and base excess (BE) were 48 +/- 18 mm Hg, 7.27 +/- 0.13, and -5.5 +/- 7.4, respectively, with five patients showing severe metabolic acidosis (BE < - 10). NIMV was applied using proportional assist ventilation. There were three early failures. These included the two patients with sepsis/ARDS who did not tolerate the mask. One patient failed because Pa CO2 and pH deteriorated despite subjective improvement. The remaining eight patients demonstrated progressive improvement, and none required intubation. The duration of NIMV was 3 h to 2 d. We conclude that when NIMV is made available on a "few minutes" basis, selected patients with severe de novo respiratory distress/failure caused by reversible medical disorders, who would otherwise have been intubated, can be given substantial relief and be spared intubation.
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PMID:Noninvasive positive-pressure ventilation in acute respiratory distress without prior chronic respiratory failure. 863 May 38

A 69-year-old alcoholic man with pneumonia and sepsis due to Aeromonas hydrophila is presented. He died of suffocation by a copious amount of hemoptysis six hours after his first symptoms of abdominal pain, diarrhea and dyspnea. Aeromonas hydrophila was isolated from blood and bronchial secretion. A fulminant form of pneumonia could develop in patients with predisposing underlying conditions such as alcoholism with chronic hepatitis and diabetes mellitus. Aeromonas hydrophila pneumonia may be characterized by hemoptysis and rapid clinical deterioration with a high mortality rate.
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PMID:Fulminant pneumonia and sepsis due to Aeromonas hydrophila in an alcohol abuser. 879 58


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