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Physically Powerful Can Be Hazardous:Negative Pressure Pulmonary Edema

Kim A. Noble, PhD, RN, CPAN

ERIANESTHESIA NURSING is a wonderfulnd demanding profession. As an academic pro-essor, working with patients in Phase I is a treatnd a nice break from tests and lectures. Asomeone who needs new experiences and stim-lation, I have found my “special place” in theACU because there is no room for compla-ency. Every so often, however, I am in need ofreminder of the demanding nature of the fieldhave chosen.

was called in one Saturday morning for aquick and easy” case: a laparoscopic appendec-omy. Experience makes me shudder at thoseords and my intuition was once again rein-

orced with this case. My patient, PL, was a0-year-old, 6’4,” 280-pound police officer with2-week history of intermittent abdominal pain

hat increased in severity and localized to hisight abdomen. He waited an additional 48ours and then presented to the emergencyepartment with vomiting, fever, and abdomi-al pain described as “12 out of 10 on the paincale.” Physical examination revealed a highlyuscular male in acute distress. His vital signs

VS) were: blood pressure (BP) 164/101, heartate (HR) 128, respiratory rate (RR) 28, andemperature 102.4° F. His lab work was normal,

Kim A. Noble, PhD, RN, CPAN, is an Assistant Professorn the Department of Nursing at Temple University,hiladelphia, PA.Address correspondence to Kim A. Noble, PhD, RN, CPAN,epartment of Nursing, Temple University, 3307 N. Broad St,hiladelphia, PA 19140; e-mail address: knoble@temple.edu.© 2007 by American Society of PeriAnesthesia Nurses.1089-9472/07/2202-0010$35.00/0

doi:10.1016/j.jopan.2007.01.008

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with the notable exception of a white blood cell(WBC) count of 19 � 103/�L and neutrophilsof 77%.1

PL was hydrated and brought to the OR andreceived general anesthesia for an open appen-dectomy. He was induced with oxygen, nitrousoxide, midazolam, fentanyl, and propofol, andfor maintenance of anesthesia, he receivedsevoflurane and atracurium. PL also received 10mg of morphine, which was administered inincremental doses over the length of the case.The surgery was completed in 55 minutes,blood loss was minimal, and a total of 1800 mLof Lactated Ringers (LR) was infused. After com-pletion of the surgery, the paralytic agent wasreversed using a maximal dose of neostigmineand atropine. PL became very agitated uponemergence. Because an oral airway tube causeda gagging reflex in PL, it was removed and PLimmediately bit down on his endotracheal tube,leading to a cessation of air exchange. Midazo-lam 1 mg and morphine sulfate 2.5 mg weregiven, PL relaxed his jaw, and ventilation wasagain restored. PL remained agitated but coop-erative. He was extubated and brought to thePhase I PACU without further incident.

PL was awake upon admission but very restlessand agitated. With 10 as a maximum level ofpain, PL reported incisional pain of 6. He alsowas noncompliant with the nasal cannula, be-cause “it was making my nose burn.” Oxygensaturation at admission was 92% and he wasswitched to a 40% face hood and the cannulawas discontinued. His admission VS were: BP

168/94, HR 66, RR 24 to 28 and shallow, and

Journal of PeriAnesthesia Nursing, Vol 22, No 2 (April), 2007: pp 132-135

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emperature 98.9° F. Bilateral breath soundsere present, but decreased; PL refused toeep breathe because it increased his abdomi-al pain. His 2 � 2 right lower quadrant abdom-

nal dressing was intact, with no swelling orcchymosis noted. He denied complaints ofausea and was noted to be very strong in histtempts to get “off this bed.” The anesthesiol-gist in attendance administered an additional.5 mg of midazolam and opioid orders wereeceived. The attending anesthesiologist andurse anesthetist then left the department toomplete an emergent cesarean section.

L remained very restless and continued to re-ort severe abdominal pain. Morphine sulfate 5g was titrated over the next 15 minutes with-

ut improvement in PL’s activity level. PL’s ox-gen saturation remained at 90% to 94%, and heegan to have an intermittent, nonproductivearsh cough. As the wrestling match continuedo keep PL on the stretcher and his oxygenask in place, his oxygen saturation continued

o decline and he began to have a productiveough of copious, blood-tinged, frothy secre-ions. He had moist crackles audible over allung fields and remained very agitated. A chestadiograph confirmed acute noncardiac pulmo-ary edema. A declining saturation, and increas-

ng agitation necessitated sedation, paralysis, re-ntubation, and mechanical ventilation withositive-end expiratory pressure until diuresisas completed. So much for a “quick and easy”

ase!

