Services on Demand
On-line version ISSN 1806-907X
Rev. Bras. Anestesiol. vol.58 no.2 Campinas Mar./Apr. 2008
Acute pulmonary edema associated with obstruction of the airways. Case report
Edema agudo pulmonar asociado a la obstrucción de las vías aéreas. Relato de caso
Flora Margarida Barra Bisinotto, TSAI; Ricardo de Paula CardosoII; Tânia Mara Vilela AbudIII
Adjunta da UFTM; Responsável pelo CET/SBA da UFTM; Doutora em Anestesiologia
IIME (2005-2008) do CET-SBA da UFTM
IIIMédica Anestesiologista do CET/SBA da UFTM; Doutora em Anestesiologia pela FMB-UNESP
OBJECTIVES: Negative pressure pulmonary edema has been defined as non-cardiogenic
edema, with transudation of fluid to the interstitial space of the lungs due
to an increase in negative intrathoracic pressure secondary to obstruction of
the upper airways. This is the case of a healthy patient who underwent general
anesthesia and developed acute pulmonary edema after extubation.
CASE REPORT: A 23-year old female patient, physical status ASA II, underwent gynecologic videolaparoscopy under general anesthesia. The procedure lasted 3 hours without intercurrence. After extubation the patient developed laryngeal spasm and reduction in oxygen saturation. The patient improved after placement of an oral cannula and administration of oxygen under positive pressure with a face mask. Once the patient was stable she was transferred to the recovery room where, shortly after her arrival, she developed acute pulmonary edema with elimination of bloody serous secretion. Treatment consisted of elevation of the head, administration of oxygen via a face mask, furosemide and fluid restriction. Chest X-ray was compatible with acute pulmonary edema and normal cardiac area. Electrocardiogram (ECG), echocardiogram and cardiac enzymes were normal. The condition of the patient improved and she was discharged from the hospital the following day, asymptomatic.
CONCLUSIONS: Acute pulmonary edema associated with obstruction of the upper airways can aggravate surgical procedures with low morbidity, affecting mainly young patients. Early treatment should be instituted because it has a fast evolution and, in most cases, resolves without lasting damages.
Key Words: AIRWAYS: negative pressure; obstruction; COMPLICATIONS: pulmonary edema.
Y OBJETIVOS: El edema pulmonar por presión negativa ha sido definido
como edema no cardiogénico, con transudación de líquido
para el intersticio pulmonar, por aumento en la presión negativa intratorácica
ocasionado por la obstrucción de las vías aéreas superiores.
Se describió el caso de paciente saludable, sometida a la anestesia general,
que presentó edema agudo pulmonar después de la extubación
RELATO DEL CASO: Paciente de 23 años, sexo femenino, estado físico ASA II, sometida a la anestesia general para videolaparoscopía ginecológica. El procedimiento duró 3 horas, sin intercurrencias. Después de la extubación, la paciente presentó laringoespasmo y disminución de la saturación de oxígeno. Hubo una mejoría después de la colocación de la cánula oral y administración de oxígeno bajo presión positiva, con máscara facial. Estabilizado el cuadro, se la llevó a la sala de recuperación postanestésica, en donde, en cuanto entró, presentó edema agudo de pulmón con eliminación de secreción sero-sanguinolenta. El tratamiento constó de elevación del dorso, oxígeno bajo máscara, furosemida y restricción hídrica. La radiografía torácica mostró una imagen compatible con edema agudo pulmonar y área cardíaca normal. El electrocardiograma (ECG), ecocardiografía y enzimas cardíacas estaban normales. La paciente presentó una buena evolución, recibiendo alta hospitalaria al día siguiente, sin síntomas.
CONCLUSIONES: El edema agudo de pulmón asociado a la obstrucción de las vías aéreas superiores es una condición clínica que puede agravar los procedimientos quirúrgicos de baja morbidez y que aparece principalmente en pacientes jóvenes. El tratamiento debe ser empezado rápidamente, pues la resolución también es rápida y en la mayoría de las veces, no quedan secuelas.
Negative-pressure pulmonary edema (NPPE) has been defined as a non-cardiogenic edema with transudation of fluid to the pulmonary interstitium in response to an increase in negative intrathoracic pressure secondary mainly to obstruction of the upper airways after extubation 1-3. It has a typical presentation with abundant pulmonary secretion, at times bloody, easily recognized clinically and radiologically. Reports of this complication are rare. The objective of this report was to describe a case of non-cardiogenic pulmonary edema triggered by an increase in intrathoracic negative pressure in a young patient undergoing gynecological videolaparoscopy and to discuss the physiopathology, diagnosis and therapeutic approach of this post-anesthetic complication.
