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

Histopathological observation was performed to clarify pathological differences of the lung between SIDS and asphyxia. In regard to pulmonary edema, there was no significant difference between SIDS and asphyxia. Occurrences of microemboli in the pulmonary vessels in cases of SIDS showing aspiration of gastric content into the lung, asphyxia and drowning were significantly high, compared with that of SIDS cases without aspiration.
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PMID:Pathological approaches to SIDS. I. Special emphasis on the histopathological differences between SIDS and asphyxia. 130 40

The original 1969 definition of SIDS as "unexpected by history" and "unexplained after thorough postmortem examination" is under review in the light of two decades of experience. Suggested modifications include restricting the age to less than 1 year, stipulating that the necropsy includes appropriate histology and laboratory tests, and requiring a review of the clinical history and examination of the death scene. The use of a protocol is recommended both by professional and parent groups. Although the diagnosis of SIDS is to some extent one of exclusion, there are several typical findings which are of value in diagnosis and suggest new avenues for research. External examination is important to exclude trauma and signs of suffocation. A recent study has confirmed that petechiae on the face are rare in SIDS and if found raise the question of deliberate or accidental suffocation. Frothy fluid escaping from the nose and mouth is seen in about half of infants who die from SIDS. Postmortem hypostatic staining as an indicator of position has assumed increased importance since prone sleeping has been shown to be a major risk factor for SIDS. Evidence of sweat in clothing suggests overwrapping. Internal examination shows subserosal petechial haemorrhages in the thymus in most cases. These may be related to age and are commoner in babies dying of SIDS than in controls. Relative sparing of the cervical extension of the thymus is strong evidence for negative intrathoracic pressure, perhaps due to upper or lower airway obstruction. Other typical findings are liquid heart blood, prominent lymph nodes, and an empty bladder (which frustrates some biochemical tests in about half of cases). The lungs are usually well inflated, arguing against surfactant deficiency as a significant cause of SIDS. Microscopic evidence of pulmonary oedema and congestion is found in infant deaths for many reasons and is not discriminatory for SIDS. Minor inflammation and infection of the respiratory tract is common in SIDS and may be important by contributing to overheating, apnoea, or sensitisation to bacterial toxins. Mild fatty change in the liver is very common in infant deaths. Panlobular microvesicular fatty change is rare and may require special stains for its recognition. It indicates the necessity of searching for inherited biochemical disorders. Although these are rare in true SIDS, they are an important cause of unexpected death in infancy. Of Naeye's "tissue markers of hypoxia'', extramedullary haemopoiesis in the liver and brainstem gliosis have been confirmed. Persistence of fetal haemoglobin and raised hypoxanthine values in vitreous humour are further pointers to periods of premortem hypoxia. Painstaking neuropathology has shown delayed myelination and maturation of dendritic spines. Changes in the brain may explain the link between antenatal factors such as smoking and SIDS. A second cot death in a family requires expert examination. Minor injuries or unexplained apnoeic spells may be important retrospective clues to non-accidental injury. Investigations mus exclude inherited disorders before the death is ascribed to SIDS. Parents demand that the pathologist takes care of their baby before, during, and after the necropsy, carries out the procedure to a high standard, checks reconstruction of the body, facilitates access, and is responsible for communicating the results of the examination. The "SIDS postmortem" presents both a practical and an intellectual challenge.
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PMID:Pathological findings in SIDS. 147 51

Immunopathological studies of SIDS share the problems of all necropsy based studies of this syndrome: the extent of autolytic changes in the material under study; and the lack of appropriate controls. Despite these problems, several studies have been performed on serum, bronchoalveolar lavage, and pulmonary tissue. Many of these studies have been inspired by the modified anaphylaxis hypothesis, based on the experiments of Coombs and coworkers. Lightly anaesthetised guinea-pigs, which had been sensitised to cows' milk protein, were shown to die after intratracheal challenge. Studies of serum IgE concentrations in SIDS initially indicated raised specific IgE for Dermatophagoides pteronyssinus, Aspergillus fumigatus, and bovine beta-lactoglobulin, but subsequent studies have not sustained these findings. Raised immunoglobulin concentrations in bronchoalveolar lavage fluid have been found in association with SIDS but this probably reflects plasma leakage rather than local secretion. Immunocytochemical analysis of lavage cells performed by the same group revealed no major difference between SIDS cases and controls, although these were limited to four cases. To date, there have been no comprehensive studies of the inflammatory cell content of the pulmonary parenchyma in SIDS. In our own studies, we have examined the mast cell and eosinophil populations in the lungs of 49 cases of infants with SIDS and in 33 infants dying of non-pulmonary causes in the first 18 months of life. We found no difference in mast cell numbers between the groups but there was a striking excess of eosinophils in the lungs of infants dying of SIDS. Because eosinophils can secrete oxygen free radicals and cytotoxic cationic proteins, we regard this as evidence of a potential mechanism for the pulmonary oedema that is characteristic of SIDS. A viral infection which might otherwise have been trivial could therefore prove fatal.
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PMID:Immunopathology of SIDS. 147 58