You Need an Intensive Care Bed forn Appendectomy?”—Thehysiology of Negative Pressureulmonary Edema

lthough a link between the generation of signif-cant negative intrapleural pressures and negativeressure pulmonary edema (NPPE) was first doc-mented in animals in the late 1920s, the firsteported case in humans was in 1977.2 Althoughare, this complication of general anesthesia iseen in approximately 0.1% of patients undergo-

ng a variety of surgical procedures.3 It is most

commonly associated with laryngospasm3; how-ever, it may be seen in any situation where highnegative pressures are produced, such as in epi-glottitis, croup, and choking.4 Most commonly,the development of this disorder is short lived andis associated with healthy, strong males who areable to produce high negative intrathoracic pres-sures.4 To completely understand the pathophys-iology of this disorder, it is first necessary to brieflyreview the normal physiology that governs themovement of fluid across capillary membranes:the Starling forces.

The Starling Forces

The Starling forces are the four forces that gov-ern the movement of fluid across the walls of allsystemic capillaries. On the arterial end of thecapillary there is a net filtration of fluid, orthe movement of fluid from the capillary into theinterstitial spaces, to the lymphatic vessels andthen the return into the venous vessels. On thevenous end of the capillary, because of variationsin the Starling forces, there is a net reabsorption offluid back into the capillary. These forces areespecially important in the thoracic cavity, be-cause there is a constant undulation of pressurewith inspiration and expiration, leading to height-ened lymphatic activity in the chest. When themaximal activity of the lymphatics is over-whelmed, interstitial edema is seen.

The Starling forces represent four rival forces:two forces favoring the movement of fluid outof the capillary, and two opposing the outwardmovement of fluid (Fig 1). On the arterial end ofthe capillary, the capillary hydrostatic pressure(CHP) represents a large outward “push” andleads to the net outward movement of fluid.The CHP is opposed inside the capillary by the

Fig 1. Starling forces.

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KIM A. NOBLE134

apillary oncotic pressure (COP), which is pro-uced by the intravascular plasma proteins, ef-ectively holding fluid within the lumen of theapillary. There are also two forces present inhe tissues that surround the capillary: the tissuencotic pressure (TOP), which promotes theutward movement of fluid, and the tissue hy-rostatic pressure (THP), which opposes fluidovement.5 Alterations in these forces can lead

o the development of edema, such as would beeen in a patient who has a decreased albuminr COP, leading to an increase in the fluid

eaving the capillary and collecting in the inter-titial spaces of the tissues.

n NPPE, there is an acute obstruction of theirway, most often as a result of laryngospasmType I) or after the relief of a chronic upperirway obstruction such as enlarged tonsils orbstructive sleep apnea (Type II).4,6 As the pa-ient struggles to inspire against an obstructedirway, the intrapleural pressure dramaticallyeclines, especially in patients with large-bodyuscle mass and increased upper body

trength. The negative intrapleural pressure fa-ors venous return and the preload of the righteart increases. This causes an increase in cap-

llary hydrostatic pressure in the pulmonary ves-els and drives fluid and blood out of the pul-onary capillary initially into the interstitial

rea, and then into the alveoli (Fig 2). Mostften, the development of NPPE is immediate,ut it may be delayed for as long as two hoursfter intubation or airway obstruction.7 As withll forms of pulmonary edema, the fluid createsbarrier to the exchange of oxygen and carbonioxide and washes out the surfactant, leadingo an increased work of breathing.7 Dependentn the degree of edema and the comfort of the

Fig 2. Negative pressure pulmonary edema mechanism.

patient, short-term mechanical ventilation anddiuresis may be needed. For other patients, theuse of a positive pressure apparatus, such ascontinuous positive airway pressure, bilevelpositive airway pressure, or supportive therapysuch as with supplemental oxygen therapy,may be all that is required. Most cases resolve in12 to 24 hours6 and intensive care monitoringshould be provided as indicated.

Implications for the PACU Patient

As in many disorders, the best treatment for NPPEis prevention and the proactive intervention(s)designed to prevent and rapidly treat laryngo-spasm8 and airway obstruction. The developmentof NPPE requires rapid nursing assessment, com-munication with the attending anesthesiologist,and treatment to prevent the development ofadditional complications. Although relatively rare,NPPE may follow any surgical procedure withgeneral anesthesia and intubation, or it may followthe manipulation of a patient’s airway. There arespecific implications for the care of a patient withNPPE in the Phase I PACU.

