Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019079 (hemoptysis)
 6,129 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Breath-hold divers may experience haemoptysis during diving. Central pooling of blood as well as compression of pulmonary gas content can damage the integrity of the blood-gas barrier, resulting in alveolar hemorrhage. The single-breath carbon monoxide test (DL,CO) was used to investigate the blood-gas barrier following diving. The study population consisted of 30 divers recruited from a training course. DL,CO levels were measured before diving and at 2, 10 and 25 min after the last of a series of four dives to depths of 10, 15, 20 and 30 m. When compared to pre-diving values, DL,CO values increased significantly at 2 min following diving in all subjects except one. Thereafter values progressively decreased toward baseline at 10 and 25 min in all subjects but one, while in four divers DL,CO values decreased below baseline. The early but transient increase in DL,CO levels shortly after diving supports the persistence of capillary pooling of red blood cells following emersion. Persistence at 25 min of high DL,CO values in one subject could be attributed by lung CT to extravasation of blood into the alveoli. Early or late DL,CO values >10% below baseline values suggest the presence of pulmonary edema. The relatively high prevalence of DL,CO alterations found suggests caution on the safety of breath-hold diving activities.
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PMID:Time course of carbon monoxide transfer factor after breath-hold diving. 1946 49

Tuberous sclerosis complex (TSC) is an autosomal-dominant disorder characterized by seizures, mental retardation, and various hamartomatous lesions, including renal angiomyolipoma (AML) and pulmonary lymphangioleiomyomatosis. A 22-year-old woman with TSC presented with multiple renal AMLs exceeding 4 cm in diameter. She underwent two transcatheter embolization procedures with a mixture of ethanol and iodized oil. She complained of dyspnea and minor hemoptysis 4 and 6 hours after the procedure. Findings on chest radiographs and computed tomographic images were indicative of pulmonary edema. The patient was treated with conservative therapy. The possible causes of the pulmonary edema are discussed in the text.
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PMID:Pulmonary edema as a complication of transcatheter embolization of renal angiomyolipoma in a patient with pulmonary lymphangioleiomyomatosis due to tuberous sclerosis complex. 1946 8

Community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) is epidemic in the United States, even rivaling HIV/AIDS in its public health impact. The pandemic clone USA300, like other CA-MRSA strains, expresses Panton-Valentine leukocidin (PVL), a pore-forming toxin that targets polymorphonuclear leukocytes (PMNs). PVL is thought to play a key role in the pathogenesis of necrotizing pneumonia, but data from rodent infection models are inconclusive. Rodent PMNs are less susceptible than human PMNs to PVL-induced cytolysis, whereas rabbit PMNs, like those of humans, are highly susceptible to PVL-induced cytolysis. This difference in target cell susceptibility could affect results of experimental models. Therefore, we developed a rabbit model of necrotizing pneumonia to compare the virulence of a USA300 wild-type strain with that of isogenic PVL-deletion mutant and -complemented strains. PVL enhanced the capacity of USA300 to cause severe lung necrosis, pulmonary edema, alveolar hemorrhage, hemoptysis, and death, hallmark clinical features of fatal human necrotizing pneumonia. Purified PVL instilled directly into the lung caused lung inflammation and injury by recruiting and lysing PMNs, which damage the lung by releasing cytotoxic granule contents. These findings provide insights into the mechanism of PVL-induced lung injury and inflammation and demonstrate the utility of the rabbit for studying PVL-mediated pathogenesis.
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PMID:Polymorphonuclear leukocytes mediate Staphylococcus aureus Panton-Valentine leukocidin-induced lung inflammation and injury. 2023 57

Swimming-Induced Pulmonary Oedema (SIPE) has been described in military combat swimmers in both the US and Israeli Navies. The pathophysiology is explained by the immersion in cold water, and its effects on central vascular volume. SIPE has been hypothesized to be caused by pulmonary capillary stress failure (PCSF) due to elevations in pulmonary capillary transmural pressure. This leads to mechanical impairment and leakage of blood cells and proteins from capillaries. Patients with SIPE can present with pronounced dyspnoea, cough, hypoxemia and profuse frothy haemoptysis. Physical examination and chest X-rays usually show evidence of pulmonary oedema. The treatment of choice is to recognize the symptoms, get the patient out of the water and follow with close observation for emergent problems. Soldiers prone to acquire SIPE should be identified as this medical condition has a high degree of recurrence. The awareness of the symptoms of SIPE will increase appropriate diagnosis and therefore inform treatment.
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PMID:Swimming-induced pulmonary oedema--a hazard in intensive military training? 2127 62

