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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To examine whether pulmonary dysfunction leads to episodes of cerebral hypoxia during recurrent seizures, measurements were made of arterial blood pressure, blood-gases, cerebral pO2, and relative changes in cytochrome a,a3 redox levels in anesthetized, paralyzed rats. Seizures were induced serially with bicuculline (BIC) or pentylenetetrazol (PTZ). During early seizures, cerebral oxygenation increased phasically. As seizures continued, a transition often occurred following which seizures were accompanied by phasic decreases in cerebral oxygenation. In addition, pulmonary edema often occurred at an unpredictable point during a series of seizures. Seizure-associated pulmonary edema was less likely to occur with pentobarbital anesthesia and PTZ seizures, than with nitrous oxide anesthesia and BIC seizures. Pulmonary edema was always accompanied by prolonged increases in blood pressure and paroxysmal electrocortical activity, and by hypoxemia, acidemia, and decreased cerebral oxygen supply. Despite the severity of these physiological changes, the transition from phasic increases to decreases in cerebral oxygenation during serial seizures occurred with virtually the same frequency in rats with and without pulmonary edema. This indicates that this transition is independent of pulmonary edema.
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PMID:Role of pulmonary edema in phasic changes of cerebral oxygenation during serial seizures. 282 May 45

We prospectively studied 56 consecutive patients with severe tricyclic antidepressant ingestion to determine the incidence of associated pulmonary complications. Among the patients meeting the entrance criteria, the mean antidepressant level was 1136 ng/ml. Other characteristics were a QRS duration of greater than or equal to 0.1 seconds in 35 (63%) and seizures in 19 (34%). Seventeen patients (30%) developed 18 abnormal chest X-ray findings which included pulmonary edema in 8 cases and aspiration pneumonia in 10. Using logistic regression, we evaluated the influence of tricyclic antidepressant level, blood pressure, QRS interval, seizures, drug co-ingestion and the use of gastric lavage vs. ipecac-induced emesis on pulmonary complications. For patients with pulmonary edema, the only significantly associated factor was hypotension on emergency department presentation. For aspiration pneumonia, no significant associations were found. Co-ingestion of another drug had no apparent influence on the development of pulmonary abnormalities. Our findings suggest that pulmonary edema and aspiration pneumonia are frequent complications of severe ingestions of tricyclic antidepressants. Pulmonary edema appears to result from hypotension or its treatment. The etiology of aspiration pneumonia is unclear. A chest X-ray should be obtained in all victims of tricyclic antidepressant overdose.
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PMID:Pulmonary consequences of severe tricyclic antidepressant ingestion. 289 71

A case of acute neurogenic pulmonary oedema following a generalized tonic clonic seizure is presented. The condition is rare and the exact pathophysiology is unknown. Pulmonary oedema is a serious complication of epileptic seizures, however, and the importance of awareness of this condition and its treatment is emphasized by a high mortality rate in older epileptics and by the demonstration of pulmonary oedema in recent series of young epileptics who died suddenly.
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PMID:Acute neurogenic pulmonary oedema following generalized tonic clonic seizure. A case report and a review of the literature. 305 77

A 32-year-old woman was examined in the Department of Internal Medicine at Saiseikai Fukuoka General Hospital after a grand mal seizure on December 29, 1985. She had a history of eclampsia 5 years before but had had no evidence of convulsive seizure. Chest examination revealed rales over the bilateral chest. The cardiac examination revealed no abnormalities. Laboratory data on admission included a total white blood cell count of 13000/mm3. The electrocardiogram also failed to reveal any abnormalities. Analysis of arterial blood with the patient breathing room air revealed a PaO2 of 51.2 mmHg, PaCO2 of 33.1 mmHg and a pH of 7.426. The chest film showed diffuse bilateral nodular-appearing alveolar infiltrate and a normal cardiac size. Cardiac function test using Swan-Ganz catheter was performed after 10 hours of onset. However, no abnormalities in pulmonary arterial pressure (PAP) and pulmonary capillary wedge pressure (PCWP) were noted. She was treated with Latamoxef and supplementally inspired oxygen. A repeat chest roentgenogram taken 7.5 hours after admission showed marked improvement. She was discharged without any residual symptoms and continued as an outpatient under the administration of sodium valproate. However, the drug was discontinued because of the presence of seizure was under suspicion. On August 24, 1986, she was readmitted for pulmonary edema after another grand mal seizure. The clinical course was uneventful and was almost the same as the previous episode. She was treated with oxygen only, via nasal catheter.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Recurrent postictal pulmonary edema--a case report]. 313 30

The effect of elevated baseline pulmonary vascular pressures on systemic and pulmonary vascular sequelae of prolonged seizures was studied in sheep. Five animals with seizures induced after baseline left atrial pressure elevations of 25 mm Hg were compared with animals treated with seizures alone. Seizure-induced elevations from baseline of systemic and pulmonary vascular pressures were identical in the two groups both in height and duration. In animals with left atrial balloon inflation prior to seizures, however, the peak pulmonary arterial and left atrial pressures were the sum of baseline elevation (induced by left atrial balloon inflation) and the seizure-induced pressure elevation. Accordingly, the resultant pulmonary vascular pressure and resultant pulmonary lymph flow elevations, were substantially greater in these animals with elevation in baseline pulmonary vascular pressures. Therefore, patients with pulmonary vascular hypertension are at greater risk for pulmonary edema during seizures.
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PMID:Effect of pulmonary vascular pressure on lung lymph flow following seizures. 333 8

