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Year : 2020  |  Volume : 3  |  Issue : 1  |  Page : 49-51

Delayed presentation of negative pressure pulmonary oedema

1 Department of Anesthesiology, All India Institute of Medical Sciences, Bathinda, Punjab, India
2 Department of Anaesthesia and Intensive Care, PGIMER, Chandigarh, India

Date of Submission20-Feb-2020
Date of Acceptance06-Apr-2020
Date of Web Publication30-May-2020

Correspondence Address:
Dr. Navneh Samagh
Department of Anesthesiology, All India Institute of Medical Sciences, Bathinda, Punjab
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ARWY.ARWY_5_20

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Negative pressure pulmonary oedema (NPPO) is a life-threatening complication occurring due to large negative intrathoracic pressures created by inspiration against a closed glottis. Timely diagnosis and management is important to prevent any fatal outcome. Although it presents acutely most of the time, its presentation may rarely be delayed. We present a case of a 21-year-old female weighing 40 kg who developed NPPO 1.5 h after warding in the post-anaesthesia care unit. Despite the delayed presentation, she was diagnosed in a timely manner and managed successfully. This case emphasises the need for extended monitoring of all patients with any respiratory difficulty in the perioperative period for delayed development of NPPO.

Keywords: Delayed presentation, negative pressure pulmonary oedema, post-anaesthesia care unit

How to cite this article:
Kaur R, Naik B N, Samagh N, Singh N. Delayed presentation of negative pressure pulmonary oedema. Airway 2020;3:49-51

How to cite this URL:
Kaur R, Naik B N, Samagh N, Singh N. Delayed presentation of negative pressure pulmonary oedema. Airway [serial online] 2020 [cited 2021 Oct 25];3:49-51. Available from: https://www.arwy.org/text.asp?2020/3/1/49/285432

  Introduction Top

Negative pressure pulmonary oedema (NPPO) is a complication which can be fatal. It occurs due to large negative intrathoracic pressures generated by forceful inspiration against an obstructed airway. Its incidence is 0.005%–0.1%, with more than half of the cases occurring in patients of post-anaesthetic laryngospasm.[1],[2],[3],[4] The presentation of NPPO can be immediate or delayed.[1],[5] We present a case of delayed NPPO in a young female following arthroscopic partial meniscectomy.

  Case Report Top

A 21-year-old female weighing 40 kg, a known case of lateral meniscal tear of the left knee, was scheduled to undergo arthroscopic partial meniscectomy. A thorough preanaesthetic evaluation revealed no comorbid illness, and systemic examination was normal. Investigations including chest X-ray and electrocardiogram (ECG) were normal. Written informed consent was obtained. The patient was found to be fasting for 15 h. General anaesthesia was administered as requested by the patient. Standard monitoring consisting of ECG, noninvasive blood pressure and pulse oximetry was initiated in the operating room. The patient was induced with intravenous (IV) fentanyl 60 μg, propofol 80 mg and atracurium 20 mg. A size 7.0 mm ID cuffed oral endotracheal tube was inserted and fixed at 18 cm at the angle of the mouth after confirming bilateral equal air entry. Anaesthesia was maintained with oxygen in nitrous oxide (50:50) and isoflurane up to 2%. Intraoperatively, the patient's vitals were stable. Considering 15 h of fasting, 700 mL of fluid was given intravenously according to Holliday–Segar formula. Blood loss was <50 mL. IV paracetamol 600 mg was given for pain management. Injection ondansetron 4 mg IV was given at the end of surgery for preventing postoperative nausea and vomiting. While the surgery lasted 50 min, the duration of anaesthesia was 70 min. Residual neuromuscular blockade was antagonised, and the patient extubated when she was generating adequate tidal volume and started moving all the four limbs. The patient was extubated as she was coughing and straining on the tube. Following extubation, it was found that the patient was not breathing adequately. Ventilation was assisted with a bag and a mask for 15 min. Assisted ventilation was adequate as revealed on the capnograph. After 15 min, the patient started swallowing, coughing and vocalising on command.

As the patient was fully conscious and generating adequate tidal volume, she was shifted to the post-anaesthesia care unit (PACU) for monitoring. In the PACU, the modified Aldrete score was 9. Vital signs revealed a heart rate of 88/min, blood pressure of 116/60 mm Hg, respiratory rate of 16/min and an SpO2 of 100% on room air. Systemic examination was essentially normal. On arrival in the PACU, TOF-Watch® SX (Organon Ltd., Ireland) neuromuscular monitor was used to check recovery from neuromuscular blockade. The TOF-Watch SX revealed a train-of-four ratio of 0.9 (indicating 90% recovery from neuromuscular blockade). Oxygen was started using a 35% venturi mask. IV fluids were given at 60 mL/h. Ninety minutes after warding in the PACU, the patient developed a dry cough. It was sudden in onset and intermittent in nature. Vital signs were normal, and respiratory rate was 14–16 breaths/min. Auscultation of the chest revealed normal breath sounds. Saline nebulisation was administered suspecting airway irritation. After another 30 min, the patient developed breathlessness and cough with pink frothy sputum. The patient desaturated to 85% on room air. The ECG monitor showed sinus tachycardia with no ST-T changes. Bilateral coarse crepitation were present in both lung fields. Arterial blood gas analysis (ABG) was done which showed hypoxia [Table 1]. Bedside chest X-ray showed the presence of bilateral pulmonary infiltrates. Ultrasound of the lungs showed presence of B lines. Diagnosis of pulmonary oedema was made. IV morphine 3 mg and intravenous furosemide 30 mg were given. The patient was put on noninvasive ventilation (NIV) with an FIO2 of 0.4, PEEP of 6 cm H2O and a pressure support of 8 cm H2O. Cardiology opinion was obtained. The 12-lead ECG and two-dimensional (2D)-echocardiography (ECHO) were essentially normal and so were the proBNP levels. The diagnosis of noncardiogenic pulmonary oedema was confirmed. Serial ABGs were sent at regular intervals [Table 1]. The patient was slowly weaned off from NIV after 2 h. Oxygen was continued via venturi mask at an FIO2 of 0.31. The patient was monitored overnight in the PACU. Cardiology review was obtained and the patient was discharged after 24 h.
Table 1: Reports of arterial blood gas analysis

