Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032290 (aspiration pneumonia)
 2,291 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

10 percent glycerol was given for 6 days to 30 patients who had had acute ischaemic cerebral infarction, and the results were compared with those obtained after treating 31 similar patients with dexamethasone (16 mg. per 24 hours for 6 days). 1 patient treated with glycerol died of haemoglobinuria and acute renal failure. 6 patients treated with dexamethasone died--3 from cerebral oedema and 3 from non-neurological complications (pulmonary embolism, myocardial infarction, and aspiration pneumonia). Improvement was significantly greater in the glycerol group after 8 and 15 days. No improvement was noted using either glycerol or dexamethasone in 7 patients with spontaneous intracerebral haemorrhage.
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PMID:Controlled trial of glycerol versus dexamethasone in the treatment of cerebral oedema in acute cerebral infarction. 4 27

A consensus conference on stroke was held on March 22, 1991. Subjects on which consensus was reached were: There are different kinds of cerebral haemorrhage and infarction, which can be differentiated by computerized tomography, and this can have practical consequences. At clinical examination special attention should be paid to cognitive impairment. Angiography is indicated only if carotid surgery or unusual causes are considered. CSF examination and EEG are performed only on special indications. Cardiological consultation is necessary in young patients, or if clinical signs of cardiogenic embolism are present. Coumarin derivatives are prescribed in some of these cardiac causes of stroke, to prevent recurrence. There is as yet no effective medical treatment for cerebral infarction. In lobar and cerebellar haemorrhage surgical treatment may be indicated. In the acute phase of stroke it is always important to prevent aspiration pneumonia, pulmonary embolism and decubitus, and to care for muscles and joints. Advantages and disadvantages of gastric tube and indwelling catheter should be weighed. Treatment of hypertension after the acute phase is indicated to prevent recurrent stroke. After TIA and minor stroke, aspirin is prescribed, which reduces the risk of cerebral and myocardial infarction by 30%. Carotid endarterectomy in symptomatic patients with carotid stenosis of 70% or more, reduces the number of fatal or disabling strokes by 50%, if perioperative complications are less than 4%. Rehabilitation after stroke reduces disability and improves the adaptation of both the patient and his environment. The patient should be stimulated and supported; good information, including the family, is essential. Supplying aids and taking special measures should be done on individual basis, after a period of training.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Consensus cerebrovascular accident]. 174 34

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

Respiratory diseases are the most heavy complications that we can meat in self-poisoning persons. Authors report 15 cases of respiratory complications appeared in 824 self-poisoning cases by drugs. Different factors involved in respiratory diseases origin are analysed but only one appears to be significant: the time between poisoning and admission in intensive care unit. The encountered complications are: acute respiratory distress syndrome, Mendelson syndrome, heavy pulmonary infections, pulmonary embolism. Authors argue about the means of prevention. This seems the fundamental aspect, alone capable to decrease the incidence of very heavy complications responsible of a height mortality range (33%).
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PMID:[Severe respiratory complications in acute voluntary drug poisoning. Apropos of 15 cases in 824 poisoning cases]. 668 85

We describe four major and five minor clinical patterns of acute phencyclidine (PCP) intoxication and give the incidence of findings in each pattern. Major patterns were acute brain syndrome (248 cases; 24.8%), toxic psychosis (166 cases; 16.6%), catatonic syndrome (117 cases; 11.7%), and coma (106 cases; 10.6%). Minor patterns included lethargy or stupor (38 cases; 3.8%), and combinations of bizarre behavior, violence, agitation, and euphoria in patients who were alert and oriented (325 cases; 32.5%). Patients with major patterns of PCP toxicity usually required hospitalization and accounted for most complications. In general, patients with minor patterns had mild intoxication and did not require hospitalization except for the treatment of injuries or autonomic effects of PCP. Various types of injuries occurred in 16%, and aspiration pneumonia occurred in 1.0% of all cases. There were 22 cases of rhabdomyolysis (2.2%), with three patients requiring dialysis for renal failure. One patient who had been comatose from PCP died suddenly. A fresh pulmonary embolism was found at autopsy.
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PMID:Acute phencyclidine intoxication: clinical patterns, complications, and treatment. 723 37

The authors reviewed all chest radiographs obtained for pregnant women at a university hospital over a 15-year period to determine the intrathoracic complications of pregnancy and diseases occurring during pregnancy. The characteristic physiologic changes seen on chest radiographs during normal pregnancy are reviewed. Examples of intrathoracic diseases that may occur in pregnant patients include pulmonary embolism, amniotic fluid embolism, beriberi, aspiration pneumonia, community-acquired pneumonia, viral pneumonia, asthma, systemic disease, trophoblastic disease and peripartum pulmonary edema. The authors discuss the radiation biology implications of performing chest radiography during pregnancy and conclude that the benefit that the fetus receives from diagnosis and treatment of the mother's disease may be greater than the risk of radiation exposure.
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PMID:Radiographic appearance of intrathoracic complications of pregnancy. 894 17

