Acute postobstructive pulmonary edema

Guffin, Thomas N.; Har‐El, Gady; Sanders, Abraham; Lucente, Frank E.; Nash, Michael R.

doi:10.1016/s0194-5998(95)70242-3

Cited by 53 publications

(37 citation statements)

References 4 publications

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“…3 There are 2 types of postobstructive pulmonary edema, which were first proposed in 1995. 4 Type I is associated with forceful inspiratory effort in an acute airway obstruction; causes include laryngospasm after extubation, epiglottitis, croup, choking and foreign-body aspiration. Type II occurs after relief of a chronic partial airway obstruction via surgical intervention (Box 1).…”

Section: Discussionmentioning

confidence: 99%

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Postobstructive pulmonary edema associated with a substernal goitre

Liu

Shih

Chen

2012

CMAJ

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A 50-year-old woman had experienced 6 months of mild shortness of breath and noise while breathing. She was obese with a body mass index of 32. Her primary care physician found a neck mass; results of a serum thyroid function test were normal. Her symptoms remitted spontaneously, and she ignored advice to seek further evaluation. Six months later, she had her first episode of dyspnea with cyanosis, followed by decreased consciousness. When the ambulance arrived, her Glasgow Coma Scale score was 7 and her peripheral oxygen saturation was 60%. A nonrebreather oxygen mask was applied during transport.On arrival at the emergency department, the patient's respiratory rate was 30 breaths/min, pulse rate was 80 beats/min, blood pressure was 107/61 mm Hg and peripheral oxygen saturation was 76%; her Glasgow Coma Scale score had deteriorated to 6. Blood gas analysis revealed pH 6.7, PCO 2 99.1 mm Hg, PO 2 91.3 mm Hg and HCO 3 11.0 mmol/L, which was consistent with mixed respiratory acidosis and metabolic acidosis. Physical examination showed diffuse rales and some wheezing. After emergent endotracheal intubation, the patient regained consciousness. The endotracheal tube contained copious amounts of a pink frothy secretion. Brain computed tomography scans were normal. Chest radiography done after intubation showed ground-glass opacities bilaterally, suggestive of pulmonary edema ( Figure 1A).Laboratory test results revealed d-dimer levels up to 10.5 (normal < 0.5) µg/mL. Computed tomography of the chest with contrast indicated no filling defect in the pulmonary arteries. There was a nodule visualized that measured 4.0 × 4.5 × 7.0 cm in the right thyroid lobe, with intrathoracic extension (Figure 2). Electrocardiography showed ST segment depressions in leads II, III, aVF, V5 and V6. Further laboratory results were as follows: creatine phosphokinase 527 (normal 26-192) U/L; creatine phosphokinasemyocardial band 40 (normal < 25) U/L and troponin I 1.73 (normal < 0.50) µg/L. Echocardiography showed hypokinesia over the anterolateral and basal septum with an ejection fraction of 40%. Coronary arteriography was normal. Results of thyroid function and virus serologic tests were negative.Subsequent chest radiography, 29 hours after intubation, showed resolution of the interstitial, patchy infiltrations ( Figure 1B). A second echocardiogram showed normal systolic function with an ejection fraction of 62%. The endotracheal tube was removed after weaning criteria were met and after a successful spontaneous breathing trial with a T-piece circuit. Two hours after extubation, the patient had a second episode of respiratory distress accompanied by stridor with hypoxemia and altered consciousness. Her condition was unresponsive to intravenous hydro cortisone and bilevel positive airway pressure ventilation. After reintubation, she recovered immediately. The patient underwent a tracheostomy and was transferred to the regular ward. She had a third episode of respiratory distress with desaturation 12 hours after the tracheostomy tube was re...

