Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Five patients received overdoses of vincristine ranging from 3.5 to 32 mg. Neurotoxicity accounted for most of the complications observed. Peripheral neuropathies, cranial nerve palsies, paralytic ileus, atony of the bladder, hypertension, hypotension, seizures, inappropriate ADH secretion, and severe bone marrow depression were all encountered. Two patients died within 72 hours of the overdose. Another patient died of sepsis 22 days after the overdose. Two patients recovered and were discharged. The three patients who survived longer than a few days showed improvement in the vincristine-induced neuropathy, and the two long-term survivors had essentially complete recovery. It appears that if a patient can be supported through the critical period following an overdose, he can be expected to recover normal neurologic function.
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PMID:Overdosage with vincristine. 18 48

Among 592 infants examined at autopsy during a four-year period, 32 (5.4%) had cerebral infarcts. Excluded were cases of traumatic hemorrhages and softening, periventricular leukomalacia, venous lesions, and any mass, including encephaloceles, with arterial distortion and infarction. Histological abnormalities were similar to those of infarcts in adults. Relatively advanced histopathological changes in some infants living only a few hours indicated that some infarctions may have occured in utero. The most common cause of arterial occlusion was embolization, with sepsis and disseminated intravascular coagulation playing a major role. The brains of term neonates were more frequently involved than those of premature infants. Multiple small infarcts occurred more often in premature infants. In most cases autonomic dysfunction with prolonged apnea, episodic seizures, and metabolic acidosis were the major associated clinical features, rather than focal neurological deficits. Similar cerebral infarcts in infants who survive with less severe systemic complications may lead to porencephaly, hemiplegia, mental and motor retardation, and recurrent seizures.
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PMID:Cerebral infarcts with arterial occlusion in neonates. 53 48

Inhibitors of nitric oxide synthase (NOS) have been reported to increase mean arterial pressure in animal models of sepsis and recently have been given to patients in septic shock. However, controlled studies to determine the effects of these agents on cardiovascular function and survival in awake animal models of sepsis have not been reported. To examine the therapeutic potential of NOS inhibition in septic shock, we challenged canines with endotoxin (2 or 4 mg/kg i.v.) and treated them with either normal saline or N omega-amino-L-arginine (10 or 1 mg/kg/h), the most specific inhibitor available for the isoform of NOS implicated in septic shock. Endotoxemic animals treated with N omega-amino-L-arginine (n = 11) had higher systemic and pulmonary vascular resistance indices (SVRI and PVRI, p less than or equal to 0.033) and decreased heart rates (p = 0.009), cardiac indices (CI, p = 0.01), oxygen delivery indices (p = 0.027), and oxygen consumption indices (p = 0.046) compared with controls (n = 6). Moreover, N omega-amino-L-arginine increased mortality rates after endotoxin challenge (10 of 11 vs. 1 of 6 controls, p = 0.005). Administration of L-arginine did not improve survival or alter the cardiopulmonary effects of N omega-amino-L-arginine, which suggests that inhibition of NOS may not have been competitive. In normal animals, N omega-amino-L-arginine alone (n = 3) increased SVRI (p = 0.0008) and mean arterial pressure (p = 0.016), and decreased CI (p = 0.01) compared with saline-treated controls (n = 3), but, at the high dose, also produced neuromuscular rigidity and seizure-like activity that was not apparent in the endotoxemic model. Thus, the mortality rate from endotoxemia increased either because of NOS inhibition per se or because of properties unique to N omega-amino-L-arginine, or both.
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PMID:N omega-amino-L-arginine, an inhibitor of nitric oxide synthase, raises vascular resistance but increases mortality rates in awake canines challenged with endotoxin. 138 77

A previously healthy breast-fed baby was admitted at 10 days of age to a hospital in the north of Pakistan with diarrhoea and fever. He was treated for suspected sepsis with intravenous cefotaxime and tobramycin. Cultures of blood and faeces at that time proved negative. At 12 days of age, seizures began and examination of CSF revealed evidence of pyogenic meningitis but bacteria were neither seen microscopically nor isolated in culture. Ceftazidime was substituted for cefotaxime and carbenicillin was given also. Since the baby's condition continued to deteriorate with persistent fever, vomiting and recurrent seizures, he was transferred to the Aga Khan University Hospital, Karachi. Examination of CSF there confirmed the diagnosis of pyogenic meningitis and revealed Gram-negative bacteria. Cultures of CSF and faeces yielded Salmonella paratyphi A but the blood culture was negative. The isolate was found to be multiple antimicrobially resistant but sensitive to ciprofloxacin. Treatment with this drug was therefore started 3 days after the baby's admission to the Aga Khan Hospital. Within 36 h, improvement was observed. From then onwards, the baby made a progressive recovery and was healthy when seen at 7 months of age.
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PMID:Eradication of a multiple drug resistant Salmonella paratyphi A causing meningitis with ciprofloxacin. 143 Nov 77

