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Negative Pressure Pulmonary EdemaArthura Moore M.D.Staff anesthesiologistSt Jude childrens research Hospital

ObjectivesUnderstand the pathophysiological mechanism of the development and resolution of the condition.Recognize and diagnose a patient with NPPEProvide swift treatment for its resolution

ALIASESPost-obstructive Pulmonary EdemaLaryngospasm-induced Pulmonary Edema

What is negative pressure pulmonary edema?

NPPE is a manifestation of upper airway obstruction, a markedly low intrathoracic pressure generated by forced inspiration against an obstructed airway which leads to exudation of fluid and red blood cells in the interstitium.Example of non-cardiogenic edemaSeen during emergence from anesthesia

Medical MythsSugar makes children hyperactiveYou lose most of your body heat from your headYou need to drink 8 glasses of water a day

Myths associated with NPPEOnly occurs with patients who have been intubatedCannot occur with patients using an LMADoes not occur in pediatricsIt is always a bilateral presentation.

History of NPPE1927- Moore and Binger- first to demonstrate in spontaneously breathing dogs1942- Warren- first description of pathophysiological correlation between the creation of negative pressure and pulmonary edema1973- Capitanio- described relationship between pulmonary edema and upper airway obstruction in 2 children with croup and epiglottis1977- Oswalt first to show the clinical significance in 3 adults after severe acute upper airway obstruction

Pathophysiology3 Major Mechanisms1: Creation of marked intrathoracic negative pressures of -50 to -100cm H20 provides the stimulus for NPPEIntrapleural pressure decreases to -50 to -100cm H2O when inspiration is attempted against a closed glottis.Muller maneuver

Mechanism #1

Mechanism #1

Hydrostatic pressure-favors movement of fluid from the capillary into the interstitiumOncotic pressure-favors movement of fluid into the vesselMechanism #2Hypoxia and hyperadrenergic state that accompany upper airway obstruction also contributes to the development of pulmonary edema.

Mechanism #2

Mechanism #3In chronic upper airway obstruction- modest level of AutoPEEP with an increase of end expiratory lung volumes. Relief of obstruction leads to edema formation

Mechanism #3

NPPE Types

Studies have shown that most of the pts who develop Type I are young.

Whereas, Type II NPPE occurs in extremes of ages.

Clinical ManifestationsUsually present immediatelyS/S of respiratory distress due to acute airway obstructionStridorSuprasternal/Supraclavicular retractionsUse of accessory muscles of inspirationDecrease of oxygen saturation

Clinical ManifestationsAuscultation of lungs

Coarse, rales

Rhonchi

WheezeClinical ManifestationTypical CXRKerley A lines- caused by distension of channels between peripheral and central lymphatics of lungsKerley B lines- represent interlobular septa, peripherally locatedPeribronchial cuffing (thickening)- occurs with excess fluid or mucus build-up in small airways causes patches of atelectasis

Clinical Manifestations

Hallmark sign of NPPE is the frothy pink, sputum

OnsetTime onset of pulmonary edema after relief of obstruction30-150 minutesLungs can accommodate increased fluid: lymphatic flow can increase 3-10X before edema forms

Stages of Pulmonary EdemaStage 1: Only interstitial pulmonary edema is presentStage 2: Fluid fills the interstitium and begins to fill the alveoliStage 3: Alveolar flooding occurs, many alveoli are completely flooded with no airStage 4: Marked alveolar flooding spills over into the airway as froth

DiagnosisBased on history of a precipitating incident and symptomsSymptoms usually develop within one hour of the event but may be delayedCXR findings support diagnosis

Incidence

Reported to be 0.05%-0.1% of all anesthetic procedures; however suggested to occur more commonly than is generally documented

According to one estimate, NPPE develops in 11% of all pts requiring active intervention for acute upper airway obstruction for example laryngospasm

The m/m of an unrecognized event of NPPE is as high as 40%

Case Reports of Postoperative Pulmonary Edema

LaryngospasmThe occlusion of the glottis secondary to contraction of the laryngeal constrictors. Defensive system of the upper airway and lungs mediated by the vagus nerveOlsen and Hallen reported that the overall incidence of laryngospasm in the adult and pediatric practice is just under 1%. The incidence doubles in children and triples in the very young ( birth to 3mths) Cause in >50% of the cases of NPPE

Risk FactorsPt with airway lesionsUpper airway surgeriesObesityH/o OSAYoung ageMale sexShort neckDifficult intubationAcromegaly

Differential DiagnosisOther causes: Cardiogenic edemaNeurogenic edemaARDSAnaphylaxisDrug-induced non-cardiogenic

ManagementFirst treatment priority is relief of the airway obstruction and correction of the hypoxemia. Treatment is primarily supportive.Maintenance of patent airwayAdministration of supplemental oxygenDiuretics are often administered