Of several toxins examined, only staphylococcal alpha and gamma toxin, endotoxin, and diphtheria toxins were lethal for 5-day-old ferrets. Their toxicities were enhanced in animals infected at 1 day old with influenza virus, from 3-fold with staphylococcal gamma toxin through 14-fold for staphylococcal alpha toxin, 84-fold for endotoxin, and 219-fold for diphtheria toxin. No increased viral replication occurred in any tissue; thus the effects of the toxins were exacerbated by the infection, not vice versa. Neonates died suddenly without clinical symptoms as in human babies dying from the sudden infant death syndrome (SIDS). Pathologic examination showed inflammation in the upper respiratory tract, lung edema and collapse, and early bronchopneumonia in the toxin- and influenza virus-treated animals but not in those treated with toxin or virus alone. Thus, bacterial toxins could play a role in SIDS, this being more likely with a concomitant influenza virus infection.
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PMID:Exacerbation of bacterial toxicity to infant ferrets by influenza virus: possible role in sudden infant death syndrome. 198 74

During summer-like outdoor temperature, a seven-month old female infant was put into a sleeping bag, wrapped up with a blanket and tied up by her mother and a friend of hers because of unrest and continuous screaming. Prior to that, between 0.30 a.m. and 0.45 a.m., occurred the rectal measurement of temperature: 37.5 degrees C. The infant died one to two hours later. At 10.00 a.m., about 8 hours after death, in the criminal investigations of the police measurements of temperature were made: rectal 38.1 degrees C; in the pharyngeal cavity 29.5 degrees C; surrounding temperature 22.2 degrees C. In the forensic autopsy, symptoms of maltreatment were noticed: hematoma of the skin at buttock and legs, no essential change of organs. The histological investigation showed an interstitial pulmonary oedema, an acute catarrhal tracheobronchitis and hyperaemic inner organs. Concerning the complete investigation results, an acute cardiac insufficiency and circulatory failure due to hyperthermy after wrapping up and immobilisation of the child were assumed to be the cause of death. In consequence of the avowal of the maltreater they were accused of murder and convicted for bodily injury with death. The difficulties of the differential diagnosis SIDS by hyperthermy and mortal hyperthermy due to maltreatment will be discussed. The necessity of a close cooperation between police and forensic physicians is emphasized as prerequisite to clarify such events.
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PMID:[The differential diagnosis of sudden infant death or child abuse--a case of fatal hyperthermia]. 281 99

Pulmonary lymphatics in a group of SIDS cases were compared with a control group of a similar age distribution. The causes of death in the controls were known to be associated with varying degrees of pulmonary edema. The surface areas of pleural, interstitial, peribronchial, periarterial and perivenous lymphatics were planimetrically measured. The data were statistically tested. The tests showed that the pulmonary lymphatics of the SIDS group were significantly more distended than those of the control group as expressed by highly significant differences in their surface areas. On the whole 2142 lymphatics were measured; 1255 in the SIDS group, which consisted of slides from 10 cases and 887 in the control group which consisted of slides from 11 controls. Although the sample size imposes a limit on the general applicability of the results, the clear distinction between the two groups as shown by the tests do indicate a possible feature of SIDS--lymphatic stasis--which might be secondary to some impairment of lymphatic drainage. This in turn could induce subtle fibrotic changes in the connective tissue framework of these lungs. The results are presented in the light of the forensic significance of the signs of asphyxia frequently found in SIDS and the diagnostic difficulties encountered in differentiating between SIDS and mechanical asphyxia e.g. due to smothering.
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PMID:Pulmonary lymphatics in SIDS--a comparative morphometric study. 322 Mar 49

The Sudden Infant Death Syndrome (SIDS) is responsible for the death of 10,000 infants annually in the U.S.A. The cause of these deaths is not known; all SIDS infants studied died during sleep in a silent fashion and there are no specific lesions observable post mortem. It may be of significance, however, that nearly half of SIDS infants had a respiratory tract infection in the last two weeks of life while forty percent had bloody froth over their mouths when found, presumably pulmonary oedema fluid. It is hypothesis that improper feeding or diarrhoea may likewise be involved in SIDS and that enterotoxins from putrefactive products are the precipitating event in this syndrome.
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PMID:Sudden infant death syndrome. The role of putrefactive toxins in respiratory paralysis and cerebral coma. 364 20