On returning from a medical meeting, we learned that sadly a patient, "Mr. B.," had passed away. His death was a completely unexpected surprise. He had been doing well nine months after a course of intensive radiotherapy for a locally advanced head and neck cancer; in his most recent follow-up notes, he was described as a "complete remission." Nonetheless, he apparently died peacefully in his sleep from a cardiac arrest one night and was found the next day by a concerned neighbor. In our absence, after Mr. B. expired, his death certificate was filled out by a physician who didn't know him in detail, but did know why he recently was treated in our department. The cause of death was listed as head and neck cancer. It wasn't long after his death before we began to receive those notorious "requests for additional information," letters from the statistical office of a well-known cooperative group. Mr. B., as it turns out, was on a clinical trial, and it was "vital" to know further details of the circumstances of his passing. Perhaps this very large cancer had been controlled and Mr. B. succumbed to old age (helped along by the tobacco industry). On the other hand, maybe the residual "fibrosis" in his neck was actually packed with active tumor and his left carotid artery was finally 100% pinched off, or maybe he suffered a massive pulmonary embolism from cancer-related hypercoagulability. The forms and requests were completed with a succinct "cause of death uncertain," adding, "please have the Study Chairs call to discuss this difficult case." Often clinical reports of outcomes utilize and emphasize the endpoint "disease specific survival" (DSS). Like overall survival (OS), the DSS can be calculated by actuarial methods, with patients who have incomplete follow-up "censored" at the time of last follow-up pending further information. In the DSS, however, deaths unrelated to the index cancer of interest are censored at the time of death; thus, a death from intercurrent disease is considered a "success" (to the investigator, that is; obviously, not to the patient and his or her family). The DSS rate will always be superior to the OS rate. Obviously, for any OS curve, if one waits long enough it will ultimately come to zero. There is thus a very logical rationale for reporting the DSS separately, particularly in diseases where death from intercurrent disease is expected to be common. Analyzing the DSS allows researchers to better compare the biologic efficacy of two or more cancer treatments, since it does not necessarily come to zero. Unlike some other endpoints, including local-regional control or freedom from progression, it takes into account the possibility of salvage therapy. DSS also focuses on an endpoint of interest to the public-death from cancer. In a recent popular media survey in which people were asked how they would choose to die if they could, 0% selected cancer. However, there are two serious potential problems with heavy dependence on the DSS. First, since patients who die from intercurrent disease are considered "cured," it seriously inflates the apparent effectiveness of a cancer treatment. Given the same biologic disease and the same treatment, the DSS as calculated in an old, sick population at high risk of intercurrent death will be better than the DSS in a younger, healthier population whose major risk is from their cancer. This problem has been discussed with respect to early stage prostate cancer, in which the conservative approach of observation has been criticized. The studies at issue rely heavily on the DSS, suggesting a comparable DSS (90% at 10 years) with "watchful waiting" to other researchers' results with aggressive therapy. The problem is that these series of conservative management focus on a patient population (as opposed to individuals) with a high risk of competing causes of mortality, which is very different from the population of patients generally treated with aggressive therapy (in which some have shown overall survivals superior to age-matched controls). It is fallacious and illogical to compare nonrandomized series of observation to those of aggressive therapy. In addition to the above problem, the use of DSS introduces another potential issue which we will call the bias of cause-of-death-interpretation. All statistical endpoints (e.g., response rates, local-regional control, freedom from brain metastases), except OS, are known to depend heavily on the methods used to define the endpoint and are often subject to significant interobserver variability. There is no reason to believe that this problem does not occasionally occur with respect to defining a death as due to the index cancer or to intercurrent disease, even though this issue has been poorly studied. In many oncologic situations-for example, metastatic lung cancer-this form of bias does not exist. In some situations, such as head and neck cancer, this could be an intermediate problem (Was that lethal chest tumor a second primary or a metastasis?.Would the fatal aspiration pneumonia have occurred if he still had a tongue?.And what about Mr. B. described above?). In some situations, particularly relatively "good prognosis" neoplasms, this could be a substantial problem, particularly if the adjudication of whether or not a death is cancer-related is performed solely by researchers who have an "interest" in demonstrating a good DSS. What we are most concerned about with this form of bias relates to recent series on observation, such as in early prostate cancer. It is interesting to note that although only 10% of the "observed" patients die from prostate cancer, many develop distant metastases by 10 years (approximately 40% among patients with intermediate grade tumors). Thus, it is implied that many prostate cancer metastases are usually not of themselves lethal, which is a misconception to anyone experienced in taking care of prostate cancer patients. This is inconsistent with U.S. studies of metastatic prostate cancer in which the median survival is two to three years. It is possible that many deaths attributed to intercurrent disease in "watchful waiting" series were in fact prostate cancer-related, perhaps related to failure to thrive, urosepsis, or pulmonary emboli. We will not know without an independent review of the medical records of individual patients; in some cases, even the most detailed review, sometimes even an autopsy, will not be conclusive. There are only a few data available describing the problems created by cause-of-death-interpretation bias. One small study, presented only in abstract form, assessed the cause of death in 50 randomly selected prostate cancer patients who died. Five experts in prostate cancer were asked to assign the cause of death as due to or not due to prostate cancer. The DSS varied from 21% to 35% among the five reviewers, a relative difference of 66%. Studies of autopsies, which are now rarely done in the U.S., have shown that fatal malignant tumors were occasionally missed by clinicians and-even more sobering-an occasional patient thought to have died from metastatic cancer is found to have no tumor but to have died from a "benign" cause such as TB. One study suggested an error rate of approximately 8%. Clearly the use of DSS is here to stay and is a useful adjunct to OS in analyzing randomized trials. There needs to be more research on the validity and interobserver reproducibility of the DSS. In the meantime, researchers should not report DSS without reporting OS and the reasons for intercurrent deaths should be described-peer reviewers should enforce this. As with so many other problems with statistics in the medical literature, it is the job of the reader to remain skeptical. The rate of intercurrent deaths in a study should reflect the age and demographics of the study population. If the DSS is far superior to the OS, the population being studied may be unusually sick (and thus unrealistic), or there may be a bias in classifying the causes of death. Similarly, if the DSS and OS are identical (unless a highly virulent malignancy is being studied), it may suggest the researchers have only included an unusually healthy (and thus unrealistic) patient population. Finally, we would also be a bit suspicious of a sizeable series that did not have any deaths that were considered of "uncertain" cause, unless the researchers specifically included them as being due to the cancer. We honestly think that everybody has a few patients like Mr. B.
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PMID:"Just Another Statistic" 1038 5