Persistent airway obstruction may necessitate an artificial airwayAdministration of succinylcholine (0.1-0.2mg/kg)Relax the jaw musclesBreak the laryngospasm

Invasive vs. Non-InvasiveAirway Support

PEEP

Auto (intrinsic) PEEPIncomplete expiration Progressive air-trapping (hyperinflation)Common in high MV, expiratory flow limitations, and expiratory resistanceApplied (extrinsic) PEEPSmall amounts ( 4-5cmH20) used to mitigate alveolar collapseHigher levels(>5 cmH20) used to improve hypoxemia

Purpose of CPAPPartially compensate respiratory function by reducing the WOBImprove alveolar recruitment Reduce left ventricular afterload and increase CO which leads to improved hemodynamics

Non-invasive

Reduce intubation ratesReduce ICU admissionsReduce hospital length of stayReduce morbidity/mortality rates

Case #1Presentation

7 y/o, 23kg, girl presented for tonsilloadenoidecotomy.History of mild OSAPremedicated with 7.5mg PO midazolamTo OR with standard ASA monitors applied. An uneventful mask induction with 70% nitrous oxide, 30% oxygen, and 8% sevoflurane22-gauge PIV insertedIntubated with 5.5cm uncuffed ETT- atraumatic on 1st attempt with airleak at 18cm H2O pressure.Pt returned to spontaneous repiration, maintained with 1.5% sevoflurane, and 50/50 nitrous oxide and oxygenShe was given 6mg dexamethasone, 2mg morphine, and 2mg zofran intraoperatively

Case #1EmergenceWhile emerging from GA, the SpOs declined from 98%-100% to 84%-87%. Attempts made to assist ventilation were unsuccessfulPt biting on tube Repeated strenuous inspiratory efforts

Case #1TreatmentPt given 20mg IV SuccinycholineControlled ventilation resumed, saturations remained in low 90s.Frothy pink sputum suctioned from ETT. 5mg Lasix given with improvement of sats to mid 90sOver next 20mins, pts condition improved. Extubation uneventful. To PACU with simple facemask at 6L/min of oxygen. Postop CXR revealed:Pt remained under observation for a few hours. Later discharged that evening.

Case #1Presentation

7 y/o, 23kg, girl presented for tonsilloadenoidecotomy.History of mild OSAPremedicated with 7.5mg PO midazolamTo OR with standard ASA monitors applied. An uneventful mask induction with 70% nitrous oxide, 30% oxygen, and 8% sevoflurane22-gauge PIV insertedIntubated with 5.5cm uncuffed ETT- atraumatic on 1st attempt with airleak at 18cm H2O pressure.Pt returned to spontaneous repiration, maintained with 1.5% sevoflurane, and 50/50 nitrous oxide and oxygenShe was given 6mg dexamethasone, 2mg morphine, and 2mg zofran intraoperatively

Pediatric pts are at risk because of their extremely compliant chest walls that can generate large negative intrapleural pressure.

Myth #1:

NPPE does not occur in pediatrics

Case #2Presentation58 y/o 90kg man presented to ED with 3-day h/o fever, worsening perineal erythema, and pain. Appropriately NPOTo OR for emergency surgical debridement of the Fourniers gangrene.Premedicated with 2mg IV midazolam Anesthesia induced with 200mg IV Propofol and 100mcg IV fentanylLMA was placed w/o difficultyAnesthesia maintained with 2-3% sevoflurane with 50/50 oxygen/air500mcg fentanyl and 1mg dilaudid for intraoperative analgesia

Case #2EmergenceConclusion of surgery, sevoflurane discontinued, before removal of LMA, pt bit LMA.LMA removed followed by laryngospasmApplication of positive pressure via face mask unsuccessful.

Case #2TreatmentIV propofol and succinylcholine and intubated with 7.5ETTSpO2 remained 85-88% despite 100% FiO2.Placed on the vent in SIMV mode with PS of 10 and PEEP 10, PEEP later increased to 12 with sats >90%Admitted to ICU and CXR revealed12hrs later FiO2 was weaned and pt extubated. F/u CXR revealed

Case #2Presentation58 y/o 90kg man presented to ED with 3-day h/o fever, worsening perineal erythema, and pain. Appropriately NPOTo OR for emergency surgical debridement of the Fourniers gangrene.Premedicated with 2mg IV midazolam Anesthesia induced with 200mg IV Propofol and 100mcg IV fentanylLMA was placed w/o difficultyAnesthesia maintained with 2-3% sevoflurane with 50/50 oxygen/air500mcg fentanyl and 1mg dilaudid for intraoperative analgesia

Majority of cases of NPPE in the literature are in associaton with ETT use. Although the increasing use of LMAs in the administration of anesthetics will provide more scenarios where NPPE can manifest.

Myth #2 and 3:It only occurs in pts who were intubated.Cannot occur with pts using an LMA.

