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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The first phase of accidental drowning begins with asphyxia, due to either laryngospasm (10-15 percent of cases) or water aspiration. The second phase is characterized by water and electrolyte changes in the blood. The physiopathological modifications caused by drowning in fresh water differ from those of drowning in sea water. The hypotonic fresh water quickly diffuses in the bloodstream. The consequences are, in many cases, hypervolemia with pulmonary edema, hemolysis, hyperkalemia with risk of ventricular fibrillation, diminution of hemoglobin, and a relative decrease in plasma concentration of Na, Cl, Ca, and albumin. Further, inactivation and washing out of the anti-atelectasis factor from the alveoli by fresh water facilitate the formation of atelectasis. In cases of accidental drowing in sea water the osmotic gradient is in inverse: the electrolytes of aspirated salt water diffuse in the circulation, whereas the blood serum and the plasma albumin pass into the alveoli. Acute pulmonary edema often follows these pathological changes. Hypovolemia with circulatory collapse, hemoconcentration with rise in hemoglobin, hematocrit, sodium, potassium and albumin, and, finally, an elevated risk of thromboembolism due to increased blood viscosity, represent further complications. On the other hand, ventricular fibrillation is rare, hemolysis is absent and atelectasis usually does not occur.
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PMID:[Physiopathology of accidental drowning]. 112 62

Noncardiogenic pulmonary edema is a well recognized complication of upper airway obstruction. We report the case of a previously healthy 18-year-old male who presented this complication following laryngospasm after anesthesia. He developed severe pulmonary edema with hypoxemia, high cardiac output and low pulmonary capillary pressures. He was managed with mechanical ventilation and PEEP. Pulmonary edema resolved within 24 hours. The clinical picture, etiology, differential diagnosis and prevention are also discussed.
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PMID:[Acute non-cardiogenic pulmonary edema secondary to upper airway obstruction. Clinical case]. 134 80

Based on the content of this article, the reader should be able to (1) identify the differences between cardiogenic and noncardiogenic pulmonary edema (NCPE); (2) identify the most common causes of airway obstruction leading to pulmonary edema; (3) state the mechanism of action for the development of NCPE following laryngospasm; (4) state the signs and symptoms of NCPE; (5) identify the treatment for NCPE; and (6) state three nursing actions that are indicated in the care of the patient with NCPE.
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PMID:The patient with noncardiogenic pulmonary edema. 174 37

Pulmonary edema secondary to postextubation laryngospasm is a potentially life-threatening problem, demanding early diagnosis and prompt treatment. We believe that this problem has been grossly underestimated in its incidence, as only seven adults have been reported in the English literature, whereas seven adults have been observed at our institution in only a 24 month period. All were young, healthy, athletic adult males (average weight, 218 pounds) who underwent relatively minor, uncomplicated surgical procedures under general anesthesia. Five of these patients were collegiate and/or professional athletes and had meticulous medical records detailing their clinical course. Clinical laryngospasm was noted immediately following extubation and anesthesia by mask with subsequent pulmonary edema. The diagnoses were confirmed by clinical examination, arterial blood gas determinations or pulse oximetry, and chest roentgenogram. Four adults required reintubation. Six of the seven adults demonstrated very rapid resolution of the pulmonary edema with prompt diagnosis and institution of a therapeutic regimen including oxygen, diuretics, reintubation, and/or positive pressure ventilation. In one patient, the problem was not immediately recognized, and progressed to florid pulmonary edema requiring emergent intubation 14 hours later in the emergency room, and 3 days of mechanical ventilation. The etiology of pulmonary edema following upper airway obstruction represents an interplay between several factors: cardiogenic and neurogenic mechanisms, as well as hypoxia contribute. In this group, excessive negative intrathoracic pressure generated by forced inspiration against a closed glottis is the most likely, consistent, and logical explanation. This study suggests that young, healthy, athletic males may be at increased risk for this complication.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Postoperative pulmonary edema in young, athletic adults. 155 59

