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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The author reviewed the complications of 700 heart catheterizations in infants and children performed between 1970 and 1978 with a frequency of 55 to 113 investigations per year. Arrhythmias occurred on 70 occasions (10%), death within 24 hours: 14 (2%), extravasation of contrast media: 11 (1,6%), perforation by catheter: 6 (0,9%), cyanotic spells 5 (0,7%), myocardial ischemia: 4 (0,6%), respiratory arrest: 4 (0,6%), convulsions: 2 (0,3%), wound infection: 2 (0,3%), icterus 2 (0.3%), lung atelactasis: 1 (0,15%), bacterial endocarditis: 1 (0,15%), pyrexia: 1 (0,15%), exanthema: 1 (0,15%), pulmonary edema: 1 (0,15%), meningitis purulenta and hepatitis as possible complications: 1 (0,15%) each. The mortality figue of 2% lies well within the range of rates reported by Ho and ass. (1972): 1,5%, Stanger and ass. (1974): 3,0%, Rowe (1978): 0,95%, and Graham (1978): 2,9%. Mortality mainly occurs in sick neonates and infants with complex cardiac malformations. It could be lowered by a more aggressive approach to diagnostic work-up of suspected cardiac disease, as well as by using more sophisticated catheterization techniques and material and by introducing intensive care principles on the infant ward. Catheter related mortality (e. g. by perforation, severe arrhythmia) could be reduced to zero during the last three years. Myocardial staining by contrast media and electrocardiographic alterations suggesting myocardial ischemia occurred comparatively often but were never followed by serious or long lasting sequelae. Their occurrence was not related to the diagnosis or to the age of the patient. Respiratory arrest and convulsions could only be observed in sick infants. The seizures were not directly related to angiocardiography. All other complications were incidental events. Arrhythmias and vascular complications are discussed in separate papers.
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PMID:[The risks involved in the heart catheter examination. A retrospective evaluation of the complications after 700 examinations. II. Complications (author's transl)]. 53 Jul 26

Septicemic disease occurred in 49 of 126 pigs several days after being transported 80 km. All affected pigs died. The main changes in acutely affected pigs were skin discoloration, pulmonary edema, arthritis, meningitis, and renal glomerular thrombosis. In peracute cases, gross findings were minimal. Haemophilus parasuis was isolated from multiple organ sites in most affected pigs. Haemophilus parasuis was isolated from nasal swab specimens from 17 of 20 clinically normal pigs on the farm of origin. Fatal acute septicemia was reproduced in 2 pigs by intravenous or intratracheal exposure to an isolant of H parasuis obtained from 1 of of the 49 fatally affected pigs. Aerosol exposure of 5 pigs resulted in mild pneumonia in 4 pigs and severe pneumonia, pleurisy, pericarditis, and terminal septicemia in 1 pig.
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PMID:Haemophilus parasuis infection in swine. 91 94

Common intracranial complications following head injury are meningitis, usually associated with a basilar skull fracture or open-depressed skull fracture; delayed hematoma; hydrocephalus; and vascular injuries. Prophylactic antibiotics are not recommended for the management of basilar skull fractures. The best means of preventing infection from open-depressed skull fractures is operative debridement and thorough irrigation, though recent evidence suggests that select cases can be safely managed without operation. Serial CT scans should be obtained in severely head-injured patients to identify delayed hematomas. CT and MRI scans obtained several weeks or months after severe head injury frequently reveal enlarged ventricles, though only a small percentage of these patients have clinical hydrocephalus. Those that do, often benefit from a shunt. Vascular injuries frequently are not detected until ischemic symptoms develop hours or days after the injury. Recommended treatment for intimal tears or dissection is full anticoagulation, but in those with cerebral contusions or other intracranial lesions, this may present an unacceptable risk for intracranial hemorrhage. Pulmonary infections frequently occur following head injury, and can be associated with admission to the ICU and intubation. A large percentage of these infections are caused by enteric gram-negative organisms, and aggressive treatment with appropriate antibiotics is necessary. Aspiration of gastric contents is common in head-injured patients and is frequently complicated by bacterial superinfection. The routine use of antacids and H2 blocking agents leads to bacterial colonization of the stomach with anaerobes and gram-negative aerobes. Thus, empiric therapy for aspiration pneumonia should include clindamycin. Sinusitis is a frequent cause of fever and leukocytosis in patients with nasotracheal or nasogastric tubes in place for several days and often subsides spontaneously with removal of the tubes. Pulmonary edema is often caused by excessive fluid administration during resuscitation of these patients, and can be avoided by monitoring central venous pressures. Pulmonary edema may also be caused by ARDS, excessive catecholamine release, or primary cardiac failure. Most of these patients will benefit from early intubation and PEEP. Pulmonary emboli most often originate from deep venous thrombi, and there is increasing evidence that prophylaxis with low-dose heparin and pulsating boots can significantly reduce the incidence of both complications. Erosive gastritis is found in the majority of severely head-injured patients and may be due to ischemia of the gastric mucosa as well as gastric hyperacidity.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Complications of head injury and their therapy. 182 50

