1/41. A case of fatal salt water intoxication following an exorcism session.In response to a recent article published in this review, we present in this paper, an unusual case of fatal salt water intoxication. In this case, we point out three special features, the type of water ingested, the physiopathologic consequences of the ingestion and the very strange context of occurrence. This complex case allows us to point out complications due to salt poisoning and others caused by water intoxication.- - - - - - - - - - ranking = 1keywords = water (Clic here for more details about this article) |
2/41. Haemoptysis after breath-hold diving.Pulmonary oedema has been described in swimmers and self-contained underwater breathing apparatus (Scuba) divers. This study reports three cases of haemoptysis secondary to alveolar haemorrhage in breath-hold divers. Contributory factors, such as haemodynamic modifications secondary to immersion, cold exposure, exercise and exposure to an increase in ambient pressure, could explain this type of accident. Furthermore, these divers had taken aspirin, which may have aggravated the bleeding.- - - - - - - - - - ranking = 0.14285714285714keywords = water (Clic here for more details about this article) |
3/41. Chemotherapy-induced noncardiogenic pulmonary edema related to gemcitabine plus docetaxel combination with granulocyte colony-stimulating factor support.Several cancer therapeutic agents have been associated with pulmonary toxicity. Herein, we describe the case of a 73-year-old woman with breast cancer metastatic to the liver, who developed noncardiogenic pulmonary edema (NPE) while on treatment with gemcitabine plus docetaxel combination with granulocyte colony-stimulating factor (G-CSF) support. Gemcitabine, a deoxycytidine analogue, is reported to produce mild self-limiting and only occasionally severe pulmonary toxicity. The microtubule stabilizer docetaxel has been associated with water retention complications. The combination of these two agents has shown promising activity in several solid tumors and is in a phase of clinical development with prophylactic G-CSF in most of the trials due to the high rate of dose-limiting neutropenia observed with this combination. In our case pulmonary toxicity resolved rapidly following the administration of corticosteroids. A possible deleterious synergy of the compounds involved in this case is discussed and the medical literature on NPE related to cancer therapy is shortly reviewed. We conclude that NPE should always be considered in patients with respiratory function deterioration while on therapy with the gemcitabine-docetaxel combination and G-CSF. Corticosteroids can provide maximum benefit if started early upon diagnosis coupled with withdrawal of the causative drugs.- - - - - - - - - - ranking = 0.14285714285714keywords = water (Clic here for more details about this article) |
4/41. Scuba diving-induced pulmonary edema in a swimming pool.SCUBA diving-induced pulmonary edema is a rare syndrome that has been previously reported to occur in cold water. We present a case of SCUBA diving-induced pulmonary edema in a 52-year-old man diving in a warm swimming pool. The pathophysiology of this syndrome is unclear, but it is unrelated to either barotrauma or decompression illness. This patient developed frank pulmonary edema while submerged, which resolved after surfacing. As with other patients who have had this syndrome, he did not have any cardiorespiratory disease. The presentation and pathophysiology of SCUBA diving-induced pulmonary edema are discussed.- - - - - - - - - - ranking = 0.14285714285714keywords = water (Clic here for more details about this article) |
5/41. methadone-induced pulmonary edema.A patient with methadone-induced pulmonary edema had increased extravascular water in the lungs and a reduced total vascular albumin space. diuresis resulted in hypotension. These observations suggest that the appropriate treatment of this condition should be ventilatory support and restoration of plasma oncotic pressure with albumin. Diuretic therapy should be used with caution.- - - - - - - - - - ranking = 0.14285714285714keywords = water (Clic here for more details about this article) |
6/41. Fatal water intoxication of an Army trainee during urine drug testing.An Army trainee developed acute water intoxication, hyponatremia, pulmonary edema, and fatal cerebral edema. This is the first report of a fatality related to urine drug testing. This resulted from supervised excessive water ingestion in an attempt to induce a sufficient urine specimen for substance abuse testing. To avoid a similar preventable death in the future, we make several recommendations. These include limiting the volume of ingested fluid to eight ounces every 30 to 45 minutes, not to exceed 40 ounces, and providing a relaxed, reassuring environment when obtaining urine specimens for substance abuse detection.- - - - - - - - - - ranking = 0.85714285714286keywords = water (Clic here for more details about this article) |
7/41. Bilateral pleural effusion and pulmonary edema caused by a fistulous aneurysm of the ductus arteriosus.We report an unusual case of pulmonary edema and rapid collection of bilateral pleural effusion caused by a fistulous large aneurysm of the ductus arteriosus (DAA). The diagnosis was performed by contrast CT and aortography. The cause of pulmonary edema and effusion was thought to be both elevated capillary pressure due to overload of the pulmonary circulation and decreased water clearance due to compression of the lymphatic system by the large DAA itself. Therefore, fistulous DAA should be considered when a continuous heart murmur and swelling in the aortic window are recognized. Once DAA is diagnosed, surgery should be performed without delay.- - - - - - - - - - ranking = 0.14285714285714keywords = water (Clic here for more details about this article) |
