Citation: Arruda BA, Miranda DB, Amorim MAS, Bezerra DM, Bastos MMA and Fagury AEA. Negative Pressure Pulmonary Edema: A Rare Complication Following Extubation. Austin J Anesthesia and Analgesia. 2017; 5(1): 1052.

Austin J Anesthesia and Analgesia - Volume 5 Issue 1 - 2017ISSN : 2381-893X | www.austinpublishinggroup.com Miranda et al. © All rights are reserved

Austin Journal of Anesthesia and AnalgesiaOpen Access

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

AbbreviationsNPPE: Negative Pressure Pulmonary Edema; SpO2: Oxygen

Saturation; NIMV: Non-Invasive Mechanical Ventilation

IntroductionNegative 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 PresentationA 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

Case Report

Negative Pressure Pulmonary Edema: A Rare Complication Following ExtubationArruda BA1, Miranda DB2*, Amorim MAS1, Bezerra DM1, Bastos MMA2 and Fagury AEA1

1Department of Anesthesiology, Santa Casa de Misericórdia de Goiânia Hospital, Brazil2Department of Medicine, Catholic University of Goiás, Brazil

*Corresponding author: Miranda DB, Department of Medicine, Catholic University of Goiás, Brazil

Received: December 29, 2016; Accepted: January 10, 2017; Published: January 12, 2017

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

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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.

DiscussionThe 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]. It’s 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

(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].

ConclusionIn 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

Figure 2: Chest X-ray 24 hours postoperative.

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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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Citation: Arruda BA, Miranda DB, Amorim MAS, Bezerra DM, Bastos MMA and Fagury AEA. Negative Pressure Pulmonary Edema: A Rare Complication Following Extubation. Austin J Anesthesia and Analgesia. 2017; 5(1): 1052.

Austin J Anesthesia and Analgesia - Volume 5 Issue 1 - 2017ISSN : 2381-893X | www.austinpublishinggroup.com Miranda et al. © All rights are reserved