Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of acute pulmonary complication following intra-arterial infusion of Lipiodol-Adriamycin emulsion for hepatocellular carcinoma was reported. Intra-arterial infusion chemotherapy was performed on a 75-year-old male with Lipiodol-Adriamycin emulsion (Lipiodol 8 ml + Adriamycin 40 mg). Severe dyspnea and cyanosis started about 30 minutes after the infusion, and blood gas analysis revealed hypoxemia and hypocapnia. Chest X-ray revealed diffuse infiltrative shadow throughout the both lungs. He was on positive end-expiratory pressure breathing for 4 days. Clinical symptoms and chest X-ray improved rapidly in the course of two weeks, he became almost asymptomatic. We concluded that the nature of this pulmonary damage was pulmonary edema due to the large amount of Adriamycin that flowed into pulmonary artery via arterio-venous shunt present in the hepatocellular carcinoma.
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PMID:[Pulmonary complication following intra-arterial infusion of lipiodol-adriamycin emulsion for hepatocellular carcinoma, report of a case]. 215 47

Presented here is a case of unilateral pulmonary edema following acute subglottic edema after removal of an endotracheal tube. A 3-year-old boy, diagnosed as having nondiphtheric croup and pectus excavatum deformity, was scheduled for repair of a cleft lip. No complication occurred during the operation. After removal of the endotracheal tube, he showed dyspnea and cyanosis and was later found to have acute subglottic edema. After reintubation of the trachea, frothy pink fluid was discharged from the tube, and chest roentgenogram showed a right-sided alveolar infiltrate. Many factors may cause unilateral pulmonary edema, but it is suggested that acute subglottic edema and unilateral bronchial fragility strongly affected this episode.
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PMID:Unilateral pulmonary edema following acute subglottic edema. 231 May 80

A case of severe vasoconstriction treated as cardiorespiratory collapse in a woman given extraamniotic PGF2alpha for midtrimester abortion is described, with comments on management of this rare reaction. The patient was having elective termination because of confirmed spina bifida with hydrocephalus by ultrasound and elevated AFP at 18 weeks gestation. She was given a 4 mg test dose of PGF2alpha (Dinoprost, Upjohn Pty, Ltd) in viscous gel (Tylose MH300, Hoechst Australia Ltd) via extraamniotic Foley catheter. She immediately developed dyspnea, abdominal and breast pain, hypotension of 50 mm Hg systolic, peripheral vasoconstriction, cyanosis and confusion. She was treated with iv Hartmann's solution 600 ml, oxygen 8 1/min, and sc adrenaline 1/1000 0.5 ml. She seemed to improve after receiving 500 ml 3.5% polygeline colloid (Haemaccel, Behringwerke AG), and 5 ml 1/10,000 adrenaline iv, as her systolic blood pressure rose to 70 mm Hg measured indirectly. 500 ml more iv colloid was given, and blood pressure rose to 90 mm Hg. Then she suddenly deteriorated with florid pulmonary edema. Oxygen saturation fell and positive pressure ventilation was begun. She was given furosemide 160 mg iv and hydrocortisone 500 mg iv. Anaphylactic reaction was ruled out on the basis of blood count; amniotic fluid embolism was ruled out because of minor changes in clotting parameters. The events seen here most likely occurred as a result of inadvertent injection of PGF2alpha into the arterial circulation, causing increased pulmonary arterial pressure and vascular resistance, systemic vasoconstriction interpreted as hypotension, all exacerbated by adrenaline and exogenous fluid load. Severe hypertension after extraamniotic PGF2alpha has been reported before in a similar case of apparent hypotension treated with agents to increase blood pressure. PGF2a should not be used without facilities to treat such adverse reactions.
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PMID:Cardiorespiratory collapse and pulmonary oedema due to intravascular absorption of prostaglandin F2 alpha administered extraamniotically for midtrimester termination of pregnancy. 260 61

Aluminium phosphide (ALP) a major suicidal agent in the developing countries is freely available as grain fumigant. It is highly toxic to lungs, heart and blood vessels causing pulmonary oedema, shock and arrhythmias. There is massive focal myocardial damage resulting in raised cardiac enzymes. Clinical manifestations were nausea and vomiting (32), dyspnoea and palpitations (25 each), cyanosis (12), hypotension (12) and shock (15). Cardiac arrhythmias were present in 28 cases and hypermagnesaemia in 13 patients. Mean serum magnesium level (1.95 +/- 0.2O, mEq/L) was significantly raised compared to mean magnesium level in control subjects (1.62 +/- 0.23 mEq/L). Hypermagnesaemia occurs due to myocardial and liver damage. Out of 32 cases studied, 22 died 18 within 24 hours of ALP ingestion. Thirty two cases of ALP were studied.
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PMID:Cardiovascular manifestations of aluminium phosphide intoxication. 238 68

Nitrofurantoin is a widely prescribed antibiotic used for the treatment of urinary tract infections. In some patients it can produce an acute pulmonary reaction ranging from mild dyspnea to noncardiogenic pulmonary edema. Symptoms include fever, dyspnea, chills, cough, and chest pain. Physical examination generally reveals an acutely ill, extremely apprehensive patient in varying degrees of respiratory distress. Fever is usually present and there is an increase in heart rate and respiratory rate. Cyanosis, rales, and a maculopapular rash are common findings. Laboratory studies typically demonstrate a leukocytosis with eosinophilia, varying degrees of hypoxia and hypocapnia, and a mild to moderate elevation of the erythrocyte sedimentation rate. The chest x-ray study may be normal but more often demonstrates bilateral lower lobe interstitial infiltrates frequently accompanied by pleural effusions. Treatment in the majority of cases requires only stopping the drug, but steroids, bronchodilators, or antihistamines may be used in selected cases. Once the diagnosis is made and the drug withdrawn, prognosis for full recovery is excellent.
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PMID:Acute pulmonary toxicity to nitrofurantoin. 270 84

