Year : 2014  |  Volume : 17  |  Issue : 2  |  Page : 161--163

Post extubation negative pressure pulmonary edema due to posterior mediastinal cyst in an infant

Prakash Kumar Dubey 
 Department of Anaesthesiology and Critical Care Medicine, Indira Gandhi Institute of Medical Sciences, Sheikhpura, Patna, Bihar, India

Correspondence Address:
Prakash Kumar Dubey
Eľ, Indira Gandhi Institute of Medical Sciences Campus, Patna - 800 014, Bihar


A 3-month-old male child underwent uneventful inguinal herniotomy under general anesthesia. After extubation, airway obstruction followed by pulmonary edema appeared for which the baby was reintubated and ventilated. The baby made a complete recovery and extubated after about 2 h. A post-operative computed tomography scan revealed a posterior mediastinal cystic mass abutting the tracheal bifurcation. Presumably, extrinsic compression by the mass on the tracheal bifurcation led to the development of negative pressure pulmonary edema.

How to cite this article:
Dubey PK. Post extubation negative pressure pulmonary edema due to posterior mediastinal cyst in an infant.Ann Card Anaesth 2014;17:161-163

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Dubey PK. Post extubation negative pressure pulmonary edema due to posterior mediastinal cyst in an infant. Ann Card Anaesth [serial online] 2014 [cited 2020 Mar 28 ];17:161-163
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Negative pressure pulmonary edema (NPPE) is a potentially fatal condition and is usually associated with post-extubation laryngospasm. Described here is a case of suspected NPPE that developed due to presence of an undiagnosed posterior mediastinal cyst abutting the tracheal bifurcation.

 Case Report

A 3-month-old male child weighing 3 kg underwent bilateral inguinal herniotomy under general anesthesia. The baby was delivered normally at term. The routine laboratory investigations were within the normal limits and physical examination was unremarkable. The parents of the child did not report any history suggestive of cardio respiratory or other illness.

In the operating room (OR), after starting monitoring with electrocardiography, non-invasive blood pressure and pulse oximetry, anesthesia was induced with fentanyl 5 μg and halothane 1% in oxygen. Ventilation was controlled easily and after administration of atracurium 2 mg, atraumatic tracheal intubation was performed with a 3 mm ID endotracheal tube. Anesthesia was continued with 0.5% halothane in nitrous oxide and oxygen. Intermittent positive pressure ventilation (IPPV) was provided as per the body weight. Surgical procedure was performed uneventfully and trachea was extubated after reversal of neuromuscular blockade with neostigmine and atropine. After extubation, the baby was moving all four limbs and crying. The duration of surgery was 75 min and volume of crystalloid infused was approximately 30 ml. A few minutes after extubation, the oxygen saturation (SpO 2 ) dropped from 98% to 86% and the respiration appeared obstructed. Suspecting upper airway-obstruction facemask was applied, oropharyngeal airway was inserted and manual ventilation was started. However, attempts to ventilate the lungs proved futile and intermittent flushing of the emergency oxygen failed to improve oxygenation. The heart rate dropped from 124 beats per minute (bpm) to 70 and SpO 2 decreased to 80%; immediately atropine 0.1 mg was administered and the trachea was reintubated without difficulty. No spasm or frothing was noted during laryngoscopy. By now, the baby had developed apnea. Positive pressure ventilation with a FiO 2 of 1 gradually improved the SpO 2 to 90%. On auscultation, fine crepitations were heard all over the chest and frothy secretion was aspirated through the endotracheal tube. Furosemide 1 mg was administered intravenously and IPPV was continued with 100% oxygen. On return of spontaneous breathing, severe indrawing of the lower chest along with vigorous diaphragmatic respiration was noticed. The clinical picture resembled airway obstruction; a sterile suction catheter was passed through the tracheal tube that went in smoothly. The respiratory-rate was 36 per minute, EtCO 2 48 mmHg but the SpO 2 remained 92%. A continuous positive airway pressure of 3 cmH2O was applied, which resulted in immediate increase of SpO 2 to 98%. Gradually, the FiO 2 was reduced and after 90 min, when the baby became fully awake, trachea was extubated. The indrawing of lower chest improved after 6 h and the baby made full recovery. Later, his mother informed that she had earlier noticed mild indrawing of lower chest when the baby was in deep sleep. A chest X-ray obtained 24 h postoperatively revealed a shadow on the right side suggestive of a mediastinal mass along with some vertebral anomalies [Figure 1]. An echocardiogram was done that did not reveal any abnormality. Computed tomography (CT) scan showed a right posterior mediastinal cyst (neuroenteric cyst) abutting the tracheal bifurcation [Figure 2].{Figure 1}{Figure 2}


NPPE usually follows upper airway obstruction due to a variety of reasons. The most common form encountered by an anesthesiologist follows the post-extubation laryngospasm. The NPPE usually disappears within few minutes after relief of obstruction and the radiographic evidence resolves within 12-24 h. The clinical presentations in the OR included decreased peripheral saturation and frothy secretions. Bronchoscopic and CT findings consistent with alveolar hemorrhage and capillary failure following post-extubation NPPE have been reported. [1] Airway obstruction manifests as stridor, suprasternal and/or supraclavicular retractions and use of accessory muscles of respiration. Treatment includes maintenance of a patent airway and administration of oxygen. [2] Furosemide is often administered in this situation. [3] Brief period of mechanical ventilation or non-invasive positive pressure ventilation may be required.