8/41. swimming-induced pulmonary edema.pulmonary edema of water immersion, which is not associated with aspiration or a closed glottis, is infrequently described in the literature. swimming-induced pulmonary edema is a syndrome whose pathophysiologic characteristics have not been fully elucidated. immersion alone has marked effects on central vascular volume, redistribution of pulmonary blood flow, and lung volumes. These changes are more prominent in cold water. These changes, coupled with an elevated cardiac output, may expose regions of the capillary bed to high pressures that favor the extravasation of fluid by hydrostatic forces and potential stress failure of the capillaries. patients with swimming-induced pulmonary edema present with dyspnea, cough, hypoxemia, and occasionally hemoptysis. physical examination and chest radiographs usually reveal evidence of pulmonary edema. Treatment is symptomatic and conservative. Improvement and resolution of symptoms are usually rapid, with radiographic normalization in 24 to 48 hours. We describe here 3 cases of swimming-induced pulmonary edema.- - - - - - - - - - ranking = 0.28571428571429keywords = water (Clic here for more details about this article) |
9/41. Pulmonary oedema in SCUBA divers: pathophysiology and computed risk analysis.SCUBA diving has become a popular sport, with an increasing number of people participating in it. Although it is an essentially very safe activity, several specific medical problems are associated with diving. The present paper addresses diving-related pulmonary oedema, which is a rarely reported condition. It has been described mostly in cold water diving, and its occurrence in warm water has not been documented before. We delineate the pathophysiology of this condition and its treatment, and use a novel computational model to analyse further the mechanisms leading to diving-related pulmonary oedema. A better understanding of diving-related pulmonary oedema may lead to earlier recognition and treatment, and, potentially, to its prevention. The physiological mechanisms likely to lead to diving-related pulmonary oedema are well recognized. Consequently, we could design and construct a bio-mechanical computer model of the alveolar septa to explore the pathophysiology of diving-related pulmonary oedema and the vulnerability of individual divers as they relate to some mechanical characteristics of their lung structure. The physiological mechanisms of diving-related pulmonary oedema and the results provided by the computational model successfully delineated the process. The model predicted that the risk of injury is significantly increased in individuals who have a stiffer lung parenchyma or lower lung compliance values.- - - - - - - - - - ranking = 0.28571428571429keywords = water (Clic here for more details about this article) |
10/41. Prolonged alveolocapillary barrier damage after acute cardiogenic pulmonary edema.OBJECTIVES: To determine whether acute cardiogenic pulmonary edema is associated with damage to the alveolocapillary barrier, as evidenced by increased leakage of surfactant specific proteins into the circulation, to document the duration of alveolocapillary barrier damage in this setting, and to explore the role of pulmonary parenchymal inflammation by determining if circulating tumor necrosis factor-alpha is increased after acute cardiogenic pulmonary edema. DESIGN: Prospective, observational study. SETTING: critical care, cardiac intensive care, and cardiology wards of a tertiary-care university teaching hospital. patients: A total of 28 patients presenting with acute cardiogenic pulmonary edema and 13 age-matched normal volunteers. INTERVENTIONS: Circulating surfactant protein-A and -B and tumor necrosis factor-alpha were measured on days 0 (presentation), 1, 3, 7, and 14. Clinical markers of pulmonary edema were documented at the same times. MEASUREMENTS AND MAIN RESULTS: Surfactant protein-A and -B were elevated on day 0 compared with controls (367 /- 17 ng/mL vs. 303 /- 17 and 3821 /- 266 ng/mL vs. 2747 /- 157 [mean /- sem], p <.05), and although clinical, hemodynamic and radiographic variables improved rapidly (p <.001), surfactant protein-A and -B rose further until day 3 (437 /- 22, p <.001, 4642 /- 353, p <.01). tumor necrosis factor-alpha was elevated at presentation (p <.05), doubled by day 1 (6.98 /- 1.36 pg/mL, p <.05), remained elevated on day 3 (5.72 /- 0.96 pg/mL, p <.05), and peak levels were related to chest radiograph extravascular lung water score (r(p) = 0.64, p =.003). CONCLUSIONS: Although the initial increase in plasma surfactant protein-A and -B may represent hydrostatic stress failure of the alveolocapillary barrier, the prolonged elevation, when hemodynamic abnormalities have resolved, and the delayed elevation of tumor necrosis factor-alpha are consistent with pulmonary parenchymal inflammation, which may further damage the alveolocapillary barrier. This prolonged physiologic defect at the alveolocapillary barrier after acute cardiogenic pulmonary edema may partly account for the vulnerability of these patients to recurrent pulmonary fluid accumulation.- - - - - - - - - - ranking = 0.14285714285714keywords = water (Clic here for more details about this article) |
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