The interest in mountain tracking and climbing has increased and there is a need for knowledge of altitude-related diseases. About one million non-acclimatized individuals annually frequent areas around 2,000 to 3,000 m above sea level and incur unpleasant symptoms in the form of acute altitude sickness or potentially fatal conditions such as pulmonary and/or cerebral oedema. Headache is the most prominent sign of acute altitude sickness but fainting fits, loss of appetite, hesitant gait, euphoria, or confusion also occur. Dyspnoea, cyanosis at rest, and a dry cough are signs of pulmonary oedema. Cerebral oedema may be feared when inexperienced climbers are afflicted by severe headaches, vomiting, and hesitant gait. Coma ensues relatively soon. Treatment consisting in descent to lower altitude, administration of oxygen, and possible medicinal therapy is effective if immediately introduced.
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PMID:[Altitude sickness]. 291 57

A case of high altitude pulmonary edema with high altitude cerebral edema was reported. A young Japanese male complained of severe palpitation and shortness of breath on the third day of climbing at 3,000 m above sea level. During the next 2 d at altitude, the following symptoms occurred: cough with foamy sputum, cyanosis, and loss of consciousness. Soon after evacuation, he showed severe hypoxemia and deep coma with decerebrate rigidity; electroencephalogram showed diffuse alpha waves, indicating "alpha wave coma." Brain computerized tomography revealed brain edema, showing small compressed ventricles and diffuse low density of the cerebrum. Pulmonary edema on chest roentgenogram disappeared by the fifth hospital day, and his consciousness recovered gradually during the next 2 weeks after the admission. He was examined serially by electroencephalography and brain computerized tomography. He recovered fully, but there were transient psychological abnormalities soon after discharge and mild brain atrophy was observed by brain computerized tomography 6 years later.
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PMID:A case of high altitude pulmonary edema followed by brain computerized tomography and electroencephalogram. 320 90

A case is reported of acute airway obstruction and pulmonary oedema of mixed origin (cardiogenic and non cardiogenic), occurring in a patient after surgical treatment for pericardial tamponade due to a mediastinal tumour. This 45 year old female patient had a non-Hodgkin lymphoma, mostly located within the anterior and middle mediastinum. When she developed cardiac tamponade, emergency cardiac decompression was carried out. The surgical procedure went well, despite an episode of severe hypotension. Immediately after extubation, she developed paradoxical breathing with retraction and cyanosis. She was reintubated and ventilated. The chest X-ray showed bilateral alveolar infiltrates, mostly around the hilar. Two hours later, she was again extubated and developed again the same respiratory failure. This time, she was intubated and ventilated for 48 h. She was then extubated with no problem. It seemed most probable that transmission to the interstitial space of a negative intrapleural pressure due to the inspiratory efforts made against an occluded airway was the principal mechanism responsible for the accumulation of fluid to this space.
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PMID:[Acute pulmonary edema following airway obstruction and cardiac tamponade related to mediastinal tumor]. 322 41

Pulmonary edema after re-expansion of a pneumothorax occurs within a maximum of 3 days of the pneumothorax and manifests by intense clinical signs (cough, abundant foamy expectoration, major cyanosis), marked hypoxia and a "white lung" radiologic image. The outcome was rapidly favorable in the case reported, despite the severity of the initial symptomatology. Currently accepted physiopathologic mechanisms implicate numerous factors in the genesis of edema due to re-expansion. The lesional pulmonary edema can be explained by alteration in alveolar capillary permeability, by the atelectasis, hypoperfusion and stretching during revascularization, and possibly by the action of free radicals. A hemodynamic edema also exists as a consequence of the reduction in pulmonary interstitial pressure. Possible prophylactic measures are discussed, the most appropriate appearing to be very progressive evacuation of the pneumothorax.
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PMID:[Reexpansion pulmonary edema after pneumothorax. Apropos of a case. Review of the literature]. 328 64

Clinical studies were performed in 27 consecutive patients with high-altitude pulmonary edema who were transported from the mountains to Shinshu University Hospital, Matsumoto, Japan. The altitude of onset was 2,680 m to 3,190 m above sea level. Symptoms included marked dyspnea, cough, and stridor. Physical findings included cyanosis, tachycardia, and rales. Neurologic disturbances, which were seen in 17 patients, included headache, vomiting, memory disturbance, clouding of consciousness, or coma. Chest roentgenograms revealed patchy infiltrates throughout the pulmonary fields, often in an asymmetric pattern, and enlargement of the right ventricle. Hemodynamic studies by right cardiac catheterization showed that high-altitude pulmonary edema was noncardiogenic. Scintiscans of the lungs with technetium-99m-macroaggregated albumin (99mTc-MAA) performed in one patient showed decreased perfusion of 99mTc-MAA in the area of infiltrates. Pulmonary edema fluid collected through the endotracheal tube in two patients was rich in protein. Computerized tomograms of the brain showed small ventricles and cisterns, disappearance of sulci, and diffuse low density of the cerebrum, indicating cerebral edema in eight of nine cases. Retinal hemorrhage and papilledema were observed in five patients.
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PMID:Clinical features of patients with high-altitude pulmonary edema in Japan. 366 94


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