Unilateral thalamic bleeding with associated intraventricular hemorrhage is reported in three full-term neonates. The first presented within 48 hours from birth with early onset streptococcal meningitis, persistent pulmonary hypertension, tonic seizures and a tense fontanelle. The second presented 6 days after birth with irritability, opisthotonus, a tense fontanelle and tonic seizures. The third was admitted three days after birth with seizures and a tense fontanelle. In the latter two infants NMR and CT imaging documented thrombosed superficial and deep cerebral veins. The etiopathogenesis of intracranial venous thrombosis in the neonate is diverse: asphyxia, dehydration, polycythemia, sepsis-meningitis and difficult delivery are the main causes. In one of our patients jugular vein compression by the collar of a negative-pressure ventilation chamber probably initiated the intracranial events. More than half of the survivors sustain severe neurological impairment.
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PMID:Deep cerebral venous thrombosis in thalamo-ventricular hemorrhage of the term newborn. 150 40

From July 1988 to March 1991, extracorporeal membrane oxygenation (ECMO) was used in 8 infants (newborn to 16 months old) with unoperated cyanotic congenital heart disease and cardiopulmonary collapse, associated with hypercyanotic spells (4 infants), pulmonary hypertensive crises (3) and sepsis (1). Indications for ECMO support were arterial saturations less than or equal to 60% accompanied by hypotension and metabolic acidosis unresponsive to mechanical ventilation with 100% oxygen, paralysis and sedation, and pharmacologic support with inotropes or vasodilators, or both. Venoarterial bypass by carotid/jugular cannulation with flow rates of 100 to 840 ml/kg/min (mean 460) stabilized all patients. Duration of ECMO support ranged from 15 to 840 hours and was associated with transient seizures (1 patient) and renal failure (1). Seven patients underwent palliative (3 patients) or corrective (4) surgical procedures while on ECMO or within 48 hours of decannulation, including 1 patient bridged to double-lung transplantation with a long (840 hours) duration of ECMO. There was 1 operative and 2 late (greater than 1 month after decannulation) deaths, for an overall survival rate of 62%. These 5 survivors all have normal growth and development, and patent neck vessels at the site of cannulation. These early results indicate that ECMO can be effective mechanical support in cardiovascular crises untreatable with maximal conventional medical therapy and can be used as a bridge to successful surgical palliation or repair.
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PMID:Extracorporeal life support in cyanotic congenital heart disease before cardiovascular operation. 154 55

Despite the generally salutary experience in recent years of managing suppurative pleuropulmonary disease, empyemas and lung abscesses have persisted and increased in incidence in hospitals such as Queens Hospital Center that serve large numbers of the socioeconomically disadvantaged. This study documents the etiology, clinical presentation, treatment, and treatment results of suppurative pleuropulmonary disease at Queens Hospital Center, which serves a large segment of the urban poor, many of whom are black. Results indicate that contributory or antecedent etiologic factors include a history of prior disease (specifically pneumonia, lung abscess, obstructive lung disease, pulmonary neoplasia, and tuberculosis); a predisposition to constitutional or immunologic deficiencies (specifically, alcoholism, anemia/malnutrition, drug abuse, and acquired immunodeficiency syndrome [AIDS]); conditions contributing to tracheobronchial aspiration (specifically, alcoholism and seizure disorders); and a miscellaneous group such as prior surgery, cardiovascular disease, and sepsis syndrome. The patients in this study were young with maximal incidence occurring in the third to fifth decades of life. Patients were predominantly male (75%) and black (66%). There were 18 deaths (23%), with sepsis being the cause in 10 (56%). Most surgical interventions were conservative, ie, bronchoscopies (48), thoracenteses (43), and tube thoracotomies (39). Thirty-one open thoracotomies were performed for drainage, decortication, or pulmonary resection. The surgical mortality was three cases or 5% of the patients who underwent surgery. The designated incidence of proven AIDS in this series (29%) was low, undoubtedly because many patients refused testing, and the multiple gram-positive and gram-negative infections that were seen did not conform to the Centers for Disease Control criteria for diagnosis and case reporting for AIDS.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of surgery in treating pleuropulmonary suppurative disease--review of 77 cases managed at Queens Hospital Center between 1986 and 1989. 160 13