The purpose of this review is to describe the pathogenesis of pulmonary oedema associated with upper airway obstruction, summarize what is known of its clinical presentation, and reflect upon its implications for the clinical management of airway obstruction. The pathogenesis of pulmonary oedema associated with upper airway obstruction is multifactorial. However, as the phrase "negative pressure pulmonary oedema" suggests, markedly negative intrapleural pressure is the dominant pathophysiological mechanism involved in the genesis of pulmonary oedema associated with upper airway obstruction. The frequency of the event is impossible to ascertain from the literature but paediatric cases requiring airway intervention for croup or epiglottitis and adults requiring airway intervention for emergence laryngospasm or upper airway tumours account for over 50 per cent of the documented cases in each age group, respectively. Individuals at risk should be observed closely while they remain at risk. The majority of cases present within minutes either of the development of acute severe upper airway obstruction or of relief of the obstruction. Resolution is typically rapid, over a period of a few hours. Rarely is anything more required for management than the maintenance of a patent airway, supplemental oxygen, and, in approximately 50 per cent of cases, mechanical ventilation and positive end-expiratory pressure.
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PMID:Pulmonary oedema associated with airway obstruction. 198 33

Pulmonary edema developing after the relief of upper airway obstruction has been reported in association with a diversity of etiologic factors, including hanging, strangulation, tumors, foreign bodies, goiter, and laryngospasm. Since 1977, 18 cases of adults with postobstructive pulmonary edema associated with anesthesia have been reported. A case is presented of a healthy 20-year-old male who developed pulmonary edema following two episodes of acute upper airway obstruction associated with general anesthesia. Postanesthetic laryngospasm has been implicated as the most frequent cause of this syndrome in adults. Risk factors for the development of upper airway obstruction have been identified in the majority of these cases. A heightened awareness among anesthesiologists of this poorly recognized and hence often perplexing syndrome may help reduce the occurrence and facilitate the treatment of this potential complication of perioperative airway management.
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PMID:Postobstructive pulmonary edema following anesthesia. 218 49

Acute pulmonary edema in the young athlete is a rare complication following arthroscopic surgery. It is not related to fluid absorption during arthroscopy, but rather to a brief period of upper airway obstruction. Pink, frothy pulmonary edema fluid appears along with other signs of hypoxia. Treatment consists of oxygenation, diuretics, and nitrates. Young athletes may be at increased risk for laryngospasm-induced pulmonary edema because they have the ability to generate large negative intrathoracic pressures. This condition must be recognized promptly to minimize morbidity and mortality.
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PMID:Acute pulmonary edema, an unusual complication following arthroscopy: a report of three cases. 220 87

A 50-year-old woman underwent laryngoscopy. Postoperatively she received naloxone and was extubated. She developed severe laryngospasm and one hour later pulmonary edema. Both naloxone administration and laryngospasm can provoke pulmonary edema; the pathophysiology is discussed. It is suggested that naloxone is administered with care to patients who in the preceding hours have had severe laryngospasm.
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PMID:Naloxone administration and laryngospasm followed by pulmonary edema. 221 64

We report the case of a 6-month-old child who developed acute pulmonary edema because of laryngeal spasm during orthopedic manipulations for congenital hip dysplasia. Laryngospasm was probably secondary to an unsuspected light level of anesthesia, maintained via face mask. No other predisposing factors, such as enlarged adenoid tonsils, laryngitis, epiglottitis, mechanical stimulation of the larynx or aspiration of foreign material were identified. Serious oxygen desaturation and bradycardia ensued, during inefficient attempts at positive pressure ventilation. After emergency intubation without muscle relaxant, copious pink secretions emerged from the airway. Negative pressure pulmonary edema was confirmed by chest X-ray, and short-lasting arterial desaturation despite positive pressure ventilation with high oxygen concentration. This type of pulmonary edema is caused by marked elevated negative intra-airway pressure, massive sympathetic discharge causing a blood shift from the systemic to the pulmonary circulation, and accentuation of physiological ventricular interdependence during forceful inspiratory effort against a closed glottis. As usual in such cases, pulmonary edema and laryngospasm resolved spontaneously without specific treatment, and extubation was carried out uneventfully two hours later. The child suffered no sequelae.
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PMID:Laryngospasm-induced pulmonary edema. 228 9

Laryngospasm during the emergent phase of anesthesia is a respected complication well known to any PACU nurse. One complication of laryngospasm is noncardiac pulmonary edema (NCPE). NCPE can be a catastrophic complication of anesthesia. A case report is presented to illustrate the signs and symptoms of laryngospasm and NCPE. The physiology of hemoptysis and hypoxemia is reviewed. The mechanism of laryngospasm-induced pulmonary edema is described. The need for PACU nurses to comprehend the pathophysiology and implications of laryngospasm and hypoxemia is paramount when determining proper treatment. PACU nurses should be particularly alert to and aware of this complication.
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PMID:Laryngospasm-induced pulmonary edema: case report. 238 66


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