Open Access

Austin Journal of Anesthesia and Analgesia

Case Report

Negative Pressure Pulmonary Edema: A Rare

Complication Following Extubation
Arruda BA1, Miranda DB2*, Amorim MAS1,
Bezerra DM1, Bastos MMA2 and Fagury AEA1
1
Department of Anesthesiology, Santa Casa de
Misericrdia de Goinia Hospital, Brazil
2
Department of Medicine, Catholic University of Gois,
Brazil
*Corresponding author: Miranda DB, Department of
Medicine, Catholic University of Gois, Brazil
Received: December 29, 2016; Accepted: January 10,
2017; Published: January 12, 2017
Abstract
We describe a case of Negative Pressure Pulmonary Edema (NPPE)
followed by laryngospasm occurred immediately after extubation. A 24-year-old
man underwent a surgical correction of unilateral inguinal hernia by laparoscopy.
The tracheal intubation was easy with grade 1 of Cormack-Lehane classification.
Anesthesia was maintained with sevoflurane 2, 5%. After fully awake extubation,
nearly total upper airway obstruction due to severe laryngospasm was observed
by a decrease in oxygen saturation and the presence of large amount frothy
pink sputum, suggestive of acute pulmonary edema. A nasal airway was
inserted, but face mask ventilation was difficult. Oxygenation of the airway was
maintained with support of non invasive ventilation for twenty four hours, with
SpO2 of 92-96 %. 48 hours later, the pulmonary edema disappeared and the
patient was discharged without complications (SpO2 96% and ambient air).
Keywords: General anesthesia; Post-extubation; Laryngospasm; Negative
pressure pulmonary edema

Abbreviations pressure, oxygen saturation (SpO2) and a peripheral vein was

NPPE: Negative Pressure Pulmonary Edema; SpO2: Oxygen
Saturation; NIMV: Non-Invasive Mechanical Ventilation
Introduction
Negative pressure pulmonary edema (NPPE) is a non common
complication of general anesthesia [1]. The incidence of NPPE is 0.05
to 0.1% in healthy adults who underwent general anesthesia [2,3].
It is even less common with the use of a laryngeal mask airway [2].
It is usually seen during emergence from anesthesia having a multi
factorial pathogenesis. The most common causes of NPPE are upper
airway infection, tumor and laryngospasm [4]. In adults about 50%
of NPPE occurrences are due to postoperative laryngospasm [5,6].
The implications of acute NPPE can be severe with mortality as high
as 11 to 40% [7]. However, if diagnosed and treated early, these rates
decrease. Previous recognition and institution of appropriate Non-
Invasive Mechanical Ventilation (NIMV) is important to ensure
successful outcomes [8]. We report a case of a previously healthy
male who developed NPPE secondary to laryngospasm shortly after
extubation following general anesthesia.
Case Presentation
A 24 year old man 72kg, with no past history of any significant
illness or allergy was admitted in the day care surgery for a correction
of unilateral inguinal hernia by laparoscopy under general anesthesia.
Patient was perfectly well before surgery, routine laboratory
findings were normal, haemodynamically stable with no respiratory
complaints. He denied previous problems with general anesthesia
and his baseline peripheral oxygen saturation was 99% in ambient
air. The patient was accepted to operation room after he was informed
and asked to sign consent form for anesthesia and surgery.
He was monitored with electrocardiogram, non-invasive blood
catheterized for infusion and drug administration. Anesthesia was
induced with intravenously propofol (150mg), fentanyl (250mcg) and
atracurium (35mg). The endotracheal intubation using tube 8.0mm
was easy with grade 1 of Cormack-Lehane classification. Anesthesia
was maintained with sevoflurane (2.0-2.5%). Surgery lasted about one
hour and during that time vital signs were normal. Patient recovered
from surgery and was extubated successfully.
Immediately after extubation, the patient developed inspiratory
stridor with severe laryngospasm followed by a decrease in oxygen
saturation, increase in respiratory rate (around 25/minute) and
increase in heart rate (about 120/min). There was large amount of
frothy pink sputum. Chest auscultation revealed bilateral generalized
coarse crackles. Immediate diagnosis of NPPE secondary to post
extubation laryngospasm was made. A nasal airway was inserted, but
face mask ventilation was difficult. The patient was moved to post
anesthetic care unit. oxygenation of the airway was maintained with
support of non invasive ventilation for twenty four hours and SpO2
ranged between 92-96% in the intensive care unit.
Computed tomography of the chest at the time showed foci of
Figure 1: Computed tomography of the chest in the immediate postoperative.

