Post-extubation Negative Pressure Pulmonary Edema Complicating Laparoscopic Appendicectomy: A Case Series

Ramya V et al | DOI: 10.65188/nurexus.1092

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Journal of MedVerse Research & Practice

ISSN: 3107-4278

Post-extubation Negative Pressure Pulmonary Edema Complicating

Laparoscopic Appendicectomy: A Case Series

V Ramya

, B Balu

Postgraduate, Professor

Department of Anaesthesia, PSP Medical Sciences, Kanchipuram

Email ID: ramyav345@gmail.Com

Submission Date: 10.06.2026

Accepted Date:18.07.2026

Published Date: 31.07.2026

DOI: 10.65188/nurexus.1092

article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted

use, distribution, and reproduction in any medium, provided the original author(s) and source are credited.

Abstract

Background: Negative pressure pulmonary edema (NPPE) is a rare but potentially life-threatening form of non-

cardiogenic pulmonary edema that occurs following acute upper airway obstruction, most commonly after post-

extubation laryngospasm. Although uncommon after laparoscopic appendicectomy, NPPE requires prompt

recognition and management to prevent significant morbidity.

Case Presentation: We report a case series of five patients who developed post-extubation negative pressure

pulmonary edema following laparoscopic appendicectomy under general anesthesia. All patients experienced acute

respiratory distress immediately after extubation, with clinical manifestations including hypoxemia, tachypnea,

bilateral coarse crepitations, and, in some cases, pink frothy sputum. Chest radiography demonstrated bilateral diffuse

pulmonary infiltrates consistent with non-cardiogenic pulmonary edema. Differential diagnoses such as aspiration

pneumonitis, cardiogenic pulmonary edema, and fluid overload were excluded based on clinical evaluation and

appropriate investigations. Management consisted of immediate airway stabilization, administration of supplemental

oxygen, positive pressure ventilation using continuous positive airway pressure (CPAP) or mechanical ventilation

with positive end-expiratory pressure (PEEP), and supportive intensive care measures. All patients showed rapid

clinical improvement with complete radiological resolution within 24–48 hours and were discharged without long-

term pulmonary complications.

Conclusion: Post-extubation NPPE is an uncommon but reversible perioperative emergency that should be suspected

in patients who develop sudden respiratory distress immediately after extubation. Early diagnosis, prompt restoration

of airway patency, and timely ventilatory support are essential for favorable outcomes. This case series highlights

the importance of vigilant postoperative airway monitoring and increased awareness among anesthesiologists and

perioperative care teams to facilitate early recognition and successful management of this rare complication.

Keywords: Negative pressure pulmonary edema; Post-extubation pulmonary edema; Laryngospasm; General

anesthesia; Laparoscopic appendicectomy; Upper airway obstruction; Non-cardiogenic pulmonary edema;

Mechanical ventilation; Perioperative complication; Case series.

Introduction

Negative pressure pulmonary edema (NPPE) is a rare but life-threatening type of non-cardiogenic

pulmonary edema which occurs following acute upper airway obstruction [1, 2]. It is defined as rapidly

accumulating fluid in the pulmonary interstitium and alveolar spaces due to the generation of severely

negative intrathoracic pressure from vigorous inspiratory efforts in an obstructed airway [2,3]. Despite only

being a small contributor to postoperative pulmonary complications, NPPE is considered an 'immediate'

perioperative emergency due to its early presentation and possible progression into severe hypoxemia

unless rapidly recognised and corrected [3,4]. Over half of reported cases involve post-extubation

laryngospasm as a triggering event for NPPE [4,5]. Other causes are endotracheal tube biting, tumors in the

CASE SERIES

ARTICLE

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upper airways (including anaphylaxis or type III hypersensitivity reactions), epiglottitis, obstructive sleep

apnoea, asfphxia from foreign-body aspiration and stridor has been documented with vocal cord paralysis

rarely seen [5,6]. This occurs often minutes after the relief of airway obstruction although late presentations

have also been reported [6]. The demographic most affected are young, healthy adults, whom we believe

can generate dangerously negative inspiratory pressures during vigorous inspiratory efforts against a closed

glottis usually −50 to −100 cmH₂O [7].

The pathophysiology of NPPE is attributed to a multifactorial interaction between hemodynamic and

mechanical mechanisms. A vigorous inspiratory effort against a closed airway results in a significant drop

in the intrathoracic pressure, an increase in venous return to the right ventricle and a rise in pulmonary

blood volume [2,7]. At the same time, the increase in transmural pressure across pulmonary capillaries

increases hydrostatic pressure, leading to disruption of the alveolar-capillary membrane and extravasation

of protein-poor fluid into pulmonary interstitium and alveoli [8]. Pulmonary edema results in impaired gas

exchange, ventilation-perfusion mismatch, decreased lung compliance, and profound hypoxemia [3,8].

