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Year : 2013  |  Volume : 57  |  Issue : 2  |  Page : 188-190  

Negative pressure pulmonary oedema following use of ProSeal LMA

Department of Anaesthesiology and Critical Care, University College of Medical Sciences and GTB Hospital, Shahdara, Delhi, India

Date of Web Publication15-May-2013

Correspondence Address:
Mahendra Kumar
47-D, Pocket-A, MIG, GTB Enclave, Shahdara, Delhi
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0019-5049.111854

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Negative pressure pulmonary oedema (NPPO) is a life threatening condition, manifested due to upper airway obstruction in a spontaneously breathing patient. Upper airway obstruction caused by classic laryngeal mask airway (cLMA) and ProSeal laryngeal mask airway (PLMA) has been reported, and NPPO has also been reported following the use of cLMA. Search of literature did not confirm NPPO following the use of PLMA. We encountered a female patient of NPPO scheduled for incision and drainage of an abscess who had signs of airway obstruction following PLMA insertion. Multiple attempts were made to get patent airway without success. PLMA was replaced with endotracheal tube following which pink frothy secretion appeared in breathing circuit. Patient was managed successfully with ICU care.

Keywords: Airway obstruction, negative pressure, negative pressure pulmonary oedema, ProSeal laryngeal mask airway

How to cite this article:
Jain R, Kumar M, Haq ZA, Banerjee A. Negative pressure pulmonary oedema following use of ProSeal LMA. Indian J Anaesth 2013;57:188-90

How to cite this URL:
Jain R, Kumar M, Haq ZA, Banerjee A. Negative pressure pulmonary oedema following use of ProSeal LMA. Indian J Anaesth [serial online] 2013 [cited 2020 Jul 2];57:188-90. Available from:

   Introduction Top

Negative pressure pulmonary oedema (NPPO) occurs in a patient breathing spontaneously against an obstructed upper airway. [1],[2] Pulmonary oedema has been observed following upper airway obstruction caused by classic laryngeal mask airway (cLMA). [3],[4] ProSeal laryngeal mask airway (PLMA) has also been reported to cause upper airway obstruction. [5] However, review of literature did not reveal any case of NPPO with the use of PLMA. We report a case of upper airway obstruction following PLMA insertion followed by pulmonary oedema in a spontaneously breathing patient.

   Case Report Top

A 10-year-old female patient weighing 25 kg presented with the complaints of painful swelling over lateral aspect of right chest wall and high-grade fever for past 4 days. She had tachycardia (PR 128/min) with normal blood pressure (114/71 mmHg). Her airway assessment revealed Mallampati class II, adequate mouth opening and short neck with limited head and neck movement. Local examination revealed a tense and tender swelling present over lateral aspect of right chest wall. On systemic examination, no abnormality was detected. Her investigations revealed anaemia (haemoglobin: 8.6 gm%) and leucocytosis (total leucocyte count: 19,500/mm 3 ). A clinical diagnosis of an abscess (?pyogenic) over right chest wall was made and patient was scheduled for incision and drainage under general anaesthesia.

In the operating room, monitoring for electrocardiography, pulse oximetry and noninvasive blood pressure (by oscillometry method) was commenced by using COLIN-306 monitor. Anaesthesia was induced with fentanyl 2 μg/kg and propofol 2.5 mg/kg, and maintained with sevoflurane 1-2% in oxygen and nitrous oxide (1:1) with spontaneous ventilation on face mask through Magill's circuit. PLMA size 2.5 was inserted without muscle relaxant and cuff was inflated with 14 ml air. The bite block was kept between the incisors. Following insertion of PLMA, difficulty in spontaneous ventilation was observed with chest retraction due to airway obstruction. Her head was almost in neutral position as sniffing position was not possible due to restricted movement of head and neck. Three attempts were made to correct the position of PLMA with restricted movement of head and neck to get an unobstructed clear airway, but no success was achieved. Resistance was felt in the bag when assisted ventilation was tried following each attempt. The value of partial pressure of end-tidal carbon dioxide (PEtCO 2 ) was zero and tracing line was touching to the base of the capnograph. The whole event of correction of position and observation of respiration took about 2 min. Meanwhile, SpO 2 started dropping to a minimum of 92% on inspired fraction of oxygen (FiO 2 ) 0.5. PLMA was removed and no difficulty on mask ventilation was observed. Her trachea was then intubated with 5.5-mm-ID cuffed endotracheal tube under the effect of atracurium (0.5 mg/kg) and intermittent positive pressure ventilation (IPPV) was started. Following intubation, anaesthesia was maintained with oxygen and nitrous oxide (1:1) with halothane (0.5-1%) through Bain's circuit. After tracheal intubation, PEtCO 2 initially observed was 47 mmHg, which later on came down to 42 mmHg with normal waveform of capnograph. However, there was no improvement in SpO 2 even on IPPV with FiO 2 0.5. Surgery was continued. On auscultation of chest, extensive coarse crepts were observed bilaterally. After few minutes, pink frothy secretions appeared in the endotracheal tube and breathing circuit with further fall in SpO 2 to a minimum value of 86% on FiO 2 1. Clinical diagnosis of pulmonary oedema was made and managed with diuretic, narcotic and IPPV under atracurium.

