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)

In this paper, the autopsy findings of a 78-year-old man mimicking primary lateral sclerosis (PLS) are reported. His clinical symptoms were slowly progressive spasticity, pseudobulbar palsy and character change. He died of sepsis 32 months after protracting the disease. The autopsy revealed severe atrophy of the frontal and temporal lobes. The histological findings were severe neuronal loss with gliosis in the precentral gyrus and left temporal lobe tip, loss of Betz cell, prominent demyelination throughout of the corticospinal tract, axonal swelling in the cerebral peduncule, severe degeneration of the amygdala, mild degeneration of the Ammon horn, normal substantia nigra, a few neuronal cells with central chromatolysis in the facial nerve nucleus and very mild neuronal cell loss in the spinal anterior horn. The anterior horn cell only occasionally demonstrated Bunina body by H & E and cystatin-C stainings, as well as, skein-like inclusion by ubiquitin staining. Thus, this is a case of uncommon amyotrophic lateral sclerosis (ALS) dominantly affecting the upper motor neuron including the motor cortex and temporal limbic system. In analysis of nine cases of putative primary lateral sclerosis in the literature, six cases showed loss of Betz cell in the precentral gyrus, and four cases very mild involvement of the lower motor neuron such as central chromatolysis and eosinophilic inclusion body. Degeneration of the limbic system was observed in two cases. We indicated a possible subgroup with concomitant involvement in the motor cortex and temporal lobe in motor neuron disease dominantly affecting the upper motor neuron.
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PMID:[An autopsied case of dominantly affecting upper motor neuron with atrophy of the frontal and temporal lobes--with special reference to primary lateral sclerosis]. 761 64

We presented a case of critical illness polyneuropathy after bacterial peritonitis. A 62-year-old male was received an emergency colectomy because of perforation of the sigmoid colon five days after the endoscopic polypectomy. He developed sepsis from peritonitis after operation in spite of the antibiotics therapy. On 15-th hospital days he developed muscle weakness and numbness of all limbs. He needed an artificial ventilator due to respiratory failure. Hematological and blood chemical findings showed a leukocytosis and metabolic acidosis with renal dysfunction because of sepsis. Serum anti-Campylobacter antibody was negative. Serial CSF examinations failed to show any abnormalities including albuminocytologic dissociation. Electrophysiological studies revealed a primary axonal degeneration, mainly in the motor, but also in the sensory nerve. Compound muscle and sensory action potentials were not elicited or markedly reduced without conduction velocity prolongation. Microscopic findings of the left sural nerve biopsy showed a primary axonal degeneration without evidence of inflammation. His prognosis was poor and three months later, he still required ventilatory assistance. Because of these clinical findings this patient was thought to have a critical illness polyneuropathy after excluding various etiologies of polyneuropathies. This case suggests that sepsis may be one of a cause of primary axonal polyneuropathy. The certain mechanism of this disease is still unknown. However cytokine, tumor necrotic factor(TNF) and/or Platelet activating factor(PAF) that secreted during sepsis may have an important role for the primary axonal degeneration.
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PMID:[A case of critical illness polyneuropathy in association with peritonitis after sigmoid colon perforation]. 766 19

The initial diagnoses of associated injuries in patients with traumatic brain injury (TBI) are often overlooked because of the priority given to life-sustaining measures. Pelvic and abdominal injuries comprise less than 5% each of the concurrent injuries associated with TBI and multiple trauma. This report describes a 32-year-old man who sustained a moderate TBI with facial, pelvic, and extremity fractures secondary to a fall. His hospital course was complicated by sepsis, acute renal failure, and retroperitoneal hemorrhage. Admitted to the rehabilitation service 6 weeks after the fall, the patient was found to have a previously undiagnosed profound quadriceps muscle weakness. A diagnosis of femoral neuropathy was confirmed by electrodiagnostic studies and was attributed to compression by pelvic hematomas. Rehabilitation management included use of a solid ankle cushion heel (SACH) wedge, a functional knee brace, a progressive ambulation program, neuromuscular stimulation, and patient and family education with an emphasis on safety. The patient progressed rapidly with his rehabilitation program, improving from moderate assistance in all skills to independence in 3 weeks. This case illustrates the importance of the physiatrist's role in the early detection of associated injuries in patients with multiple trauma and TBI; it also illustrates some of the rehabilitation techniques that may be employed to aid a patient with a femoral neuropathy to regain junctional ability.
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PMID:The rehabilitative management of the traumatic brain injury patient with associated femoral neuropathy. 774 23