Alteration in Gas Exchange

Oxygenation is always the first priority of apatient emerging from general anesthesia and,although the patient in this case study devel-oped NPPE as a result of an event in the OR,postintubation laryngospasm may occur in thePACU as well. Rapid assessment and interven-tion(s) for the management and treatment oflaryngospasm are needed.7 Laryngospasm maybe broken with the administration of positivepressure ventilation with 100% oxygen via abag–mask apparatus.8 This may require the ac-tivity of two personnel to maintain optionalhead position and a tight seal to deliver thepressure to force open the vocal cords andeliminate spasm.7 If the spasm is not brokenwith the use of a bag–mask device, the admin-istration of sedative and paralytic agents andreintubation may be required.8

The PACU nurse needs to be constantly vigilant

for patients at risk for the development of NPPE.

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ngoing assessment using continuous pulseximetry and incremental pulmonary auscultation

s imperative. If the patient’s BP is stable, the headf the bed may be raised to a 45-degree angle toase the work of breathing. The provision forigorous pulmonary toilet should be continuouslyvailable, with frequent oral or nasotrachealuctioning as needed. Suction equipment shoulde immediately available. Sedatives are adminis-ered as ordered. Intubation equipment shouldlso be readily available and the perianesthesiaurse available to assist with intubation as need-d.4 Finally, after the development of a partial oromplete airway obstruction, the patient willeed to remain in the Phase I PACU for monitor-

ng and may require an overnight stay in thentensive care unit (ICU).

lteration in Fluid and Electrolyte Balance

he use of diuresis for the treatment of NPPEemains controversial because its origination isot related to overhydration. Instead, the devel-pment of NPPE follows an occurrence of fluid

eaking from the pulmonary capillaries, and op-osing treatment recommendations are found

n the literature. Several references report theestriction of intravenous fluid and the “wait-it-ut” approach,3,7 whereas other references in-lude the use of diuretics to assist with clear-nce of the excess fluid from the alveoli.6

egardless of the treatment approach, vigilantntake and output and frequent pulmonary aus-ultation and saturation measurement must beompleted to evaluate the effectiveness of thehosen treatment modality. The administrationf diuretics may necessitate the insertion of a

rinary catheter for closer monitoring of the

Referen

nesthesia emergency. J Perianesth Nurs. 2003;18:317-323.

urinary output. If this treatment is chosen, care-ful explanation of the procedure must be pro-vided to the patient and significant other(s).

Potential for Anxiety and Incisional Pain

Because the development of NPPE is an unex-pected and frightening complication of generalanesthesia, the provision of calm and clear ex-planations of the patient’s status and treatmentprogress must be offered to the patient andsignificant others. Anxiolytics and opioidsshould be administered as ordered by the at-tending anesthesiologist for the comfort of thepatient. Because this disorder is of short dura-tion and generally unexpected, keeping the pa-tient and family informed of the patient’sprogress is also important.

Alteration in Gastrointestinal Functioning

Because PL has undergone the excision of anacute appendix, the assessment of bowelsounds and the return of gastrointestinal func-tion must be monitored. The administration ofantiemetic agents may be needed to decreasenausea and prevent the potential for the devel-opment of additional pulmonary complications.Finally, part of the ongoing nursing assessmentmust include the assessment of the incisionalarea for any drainage or potential for bleeding.

In conclusion, PL experienced a rare and frighten-ing complication of general anesthesia and themanipulation of his airway. With careful assess-ment and rapid communication with the attend-ing anesthesiologist and medical interventions asrequired, the perianesthesia nurse may minimize

the consequences of NPPE in similar situations.

ces

1. McMorrow ME, Malarkey L. Laboratory and Diagnostic

ests: A Pocket Guide. Philadelphia, PA: WB Saunders; 1998.2. Deepika K, Kenaan CA, Barrocas AM, et al. Negative

ressure pulmonary edema after acute airway obstruction.Clin Anesth. 1997;9:403-408.3. Perez RO, Bresciani C, Jacob CE, et al. Negative pressure

ost-extubation pulmonary edema complicating appendectomyn a young patient: Case report. Curr Surg. 2004;6:463-465.

4. Tarrac SE. Negative pressure pulmonary edema—A post-

5. McCance KL, Huether SE. Pathophysiology: The BiologicBasis for Disease in Adults and Children. 4th ed. St Louis, MO:Mosby; 2006.

6. Mehta VM, Har-El G, Goldstein NA. Postobstructive pul-monary edema after laryngospasm in the otolaryngology pa-tient. Laryngoscope. 2006;116:1693-1696.

7. Murray-Calderon P, Cannolly MA. Laryngospasm and non-cardiac pulmonary edema. J Perianesth Nurs. 1997;12:89-94.

8. Drain CB. PeriAnesthesia Nursing: A Critical Care Ap-

proach. 4th ed. St Louis, MO: Saunders; 2003.