Cases reported "Pulmonary Edema"

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1/31. 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.
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2/31. Unilateral negative pressure pulmonary edema during anesthesia with a laryngeal mask airway.

    PURPOSE: To present a case of unilateral pulmonary edema after upper airway obstruction. CLINICAL FEATURES: In a 21-yr-old man, anesthesia was induced with propofol and maintained with N2O/O2/isoflurane via an LMA. After being placed in the lateral position, he had an episode of upper airway obstruction while breathing spontaneously. Hypoxemia (SpO2 80-83%) refractory to the administration of oxygen (F1O2 1.0) ensued following relief of the obstruction. Chest X-ray showed edema of the dependent lung. Treatment consisted of placing the patient in the sitting position and supplemental oxygen. The situation resolved over a few hours. CONCLUSION: If airway obstruction occurs in the lateral position, development of negative pressure pulmonary edema (NPPE) in the dependent lung is favoured by hydrostatic forces and possibly the elevated resting position of the dependent hemidiaphragm.
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3/31. Exacerbation of acute pulmonary edema during assisted mechanical ventilation using a low-tidal volume, lung-protective ventilator strategy.

    STUDY OBJECTIVES: To assess the magnitude of negative intrathoracic pressure development in a patient whose pulmonary edema acutely worsened immediately following the institution of a low-tidal volume (VT) strategy. DESIGN: Mechanical lung modeling of patient-ventilator interactions based on data from a case report. SETTING: Medical ICU and laboratory. PATIENT: A patient with suspected ARDS and frank pulmonary edema. INTERVENTIONS: The patient's pulmonary mechanics and spontaneous breathing pattern were measured. Samples of arterial blood and pulmonary edema fluid were obtained. MEASUREMENTS: A standard work-of-breathing lung model was used to mimic the ventilator settings, pulmonary mechanics, and spontaneous breathing pattern observed when pulmonary edema worsened. Comparison of the pulmonary edema fluid-to-plasma total protein concentration ratio was made. RESULTS: The patient's spontaneous VT demand was greater than preset. The lung model revealed simulated intrathoracic pressure changes consistent with levels believed necessary to produce pulmonary edema during obstructed breathing. A high degree of imposed circuit-resistive work was found. The pulmonary edema fluid-to-plasma total protein concentration ratio was 0.47, which suggested a hydrostatic mechanism. CONCLUSION: Ventilator adjustments that greatly increase negative intrathoracic pressure during the acute phase of ARDS may worsen pulmonary edema by increasing the transvascular pressure gradient. Therefore, whenever sedation cannot adequately suppress spontaneous breathing (and muscle relaxants are contraindicated), a low-VT strategy should be modified by using a pressure-regulated mode of ventilation, so that imposed circuit-resistive work does not contribute to the deterioration of the patient's hemodynamic and respiratory status.
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4/31. Fulminant pulmonary edema after intramuscular ketamine.

    PURPOSE: To report an unusual case of pulmonary edema following intramuscular ketamine administration. CLINICAL FEATURES: An eight-year-old, healthy girl presented for dressing of first degree burns on dorsum of hand. Ten minutes after administration of 125 mg ketamine im, she developed laboured breathing, cyanosis, and bilateral crepitations and arterial blood gas analysis showed PaO2 55 mmHg. There was no evidence of upper airway obstruction. On intubating the trachea, pink frothy fluid emerged from the tube. She was diagnosed as a case of neurogenic pulmonary edema. She was managed with positive pressure ventilation with positive end expiratory pressure, morphine and furosemide. With this treatment she showed a favourable recovery. CONCLUSION: ketamine was given im to aid burns dressing in this case because it has distinct advantages above the other anesthetic agents including that of being a good analgesic which is absorbed by im route. Its use led to the development of pulmonary edema.
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5/31. Rapid and complete occlusion of a heat and moisture exchange filter by pulmonary edema (clinical report).

    PURPOSE: A case of near fatal obstruction of a breathing system is described, due to occlusion of a heat and moisture exchange filter in a patient with pulmonary edema. Previous reports have described cases of mechanical obstruction to fresh gas flow due to an accumulation of a bolus of fluid within the filter housing. However, in this case, the cause of occlusion was due to the protein and cell debris contained in a small amount of pulmonary edema fluid interacting with the filter membrane. CLINICAL FEATURES: Obstruction occurred rapidly and without warning, and was difficult to differentiate from the more common diagnoses of bronchospasm or tension pneumothorax. Outwardly the filter appeared normal, and routine protocol for emergency management of suspected breathing system obstruction initially failed to identify the site of occlusion. CONCLUSION: Minimal contamination by proteinaceous fluid may cause rapid and complete occlusion of a breathing system filter. Blockage of the breathing system filter and catheter mount should be considered in cases of unexplained breathing system occlusion. The use of a fresh breathing system without a filter for each patient, as recommended by The American Center for disease Control and the American Society of Anesthesiologists, would have prevented this scenario from occurring.
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6/31. pulmonary edema and respiratory insufficiency in acute pancreatitis.