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  Discussion Top

NPPO is an acute life-threatening condition of noncardiogenic origin occurring intraoperatively or postoperatively. The incidence of NPPO is 0.005%-0.1% of all anaesthetic practices.[1] In adults, about 50% of NPPO are due to postoperative laryngospasm.[2],[3],[4] Clinically, patients present with cough with pink frothy sputum, breathlessness and agitation. On examination, there is tachypnoea, tachycardia, desaturation and presence of bilateral crepitation. Chest X-ray shows diffuse interstitial and alveolar infiltrates. Computed tomography reveals nondependent, mainly central, ground-glass attenuation paralleling interstitial and pleural pressure gradients. Ultrasound of the lungs shows B lines. Normal ECG and ECHO in cases of NPPO support its noncardiogenic origin.

NPPO can be classified into type 1 and type 2 based on aetiology. Causes of type 1 NPPO include post-extubation laryngospasm, epiglottitis, croup, choking, strangulation, hanging, endotracheal tube obstruction due to biting or secretions and postoperative vocal cord paralysis. Type 2 NPPO occurs after relief of chronic obstruction and is seen following tonsillectomy, adenoidectomy and removal of upper airway tumours. Relief of chronic obstruction removes the PEEP and returns lung volumes and pressures to normal. Sudden removal of PEEP leads to interstitial fluid transudation and pulmonary oedema.

Our patient was extubated in deep plane of anaesthesia and had inadequate respiratory efforts in the immediate postoperative period. Thus, there might have been some elements of obstruction in the airway, which could have resulted in the development of NPPO. Although the symptoms of NPPO usually develop immediately after extubation, sometimes, the onset may be delayed up to a few hours into the postoperative period,[6],[7],[8] as happened in our patient. Our patient presented with sudden onset of cough and breathlessness with pink frothy sputum 1.5 h after warding in the PACU. A full-blown picture of pulmonary oedema was noticed 2 h into the PACU stay. Chest auscultation revealed bilateral crepitation. Chest X-ray showed bilateral pulmonary infiltrates, with ultrasound of lungs showing the pathognomonic B lines suggestive of pulmonary oedema. As the ECG and 2D ECHO were normal, it was clear that pulmonary oedema was noncardiogenic in origin. A possible explanation for this delayed manifestation is the positive pressure created by forceful expiration against a closed glottis, opposing fluid transudation. As airway obstruction is relieved, increased venous return causes blood shift from peripheral to central circulation and hydrostatic transudation, leading to pulmonary oedema.[9] Thus, increased vigilance is a must to diagnose such cases on time. A high index of suspicion needs to be exercised in patients having respiratory symptoms in the perioperative period to diagnose NPPO. Such patients should be closely monitored postoperatively for an extended period of time.

  Conclusion Top

NPPO can have a delayed presentation. Patients at risk for development of NPPO should be closely monitored in the postoperative period for an extended period of time.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her clinical information to be reported in the journal. The patient understands that her name and initials will not be published and due efforts will be made to conceal her identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.

  References Top

McConkey PP. Postobstructive pulmonary oedema – A case series and review. Anaesth Intensive Care 2000;28:72-6.  Back to cited text no. 1
Mamiya H, Ichinohe T, Kaneko Y. Negative pressure pulmonary edema after oral and maxillofacial surgery. Anesth Prog 2009;56:49-52.  Back to cited text no. 2
Tebay A, Bouti K, Tebay N. Negative pressure pulmonary edema following a cholecystectomy – A case report. Rev Pneumol Clin 2017;73:267-71.  Back to cited text no. 3
Chen Y, Zhang X. Acute postobstructive pulmonary edema following laryngospasm in elderly patients A case report. J Perianesth Nurs 2019;34:250-8.  Back to cited text no. 4
Timby J, Reed C, Zeilender S, Glauser FL. “Mechanical” causes of pulmonary edema. Chest 1990;98:973-9.  Back to cited text no. 5
Habtegebriel Y, Nfonoyim J, Mehari A. Delayed negative pressure edema in a young athletic man. InB40. Dyspnea: Case Reports. Am J Respir Crit Care Med 2016;193:A3438.  Back to cited text no. 6
Liu R, Wang J, Zhao G, Su Z. Negative pressure pulmonary edema after general anesthesia: A case report and literature review. Medicine (Baltimore) 2019;98:e15389.  Back to cited text no. 7
Hong SO, Chung JY, Lee DW. Quick and accurate measures in negative pressure pulmonary edema: A guideline for orthognathic surgeons. J Craniofac Surg 2014;25:e433-5.  Back to cited text no. 8
Westreich R, Sampson I, Shaari CM, Lawson W. Negative-pressure pulmonary edema after routine septorhinoplasty: Discussion of pathophysiology, treatment, and prevention. Arch Facial Plast Surg 2006;8:8-15.  Back to cited text no. 9


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