After surgery, she was put on ventilator for IPPV with positive end expiratory pressure (PEEP) in ICU. She responded well to the therapy. She was weaned off from ventilator and her trachea was extubated after 11 h of mechanical ventilation. Her 12-lead electrocardiogram, arterial blood gas analysis (PaO 2 111 mmHg, PaCO 2 31 mmHg, pH 7.37) and X-ray chest were within normal limits. She was discharged from ICU after 24 h in a satisfactory condition.

   Discussion Top

NPPO following upper airway obstruction is well documented. [1],[2] Multiple causes including airway devices, e.g. cLMA and PLMA have been reported to cause upper airway obstruction. [3],[4],[5]

The mechanism of pathogenesis of NPPO is multifactorial. [6] Creation of marked negative intrathoracic pressure by the forceful inspiratory efforts against an obstructed glottis or upper airway promotes increased blood flow to the pulmonary circulation, thereby increasing the pulmonary arterial pressure. [6] Marked negative pressure also causes a rise in transcapillary pressure gradient that favours shift of fluid from the capillaries into alveoli. Also, the hypoxaemia due to upper airway obstruction triggers intense sympathetic discharge which results in increased pulmonary arterial constriction and pressure, damaging pulmonary capillaries with increased permeability which further worsens pulmonary oedema [6] [Figure 1]. Management of NPPO depends on severity of pulmonary oedema and hypoxia. Effective airway management and immediate treatment with oxygen and diuretics is sufficient in most of the cases of NPPO. [6] Continuous positive airway pressure (CPAP) or PEEP is recommended in patients of NPPO requiring mechanical ventilatory support. [2],[7]
Figure 1: Pathophysiology of negative pressure pulmonary oedema following airway obstruction

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Three mechanisms of upper airway obstruction caused by PLMA have been described: (1) PLMA tip (and drain tube) enters in the glottis, leading to obstruction; (2) sides of PLMA bowl fold inwards with glottic occlusion; and (3) PLMA tip behind the larynx compresses the posterior larynx causing arytenoid malfunction. [7] The above-mentioned problems also occur with cLMA, but are more frequent with PLMA due to its larger size and softer material. [8] Laryngospasm triggered by LMA and downfolding of epiglottis caused by LMA are also well-known causes of airway obstruction. [4],[9]

Mechanical closure of the vocal cords with PLMA has also been observed in neutral position of head and neck despite easy and correct placement of PLMA that was relieved in sniffing position. [5] In our patient, proper sniffing position could not be achieved due to restricted neck movements and almost neutral position of the head might be the possible cause of upper airway obstruction with PLMA.

Stix et al. observed supraglottic or glottic obstruction caused by PLMA in 15 out of 317 patients and confirmed by fibreoptic examination that the mask was folded medially, a malposition that was also noted by Archie Brain using prototype masks of similar construction. [10],[11] In our patient, fibreoptic examination could not be done due to desaturation. The cause of airway obstruction in our patient was supposed to be PLMA with restricted movement of head and neck. The reason of restricted movement of head and neck was not clear.

On the basis of our observations, it may be concluded that airway obstruction caused by PLMA may lead to NPPO. Difficult sniffing position due to restricted head and neck movement may contribute to airway obstruction with PLMA.

   References Top

1.Depica K, Kenaan CA, Barrocas AM, Fonseca JJ, Bikazi GB. Negative pressure pulmonary edema after acute upper airway obstruction. J Clin Anesth 1997;9:403-8.  Back to cited text no. 1
2.Massad I, Halawa SA, Badran I, Al-Barzangi B. Negative pressure pulmonary edema - five case reports. Middle East J Anesthesiol 2006;18:977-84.  Back to cited text no. 2
3.Ezri T, Priscu V, Szmuk P, Soroker D. Laryngeal mask and pulmonary edema. Anesthesiology 1993;78:219.  Back to cited text no. 3
4.Nishikava M, Tajima K, Hoshi T, Mizutani T, Toyooka H. Pulmonary edema in a child following laryngospasm triggered by a laryngeal mask airway. Masui 2001;50:304-6.  Back to cited text no. 4
5.Brimacombe J, Richardson C, Keller C, Donald S. Mechanical closure of the vocal cords with the laryngeal mask airway Proseal. Br J Anaesth 2002;88:296-7.  Back to cited text no. 5
6.Bhaskar B, Fraser JF. Negative pressure pulmonary edema revisited: Pathophysiology and review of management. Saudi J Anaesth 2011;5:308-13.  Back to cited text no. 6
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7.Saqib M, Ahmad M, Khan RA. Development of negative pressure pulmonary oedema secondary to postextubation laryngospasm. Anaesthesia, Pain and Intensive Care 2011;15:42-4.  Back to cited text no. 7
8.Cook TM, Lee G, Nolan JP. The ProSeal™ laryngeal mask airway: A review of the literature. Can J Anaesth 2005;52:739-60.  Back to cited text no. 8
9.Brimacombe J. Analysis of 1500 laryngeal mask uses by one anaesthetist in adults undergoing routine anaesthesia. Anaesthesia 1996;51:76-80.  Back to cited text no. 9
10.Stix MS, O'Connor CJ Jr. Maximum minute ventilation test for the ProSeal™ Laryngeal mask airway. Anesth Analg 2002;95:1782-7.  Back to cited text no. 10
11.Brain A. Esophageal breathing and upper airway obstruction with ProSeal TM laryngeal mask. Anesth Analg 2002;94:1669-70.  Back to cited text no. 11


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