Sudden infant death syndrome (SIDS) is the most common cause of postneonatal mortality in the UK. Pathological investigations have shown evidence suggestive of respiratory obstruction with subsequent hypoxia leading to death. We examined 48 infants who died of SIDS and 30 who died of other, non-pulmonary, causes and identified pulmonary eosinophil and neutrophil leucocytes, mast cells, and T and B lymphocytes by immunocytochemistry. Positively stained cells were counted in the parenchyma and around the bronchi without knowledge of the tissue source. The results showed three times more eosinophils in the lungs of infants who died of SIDS (27.61 vs 7.91 [99% CI 1.76-5.87] cells/mm2 for parenchyma) accompanied by increased T lymphocytes and B lymphocytes. There were more peribronchial mast cells in the SIDS group (22.1 vs 14.7 [1.03-2.10] cells/mm2) and insignificant differences in neutrophils and parenchymal mast cells. There were significant associations between eosinophil, B lymphocyte, and T lymphocyte numbers. These findings provide evidence for an abnormal T lymphocyte-mediated pulmonary inflammatory response in SIDS. Products of eosinophil degranulation can cause epithelial damage and pulmonary oedema, which could cause the respiratory obstruction and hypoxia associated with SIDS.
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PMID:Pulmonary immunopathology of sudden infant death syndrome. 791 Aug 83

The incidence of ascites in chicks raised in a high-altitude chamber doubled from 6500 feet to 8000 feet. A similar condition developed in calves transported to pasture at high altitude. Chicks raised in a high-altitude chamber (compared to controls) produced more plasma cells in the germinal centres of the spleen about four days after an antigen challenge. Children usually suffering from a mild respiratory infection at sea level often developed pulmonary edema (HAPE) on transfer to high altitude. Sudden infant death syndrome (SIDS) victims produced more plasma cells in the germinal centers of the spleen. In one survey of SIDS, about half of the infants suffered an upper respiratory tract infection in the two weeks prior to death and the lungs were filled with fluid at autopsy. Elevated levels of hypoxanthine indicated hypoxemia before death, and a presumed response to hypoxemia in SIDS was the presence of extramedullary hematopoiesis in the liver. The effect of prolonged hypoxemia and infection are additive in increasing vascular permeability and the accumulation of edema fluid. The preferential uptake of zinc by edema fluid proteins at the expense of inflammatory cells increases the motility and metabolism of zinc-deprived activated macrophages. Activated macrophages release cytokines which in turn stimulate the release of pro-inflammatory peptides which increase vascular permeability and mortality. These inflammatory peptides are under proteolytic control. The neutral endopeptidase (NEP) is a cell-surface zinc metalloproteinase which modulates toxic shock.Zinc also modulates the inflammatory response of the activated macrophage. Interleukin-12 (IL-12), predominantly a product of macrophages, is involved in regulating both hematopoiesis and the adaptive immune response. IL-12 promotes interferon gamma (IFNgamma) production by T cells. IFNgamma acts on macrophages to release large amounts of nitric oxide (NO). An elevated immune response leads to NO overload, dilation of the cardiovascular system and toxic shock. A mechanism resulting in cardiovascular failure and a shock-like sequence is described in some cases of SIDS.Bradycardia, recorded on cardiorespiratory monitors in six SIDS infants, was considered a late event. Cytokines regulate all aspects of the immune response. Extramedullary hematopoiesis in the liver was one anatomical marker of hypoxemia in SIDS. This survey traces the function of the activated macrophage with the cytokines regulating extramedullary hematopoiesis and the precocious immune response in SIDS.
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PMID:Sudden infant death syndrome Part 2: the response of the reticuloendothelial system to hypoxemia and infection. 1142 19

The first limiting factor of dietary zinc deficiency has been described as a loss of the protective role of zinc against auto-oxidation of membrane sulfhydryl (SH) compounds. It has now been established that the prohormones (nutriuretic peptides) of the intestinal guanylin family are activated extracellularly by conversion of cysteines in the peptide to disulfide bridges. The induction of uroguanylin mRNA is elevated in intestinal zinc deficiency and nutriuretic peptides regulate epithelial transport of salt and water. Nitric oxide (NO) is also a modulator of salt and water transport. The constitutive forms of nitric oxide synthase (cNOS) in neurons and endothelial cells are calcium-dependent. The inducible form of nitric oxide synthase (iNOS) is activated by bacterial entero-toxins and damaged mucosa with NO penetrating the cell and acting directly on guanylate cyclase. The activated receptor-guanylate cyclases initiating the intracellular cycle 3'-5' guanasine monophosphate (cyclic GMP) cascade in target cells results in a flux of chloride and water into the intestinal lumen. Most of the actions of NO are mediated by activation of cyclic GMP. High-altitude pulmonary edema (HAPE) is associated with a defect in transepithelial water transport. It is suggested that dietary zinc, by modulating thiol oxidation to disulfides in guanylin prohormones to active hormones, is associated with salt and water secretion such that the overworked heart in hypoxemia increases the production and release of natriuretic peptides to activate guanylate cyclase receptors in target tissue in sudden infant death syndrome.
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PMID:Sudden infant death syndrome: is it a transepithelial transport disorder? 1232 27


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