A 36 years-old male with AIDS, presented with left hemiparesis revealing a right parietal tumour. Stereotactic biopsy demonstrated a malignant non-Hodgkin's lymphoma. His condition partially improved following radiotherapy and chemotherapy. Three months later he was re-admitted with progressive bilateral root pain and urinary incontinence resulting in paraplegia with sensory loss below T10. He died one month later from generalized sepsis. Neuropathology confirmed an immunoblastic B-cell malignant non-Hodgkin's lymphoma in the white matter of the right parietal lobe and revealed a centrospinal localisation of the lymphoma in the thoracic cord at T10. There was no visceral localisation of the tumour. Secondary spread to the spinal cord of malignant non Hodgkin's lymphomas, usually causes meningo-myelo-radiculitis. Intraspinal deposits of primary cerebral lymphomas are uncommon and have never been previously described in AIDS, to our knowledge. Their pathogenesis is unclear. In our case, neuropathological findings are consistent with diffusion of the primary tumour to leptomeninges and secondary infiltration of the spinal cord along the perivascular spaces.
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PMID:[Intramedullary localization of a primary cerebral lymphoma in AIDS]. 774 1

A 26-year-old man was admitted to our hospital with a 10-day history of sore throat, high fever, and right knee joint pain. On physical examination, the pharynx was considerably inflamed, and the right knee joint was swollen and extremely tender. Chest radiography showed multiple, bilateral nodules and masses with pleural effusions. Fusobacterium necorforum grew from samples of blood, pleural effusion, and pus taken from the knee joint. The patient was treated with intravenous clindamycin, ventilatory support, and continuous chest and knee joint drainage. His condition progressively improved and he was discharged on the 66th hospital day. A disease caused by an oropharyngeal infection with secondary suppurative thrombophlebitis of the internal jugular vein, and complicated by multiple metastatic infections is called postanginal septicemia, or Lemierre syndrome. Before the discovery of antibiotics, this disease usually was fatal. The widespread use of antibiotics for treat oropharyngeal infections may have caused a number of reported cases. Lemierre syndrome is an uncommon complication of oropharyngeal infection, and it may be fatal if diagnosis is delayed. Careful attention must be directed to patients with oropharyngeal infection who have signs and symptoms that suggest metastatic infection.
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PMID:[A case of Fusobacterium necroforum sepsis]. 781 62

Concentrations of amino acids in plasma and whole blood in response to 10 hours of food deprivation were determined in healthy 2-day-old foals (n = 8) and were compared with control values in foals of the same age (n = 8) allowed free access to suckle. In addition, response of concentrations of amino acids in plasma to 15 minutes of free-access suckling was determined at the end of the 10-hour period in both groups. Response of 13 amino acids in plasma of food-deprived foals was significantly (P < 0.05) different, compared with that in control foals. Concentrations of 3 amino acids (alanine, glycine, and phenylalanine) in plasma increased significantly (P < 0.05), whereas concentrations of 7 amino acids (asparagine, citrulline, histidine, ornithine, proline, tryptophan, and tyrosine) in plasma decreased significantly (P < 0.05) during food deprivation. Response of concentrations of 2 amino acids (glycine and histidine) in whole blood was significantly (P < 0.05) different from that in plasma of food-deprived vs control foals. Refeeding of food-deprived foals resulted in significantly (P < 0.05) different responses for concentrations of all but 2 amino acids (cystine and taurine) in plasma, compared with responses in controls. Changes in concentrations of amino acids in plasma and whole blood of foals in response to food deprivation are similar to those in foals with septicemia and in children with grade 1 or 2 kwashiorkor. The significantly different response of food-deprived foals to refeeding may be attributable to increased protein intake or altered physiologic state.
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PMID:Concentrations of amino acids in plasma and whole blood in response to food deprivation and refeeding in healthy two-day-old foals. 797 19