The findings in 44 patients (42 of whom were chronic alcoholics) with central pontine myelinolysis show that the outcome does not depend on the severity of neurological deficits during the acute phase of the condition or on concomitant internal diseases, including the degree of hyponatremia. Of the 34 patients for whom follow-up data were available, 32 survived. Of these 11 completely recovered, 11 had some deficits but were independent, and 10 were dependent (4 through disorders of memory or cognition, 3 with tetraparesis, 2 with cerebellar ataxia, 1 with polyneuropathy). The electrophysiological findings did not contribute usefully to the prediction of outcome. Additional neuroradiological diagnostic testing with magnetic resonance imaging was also of no prognostic significance. The extent of the initial pontine lesion was not correlated with the severity of clinical findings during the acute phase of disease, nor was persistence of the pontine lesion as usually seen on magnetic resonance imaging correlated with clinical improvement. We conclude that patients with cerebral myelinolysis survive if the nonspecific secondary complications of transient illnesses such as aspiration pneumonia, ascending urinary tract infection with subsequent septicemia, deep venous thrombosis, and pulmonary embolism can be avoided.
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PMID:Outcome of central pontine and extrapontine myelinolysis (n = 44). 1046 Apr 48

We report on the age and the causes of death in 16 patients with mitochondrial diseases. Nine patients with mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) died at a mean age of 34 years and three patients with chronic progressive external ophthalmoplegia at a mean age of 56 years. The causes of death were cardiopulmonary failure (n = 5), status epilepticus (n = 4), aspiration pneumonia (n = 2), pulmonary embolism (n = 2), renal failure (n = 1), metabolic disturbance (n = 1), and unknown causes (n = 1). Thus, many patients in this series died of medical complications, some of which may be prevented.
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PMID:Age and cause of death in mitochondrial diseases. 1048 54

Neuroleptic malignant syndrome is an uncommon but potentially fatal side effect of antipsychotic drug treatment. Several serious complications have been associated with neuroleptic malignant syndrome, such as acute renal failure, deep venous thrombosis, pulmonary embolism and aspiration pneumonia. Reports on infections other than aspiration pneumonia appear, from the literature, to be uncommon. Four cases of infection (three cases of upper respiratory tract infection and one case of urinary tract infection) which developed during the course of neuroleptic malignant syndrome are reported and pathophysiological mechanisms underlying their presentation are suggested.
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PMID:Infections as complications of neuroleptic malignant syndrome. 1860 25


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