A 17-year-old man presented with acute febrile, obtundation, nuchal rigidity and CSF pleocytosis with polymorphonuclear cell predominate. He developed acute pulmonary edema which could not be explained by other mechanisms. Meningitis appears to be another cause of neurogenic pulmonary edema.
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PMID:Neurogenic pulmonary edema associated with meningitis. 226 59

Between July 1981 and June 1985, 49 cases (36 boys (73%) and 13 girls (27%] of mumps meningo-encephalitis confirmed by culture of the virus from the cerebrospinal fluid (CSF) were seen. Patients presented particularly in the late spring and early summer. A CSF cell count greater than 500 X 10(6)/l was obtained in 14 cases (28%), a total CSF protein greater than 0.8 g/l in 6 cases (12%) and a CSF glucose of less than 2.2 mmol/l in 2 cases (4%). Two cases are reported to illustrate the diagnostic problems which the infection may cause, particularly when the CSF changes resemble those of tuberculous meningitis. In 1 case neurogenic pulmonary oedema developed after a convulsion; this caused further diagnostic uncertainty.
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PMID:Mumps meningo-encephalitis. 356 52

We have studied retrospectively 30 cases of leptospirosis observed in Aquitaine (South West France) from 1980 till 1992. This review was made in three internal and a nephrology department in Bordeaux hospital. Most cases occurred by indirect contact with infected animals or by occupational exposures. Onset was brutal with fever often associated with painful syndrome and sometimes conjunctival suffusion. Jaundice (70%), acute renal failure (67%), meningitis (50%) and hemorrhagic signs (50%) were among the major visceral manifestations. Diagnosis was always confirmed by micro-agglutination test. Leptospira ictero-hemorrhage was the predominant serogroup found. The outcome was favorable in 22 patients; reversible complications were seen in six cases (five acute renal failure with hemodialysis myocarditis and pulmonary edema in two hemodialysed patients, polyradiculoneuritis). Two patients died (acute respiratory failure and meningo-encephalitis with diffuse hemorrhagic syndrome). The characteristic of our series is the high frequency of hepatorenal syndrome due to the importance of our nephrologist recruitment. Furthermore our study confirm the vital prognostic characters of the pulmonary, renal, hemorrhagic and neurologic complications. No absolute relationship was found between the clinical and laboratory findings and the serotype of leptospira. Penicillin remains the treatment of choice and should be started as soon as possible the avoid the life threatening visceral complications.
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PMID:[Epidemiological, clinical, biological and developmental aspects of leptospirosis: apropos of 30 cases in Aquitaine]. 793 56

32 cases (21 acute severe malaria and 11 chronic malaria syndrome), who developed unusual complications and/or manifestations are reported. The acute manifestations were unexplained tachypnoea 4, pulmonary oedema 5 and shock due to multiple organ dysfunction syndrome 3, melena 2 and E coli septicaemia in one. The other features were concomitant salmonellosis 2, meningitis 1, renal failure 3, hepatorenal syndrome 2, hepatitis like illness 7, neck stiffness with normal CSF 3, urticaria and subconiunctival haemorrhage 2 each, apyrexial spell with anaemia 4, thromocytopenia 3, and hypoglycaemia 3 (two pretreatment and one while on quinine in 5% glucose drip). The chronic syndrome noted were hyperreactive malaria syndrome (Tropical splenomegaly) 3, repeated haemolysis 2, chronic simple malaria with positive parasitaemia and normal Igm levels 4, and cerebellar ataxia with tremors 3. Bone marrow in these cases was hypercullular with increase plasma cells. Liver biopsy revealed lymphocytic infiltration. There was no case with permanent neurogical deficit. All patients with pulmonary oedema and multiple organ dysfunction died but chronic syndrome patients recovered fully. Early recoginition of atypical manifestation and prompt treatment will decrease the mortality and morbidity due to malaria.
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PMID:Unusual acute and chronic complications of malaria. 928 1