    pulmonary edema, cardiac enlargement, and respiratory insufficiency may occur in patients with acute pancreatitis. The mechanisms are complex and incompletely understood, but probable etiologic factors include fluid overload, left ventricular failure, impaired respiratory excursion and microatelectasis, and a nonspecific response of the lung to various types of pulmonary injury including hypotension, intravenous crystalloids, and the effects of circulating pancreatic enzymes. Recognition of the association of pulmonary edema and respiratory insufficiency with pancreatitis is importance because early treatment with positive pressure breathing, careful fluid management and diuretics, and corticosteroids may prevent the development of irreversible respiratory failure.
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7/31. pulmonary edema in scuba divers: recurrence and fatal outcome.

    pulmonary edema occurring in divers using a self-contained underwater breathing apparatus (scuba) is an uncommon, probably under-reported, but potentially life-threatening and recurrent condition. We report six episodes of pulmonary edema in five scuba divers seen during a period of 15 months. The four men and one woman ranged in age from 37 to 56 years and two were treated for hypertension. Symptoms were mostly dyspnea onset at depth, cough, hemoptysis and hypoxemia, which in the recurrent case led to cardiac arrest and death. All cases occurred in rather cold water. Findings on thoracic computed tomography (CT) scanning ranged from pleural effusion to ground-glass opacities restricted to a few areas of the lung. The complex underlying mechanisms that would contribute to a raised transalveolar pressure or to a disruption of the blood-gas barrier are discussed. It is important for emergency care providers to be aware of this syndrome for prompt recognition and optimal treatment.
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8/31. Case with bromine exposure leading to respiratory insufficiency.

    A 21-year-old male had a chemical burn on the right forearm when he inadvertently spilled bromine during an experiment. Since he inhaled vaporized bromine and had dyspnea and pharyngalgia, he arrived at our hospital in an ambulance as an emergency patient. On arrival, he kept a clear consciousness with a pulse rate of 98, body temperature of 36.8 degrees C, blood pressure of 132/80 mmHg, respiratory rate of 25, and oxygen saturation of 100%. (10 L/min of oxygen were administered.) He had marked dry coughs. His clothes had a foreign odor with mucosal irritation. Arterial blood gas analysis and blood biochemistry were normal. Based on these findings, he was diagnosed with chemical airway damage and bulbar conjunctiva from the exposure to bromine and a chemical burn on the right forearm. His respiratory condition became worse after admission, resulting in pulmonary edema. He was endotracheally intubated and controlled with an artificial ventilator on Day 3 after his injury. He was continuously treated with steroids and sivelestat sodium hydrate, which gradually improved his respiration. He was released from the artificial ventilator and extubated on Day 7. Although dyspnea associated with body movement and hoarseness persisted after extubation, the symptoms decreased and he was discharged on Day 41. This rare case is worth attention because serious respiratory insufficiency requiring artificial ventilation due to pulmonary edema from bromine exposure has not been reported in japan.
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9/31. Bilateral negative airway pressure pulmonary edema (NPPE)--a case report--.

    A case of negative pressure bilateral pulmonary edema in a 28 years old healthy female patient, scheduled for diagnostic pelvic laparoscopy for infertility. Following extubation and apparent recovery from anesthesia, she had strong inspiratory efforts due to airway obstruction caused by coughing and laryngeal spasm, that lead to negative pressure bilateral pulmonary edema. The pulmonary edema disappeared within few hours. She was breathing spontaneously through CPAP system (mask-bag-expiratory valve). diuretics and lungs physiotherapy helped in controlling patient's complication.
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10/31. Acute pulmonary oedema on the Ruwenzori mountain range.

    A 40 year old man had an episode of severe pulmonary oedema at 4000-5000 m during the ascent of the Margherita peak (5109 m) of Mount Stanley on the Ruwenzori. He had taken acetazolamide and high dose dexamethasone to treat symptoms of acute mountain sickness. Six years before he had been studied by right heart catheterisation as a healthy volunteer during hypoxic breathing at sea level. His pulmonary vascular reactivity had been within the normal range for 32 healthy subjects. This man had high altitude pulmonary oedema despite currently recommended treatments for acute mountain sickness and normal pulmonary vascular reactivity to hypoxia at sea level.
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