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

Children who have been exposed to smoke in a confined space or who have soot or burns, however minimal, on the face should be admitted to hospital. Respiratory distress may be delayed, but if it is progressive the patient should be curarised, intubated, and mechanically ventilated. Unless ventilation continues for 48 hours, followed by 24 hours' spontaneous respiration against a positive airway pressure, stridor and pulmonary oedema may recur. An endotracheal tube small enough to allow a leak between it and the oedematous mucosa must be passed to prevent laryngeal damage and subsequent subglottic stenosis. High humidity of inspired gases keeps secretions fluid and the endotracheal tube patent. A high oxygen concentration compensates for deficient oxygen uptake and transport caused by pulmonary lesions and the presence of poisonous compounds interfering with oxygen transport. Dexamethasone to minimise cerebral oedema and antibiotics to reduce the incidence of chest infections should be given.
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PMID:Management of airway complications of burns in children. 58 69

In summary, there are a number of important respiratory manifestations of endocrine diseases. Hypothyroidism may be associated with respiratory failure that can be caused by a reduction in central respiratory drive, upper airway obstruction, and associated restrictive pulmonary function from pleural effusions or an intrinsic decrease in lung volumes. Hyperthyroidism can present with dyspnea as a major clinical manifestation because of the increase in central respiratory drive associated with thyrotoxicosis. Cardiac dysfunction associated with hyperthyroidism may lead to pulmonary edema in some patients. Hypoparathyroidism may occur acutely, especially after thyroid surgery and be associated with hypocalcemia and acute tetany, laryngeal stridor, and muscle weakness. Ovarian tumors, both benign and malignant, may present with unilateral or bilateral effusions. Finally, patients with diabetes mellitus are at increased risk of developing a variety of pulmonary disorders. Acute and chronic pulmonary infections are the most common respiratory abnormalities in patients with diabetes, although cardiogenic and noncardiogenic pulmonary edema can also be a complication of their disease.
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PMID:Pulmonary manifestations of endocrine and metabolic disorders. 268 69

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

Children with a history of exposure to smoke in a confined space or showing soot or burns, however minimal, on the face should be admitted to hospital. Respiratory distress may be delayed, but if it is progressive the patient should be curarized, intubated, and mechanically ventilated. Ventilation should be continued for a minimum of 48 hours, followed by 24 hours of spontaneous respiration against a positive airway pressure. It treatment is stopped sooner, a recurrence of stridor and pulmonary oedema is likely. It is mandatory to pass an endotracheal tube small enough to allow a leak between it and the oedematous mucosa, in order that laryngeal damage and subsequent subglottic stenosis may be avoided. It is important tu use high humidity of inspired gases to keep secretions fluid and the endotracheal tube patent. Dexamethasone should be given to minimise cerebral oedema and antibiotics to reduce the incidence of chest infections.
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PMID:Inhalation injury to the respiratory tract of children. 722 Oct 6

A case of severe head injury associated with fulminant pulmonary edema considered as neurogenic which developed within short time after the injury was presented. A five-year-old boy who had no previous history of cardiopulmonary disease was struck on his right frontal region by car accident at 15.30 PM on July 5 of 1979. Immediately after the impact he lost his consciousness and subsequently transferred to a local hospital where bilateral dilated pupil and flaccid paralysis of the limbs were noted. On transmission of the patient to Omuta City Hospital 30 minutes after the injury, massive foamy fluid was discharged from the tracheal tube. On admission, he was comatous, with bilateral dilated and fixed pupils and flaccid paralysis of the limbs. There was no retinal bleeding. He showed ataxic respiration with severe stridor and massive discharge of foamy fluid pinkish in colour from the trachea characteristic in pulmonary edema was significant. Chest x-ray film demonstrated perihilar densities suggesting pulmonary edema. CT scan showed extremely small ventricle on both sides without manifestations of intracranial hematomas or cerebral contusion. With an intensive medical treatments including corticosteroids, alkalizing agents and alpha-blocker were administered under controlled respiration, the discharge of edema fluid was gradually decreased and the findings on blood gases were also improved. However neurological signs were aggravated and he died 8 hours after the injury. Central venous pressure was maintained at the level between 8 to 10 cm. From these clinical findings the pulmonary edema was concluded as neurogenic. Direct or indirect injury to the hypothalamic efferent pathway at the level of lower brain stem seemed to be important as the cause of neurogenic pulmonary edema in this case. The possible pathophysiology of neurogenic pulmonary edema associated with brain stem injury and intracranial hypertension was discussed with other related literature.
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PMID:[Neurogenic pulmonary edema following severe head injury--case report (author's transl)]. 724 16

