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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

As the mortality rate for penetrating colonic injuries approaches zero, emphasis has shifted toward reducing associated morbidity. This study was done to identify patients at low risk for colon-related extensive morbidity after primary repair of a penetrating colonic injury. The records of 100 consecutive patients admitted to the District of Columbia General Hospital (DCGH) between 1984 to 1990, surviving more than 24 hours after full-thickness penetrating colonic injuries, were retrospectively reviewed. Data collection included mechanism, management and anatomic location of the colonic injury. Severity of injury was evaluated by the Trauma Score (TS), Penetrating Abdominal Trauma Index (PATI), Flint Colon Injury Score (FCIS), time in the operating room, blood transfused during the first 24 hours and presence of preoperative shock (systolic blood pressure less than 90 millimeters of mercury). Mechanism of injury included 97 gunshot wounds and three stab wounds. Fifty-seven patients had primary repair (17 having resection and anastomosis) and 43 had colostomy. The anatomic location of injury was right colon in 37, transverse colon in 27, left colon in 35 and multiple sites (two) in one patient. In this series, only two patients had colon-related extensive morbidity--a parastomal hernia and wound dehiscence, both requiring operative intervention. There were no instances of intraperitoneal abscess formation. One patient died from overwhelming pneumonia after segmental resection of the colon with primary anastomosis. The literature reports a 12 to 42 percent colon-related morbidity rate in patients sustaining penetrating colonic injuries. This series from DCGH represents the lowest colon-related extensive morbidity and mortality rates reported to date in any substantial series of penetrating abdominal trauma. We attribute the 2 percent extensive morbidity rate to high TS (mean of 15.7), low PATI (mean of 24.2), low FCIS (mean of 1.9) and few associated intra-abdominal injuries (59 percent of patients with less than two). We have identified a group of patients with full-thickness penetrating injuries to the colon, few associated intra-abdominal injuries, high TS, low PATI and low FCIS who can be managed safely and judiciously by primary repair without undue morbidity and mortality.
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PMID:Identifying the low-risk patient with penetrating colonic injury for selective use of primary repair. 835 96

Mercury vapour inhalation is a rare cause of acute toxic injury to the lungs and is often fatal in infants. A 5 month-old girl with mercury vapour poisoning who developed chemical pneumonitis with bilateral pneumothoraces is reported. She was managed successfully in an intensive care unit with respiratory support, without chelation therapy.
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PMID:Acute mercury vapour poisoning in an infant. 917 79

Chronic mercury toxicity was induced in goats by administering mercuric chloride at 100 micrograms/ml in deionized drinking water offered ad libitum for 90 days. Toxic signs of gastrointestinal disturbances and renal dysfunction developed from 43 days onwards without any mortality. The toxicity also induced nephrosis and tubular nephritis; centrilobular necrosis of liver; mild to moderate necrosis in spleen, intestine and lymph node; Zenker's degeneration of cardiac muscles; exudative pneumonia; and pial congestion, oedema and vacuolation in the brain. In addition, hyperaemia, oedema and tissue haemorrhages were evident in most of the organs. The kidneys contained the largest residues of mercury, followed by liver, spleen, intestine, lymph node, skeletal muscles, lungs, heart, brain and the omental fat. The intensity of the cytotoxic changes in the various organs was proportional to the amount of mercury accumulated.
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PMID:The chronic toxicity of inorganic mercury in goats: clinical signs, toxicopathological changes and residual concentrations. 956 71

Acute mercury inhalation poisoning is a rare cause of acute lung injury. It is usually fatal because of progressive pulmonary failure. We experienced a patient with acute respiratory distress syndrome (ARDS) after illicit use of mercury vapor for hemorrhoid treatment; he developed acute chemical pneumonitis following exposure to mercury vapor. Prompt treatment with corticosteroids and penicillamine for acute chemical pneumonitis was instituted; radiologic pulmonary infiltrates disappeared within a week, but late phase neurologic sequelae and pulmonary interstitial fibrosis progressed.
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PMID:Mercury inhalation poisoning and acute lung injury. 973 69