Only in even worse circumstances, sympathetic activation emerges owing to hypoxia and adds to

pulmonary vascular stresses, aggravating pulmonary edema [8,9].

The incidence of NPPE after general anesthesia has been reported at between 0.05% and 0.1%, although,

as mild cases resolve rapidly and may not be recognized or reported, the true incidence is probably

underreported [4,9]. Risk factors or predictors include difficult airway, obesity, short neck, upper airway

surgery, recent history of upper respiratory tract infection (URTI), excessive airway secretions, multiple

attempts at extubation, vigorous coughing during emergence and incomplete reversal of neuromuscular

blockade [5,10]. Even so, anesthesiologists and perioperative physicians should always assume a high index

of suspicion in any patient who experiences acute respiratory distress immediately following extubation

[3,10]. Clinically, NPPE typically manifests with rapid onset of respiratory distress, tachypnea, tachycardia

and agitation in addition to oxygen desaturation and bilateral inspiratory crackles immediately after

extubating [1,11]. Pink frothy sputum, a classic manifestation, is not always seen [11]. Chest X rays

typically show bilateral diffuse alveolar infiltrates (without cardiomegaly), while arterial blood gas analysis

shows various degrees of hypoxemia and occasionally hypercapnia [12]. Diagnosis is mainly clinical and

must be differentiated from cardiogenic pulmonary edema, aspiration pneumonitis, acute respiratory

distress syndrome (ARDS), pulmonary embolism (PE), fluid overload or anaphylaxis [12, 13].

NPPE is usually reversible if properly managed; therefore, early diagnosis and management are important

[2, 13].

Among the most common emergency surgery it is laparoscopic appendicectomy, which in practice usually

has little or no postoperative respiratory complication [15]. NPPE after an otherwise straightforward

laparoscopic appendicectomy is consequently a rare complication and may prove troublesome to diagnose

early post-operatively [15, 16]. It is essential to report these cases in order to raise awareness among

anaesthesiologists and surgeons, allowing for early recognition and reinforcing evidence-based

management strategies [14,16]. We describe the case of a patient who developed post-extubation negative

pressure pulmonary edema following laparoscopic appendicectomy, and in particular highlight its clinical

presentation, investigative work-up, management, and key take-home messages to reduce the risk of this

potentially life-threatening but reversible complication.

Case Series

Case 1

A 24-year-old previously healthy male presented with acute right iliac fossa pain and was diagnosed with

acute appendicitis. He underwent an uneventful laparoscopic appendicectomy under general anesthesia.

Ramya V et al | DOI: 10.65188/nurexus.1092

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The surgery lasted 55 minutes with minimal blood loss. Neuromuscular blockade was adequately reversed,

and extubation was attempted after the patient regained spontaneous breathing. Immediately following

extubation, the patient developed severe laryngospasm associated with paradoxical chest movements and

oxygen desaturation from 99% to 72%. Positive pressure ventilation and intravenous propofol were

administered to relieve the airway obstruction. Soon after, the patient developed respiratory distress with

pink frothy sputum and bilateral coarse crepitations. Chest radiography demonstrated diffuse bilateral

perihilar alveolar infiltrates consistent with pulmonary edema. Arterial blood gas analysis revealed

hypoxemia (PaO₂ 58 mmHg). He was re-intubated and mechanically ventilated with positive end-expiratory

pressure (PEEP). Intravenous furosemide and supportive therapy were initiated. Pulmonary infiltrates

resolved within 24 hours, and the patient was successfully extubated the following day with complete

recovery.

Case 2

A 32-year-old woman with no significant medical history underwent emergency laparoscopic

appendicectomy for perforated appendicitis. General anesthesia and surgery were uneventful. During

emergence, vigorous coughing followed by transient laryngospasm occurred immediately after extubation.

Oxygen saturation rapidly decreased to 80%, and the patient complained of acute breathlessness. Bilateral

basal crackles were audible on chest auscultation. Chest radiography revealed diffuse bilateral pulmonary

infiltrates without cardiomegaly, while echocardiography showed normal cardiac function. She was

managed with continuous positive airway pressure (CPAP), high-flow oxygen therapy, intravenous

corticosteroids, and careful fluid restriction. Respiratory status improved progressively, and repeat chest

radiography after 36 hours demonstrated complete resolution of pulmonary edema. The patient was

discharged on the fourth postoperative day without residual complications.

Case 3

A 19-year-old athletic male underwent laparoscopic appendicectomy for uncomplicated acute appendicitis.