An eight-year-old Highland pony which had previously shown normal laryngeal function, underwent general anaesthesia for surgical treatment of a mandibular sinus. During its recovery from the anaesthesia, the pony suffered great respiratory distress and stridor, due to total bilateral laryngeal paralysis and pulmonary oedema. The animal was immediately given a temporary tracheostomy. Some hours later, postoperative myositis developed; it resolved within two days and the pony's laryngeal function returned to normal during the following year.
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PMID:Temporary bilateral laryngeal paralysis in a horse associated with general anaesthesia and post anaesthetic myositis. 844 33

A case of post-extubation laryngospasm complicated by negative pressure pulmonary edema in a 26 year-old healthy male undergoing right herniorrhaphy is presented. Immediately after extubation laryngeal stridor was noted, which rapidly developed in severe laryngospasm. Two minutes after the laryngospasm, reintubation was accomplished, but pulmonary edema was soon noted. After supportive treatment his condition improved and the endotracheal tube was removed in the next day. The patient was discharged home uneventfully on the 4th postoperative day. The cause, mechanism, treatment and how to prevent such complications are discussed.
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PMID:Pulmonary edema complicated by post-extubation laryngospasm: a case report. 950 61

A 33-year-old male was scheduled for tonsillectomy and pharyngoplasty due to sleep apnea syndrome. The intubation was uneventful following induction with thiamylal and vecuronium. Anesthesia was maintained with O2-N2O-sevoflurane. No complications were observed during the 90 min operation. After the termination of the anesthesia, a hyperadrenergic state was observed: arterial pressure and heart rate rose to 230/135 mmHg and 135 bpm, respectively. Immediately after extubation, he developed dyspnea with tracheal tag and stridor, and became cyanotic despite the use of a simple oxygen mask and assisted ventilation. Laryngospasm was suspected. The patient was reintubated and suctioned; pink, frothy sputum was not obtained. Arterial blood gases 5 minutes after reintubation revealed a pH of 7.24, Pao2 86 mmHg (FIo2 1.0), and Paco2 54 mmHg. Chest X-ray 30 minutes after reintubation revealed bilateral diffuse alveolar infiltration. The diagnosis was interstitial pulmonary edema. The patient was ventilated mechanically by applying a positive end-expiratory pressure of 5cm H2O, and furosemide and dopamine were administered intravenously. The patient was extubated the next day, and discharged from hospital ten days later. We considered that the lung edema was induced by the severe negative pressure generated by inspirating against a closed upper airway, as well as by the hyperadrenergic state and severe hypoxemia observed during and after extubation.
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PMID:[Pulmonary edema due to acute airway obstruction immediately after tracheal extubation]. 985 97