Austin J Anesthesia and Analgesia - Volume 5 Issue 1 - 2017 Citation: Arruda BA, Miranda DB, Amorim MAS, Bezerra DM, Bastos MMA and Fagury AEA. Negative Pressure
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Miranda et al. All rights are reserved 1052.
Miranda DB
Figure 2: Chest X-ray 24 hours postoperative.
consolidation with confluent aspect in frosted glass in the upper
lobes of both lungs in the middle lobe and lingula, consistent with
the diagnosis of pulmonary edema (Figure 1). Patient gradually
started improving; after six hours was moved to intensive care unit
with SpO2 up to 96% in NIMV and the crackles on his chest markedly
decreased. Patient continued to improve during the next 24 hours
and was completely asymptomatic at this time. A comparison
between the chest X-ray after extubation and about 24 hours after
the event showed marked improvement; however, residual interstitial
infiltrate persisted with small alveolar consolidations (Figure 2). He
was discharged from the hospital within 48 hours of the event.
Discussion
The incidence of NPPE is around 0.05-0.1 % of all anesthetic
procedures [5,9]. This statistic increases to 11% when considering all
patients requiring intervention for acute upper airway obstruction [5].
The same statistics are shared by different authors [10,11]. Its more
common in healthy and young males who are more pre disposed to
major negative pressure differences [3,10]. In adults, 50% of cases are
due to laryngospasm postoperatively, but can also occur by occlusion
of the endotracheal tube by biting and less frequently after foreign
body aspiration, oropharyngeal surgery or residual neuromuscular
blockade [5].
Post-extubation NPPE is associated with a higher incidence
of cases, which are mostly due to laryngospasm. Laryngospasm
is defined as glottic occlusion, secondary to laryngeal constrictor
muscles contraction (interarytenoids, lateral cricoarytenoids and
internal and external thyroarytenoids), in response to a stimulus
[3]. Laryngospasm and bronchospasm are manifestations of upper
airways and lungs defensive reflex system. During laryngospasm,
spasm is a response to mechanical or chemical stimulation intrinsic
or extrinsic to painful stimulation, involving all laryngeal and
chest wall muscles and tracheobronchial tree smooth muscles. This
protective reflex is mediated by the vagus nerve [2]. Laryngospasm is
more often seen in anesthetic emergence during extubation [2], both
with tracheal tubes and laryngeal mask [5]. However, it may be less
frequent when there is a major noxious stimulation in the surgical
site during anesthesia recovery. This may generate high intra pleural
negative pressure levels and cause pulmonary edema [1].
NPPE begins with a significant obstruction of the upper airway
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(as mentioned in most by laryngospasm), increasing inspiratory
efforts (50-100 cm H2O, when normal is 3-10 cm of H2O) to overcome
the obstruction for generate pleural and very negatives alveolar
pressures. The pressure gradient difference causes the fluid to move
out of the pulmonary capillaries and flood the interstitial and alveolar
spaces. There are four primary mechanisms: interstitial fluid in the
capillary bed of the lungs or, (conversely, a decrease in pressure in
the interstitium) decreased the plasma osmotic pressure, increased
membrane permeability and decreased fluid to return through the
lymphatic route [3,7].
The intra thoracic negative pressures cause an increase in systemic
venous return to the heart with a decreased cardiac output. Sudden
increase in pulmonary capillary pressure causes fluid to move rapidly
in interstitial and alveolar spaces and edema persists even after the
relief airway obstruction [8]. This generates a hypoxemia increasing
of pulmonary vascular resistance pre and post capillary which in turn
precipitate hyper adrenergic state, mimcking neurogenic pulmonary
edema [8].
Pulmonary edema presents with snores and rales on auscultation,
dyspnea, cyanosis and pink puff secretion [5]. The differential
diagnosis includes hidden heart disease, fluid overload and
anaphylaxis. Fast and effective radiography simple chest shows edema
with alveolar-interstitial pattern diffuse, in their bilateral majority,
centralized with pulmonary pedicle extended and cardiac normal.
Unilateral pulmonary edema is rarely found and has been associated
with the positioning of the patient when the gravitational effects
could interfere the presentation of the table [10,12]. In the absence of
these differential diagnoses and evidence of acute obstruction of the
upper airways is with the opportune diagnosis of NPPE [3,5].
It is essential to re establish ventilation of the patient, consisting in
most cases NIMV or re intubation [13]. Early relief of laryngospasm
and assistance in new intubation can be achieved at the expense of
neuromuscular blockers. The succinylcholine and rocuronium in
double rates could favor this role [11,12,14]. The use of diuretics
remains controversial as well as steroids [5,13].
Prevention is not easy but one should know the clinical and
associated factors for an accurate diagnosis and prompt treatment.
The extubation in deep plan could be associated with prevention,
but some studies have shown that the incidence of laryngospasm
in children is higher in the anesthetized group as compared to the
awaken group[15]. In most case reports in this age group, the tracheal
tube had been removed before the awakening [16,17].
Most cases present resolution within 24 hours and these patients
should be observed for a longer period of post-anesthetic recovery.
NIMV is an important strategy to prevent/treat acute respiratory
failure by NPPE and reduce the chance of intubation, length of
hospital stay, morbidity and mortality [5].
Conclusion
In conclusion, although a frequently benign condition, NPPE
secondary to laryngospasm is an important cause of morbidity,
hospitalization in intensive care unit and occasionally mortality
in young and healthy individuals. It is a well-described clinical
syndrome, but probably under-recognized, with the exact mechanism
still unclear. Early recognition of the disease was a key point that
Austin J Anesthesia and Analgesia 5(1): id1052 (2017) - Page - 02
Miranda DB
allowed the immediate application of positive airway pressure
leading to a rapid resolution of the frame, thus ensuring the favorable
developments in this case. We encourage our colleagues to be vigilant
in recognizing NPPE in the presence of laryngospasm.
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Austin J Anesthesia and Analgesia - Volume 5 Issue 1 - 2017 Citation: Arruda BA, Miranda DB, Amorim MAS, Bezerra DM, Bastos MMA and Fagury AEA. Negative Pressure
ISSN : 2381-893X | www.austinpublishinggroup.com Pulmonary Edema: A Rare Complication Following Extubation. Austin J Anesthesia and Analgesia. 2017; 5(1):
Miranda et al. All rights are reserved 1052.
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Austin Publishing Group
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