Extubation was initially uneventful; however, within five minutes, he developed inspiratory stridor, severe

dyspnea, tachypnea (36 breaths/min), and oxygen saturation of 75%. Pink frothy sputum was noted during

suctioning. Chest radiography demonstrated bilateral diffuse alveolar opacities, and arterial blood gas

analysis confirmed severe hypoxemia. A diagnosis of post-extubation negative pressure pulmonary edema

secondary to acute upper airway obstruction was made. The patient required immediate re-intubation and

mechanical ventilation with PEEP. Supportive intensive care management resulted in rapid clinical

improvement, allowing extubation after 18 hours. Follow-up chest radiography showed complete

resolution, and he was discharged on postoperative day three.

Case 4

A 41-year-old obese woman (Body Mass Index 34 kg/m²) underwent laparoscopic appendicectomy under

general anesthesia. Shortly after extubation, upper airway obstruction due to soft tissue collapse resulted in

forceful inspiratory efforts and progressive oxygen desaturation. She developed tachycardia, bilateral

pulmonary crackles, and expectoration of blood-tinged frothy sputum. Chest radiography demonstrated

bilateral pulmonary edema with normal cardiac size. Electrocardiography and cardiac biomarkers excluded

myocardial ischemia. The patient was managed with non-invasive ventilation using CPAP, intravenous

diuretics, supplemental oxygen, and close monitoring in the intensive care unit. Her respiratory symptoms

resolved within 48 hours, and she was discharged in stable condition on postoperative day five.

Case 5

A 27-year-old male underwent emergency laparoscopic appendicectomy under general anesthesia. During

extubation, he bit the endotracheal tube, causing transient airway obstruction followed by forceful

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inspiratory efforts after tube removal. Within minutes, he developed severe hypoxemia (SpO₂ 68%),

tachycardia, diffuse bilateral crepitations, and production of pink frothy secretions. Chest radiography

demonstrated bilateral pulmonary infiltrates suggestive of non-cardiogenic pulmonary edema. Bedside

echocardiography showed preserved ventricular function, excluding cardiogenic pulmonary edema. The

patient was immediately re-intubated and ventilated with PEEP. Supportive management, including oxygen

therapy and cautious fluid management, resulted in marked improvement within 24 hours. He was

extubated the following day successfully and discharged home on postoperative day four without

respiratory sequelae.

Result

Variable

Case 1

Case 2

Case 3

Case 4

Case 5

Age (years)

Sex

Male

Female

Male

Female

Male

BMI

(kg/m²)

22.1

24.6

21.8

34.0

23.4

ASA Grade

Diagnosis

Acute

appendicitis

Perforated

appendicitis

Acute

appendicitis

Acute

appendicitis

Acute

appendicitis

Procedure

Laparoscopic

appendicectom

Laparoscopic

appendicectom

Laparoscopic

appendicectom

Laparoscopic

appendicectom

Laparoscopic

appendicectom

Duration of

surgery

(min)

Trigger for

NPPE

Laryngospasm

Vigorous

coughing with

transient

laryngospasm

Acute upper

airway

obstruction

Airway

collapse after

extubation

Endotracheal

tube biting

Time to

symptom

onset

Immediate

2 min

5 min

Immediate

3 min

Lowest

SpO₂ (%)

Pink frothy

sputum

Yes

Bilateral

crepitations

Yes

Chest X-ray

Bilateral diffuse

infiltrates

Bilateral

infiltrates

Diffuse alveolar

edema

Bilateral

pulmonary

edema

Bilateral diffuse

infiltrates

ABG

finding

Severe

hypoxemia

Moderate

hypoxemia

Severe

hypoxemia

Moderate

hypoxemia

Severe

hypoxemia

Ventilatory

support

Re-intubation +

PEEP

CPAP

Re-intubation +

PEEP

CPAP

Re-intubation +

PEEP

ICU

admission

Yes

Ramya V et al | DOI: 10.65188/nurexus.1092

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Duration of

ventilation

24 hours

CPAP for 12

hours

18 hours

CPAP for 24

hours

24 hours

Radiologica

l recovery

24 hours

36 hours

24 hours

48 hours

24 hours

Hospital

stay

4 days

3 days

5 days

4 days

Outcome

Complete

recovery

Complete

recovery

Complete

recovery

Complete

recovery

Complete

recovery

Discussion

Negative pressure pulmonary edema (NPPE) is an uncommon but potentially life-threatening cause of acute

postoperative respiratory failure resulting from forceful inspiratory efforts against an obstructed upper

airway [1–3]. Although the reported incidence following general anesthesia is relatively low, ranging from

0.05% to 0.1%, delayed recognition may lead to severe hypoxemia, prolonged mechanical ventilation, and

increased morbidity [4,5]. Post-extubation laryngospasm remains the most common precipitating factor,

accounting for the majority of reported cases, particularly in young, healthy individuals capable of

generating high negative intrathoracic pressures [5,6].