We report a 54-year-old man with progressive generalized muscle atrophy and ophthalmoparesis in the terminal stage. He was well until 44 years of age (1982) when he noted weakness in his right hand and muscle atrophy; in May of 1985, he noted weakness in his left hand and in both legs. His weakness had become progressively worse, and he became unable to walk in November of 1985. He noted dysarthria one month later, and dysphagia in March of 1986. His difficulty in swallowing had also become worse; he regurgitated foods into the trachea in September of that year, and he developed a low grade fever on the same day. He was admitted to our service on September 24, 1987. On physical examination, general findings were unremarkable, except for low grade fever (37.3 degrees C). On neurologic examination, he was alert and mentally sound. He had normal vision and visual fields; ocular movements were normal. He had moderate weakness in facial muscles, dysarthria, dysphagia, and atrophy in his tongue. He had marked generalized muscle atrophy with fasciculation. He was unable to stand or walk. His muscle strength was not more than 1/6 in any part. The lower extremities were spastic. Deep reflexes were exaggerated in both lower extremities but were normal in upper extremities. Sensation was intact. Laboratory examination was unremarkable, and so was the cranial CT scan. He was treated with nasogastric feeding. He was able to communicate smoothly using his eyes, but a restriction in the vertical gaze was noted in February of 1989. The range of ocular movement was better in the oculocephalic reflex compared with his spontaneous vertical eye movements. In April of 1990, his horizontal gaze also had become slow, and he was complicated by bronchial asthma. He was treated with 20 mg/day of prednisolone; after the institution of prednisolone, his horizontal eye movement showed much improvement. In the terminal stage, he was able to move his eyes only very slowly; vertical gaze was impossible. His subsequent course was complicated by respiratory tract infection and septicemia, and he expired on July 15, 1992. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that this patient had amyotrophic lateral sclerosis with oculomotor paresis. Post-mortem examination revealed spongy change involving the posterior column and the posterior spinocerebellar tract, in addition to severe degenerative change in the upper and the lower motoneurons, which were consistent with amyotrophic lateral sclerosis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 54-year-old man with generalized muscle atrophy and oculomotor paresis]. 799 50

The examination of septic children has revealed characteristics of iron and red cell metabolism: deep and persistent hypotransferrinemia, normo- or hypersideremia, normal ferritin levels. Red cells of septic children contain low concentrations of ATPase, histidine, lipoproteins, there is compensatory enhancement of 2,3-DPG, G-6-PD SH-group activity. In terminal sepsis the activity of the above parameters drastically falls entailing hemolysis, anemia and severe hypoxia.
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PMID:[The metabolic activity of the erythrocytes and the characteristics of ferrokinetics in children with sepsis]. 802 Jul 13

The patient was a 26-year-old man who complained of headache and vomiting. On examination, there was nothing abnormal, but the edge of the right optic papilla was not clear. His temperature was 38.5 degrees C, pulse 96/min, blood pressure 120/80 mmHg. A space-occupying lesion in his fronto-dextra cupular part was found by CT scanning. He had a 12-year history of chronic purulent otitis. The diagnosis was a brain abscess in the fronto-dextra cupular part. The brain abscess was extracted and Pasteurella multocida was isolated from the dark brown pus draining from the abscess. The patient recovered through proper antibiotic therapy based on a sensitivity test. Reports of infections caused by this organism in foreign countries very widely from local infections due to bites and scratches by cats, dogs etc. to general infections such as infections of the respiratory tract, sepsis and meningitis. However, Pasteurella multocida brain abscesses are rare. Pasteurella multocida is a Gram-negative short rod which is best known as part of the mouth flora and as a pathogen causing septicemia in many domestic animals, such as cats, dogs etc.. Infection in man results mainly from animal bites or scratches. It has been reported that Pasteurella multodida can cause human septicemia, meningitis, respiratory tract infection, conjunctivitis and other infections. We isolated a strain of Pasteurella multocida from the pus of a brain abscess following chronic purulent otitis on August 6, 1990.
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PMID:Brain abscess due to Pasteurella multocida. 817 82

In 110 patients undergoing elective heart surgery on extracorporeal circulation, various parameters were studied regarding the early assessment of septic complications. In a first step, the Elebute score definition for postoperative sepsis validated in general surgery patients (score > or = 12) could be confirmed in an extended form (> or = 12 on > or = 2 days) for cardiac surgery patients. According to this definition (overall classification accuracy for clinically defined sepsis-related mortality: 94%), septic complications occurred in 16 patients and were associated with a significantly worse prognosis than in non-septic patients (mortality 69% vs. 1%, p < 0.0001). In contrast, SIRS (best classification criterion: positive on > or = 3 days) displayed a lower specificity for clinically defined sepsis-related mortality, at least during the early postoperative course (accuracy: 67%). Based on the Elebute score classification, other more practicable parameters were investigated regarding their usefulness for an early sepsis risk assessment in post cardiac surgical patients. Five additional severity scores (APACHE II, MOF-Goris, HIS, SAPS, SSS) were comparable (ROC area: 0.94 to 0.96) and superior to plasma PMN-elastase and neopterin, haemodynamics and clinical parameters in predicting the risk for septic complications as early as by the first postoperative day.
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PMID:Evaluation of definitions and parameters for sepsis assessment in patients after cardiac surgery. 818 48


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