Pulmonary edema has been reported in SCUBA divers, apnea divers, and long-distance swimmers however, no instances of pulmonary edema in triathletes exist in the scientific literature. Pulmonary edema may cause seizures and loss of consciousness which in a water environment may become life threatening. This paper describes pulmonary edema in three female triathletes. Signs and symptoms including cough, fatigue, dyspnea, haemoptysis, and rales may occur within minutes of immersion. Contributing factors include hemodynamic changes due to water immersion, cold exposure, and exertion which elevate cardiac output, causing pulmonary capillary stress failure, resulting in extravasation of fluid into the airspace of the lung. Previous history is a major risk factor. Treatment involves immediate removal from immersion and in more serious cases, hospitalization, and oxygen administration. Immersion pulmonary edema is a critical environmental illness of which triathletes, race organizers, and medical staff, should be made aware.
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PMID:Immersion pulmonary edema in female triathletes. 2166 Feb 30

We report the case of a healthy 21-year-old woman who performed iterative breath-hold dives in relatively cold water, not exceeding depths of 5 meters but with "empty lungs." At the end of a dive, after experiencing an intense involuntary diaphragmatic contraction underwater, she presented hemoptysis followed by chest pain and cough. Chest radiography and computed tomography were performed 24 hours later, confirming the diagnosis of pneumomediastinum. The clinical course was benign: However, chest pain and effort dyspnea lasted for a few weeks. The pathophysiology of this accident may be explained by a combination of mechanisms involved in several clinical entities, namely pulmonary edema of immersion, pulmonary barotrauma and spontaneous pneumomediastinum.
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PMID:Hemoptysis and pneumomediastinum after breath-hold diving in shallow water: a case report. 2172 55

Acute pulmonary edema complicating electroconvulsive therapy is an extremely uncommon event that has rarely been described in the literature. Different theories, including one suggesting a cardiogenic component, have been proposed to explain its genesis. The present report describes a classic presentation of this condition with review of its potential mechanisms and diagnostic approach. After successful completion of a session of electroconvulsive therapy, a 42-year-old woman with major depressive disorder developed acute systemic high blood pressure, shortness of breath, and hemoptysis. A chest radiograph demonstrated diffuse bilateral pulmonary infiltrates. Initially cardiogenic pulmonary edema was presumed, but an extensive diagnostic work-up demonstrated normal systolic and diastolic left ventricular function, and with only supportive measures, a complete clinical and radiographic recovery was achieved within 48 hours. The present case does not support any cardiogenic mechanism in the genesis of this condition.
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PMID:Non-cardiogenic pulmonary edema complicating electroconvulsive therapy: short review of the pathophysiology and diagnostic approach. 2203 75

In children, post-obstructive pulmonary edema is a rare condition, caused by a sudden change in upper airway patency. It causes dyspnea, tachypnea, hypoxemia, and at times hemoptysis and respiratory insufficiency. It occurs as a complication in the immediate post-operative period. Pediatricians should be aware of this clinical entity.
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PMID:Hemoptysis after orthopedic surgery in an adolescent boy. 2203 84

Hemoptysis and pulmonary edema associated with nonsteroidal anti-inflammatory drug use is a known condition, but is probably underreported. The mechanisms of induction of pulmonary toxicity are still not well understood. We describe a case of hemoptysis and dyspnea in a scuba diver who was taking diclofenac.
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PMID:Hemoptysis and pulmonary edema in a scuba diver using diclofenac. 2235 73

This study's aim was to define the clinical manifestations and long-term outcome of pediatric patients living at altitude with isolated pulmonary artery (PA) of ductal origin (IPADO). This was a retrospective cohort study of 17 consecutive cases of IPADO at a single center. All patients lived at modest altitude (median 2050 m [range 1700 m to 3050 m]). Fifteen children (88%) were symptomatic at presentation. High-altitude pulmonary edema was present in 2 patients (12%) at diagnosis, and only 1 patient had episodes of hemoptysis during follow-up. Fourteen patients (82%) demonstrated evidence of pulmonary arterial hypertension (PAH). Among 14 patients with PAH, 11 patients had surgical interventions. PAH resolved in 5 of 11 patients (45%) undergoing surgical rehabilitation. One patient died during follow-up, and 7 patients are receiving oral vasodilator therapies due to residual PAH; 14 patients remained asymptomatic. Our study showed that early intervention in patients with IPADO at modest altitude can potentially rehabilitate the isolated PA and reverse PAH. Whether surgery is indicated for patients with this disorder in the absence of PAH is unknown.
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PMID:Clinical manifestations and long-term follow-up in pediatric patients living at altitude with isolated pulmonary artery of ductal origin. 2243 Mar 74


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