In the present case series, all patients developed acute respiratory distress within minutes of extubation

following laparoscopic appendicectomy, consistent with the classical presentation described in previous

reports [5,7]. Clinical manifestations included sudden oxygen desaturation, tachypnea, bilateral

crepitations, and radiographic evidence of diffuse pulmonary infiltrates without features suggestive of

cardiogenic pulmonary edema. These findings highlight the importance of considering NPPE as a

differential diagnosis in patients who deteriorate immediately after extubation despite an otherwise

uneventful surgical procedure.

The underlying mechanism involves marked negative intrathoracic pressure generated during inspiratory

efforts against an obstructed airway, resulting in increased venous return, elevated pulmonary capillary

hydrostatic pressure, disruption of the alveolar-capillary membrane, and rapid accumulation of fluid within

the pulmonary interstitium and alveoli [2,7,8]. Hypoxia-induced sympathetic stimulation further aggravates

pulmonary vascular pressure and edema formation [8]. Young adults are particularly vulnerable because of

their ability to generate strong inspiratory forces during laryngospasm or transient airway obstruction [6,9].

Prompt diagnosis and aggressive supportive management are essential for favorable outcomes. Early

restoration of airway patency, administration of high-flow oxygen, application of continuous positive

airway pressure (CPAP) or positive end-expiratory pressure (PEEP), and re-intubation with mechanical

ventilation when required remain the cornerstone of treatment [10,11]. In the present series, all patients

responded well to early airway stabilization and ventilatory support, with complete clinical and radiological

recovery within 24–48 hours, similar to outcomes reported in previous studies [11,12]. Although diuretics

such as furosemide were administered in selected cases, their routine use remains controversial because

NPPE is primarily a hydrostatic rather than a volume-overload phenomenon [12,13].

This case series emphasizes the importance of preventive measures, including adequate reversal of

neuromuscular blockade, gentle airway manipulation, complete suctioning of secretions, and prompt

treatment of laryngospasm during emergence from anesthesia [5,13]. Although limited by the small sample

size, the consistent presentation and favorable recovery observed in all cases reinforce existing evidence

that NPPE is a rapidly reversible condition when recognized and managed promptly. Increased awareness

among anesthesiologists, surgeons, and perioperative physicians is essential for early diagnosis and optimal

patient outcomes [14–16].

Ramya V et al | DOI: 10.65188/nurexus.1092

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Summary

Post-extubation negative pressure pulmonary edema (NPPE) is a rare but potentially life-threatening

complication that may occur following acute upper airway obstruction, most commonly due to

laryngospasm after general anesthesia. Although laparoscopic appendicectomy is generally associated

with an uneventful postoperative course, the development of NPPE can result in rapid respiratory

deterioration requiring immediate recognition and intervention. The cases presented in this series

highlight the characteristic clinical features of acute hypoxemia, respiratory distress, bilateral pulmonary

infiltrates, and prompt response to supportive respiratory management. Early diagnosis, timely

restoration of airway patency, administration of supplemental oxygen, application of positive pressure

ventilation, and re-intubation when necessary are the cornerstones of successful management. With

prompt treatment, NPPE is typically reversible and associated with an excellent prognosis, with most

patients achieving complete clinical and radiological recovery within 24–48 hours.

This case series emphasizes the importance of maintaining a high index of suspicion for NPPE in

patients who develop sudden respiratory compromise immediately after extubation. Increased

awareness among anesthesiologists, surgeons, and perioperative physicians, along with adherence to

preventive airway management strategies, can facilitate early diagnosis, minimize morbidity, and

improve postoperative outcomes.

Conclusion

Post-extubation negative pressure pulmonary edema is an uncommon but potentially life-threatening

perioperative complication that requires a high degree of clinical suspicion for timely diagnosis. Although

rare following laparoscopic appendicectomy, it should be considered in any patient who develops sudden

hypoxemia, respiratory distress, or pink frothy sputum immediately after extubation, particularly in the

presence of laryngospasm or other forms of acute upper airway obstruction. Early recognition, prompt

restoration of airway patency, appropriate oxygen therapy, positive pressure ventilation, and re-intubation

when indicated are essential for preventing severe complications and ensuring favorable outcomes. The

cases presented demonstrate that with rapid diagnosis and supportive management, NPPE is a reversible

condition with complete clinical and radiological recovery in most patients. Increased awareness among

anesthesiologists, surgeons, and perioperative care teams, together with meticulous airway management

and preventive strategies during emergence from anesthesia, is crucial to reduce morbidity and optimize

postoperative patient safety.

Declaration

Consent: Written informed consent was obtained from the patient. All patient information has been

anonymized to maintain confidentiality.

Conflict of Interest: The authors declare that they have no competing interests or conflicts of interest

related to this work.

Funding: Nil

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