Sixty four patients who presented to the emergency department following severe acute tricyclic antidepressant (TCA) overdose (defined as an antidepressant ingestion associated with a QRS interval greater than or equal to 0.10 seconds, TCA level greater than or equal to 500 ng/mL, or grade IV coma) were prospectively evaluated to determine the incidence of hypotension and the factors associated with its development. Among these patients, the mean antidepressant level was 1,094 ng/mL. The overall frequency of admission hypotension (systolic BP less than 95 mmHg) was 34% (22 of 64 patients). Using regression analysis, systolic BP showed poor correlation with TCA level (r = -.37) and maximal QRS interval (r = -.17) following severe TCA overdose. Using multivariate analysis with a logistic regression model, the influence of BP (as well as TCA level, QRS interval, and coingestion of another drug) was evaluated on four clinical outcomes: seizures, arrhythmias, aspiration pneumonia, and pulmonary edema. The occurrence of arrhythmias and pulmonary edema was significantly associated (inversely) with hypotension (P less than .01). Seizures and aspiration pneumonia were unrelated to admission BP. These results suggest that hypotension is common after severe TCA overdose and occurs independently of TCA level and prolongation of the QRS interval. Hypotension is strongly associated with the development of arrhythmias and pulmonary edema. Seizures and aspiration pneumonia may occur regardless of initial BP.
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PMID:Hypotension in severe tricyclic antidepressant overdose. 341 35

Neurogenic pulmonary edema may be a consequence of a number of diverse central nervous system insults, including resection of an acoustic neuroma. Brainstem lesions in particular seem to cause neurogenic pulmonary edema. Diagnosis requires a high index of suspicion, especially in the case of respiratory decompensation following a seizure.
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PMID:Neurogenic pulmonary edema. 349 52

Cerebral partial pressure of O2 (PO2), relative changes in the ratio of reduced/oxidized cytochrome aa3, blood flow, and the arteriovenous difference in O2 content were measured during seizures with and without pulmonary edema. Seizures were induced with bicuculline (0.2-1.2 mg/kg iv) in rats anesthetized with 70% N2O and paralyzed with curare. Briefer seizures were accompanied by increased cerebral PO2 and increased oxidation of cytochrome aa3. Lung water content and arterial O2 partial pressure (PaO2) remained normal. Longer duration seizures were also accompanied initially by increases in cerebral oxygenation. Within minutes, however, PaO2 fell from a mean of 118 to 51 mmHg, and lung water content increased from 76.2 to 83.6%. Cerebral PO2 fell but most often rose back to or above control levels, while cytochrome aa3 became markedly reduced. Simultaneously, cerebral blood flow increased more than 300% above preseizure values and O2 delivery increased more than O2 consumption. The reductive shift of cytochrome aa3 was greater than that produced by lowering PaO2 to equivalent values in seizure-free rats. The reductive shift of cytochrome aa3, despite increased O2 delivery, may be indicative of derangements in cerebral O2 diffusion or energy metabolism.
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PMID:Seizure-associated pulmonary edema and cerebral oxygenation in the rat. 355 25

There is evidence from pediatric tertiary care centers in the United States that childhood deaths from asthma in hospitalized patients are becoming increasingly rare, while asthma mortality outside the hospital appears to be on the rise. When a young outpatient with asthma dies, the event is apt to be sudden and unanticipated and the victim is likely to be a preadolescent or adolescent who has suffered from asthma most of his or her life and who, despite ongoing bronchodilator therapy, requires hospitalizations for treatment of status asthmaticus. Patients in this age cohort have a strong tendency to underuse, overuse, or neglect to use prescribed medications, possibly as a gesture of emerging independence or because of the depression engendered by a chronic illness. In some instances serious psychosocial pathology accounts for noncompliance. For a patient with chronic asthma with a high-risk profile, any departure from an ongoing treatment regimen may result in respiratory failure. Pathologic complications of asthma may also act to upset the precarious physiologic equilibrium these patients have established. Unsuspected chronic pneumonia may lead to further increases in a chronically high degree of oxygen desaturation. Hypoxic seizures during an asthma attack may precipitate pulmonary edema. Tension pneumothorax has an even greater fatality potential for high-risk patients with asthma than it has for other patients with asthma, and pulmonary hypertension with cor pulmonale may develop because of chronic hypoxia. Some sudden deaths in children with chronic, severe asthma are unassociated with any of the above, making it necessary to entertain still other hypotheses.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:An analysis of fifteen childhood asthma fatalities. 362

We report three patients with recurrent tonic-clonic seizures associated with unilateral pulmonary edema. Each lung was involved on separate occasions in one patient. The mechanisms of seizure-related pulmonary edema are discussed. Although accurate diagnosis of unilateral postictal pulmonary edema may be difficult because of its rarity, not all pulmonary abnormalities that follow seizures represent pneumonia.
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PMID:Epileptic seizures as a cause of unilateral pulmonary edema. 379 88


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