Case #3Presentation21y/o young male, previous h/o multiple trauma victim, presented for elective removal of a right intramedullarly femoral nail. Medical h/o mild asthmaNo premedicationTo OR routine monitors applied. Anesthesia induced with 200mcg fentanyl and 200mg propofol IV#4 LMA placed. Pt moved into the left lateral positionDuring positioning, pt began to cough and clenched his teeth upon the LMA.

Case #3TreatmentHe was given 100mg Propfol and 60mg Sux.Ventilation reestablished.Oxygen saturations dropped to the low 80s100% oxygen administered with attempts to assist ventilation and provide PEEP. Despite these measures, the SpO2 remained 84-86%Auscultation revealed coarse BS, L>R, no wheeze, and no notable prolongation of the expiratory phase. No material found with suctioning of the LMA. Procedure abandoned, pt returned to supine with improvement of sats to 92-93%. LMA removed continued to breath 100% oxygen with sats 91%Pt to PACU received high-flow oxygen and nebulized albuterol

Case #3

CXR- marked left-sided extravascular lung water and normal right side. Pt improved rapidly, w/I 2hrs sats were 90%RA and 95%on 3L. Monitored overnight with complete resolution of CXR in 24hrs.

Case #3Presentation21y/o young male, previous h/o multiple trauma victim, presented for elective removal of a right intramedullarly femoral nail. Medical h/o mild asthmaNo premedicationTo OR routine monitors applied. Anesthesia induced with 200mcg fentanyl and 200mg propofol IV#4 LMA placed. Pt moved into the left lateral positionDuring positioning, pt began to cough and clenched his teeth upon the LMA.

If airway obstruction occurs in the lateral position, development of NPPE in the dependent lung is favored by hydrostatic forces and possibly the elevated resting position of the dependent diaphragm.

Myth #4: It is always a bilateral presentation

PreventionAvoid airway irritationAdminister topical lidocaine to the laryngotracheal areaCareful suction of the oropharynxExtubation of trachea in Stage 1

Stages of Anesthesia

Stage 1From administration of anesthesia to loss of consciousnessDizziness, exaggerated hearing and feelingStage 2From Loss of consciousness to loss of eyelid reflexAny kind of stimulation intensifies the pts excitementMay vomit, hold breath, or struggleIncreased muscle tone and involuntary muscle activityStage 3Surgical anesthesiaSpinal reflexes dulled and relaxation of skeletal muscles obtainedFurther divided into 4 planes ( 1-lightest, 4-deepest)Stage 4Medullary ParalysisAnoxiaCardiac/respiratory paralysis and death

ConclusionPrompt diagnosis and therapeutic action NPPE resolution w/I 24hrs.Early recognition crucial to morbidityHigh index of suspicion for NPPE in pts who experienced postextubation laryngospasm.Those who have experienced postanesthetic laryngospasm monitored longer in PACURecommended monitoring period ranges from 2-12 hrs.

ReferencesRasheed, Asim; Urmila Palaria, Dolly Rani, and Shatrunjay Sharm. A case of negative pressure pulmonary edema in an asthmatic patient after laproscopic cholecystectomy: Anesthesia Essays and Researches, 2014 Jan-Apr;8(1):88-86Bhaskar, Balu and John F. Fraser. Negative pressure pulmonary edema revisited: Pathophysiology and review of management: Saudi Journal of Anesthesia. 2011 Jul-Sep; 5(3):308-313Vandse, Rashmi, Deven Kothari, Ravi Tripathi, Luis Lopez, Stanislow Stawicki, and Thomas Papadimos. Negative pressure pulmonary edema with laryngeal mask airway use: Recognition, pathophysiology, and treatment modalities: International Journal of Critical Illness & Injury Science. 2012 May-Aug; 2(2):98-103Saqib, Muhammad, Maqsood Ahmad, Raheel Azhar Khan. Development of negative pressure pulmonary edema secondary to postextubation laryngospasm. Anesthesia, Pain & Intensive Care. 2011;15(1)June 2011Davidson, Susan, Cherry Guinn, Daniel Gacharna. Diagnosis and Treatment of negative pressure pulmonary edema in a pediatric patient: A case report. AANA Journal, October 2004/Vol 72, No 5Sullivan, Michael. Unilateral negative pressure pulmonary edema during anesthesia with a laryngeal mask airway. Canadian Journal of Anesthesia 1999/46:11/1053-1056Massad, Islam, Sami Abu Halawa, Izdiad Badran, and Bassam Al-barzangi. MEJ Anesthesia 18(5), 2006, 977-982Video: http://www.calshipleymd.com/ Audio: Copyright, 2010, MedEdu LLC; Copyright (c), Keroes-Lieberman LLC, 2010

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RhonchiHeart And Lung Sounds Reference Library, track 512460.371Copyright, 2010, MedEdu LLCnull5041.644