Acute mercury vapour poisoning is a serious, potentially fatal but fortunately rarely encountered problem. It is most commonly due to industrial accidents. The vapour is a direct respiratory tract irritant as well as a cell poison, exerting its greatest effects in the lungs, nervous system, kidneys and liver. We present a case of mercury vapour poisoning in a shipyard workers presenting as an acute chemical pneumonitis, which resolved with aggressive supportive therapy. Further investigations later revealed transient mild neuropsychiatric symptoms, and residual peripheral neuropathy. No chelation therapy was instituted. The detailed investigative work that led to the discovery of the source of mercury is also presented. This case alerts us to the potential hazard to shipyard workers who may work in ships previously carrying oil contaminated with mercury. There have been no previous reports of mercury poisoning in shipyard workers. A high index of suspicion leading to early diagnosis and institution of appropriate supportive measures in suspected cases can be life-saving.
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PMID:Acute mercury vapour poisoning in a shipyard worker--a case report. 1049 87

Differences in pathology were found between acute and chronic exposure to methylmercury, mercury vapor, and inorganic mercury. Characteristic pathologic changes produced by organic mercury in the brain have previously been described in patients with Minamata disease. The brains of patients who presented with acute onset of symptoms and died within 2-mo showed loss of neurons with reactive proliferation of glial cells, microcavitation, vascular congestion, petechial hemorrhage, and edema in the cerebral cortices, predominantly in the calcarine, pre- and postcentral, and transverse temporal cortices and in the cerebellar cortex. The neuropathologic changes in the patients with acute onset of symptoms who survived for a long period (>10 yr) were also included neuronal loss with reactive proliferation of glial cells in similar anatomic locations. The neuropathologic changes in patients with inorganic mercury poisoning are quite different. Autopsies performed on 3 individuals with fatal cases of acute inorganic mercury poisoning who were exposed to mercury vapor for about 2 wk revealed diffuse organized pneumonia, renal cortical necrosis, disseminated intravascular coagulopathy, and infarctions in the brain and kidneys. In 2 other patients who worked in mercury mines for about 10 yr and who suffered from chronic inorganic poisoning, no specific lesions were demonstrated in the brain. However, the assay and the histochemistry of mercury revealed that inorganic mercury was present in the brain in all 3 groups irrespective of the brain lesions and the duration of clinical signs.
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PMID:Differential diagnosis between organic and inorganic mercury poisoning in human cases--the pathologic point of view. 1058 47

Mercury contamination is a serious environmental problem worldwide. Two primary sources of contamination are dumping of large quantities of inorganic mercury and exposure in the mining industry. Although the actual fatal level of mercury vapor is not known, exposure to more than 1-2 mg/m3 of elemental mercury vapor (Hg0) for a few hours causes acute chemical bronchiolitis and pneumonitis. Two hours after exposure, lung injury appears as hyaline membrane formation, and finally, extensive pulmonary fibrosis occurs. Clinical findings correlate with the duration of exposure, the concentration of mercury, and the survival time after exposure. There is no correlation between pathological findings and the concentration of mercury in the tissues. Necrosis of proximal convoluted tubules may be attributed to the disruption of the enzyme systems of Hg2+-sulfhydryl compounds. Metallothionein protein (MT), induced by the accumulation of Hg2+ in the kidneys, may play an important role in detoxication after it forms a non-toxic Hg2+-MT compound. Despite the deposition of mercury in the brain, compared with organic mercury, inorganic mercury did not seem to damage the neurons. Drugs such as chelating agents and corticosteroids appear to effectively decrease the inflammation and delay pulmonary fibrosis.
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PMID:Review article: acute inorganic mercury vapor inhalation poisoning. 1079 79

