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Negative pressure pulmonary oedema following use of ProSeal LMA.
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PMID:  23825821     Owner:  NLM     Status:  PubMed-not-MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Richa Jain; Mahendra Kumar; Zainab A Haq; Ashim Banerjee
Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Indian journal of anaesthesia     Volume:  57     ISSN:  0019-5049     ISO Abbreviation:  Indian J Anaesth     Publication Date:  2013 Mar 
Date Detail:
Created Date:  2013-07-04     Completed Date:  2013-07-05     Revised Date:  2013-07-08    
Medline Journal Info:
Nlm Unique ID:  0013243     Medline TA:  Indian J Anaesth     Country:  India    
Other Details:
Languages:  eng     Pagination:  188-90     Citation Subset:  -    
Affiliation:
Department of Anaesthesiology and Critical Care, University College of Medical Sciences and GTB Hospital, Shahdara, Delhi, India.
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Journal Information
Journal ID (nlm-ta): Indian J Anaesth
Journal ID (iso-abbrev): Indian J Anaesth
Journal ID (publisher-id): IJA
ISSN: 0019-5049
ISSN: 0976-2817
Publisher: Medknow Publications & Media Pvt Ltd, India
Article Information
Copyright: © Indian Journal of Anaesthesia
open-access:
Print publication date: Season: Mar-Apr Year: 2013
Volume: 57 Issue: 2
First Page: 188 Last Page: 190
PubMed Id: 23825821
ID: 3696269
Publisher Id: IJA-57-188
DOI: 10.4103/0019-5049.111854

Negative pressure pulmonary oedema following use of ProSeal LMA
Richa Jainaff1
Mahendra Kumaraff1
Zainab A Haqaff1
Ashim Banerjeeaff1
Department of Anaesthesiology and Critical Care, University College of Medical Sciences and GTB Hospital, Shahdara, Delhi, India
Correspondence: Address for correspondence: Dr. Mahendra Kumar, 47-D, Pocket–A, MIG, GTB Enclave, Shahdara, Delhi, India. E-mail: mahendramohit@yahoo.com

INTRODUCTION

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

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/mm3). 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 (PEtCO2) 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, SpO2 started dropping to a minimum of 92% on inspired fraction of oxygen (FiO2) 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, PEtCO2 initially observed was 47 mmHg, which later on came down to 42 mmHg with normal waveform of capnograph. However, there was no improvement in SpO2 even on IPPV with FiO2 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 SpO2 to a minimum value of 86% on FiO2 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 (PaO2 111 mmHg, PaCO2 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

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]

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.


Notes

Source of Support: Nil

Conflict of Interest: None declared

REFERENCES
1. Depica K,Kenaan CA,Barrocas AM,Fonseca JJ,Bikazi GB. Negative pressure pulmonary edema after acute upper airway obstructionJ Clin AnesthYear: 1997940389257208
2. Massad I,Halawa SA,Badran I,Al-Barzangi B. Negative pressure pulmonary edema – five case reportsMiddle East J AnesthesiolYear: 2006189778417094538
3. Ezri T,Priscu V,Szmuk P,Soroker D. Laryngeal mask and pulmonary edemaAnesthesiologyYear: 1993782198379969
4. Nishikava M,Tajima K,Hoshi T,Mizutani T,Toyooka H. Pulmonary edema in a child following laryngospasm triggered by a laryngeal mask airwayMasuiYear: 200150304611296448
5. Brimacombe J,Richardson C,Keller C,Donald S. Mechanical closure of the vocal cords with the laryngeal mask airway ProsealBr J AnaesthYear: 200288296711878665
6. Bhaskar B,Fraser JF. Negative pressure pulmonary edema revisited: Pathophysiology and review of managementSaudi J AnaesthYear: 201153081321957413
7. Saqib M,Ahmad M,Khan RA. Development of negative pressure pulmonary oedema secondary to postextubation laryngospasmAnaesthesia, Pain and Intensive CareYear: 201115424
8. Cook TM,Lee G,Nolan JP. The ProSeal laryngeal mask airway: A review of the literatureCan J AnaesthYear: 2005527396016103390
9. Brimacombe J. Analysis of 1500 laryngeal mask uses by one anaesthetist in adults undergoing routine anaesthesiaAnaesthesiaYear: 19965176808669573
10. Stix MS,O’Connor CJ Jr. Maximum minute ventilation test for the ProSeal™ Laryngeal mask airwayAnesth AnalgYear: 2002951782712456459
11. Brain A. Esophageal breathing and upper airway obstruction with ProSeal™ laryngeal maskAnesth AnalgYear: 20029416697012032050

Figures

[Figure ID: F1]
Figure 1 

Pathophysiology of negative pressure pulmonary oedema following airway obstruction



Article Categories:
  • Case Report

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

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