Hydrogen peroxide is an oxidising agent that is used in a number of household products, including general-purpose disinfectants, chlorine-free bleaches, fabric stain removers, contact lens disinfectants and hair dyes, and it is a component of some tooth whitening products. In industry, the principal use of hydrogen peroxide is as a bleaching agent in the manufacture of paper and pulp. Hydrogen peroxide has been employed medicinally for wound irrigation and for the sterilisation of ophthalmic and endoscopic instruments. Hydrogen peroxide causes toxicity via three main mechanisms: corrosive damage, oxygen gas formation and lipid peroxidation. Concentrated hydrogen peroxide is caustic and exposure may result in local tissue damage. Ingestion of concentrated (>35%) hydrogen peroxide can also result in the generation of substantial volumes of oxygen. Where the amount of oxygen evolved exceeds its maximum solubility in blood, venous or arterial gas embolism may occur. The mechanism of CNS damage is thought to be arterial gas embolisation with subsequent brain infarction. Rapid generation of oxygen in closed body cavities can also cause mechanical distension and there is potential for the rupture of the hollow viscus secondary to oxygen liberation. In addition, intravascular foaming following absorption can seriously impede right ventricular output and produce complete loss of cardiac output. Hydrogen peroxide can also exert a direct cytotoxic effect via lipid peroxidation. Ingestion of hydrogen peroxide may cause irritation of the gastrointestinal tract with nausea, vomiting, haematemesis and foaming at the mouth; the foam may obstruct the respiratory tract or result in pulmonary aspiration. Painful gastric distension and belching may be caused by the liberation of large volumes of oxygen in the stomach. Blistering of the mucosae and oropharyngeal burns are common following ingestion of concentrated solutions, and laryngospasm and haemorrhagic gastritis have been reported. Sinus tachycardia, lethargy, confusion, coma, convulsions, stridor, sub-epiglottic narrowing, apnoea, cyanosis and cardiorespiratory arrest may ensue within minutes of ingestion. Oxygen gas embolism may produce multiple cerebral infarctions. Although most inhalational exposures cause little more than coughing and transient dyspnoea, inhalation of highly concentrated solutions of hydrogen peroxide can cause severe irritation and inflammation of mucous membranes, with coughing and dyspnoea. Shock, coma and convulsions may ensue and pulmonary oedema may occur up to 24-72 hours post exposure. Severe toxicity has resulted from the use of hydrogen peroxide solutions to irrigate wounds within closed body cavities or under pressure as oxygen gas embolism has resulted. Inflammation, blistering and severe skin damage may follow dermal contact. Ocular exposure to 3% solutions may cause immediate stinging, irritation, lacrimation and blurred vision, but severe injury is unlikely. Exposure to more concentrated hydrogen peroxide solutions (>10%) may result in ulceration or perforation of the cornea. Gut decontamination is not indicated following ingestion, due to the rapid decomposition of hydrogen peroxide by catalase to oxygen and water. If gastric distension is painful, a gastric tube should be passed to release gas. Early aggressive airway management is critical in patients who have ingested concentrated hydrogen peroxide, as respiratory failure and arrest appear to be the proximate cause of death. Endoscopy should be considered if there is persistent vomiting, haematemesis, significant oral burns, severe abdominal pain, dysphagia or stridor. Corticosteroids in high dosage have been recommended if laryngeal and pulmonary oedema supervene, but their value is unproven. Endotracheal intubation, or rarely, tracheostomy may be required for life-threatening laryngeal oedema. Contaminated skin should be washed with copious amounts of water. Skin lesions should be treated as thermal burns; surgery may be required for deep burns. In the case of eye exposure, the affected eye(s) shod eye(s) should be irrigated immediately and thoroughly with water or 0.9% saline for at least 10-15 minutes. Instillation of a local anaesthetic may reduce discomfort and assist more thorough decontamination.
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PMID:Hydrogen peroxide poisoning. 1529 93

Negative-pressure pulmonary edema (NPPE) is a clinical entity of anaesthesiologic relevance, perioperatively caused by obstruction of the conductive airways (upper airway obstruction, UAO) due to laryngospasm in approx. 50% of the cases, its early recognition and treatment by the anaesthesist is mandatory. NPPE, also addressed as post-obstructive pulmonary edema (POPE) presents in most cases as a complex of symptoms with rapid onset, consisting of acute respiratory failure with dyspnea, tachypnea, and strained respiratory efforts. Additional signs are paradoxe ventilation, pink frothy sputum, stridor, and severe agitation. UAO produce extreme reduction of intrathoracic pressure during spontaneous ventilation, consecutively causing increase in venous return to the right ventricle and in intrathoracic blood volume, resulting in elevated hydrostatic pressures and interstitial transudation of fluids. Partially due to largely differing criteria used for diagnosis, opinions about incidence and prevalence of NPPE are unhomogenous in medical literature. It has been shown that generation of NPPE is not only limited to patients being intubated and ventilated, but occurs also in patients requiring higher fractions of oxygen.
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PMID:[Negative-pressure pulmonary edema (NPPE)]. 1649 58


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