In recent years the greatest progress in our understanding of pneumoconioses, other than those produced by asbestos, silica, and coal, has been in the arena of metal-induced parenchymal lung disorders. Inhalation of metal dusts and fumes can induce a wide range of lung pathology, including airways disorders, cancer, and parenchymal diseases. The emphasis of this update is on parenchymal diseases caused by metal inhalation, including granulomatous disease, giant cell interstitial pneumonitis, chemical pneumonitis, and interstitial fibrosis, among others. The clinical characteristics, epidemiology, and pathogenesis of disorders arising from exposure to aluminum, beryllium, cadmium, cobalt, copper, iron, mercury, and nickel are presented in detail. Metal fume fever, an inhalation fever syndrome attributed to exposure to a number of metals, is also discussed. Advances in our knowledge of antigen-specific immunologic reactions in the lung are particularly evident in disorders secondary to beryllium and nickel exposure, where immunologic mechanisms have been well characterized. For example, current evidence suggests that beryllium acts as an antigen, or hapten, and is presented by antigen-presenting cells to CD4+ T cells, which possess specific surface antigen receptors. Other metals such as cadmium and mercury induce nonspecific damage, probably by initiating production of reactive oxygen species. Additionally, genetic susceptibility markers associated with increased risk have been identified in some metal-related diseases such as chronic beryllium disease and hard metal disease. Future research needs include development of biologic markers of metal-induced immunologic disease, detailed characterization of human exposure, examination of gene alleles that might confer risk, and association of exposure data with that of genetic susceptibility.
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PMID:Inorganic dust pneumonias: the metal-related parenchymal disorders. 1093 87

We investigate whether long-term exposure to heavy metals, including immunosuppressive metals like mercury (Hg), is associated with infectious disease in a wild cetacean. Post-mortem investigations on 86 harbour porpoises, Phocoena phocoena, found dead along the coasts of England and Wales revealed that 49 of the porpoises were healthy when they died as a consequence of physical trauma (most frequently entrapment in fishing gear). In contrast, 37 porpoises died of infectious diseases caused by parasitic, bacterial, fungal and viral pathogens (most frequently pneumonia caused by lungworm and bacterial infections). We found that mean liver concentrations of Hg, selenium (Se), the Hg:Se molar ratio, and zinc (Zn) were significantly higher in the propoises that died of infectious disease compared to healthy porpoises that died from physical trauma. Liver concentrations of lead (Pb), cadmium (Cd), copper (Cu) and chromium (Cr) did not differ between the two groups. Hg, Se, and the Hg:Se molar ratio were also positively correlated with age. The association between Zn concentration and disease status may result from Zn redistribution in response to infection. Further work is required to evaluate whether chronic exposure to Hg may have presented a toxic challenge to the porpoises that succumbed to infectious disease.
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PMID:Exposure to heavy metals and infectious disease mortality in harbour porpoises from England and Wales. 1120 52

Mercury is a toxic and hazardous metal that occurs naturally in the earth's crust. Natural phenomena such as erosion and volcanic eruptions, and anthropogenic activities like metal smelting and industrial production and use may lead to substantial contamination of the environment with mercury. Through consumption of mercury in food, the populations of many areas, particularly in the developing world, have been confronted with catastrophic outbreaks of mercury-induced diseases and mortality. Countries such as Japan, Iraq, Ghana, the Seychelles, and the Faroe Islands have faced such epidemics, which have unraveled the insidious and debilitating nature of mercury poisoning. Its creeping neurotoxicity is highly devastating, particularly in the central and peripheral nervous systems of children. Central nervous system defects and erethism as well as arrythmias, cardiomyopathies, and kidney damage have been associated with mercury exposure. Necrotizing bronchitis and pneumonitis arising from inhalation of mercury vapor can result in respiratory failure. Mercury is also considered a potent immunostimulant and -suppressant, depending on exposure dose and individual susceptibility, producing a number of pathologic sequelae including lymphoproliferation, hypergammaglobulinemia, and total systemic hyper- and hyporeactivities. In this review we discuss the sources of mercury and the potential for human exposure; its biogeochemical cycling in the environment; its systemic, immunotoxic, genotoxic/carcinogenic, and teratogenic health effects; and the dietary influences on its toxicity; as well as the important considerations in risk assessment and management of mercury poisoning.
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PMID:Environmental exposure to mercury and its toxicopathologic implications for public health. 1274 Aug 2


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