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Section: Discussionmentioning

confidence: 99%

“…Type II occurs after relief of a chronic partial airway obstruction via surgical intervention (Box 1). 4,5 Subsequent case series, primarily reported by anesthesiologists, indicate that the most common cause is laryngospasm during intubation or extubation. The incidence is as high as 1 in 1000 cases of general anesthesia (0.094%).…”

Section: Discussionmentioning

confidence: 99%

Postobstructive pulmonary edema associated with a substernal goitre

Liu

Shih

Chen

2012

CMAJ

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“…There are two recognized forms of POPE [2]. Type I follows a sudden, severe episode of upper airway obstruction and can be seen in association with any cause of acute upper airway obstruction such as postextubation laryngospasm, endotracheal tube occlusion, epiglottitis and croup and choking.…”

Section: Discussionmentioning

confidence: 99%

“…Survivors of suicidal hanging have been found to suffer morbidity due to upper airway obstruction caused by ligature strangulation [4]. Type II POPE develops after surgical relief of chronic upper airway obstruction and has been reported after tonsillectomy [2].…”

Section: Discussionmentioning

confidence: 99%

Pulmonary Oedema in a survivor of Suicidal Hanging

Aggarwal

Anant

Vardhan

2004

Medical Journal Armed Forces India

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bilateral nonhomogeneous opacities while X-ray cervical spine did not reveal any bony lesion. Fundoscopy revealed no abnormality. After institution of mechanical ventilation, pulse rate stabilised at 130-140/min, blood pressure varied from 110-130/60-70mm of Hg and SpO 2 ranged from 90-92%.Patient was conscious the next morning and was responding to verbal commands, pulse rate was 140/min and blood pressure 130/80mm of Hg. PEEP was gradually increased to 15cm of H 2 O and FiO 2 was simultaneously decreased to 0.6, maintaining SpO 2 between 91% and 96%. Throughout the day dopamine at the rate of 3-5µg/Kg/min had to be infused intermittently to maintain systolic blood pressure above 90mm of Hg. On the third day of hospitalisation patient's general condition remained same. She was conscious and tolerated endotracheal tube well, pulse rate varied between 120-136/min and blood pressure varied between 85-90/50-70mm of Hg. Bronchial breath sounds were auscultated bilaterally with no adventitious sounds, but chest X-ray did not reveal any improvement over previous radiological findings. Hemogram and all biochemical parameters were within normal limits and tracheal secretions were sent for culture (which did not grow any organism after 48 hours of incubation). Amikacin and ceftazidime were instituted empirically. Dopamine was continued. Attempts to decrease PEEP keeping FiO 2 less than 0.6 failed and ventilatory parameters were left unchanged with SpO 2 varying from 91%-96%. Patient was sedated with morphine 3 mg IV every four hours. On the fourth day of hospitalisation PEEP was reduced to 10 cm of H 2 O and FiO 2 to 0.5. Dopamine was gradually withdrawn and blood pressure during the day ranged between 90-100/60-70 mm of Hg. On the fifth day of hospitalisation, patient was found to be conscious with pulse rate of 88/ minute, blood pressure of 100/60mm of Hg and SpO 2 of 99%. Chest was clinically clear but X-ray chest showed only minimal improvement. Weaning from artificial ventilation was attempted using SIMV mode with decreasing rate of ventilation followed by a spontaneous breathing trial with Ttube for two hours, but patient failed to maintain adequate SpO 2 and hemodynamic stability and ventilatory support was reinstituted with PEEP of 4 cm of H 2 O and FiO 2 of 0.4. On the sixth day of hospitalisation patient was successfully weaned off the ventilator. Post extubation pulse rate was 104/min, blood pressure was 100/67mm of Hg, SpO 2 98% and respiratory

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“…2 Post obstructive pulmonary edema usually develops within 60 min of relief from acute upper airway obstruction, although in some cases it has been reported to be delayed up to 6 hrs. 3 However, in the present patient the onset was delayed beyond 12 hrs after the precipitating event.…”

Section: Sirmentioning

confidence: 99%