We report a case of neurogenic pulmonary oedema occurring in association with bacterial meningitis. An 87 year old man suddenly developed severe dyspnoea without cardiac failure (MUGA scan ejection fraction 47%). Radiographs showed pulmonary oedema. A few hours later he developed signs of meningitis and lumbar puncture suggested a partially treated bacterial meningitis. We suspect that the bacterial meningitis had induced neurogenic pulmonary oedema.
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PMID:Neurogenic pulmonary oedema induced by bacterial meningitis: a case report. 1167 42

Mycoplasma alligatoris was the suspected etiology of an epidemic of acute multisystemic inflammatory disease which emerged in captive American alligators (Alligator mississippiensis) in Florida (USA) in 1995. In an experimental inoculation study conducted from April through October 1999, 18 alligators were inoculated with 10(2), 10(4), or 10(6) colony forming units (CFU) of M. alligatoris by instillation into the glottis. As early as 1 wk post-inoculation (PI), mycoplasma were cultured from blood of three of six alligators inoculated with 10(6) CFU. Two of those died and the third was euthanatized within 4 wk PI. Necropsy gross findings included fibrinous polyserositis and polyarthritis. Histopathologic changes in affected individuals included pulmonary edema, interstitial pneumonia, pericarditis, myocarditis, meningitis, and synovitis. Mycoplasma were cultured quantitatively in high numbers from trachea, lung, coelomic cavity, liver, spleen, interior of pericardial sac, heart, blood, brain, and limb joints. In alligators inoculated with 10(6) CFU, heterophilia and moderate hyperglycemia peaked about 4 wk PI, and seroconversion occurred by 6 to 8 wk PI. Necropsy gross and histologic findings were generally unremarkable for the surviving alligators inoculated with 10(6) CFU, alligators inoculated with 10(2) or 10(4) CFU, and four uninoculated control alligators. Mycoplasma were not cultured at any time point from those alligators. The findings confirm that M. alligatoris can cause fulminant inflammatory disease and rapid death of alligators.
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PMID:Pathology of experimental mycoplasmosis in American alligators. 1176 30

Fever is often an indication of a serious illness in children. In areas endemic to malaria, hospital workers should check a febrile child for malaria parasites. Children with a fever associated with meningitis or malaria need immediate attention. To diagnose meningitis: microscopic examination of cerebrospinal fluid obtained by lumbar puncture is the only reliable method. If a febrile child also has a stiff neck, health workers should immediately administer antibiotic treatment without waiting for the results of the lumbar puncture. If available and in epidemic situations, oily chloramphenicol may be administered, since it is effective in a single dose. Treatment with other antibiotics should last for 10 days in children and 14-21 days for young infants. To diagnose malaria in endemic areas: laboratory technicians should examine thick and thin blood films of sick children with fever. Health workers must consider as medical emergencies children who have a slide positive for malaria parasites plus severe anemia, hypoglycemia, deep rapid breathing, any indication of kidney malfunction or failure, or altered consciousness. They should begin antimalarial treatment with quinine, the drug of choice for severe and complicated malaria. In cases of convulsions lasting longer than 5 minutes, health workers should administer anticonvulsants and take actions to prevent aspiration pneumonia. If the fever persists for 14 days or if the child does not emerge from unconsciousness and someone in the family has active tuberculosis, health workers should consider tuberculous meningitis. If a child with malaria has low hemoglobin levels (5 g/dl) and many malaria parasites in the blood and is in heart failure, a blood transfusion (15-20 ml/kg whole blood over 4 hours) and infusion of 1 mg/kg fursemide (to prevent cardiac failure) are needed. If the preceding case has pulmonary edema, a single dose of fursemide at the same dosage is needed to prevent overloading of the circulation. Health workers should closely monitor that intravenous fluids not exacerbate brain swelling.
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PMID:Managing meningitis and severe malaria. 1229 72


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