The pathogenesis of NPPE is well described. Highly negative intrapleural pressure caused by vigorous inspiratory efforts against an obstructed airway decrease the interstitial hydrostatic pressure favoring transudation of edema fluid from pulmonary capillaries. Concomitant increase in pulmonary blood flow due to increased venous return to the right heart, further augment interstitial edema. Sympathetic stimulation associated with catastrophic airway obstruction cause systemic hypertension and central pooling of blood volume further increasing venous return to the right heart and pulmonary blood flow contributing to edema. Hypoxic vasoconstriction also increases capillary pressure and favors movement of fluid into the interstitium. All these factors increases the transcapillary pressure gradients and lead to pulmonary edema. [2] Additionally, the negative pleural pressure expose the left ventricle to an afterload stress during systole, when afterload is expressed as the transmural aortic root pressure (i.e., mean aortic pressure minus pleural pressure). This can cause a decrease in left ventricular stroke volume and increases in both ventricular end-systolic and end-diastolic volumes. Theoretically, this increase in left ventricular afterload could increase pulmonary capillary hydrostatic pressure and contribute to fluid transudation.

This patient had a right posterior mediastinal cyst (neuroenteric cyst) abutting the tracheal bifurcation. The posterior mediastinum is outlined by the pericardium and great vessels anteriorly, vertebral column posteriorly and the parietal pleura laterally. Its contents include esophagus, trachea, main bronchi and other neurovascular structures. The mediastinal lesions produce clinical symptoms due to their mass effect depending on their exact location within the thorax. Posterior mediastinal masses can be quite large and yet asymptomatic, often discovered incidentally on a chest radiograph obtained for other indications. [4] We believe in the present case the posterior mediastinal cyst caused airway obstruction at the level of tracheal bifurcation.

At the time of induction, ventilation by face-mask must have countered the pressure exerted by the mediastinal mass preventing a collapse of the airway. IPPV during surgery did not allow this compression to appear clinically. The patient's intrinsic muscle tone was less than normal immediately after extubation. This led to the pressure effect on the tracheal bifurcation creating a picture of airway obstruction and NPPE. The site of obstruction was at the tracheal bifurcation that is why it was not relieved by endotracheal intubation alone. Application of a continuous positive airway pressure overcame the compression caused by the cyst. Added factor was an improving muscle tone that gradually relieved the obstruction and the symptoms. The indrawing of the lower chest was analogous to the supraclavicular or suprasternal retraction seen in upper airway obstruction. A lower muscle tone caused the cyst to press the tracheal bifurcation, a fact corroborated by the mother also who witnessed the same phenomenon during sleep albeit in a milder form.

The other possibilities leading to this situation could have been laryngospasm, aspiration of gastric contents, intravascular volume overload or cardiac abnormalities. Laryngospasm was not seen during both atraumatic intubations and fluid overload was ruled out. Cardiac abnormalities were ruled out post-operatively. Aspiration of gastric contents is not that easily resolved by the measures taken by us. The flow volume loop and fiberoptic bronchoscopy could have settled the issue in this situation but unfortunately the facilities were not available.

Partial bronchial compression during inspiration upon emergence from anesthesia has been reported in a 16-year-old patient having anterior mediastinal mass. [5] Development of NPPE due to such compression is unusual. We believe a similar mechanism was operating in our patient but the lesion causing compression was posterior to the trachea. The bronchial smooth muscle is relaxed during anesthesia leading to increased compressibility of the large airways. This exacerbated the effects of extrinsic compression by the cyst. During emergence, a diaphragmatic mode of respiration with a minimal chest wall movement can cause an intrathoracic mass to obstruct the airway during inspiration in the supine position. [5] Later on, when the chest wall contractility became more prominent, the obstruction gradually relieved. Positive pressure ventilation preempted this obstructive pattern during induction and intra operatively. The problem led to NPPE after the child resumed spontaneous respiration and resurfaced during spontaneous breathing after reintubation. NPPE can occur due to a mediastinal mass; prompt and appropriate management can prevent an adverse outcome. A history of indrawing of lower chest during sleep may provide some clue to the possibility of airway compromise/NPPE during weaning or after extubation.


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