Postobstructive Pulmonary Edema Research Articles

Incidence of pulmonary edema after tracheotomy for obstructive sleep apnea

Objective: The phenomenon of postobstructive pulmonary edema (POPE) has been associated with the relief of upper airway obstruction, which itself is fundamental to the pathophysiology of obstructive sleep apnea (OSA). A review of patients with OSA undergoing tracheotomy was performed to characterize this process. Study Design: Retrospective chart review of study patients with OSA undergoing tracheotomy and of control patients without OSA undergoing tracheotomy for unrelated problems. Chest radiographs were reviewed in a double-blind fashion to score posttracheotomy changes in pulmonary status. Setting: Academic tertiary referral center. Results: Thirty (67%) of 45 OSA patients treated by tracheotomy had evidence of POPE, whereas only 5 (20%) of 25 control group patients had increased pulmonary edema. The remaining 15 (33%) of 45 OSA patients and 20 (80%) of 25 control patients had either no change or an improved pulmonary status. Those with OSA that developed POPE were mostly graded as having mild pulmonary edema (22/30, 73%). Far fewer were graded as having moderate pulmonary edema (6/30, 20%), and fewer still with severe pulmonary edema (2/30, 7%). Two (7%) of 45 patients with severe POPE died of complications related to cor pulmonale in the postoperative period. Conclusion: Results support maintaining a high index of suspicion for the development of postobstructive pulmonary edema in patients treated for OSA. Treatment options, such as positive pressure ventilation and diuresis, and an increased awareness of this condition may help reduce the morbidity and mortality associated with treatment of this disease. (Otolaryngol Head Neck Surg 2001;125:319-23.)

Das postobstruktive Lungenödem als Komplikation einer Endotrachealtubusokklusion

Pulmonary edema following acute or chronic upper airway obstruction is a threatening complication. A case is presented in which a 15 year old boy developed a massive pulmonary edema after a acute endotracheal tube obstruction during emergence from anesthesia. Leading pathophysiologic cause for the formation of the edema is a markedly negative intrapleural pressure due to the forceful inspiration against the obstructed airway. Treatment modalities include the instantaneous solution of the obstruction, a rapid reoxigenation and the ventilation with PEEP or CPAP. Sound knowledge of the disease increases the vigilance of the caring anaesthesiologist and helps to identify patients at risk. Preventing measures may further reduce the risk of occurrence of the postobstructive pulmonary edema.

Clinical and radiologic features of pulmonary edema.

Pulmonary edema may be classified as increased hydrostatic pressure edema, permeability edema with diffuse alveolar damage (DAD), permeability edema without DAD, or mixed edema. Pulmonary edema has variable manifestations. Postobstructive pulmonary edema typically manifests radiologically as septal lines, peribronchial cuffing, and, in more severe cases, central alveolar edema. Pulmonary edema with chronic pulmonary embolism manifests as sharply demarcated areas of increased ground-glass attenuation. Pulmonary edema with veno-occlusive disease manifests as large pulmonary arteries, diffuse interstitial edema with numerous Kerley lines, peribronchial cuffing, and a dilated right ventricle. Stage 1 near drowning pulmonary edema manifests as Kerley lines, peribronchial cuffing, and patchy, perihilar alveolar areas of airspace consolidation; stage 2 and 3 lesions are radiologically nonspecific. Pulmonary edema following administration of cytokines demonstrates bilateral, symmetric interstitial edema with thickened septal lines. High-altitude pulmonary edema usually manifests as central interstitial edema associated with peribronchial cuffing, ill-defined vessels, and patchy airspace consolidation. Neurogenic pulmonary edema manifests as bilateral, rather homogeneous airspace consolidations that predominate at the apices in about 50% of cases. Reperfusion pulmonary edema usually demonstrates heterogeneous airspace consolidations that predominate in the areas distal to the recanalized vessels. Postreduction pulmonary edema manifests as mild airspace consolidation involving the ipsilateral lung, whereas pulmonary edema due to air embolism initially demonstrates interstitial edema followed by bilateral, peripheral alveolar areas of increased opacity that predominate at the lung bases. Familiarity with the spectrum of radiologic findings in pulmonary edema from various causes will often help narrow the differential diagnosis.

Acute postobstructive pulmonary edema: Case presentation and review

Reprint no. 7411 J9248l Case Presentation An outlying hospital requested air medical transport of a y oxygen was being administered through a nonrebreather mask at 15 L/minute. The patient was moved to the aircraft and transported to Children’s Hospital. His respiratory status improved somewhat in transport as his SpOz increased to 100%. He was admitted directly to the pediatric intensive care unit (PICU). Initial evaluation by the pediatric intensivist revealed significant tons&r hypertrophy with exudate. Admission chest radiograph demonstrated pulmonary edema. The patient continued to exhibit respiratory distress. Otolaryngology and anesthesia professionals were consulted,

Unexplained Transient Postoperative Myocardial Dysfunction in a Previously Healthy Child

Unexplained Transient Postoperative Myocardial Dysfunction in a Previously Healthy Child

Bronchoscopic findings in post-obstructive pulmonary oedema

To present the first photographed bronchoscopic findings associated with negative pressure pulmonary oedema (NPPE). A previously healthy patient underwent anterior C3-C4 disc removal and arthrodesis. Following tracheal extubation he developed acute respiratory distress manifested as stridor, tachypnoea, restlessness, and desaturation. Once the trachea was reintubated, he displayed the classic findings of pulmonary oedema. Bronchoscopy was performed to confirm tracheal tube position and to rule out tracheal injury secondary to surgical manipulation. Diffuse punctate haemorrhages were noted throughout the visualised tracheobronchial tree. We believe that these haemorrhages represent disruption of the bronchial vasculature and may contribute to the clinical presentation of NPPE.