Hypovolemic hyponatremia attributable to severe fluid and electrolyte alterations was diagnosed in a foal with diarrhea. Subsequent consumption of water resulted in rapid reduction of serum sodium concentration and serum osmolar depression. Clinical signs of neurologic disease developed including blindness, loss of menace response, and seizures. Treatment of this condition with IV administered fluids included hypertonic saline solution (7.2%; 2 ml/kg of body weight), and frequent monitoring of serum electrolyte concentrations and osmolality resulted in gradual correction of the fluid and electrolyte imbalance and resolution of the neurologic signs. Hyponatremia has been recognized in foals with renal failure, ruptured urinary bladder, and iatrogenic water overload. The key to diagnosis and management of profound hyponatremia is accurate diagnosis of the status of plasma volume and association of the electrolyte imbalance with clinical signs of neurologic disease. This report describes an unusual complication of a commonly encountered problem in equine practice and documents that the severe metabolic and electrolyte abnormalities associated with diarrhea can result in clinical neurologic disease. The differential diagnosis also should include bacterial sepsis, parasitism, thoracic mass, acute renal failure, congenital neurologic deficit, or seizure syndrome. Serum electrolyte disorders should be considered as a potential cause of signs of neurologic disease in foals with diarrhea.
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PMID:Hypovolemic hyponatremia and signs of neurologic disease associated with diarrhea in a foal. 160 18

Hemorrhagic shock and encephalopathy syndrome (HSES) is a devastating symptom complex that affects previously healthy infants and is associated with significant mortality and neurologic morbidity. The syndrome was first reported less than ten years ago, and there continues to be debate regarding whether HSES actually represents a distinct clinical entity or instead is a manifestation of heat illness, occult sepsis or endotoxic shock, or perhaps toxic ingestion. Nevertheless, the signs and symptoms described as HSES present in a typical fashion in the emergency department with sudden onset of shock, encephalopathy, seizures, and coagulopathy. Even with the initiation of intensive support in the ED, the outcome is probably dismal. We describe a case of HSES and review the presentation, proposed etiologies, and management of this catastrophic illness.
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PMID:Hemorrhagic shock and encephalopathy syndrome. 174 41

In the immunocompromised patient, even mild forms of any combination of headache, meningismus, altered mental status, or focal neurologic signs should initiate an evaluation for possible CNS infection. The limited signs and symptoms of acute CNS infection are not due to specific organisms but to pathologic changes at the neuroanatomic site of infection. The initial clinical history, examination, laboratory, and neuroradiographic data will narrow the problem to one of several groups of agents, although it may not be possible to specify a single causative agent. It should be remembered that several concurrent infections (i.e., CMV and toxoplasmosis, aspergillosis, and bacterial sepsis) may be present. Thus, the clinician should rely on broad antibiotic coverage appropriate to the suspected causative agent or agents at the site of infection. It may be necessary to offer broad-spectrum antibiotic coverage for a CSF presentation that is subsequently found to result from a viral illness or from a noninfectious cause. However, one should avoid undertreating those infections for which specific therapy can be offered, and broad-spectrum treatment usually will not be regretted. Uncertainty in diagnosis following noninvasive procedures should lead to a brain biopsy. Although many of the infections discussed in this article have a poor prognosis, some of the most common pathogens, such as Cryptococcus, Listeria, and Toxoplasma, have effective specific therapies to which the patient should have access as rapidly as possible. The clinician who has successfully treated a patient with CNS infection should remain vigilant for late sequelae or recurrence of infection. Chronic treatment of some infections, such as toxoplasmosis or aspergillosis, may be necessary. The reintroduction of steroids for the treatment of an underlying cancer may reactivate previously treated disease, such as cryptococcosis, and periodic CSF surveillance is appropriate under these circumstances. Recurrence of the symptoms should raise the suspicion of recurrent or new infection, and the patient also should be evaluated with CT or MRI for the development of hydrocephalus or for new metastatic disease. In patients who have had varicella-zoster infection, postherpetic neuralgia and delayed arteritis may develop. Seizures, hearing loss, and neuropsychologic sequelae may follow any meningoencephalitis. The patient should always be reevaluated for the possibility of infection with a different opportunistic organism. CNS infections remain a major cause of morbidity and mortality in immunosuppressed patients with malignancies. In one series, 60% of such patients died as a result of their CNS infection, many at a time when the underlying disease had an otherwise good prognosis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Central nervous system infections in cancer patients. 175 29


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