Cases reported "Pulmonary Edema"

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1/1156. Negative-pressure pulmonary edema: a complication of shoulder arthroscopy.

    Negative-pressure pulmonary edema has been increasingly reported in surgical literature since 1977, yet there are no references to this condition in current orthopedic textbooks. We report a case of negative-pressure pulmonary edema occurring during arthroscopic surgery of the shoulder. The patient required reintubation for 5 days and hospitalization for 1 week. Because arthroscopic surgery is widely believed to be without complications, we want to make orthopedic surgeons aware of the possibility of negative-pressure pulmonary edema. ( info)

2/1156. Massive gastrointestinal hemorrhage after transoesophageal echocardiography probe insertion.

    PURPOSE: To describe a case of a massive gastric bleeding following emergency coronary artery bypass surgery associated with transoesophageal echocardiographic (TEE) examination. CLINICAL FEATURES: A 50-yr-old man was referred for an acute myocardial infarction and pulmonary edema (Killip class 3). Twelve hours after his myocardial infarction, he was still having chest pain despite an i.v. heparin infusion. coronary angiography revealed severe three-vessel disease with multifocal stenosis of the left anterior descending, circumflex and total occlusion of the right coronary artery. The patient was transferred to the operating room for emergency coronary artery bypass graft surgery. After total systemic heparinization (3 was obtained for cardiopulmonary bypass, a multiplane TEE probe was inserted without difficulty to monitor myocardial contractility during weaning from CPB. During sternal closure, the TEE probe was removed and an orogastric tube was inserted with immediate drainage of 1,200 ml red blood. Endoscopic examination demonstrated a mucosal tear near the gastro-oesophageal junction and multiple erosions were seen in the oesophagus. These lesions were successfully treated with submucosal epinephrine injections and the patient was discharged from the hospital eight days after surgery. CONCLUSION: This is a report of severe gastrointestinal hemorrhage following TEE examination in a fully heparinized patient. This incident suggest that, if the use of TEE is expected, the probe should preferably be inserted before the administration of heparin and the beginning of CPB. ( info)

3/1156. 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. ( info)

4/1156. hydrochlorothiazide-induced pulmonary edema and associated immunologic changes.

    OBJECTIVE: To describe a patient with noncardiogenic acute pulmonary edema induced by hydrochlorothiazide and to investigate the possible involvement of an immunologic mechanism in this adverse reaction. CASE SUMMARY: A 66-year-old Hispanic woman developed acute pulmonary edema 30 minutes after the ingestion of one tablet of triamterene 75 mg/hydrochlorothiazide 50 mg. The reaction was associated with hemoconcentration; a decreased white blood cell count with a shift to a predominance of polymorphonuclear cells; decreased serum immunoglobulin (Ig) G, IgG1, and IgG4; and increased serum IgM and complement 3 concentrations. DISCUSSION: Although there have been 35 reports of cases of hydrochlorothiazide-induced pulmonary edema, the etiology of this adverse reaction remains unknown. The observations presented in this case report, along with commonalities with previously reported cases, suggest that granulocytic infiltration into the lungs and IgG deposition in alveolar membranes may play a role in hydrochlorothiazide-induced pulmonary edema. CONCLUSIONS: Noncardiogenic pulmonary edema may be an immunologically mediated rare idiosyncratic reaction to hydrochlorothiazide. ( info)

5/1156. pulmonary edema after resection of a fourth ventricle tumor: possible evidence for a medulla-mediated mechanism.

    A well-recognized fact is that some patients may have development of pulmonary edema in association with disorders of the central nervous system. The origin of this phenomenon, known as neurogenic pulmonary edema, is unclear but may result, in part, from select pulmonary venoconstriction modulated by autonomic outflow from the medulla oblongata. We describe a 21-year-old man who had development of pulmonary edema in association with surgical resection of a brain tumor that was close to the medulla. Other than the possibility of medullary dysfunction, which could have occurred after surgical manipulation, no other risk factor for pulmonary edema was identified. Of note, the patient's blood pressure remained normal throughout the perioperative period, and no fluid overload or primary cardiac dysfunction was evident. This case supports the theory that the medulla is an important anatomic site of origin for neurogenic pulmonary edema and that alterations in medullary function can induce pulmonary edema in humans, independent of systemic hypertension. ( info)

6/1156. Postoperative pulmonary edema.

    BACKGROUND: Noncardiogenic pulmonary edema may be caused by upper airway obstruction due to laryngospasm after general anesthesia. This syndrome of "negative pressure pulmonary edema" is apparently well known among anesthesiologists but not by other medical specialists. methods: We reviewed the cases of seven patients who had acute pulmonary edema postoperatively. RESULTS: There was no evidence of fluid overload or occult cardiac disease, but upper airway obstruction was the most common etiology. Each patient responded quickly to therapy without complications. CONCLUSIONS: Of the seven patients with noncardiogenic postoperative pulmonary edema, at least three cases were associated with documented laryngospasm causing upper airway obstruction. This phenomenon has been reported infrequently in the medical literature and may be underdiagnosed. Immediate recognition and treatment of this syndrome are important. The prognosis for complete recovery is excellent. ( info)

7/1156. ehrlichiosis with severe pulmonary manifestations despite early treatment.

    It is generally thought that if patients with ehrlichiosis are treated promptly, life-threatening illness can be avoided. We report a patient who sought medical attention 1 day after the onset of symptoms, was immediately given doxycycline, and still had serious illness with generalized edema, pulmonary infiltrates, acute respiratory distress syndrome, and noncardiogenic pulmonary edema, while receiving replacement intravenous fluids. This case alerts physicians to the serious end of the disease spectrum that can occur even though patients are given prompt, appropriate drug treatment at the onset of illness. Further studies are needed to clearly define the mechanisms involved in pulmonary complications and generalized edema, including noncardiogenic pulmonary edema, in patients with ehrlichiosis. ( info)

8/1156. Drug-induced lung disease.

    Since there are no diagnostic studies to confirm the presence of a drug-induced lung reaction the physician will make a correct diagnosis only if he is aware of the drugs which have been identified to cause pulmonary reactions and their specific manifestations. Failure to recognize a drug-induced lung disease can lead to significant morbidity and in some cases mortality. The major drug-induced lung diseases are reviewed, the drugs being presented in the context of their clinical use and the reactions on the basis of common pathogenetic mechanisms. ( info)

9/1156. Negative pressure pulmonary hemorrhage.

    Negative pressure pulmonary edema, a well-recognized phenomenon, is the formation of pulmonary edema following an acute upper airway obstruction (UAO). To our knowledge, diffuse alveolar hemorrhage has not been reported previously as a complication of an UAO. We describe a case of negative pressure pulmonary hemorrhage, and we propose that its etiology is stress failure, the mechanical disruption of the alveolar-capillary membrane. ( info)

10/1156. 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. ( info)
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