Nasal BiPAP Treats Hypoxia from Postobstructive Pulmonary Edema

Nasal BiPAP Treats Hypoxia from Postobstructive Pulmonary Edema

Acute postobstructive pulmonary edema.

Acute postobstructive pulmonary edema may occur after airway obstruction. A decrease in intrathoracic and intraalveolar pressures causes an increased blood flow into the pulmonary vasculature and favors the development of pulmonary edema. Two mechanisms for the development of acute postobstructive pulmonary edema are proposed: type 1 follows acute airway obstruction, and type 2 follows relief of chronic airway obstruction.

Acute postobstructive pulmonary edema

Acute postobstructive pulmonary edema may occur after airway obstruction. A decrease in intrathoracic and intraalveolar pressures causes an increased blood flow into the pulmonary vasculature and favors the development of pulmonary edema. Two mechanisms for the development of acute postobstructive pulmonary edema are proposed: type 1 follows acute airway obstruction, and type 2 follows relief of chronic airway obstruction. (OTOLARYNGOL HEAD NECK SURG 1995;112:235-7.)

Death from Adult Respiratory Distress Syndrome and Multiorgan Failure following Acute Upper Airway Obstruction

In adults with acute epiglottitis, transient noncardiogenic pulmonary edema may follow relief of upper airway obstruction, but typically does not progress to more severe pulmonary derangements. We describe a patient with post-obstructive pulmonary edema whose course was complicated by ARDS, multiorgan failure, and death. Recognition of UAO and expedient treatment depends heavily on the judgment and skills of the clinician and the available resources of the institution. Physicians caring for patients with AE should be aware of the potential for delayed morbidity and mortality following upper airway obstruction, even after establishing an adequate artificial airway. This case provides additional justification for aggressive airway management and intensive care support of patients with AE in order to avoid serious complications.

Impaired ventilatory capacity after recovery from Guillain-Barré syndrome

A 48-year-old woman who failed to disclose significant past medical history presented for laparoscopic-assisted vaginal hysterectomy with general anesthesia. After the uneventful induction of anesthesia, her trachea could not be intubated due to an extremely anterior larynx, and she was allowed to awaken. However, she developed upper airway obstruction and displayed marked muscle weakness with inadequate tidal volumes and marginal oxygen saturation. A history of prior Guillain-Barré syndrome was disclosed by the attending gynecologist. The patient's recovery was complicated by the development of postobstructive pulmonary edema and by respiratory insufficiency requiring the use of mask continuous positive airway pressure (CPAP). Despite vigorous diuresis, her respiratory status and muscle weakness did not significantly improve until she received a trial of aminophylline by infusion, after which she was able to be weaned from mask CPAP support. The patient was discharged home and returned 8 weeks later for surgery. She underwent awake fiberoptic intubation, after which general anesthesia was induced and maintained without complication. An aminophylline infusion was used in the perioperative period until the patient was successfully awakened and her trachea extubated. The frequency of residual muscle weakness after apparent full recovery from Guillain-Barré syndrome is discussed, along with the rationale for the use of aminophylline in this patient's clinical management.

Adult epiglottitis and postobstructive pulmonary edema in a patient with severe coronary artery disease

Epiglottitis is a rare cause of upper airway obstruction that may lead to death in the adult. We report the case of a patient with severe coronary artery disease with adult epiglottitis who required emergency endotracheal intubation. Relief of the airway obstruction was followed by the development of postobstructive pulmonary edema. The literature is reviewed and the following recommendations are made: Patients with adult epiglottitis should be intubated in the presence of any respiratory signs or symptoms. All others should be observed in an intensive care unit with a skilled anesthesiologist available to carry out emergency endotracheal intubation. Inhalation induction with halothane in oxygen should be considered initially; failing that, rigid bronchoscopy, tracheostomy, or transtracheal ventilation should be available. Postobstructive pulmonary edema should be anticipated after relief of airway obstruction has occurred; it can be treated with fluid restriction, diuretics, and continuous positive airway pressure.

Postobstructive pulmonary edema as a sequela of temporomandibular joint arthroscopy: A case report

Postobstructive pulmonary edema as a sequela of temporomandibular joint arthroscopy: A case report

Postobstructive pulmonary edema following anesthesia

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 operioperative airway management.

Postobstructive Pulmonary Edema

Postobstructive Pulmonary Edema