A 23-year old white female, 50 kg, 1.75 m, physical status ASA II, with a history of primary infertility and persistent adnexal cyst suggestive of endometrioma on ultrasound was scheduled for a diagnostic videolaparoscopy. Pre-anesthetic evaluation was done as an outpatient, according to the routine of the Anesthesiology Service 4. The patient had a history of smoking 20 cigarettes a day for more than 10 years and allergy to sulfa. Physical exam, laboratory tests and chest X-ray were normal. Upon admission to the hospital there were no changes from the pre-anesthetic evaluation. In the operating room, an 18G catheter was used for venipuncture in the upper limb and monitoring with pulse oximeter, non-invasive blood pressure and continuous electrocardiogram (EKG) on DII was initiated. Anesthesia was induced with midazolam (3 mg), fentanyl (100 µg) and propofol (100 mg). Tracheal intubation with a 7.5 ETT was facilitated by using atracurium (25 mg). Mechanical controlled ventilation was instituted with a tidal volume of 400 mL and respiratory rate adjusted by capnography. Anesthesia was maintained with 100% oxygen and enflurane. Intravenous ondansetron (4 mg) and cephalothin (1 g) were also administered. After confirmation of moderate endometriosis the areas of endometriosis were treated with electrofulguration and the adnexal mass was removed. The procedure lasted 3 hours without intercurrences. The patient was hydrated with Ringer's lactate (1,500 mL) and final urine output was of 330 mL. Dypirone (2 g) and tramadol (50 mg) were administered for postoperative analgesia, 15 minutes before the end of the surgery. At the end, after reversion of the neuromuscular blockade with 0.75 mg of atropine and 1.5 mg of neostigmine, the patient was allowed to breathe spontaneously for 5 minutes and extubated afterwards. Shortly after extubation the patient developed respiratory distress and obstruction of the airways with severe inspiratory effort and reduction in oxygen saturation to 80%. A diagnosis of laryngeal spasm was made, an oropharyngeal cannula was inserted and 100% oxygen was administered under pressure with a face mask. After the patient was stable she was transferred to the post-anesthesia recovery unit (PACU) where she received 5 L.min-1 of oxygen with a face mask and monitored with pulse oximeter and non-invasive blood pressure. Ten minutes after her arrival to the PACU the patient became agitated, developed dyspnea, tachypnea (RR > 20 bpm), cyanosis, productive cough with the elimination of large amounts of pink-reddish secretion. On physical exam the patient had disseminated rales especially in the bases and tachycardia, but her blood pressure remained normal. Acute pulmonary edema (APE) was diagnosed and the following treatment was instituted: the head of the bed was raised, the flow of oxygen administered with a face mask was increased, furosemide (80 mg), water restriction and rigorous monitoring of respiratory parameters and urine output. Arterial blood gases, chest X-ray, EKG, echocardiogram and serum level of cardiac enzymes (troponin and CK-MB) were requested. After thirty minutes the patient referred improvement of the respiratory discomfort with a reduction in the amount of pink expectoration and a urine output of 850 mL. Arterial blood gases revealed pH 7.20, PCO2 = 52 mmHg, PO2 = 89 mmHg, BE = 12 mmol.L-1, bicarbonate = 21 mEq.L-1. Chest X-ray showed an increase in vascular markings and diffuse alveolar-interstitial infiltrate and normal cardiac area. The electrocardiogram was normal in all derivations.
Three hours after her arrival to the recovery room the patient was stable, eupneic with complete restoration of normal respiratory parameters, lungs with normal breath sounds on auscultation, HR 80 bpm, BP 120 x 60 mmHg and urine output of 2,200 mL. Echocardiogram was normal. Troponin and CK-MB were normal. The patient was transferred to a regular ward and discharged from the hospital the following day, asymptomatic.
The case of a young patient who underwent general anesthesia and developed acute pulmonary edema after extubation secondary to laryngeal spasm is reported here. Vigorous inspiratory efforts against the obstruction lead to the development of NPPE.
The development of non-cardiogenic pulmonary edema has been observed after different types of obstruction of the upper airways and it is more frequent in the presence of laryngeal spasm (50% of reported cases), which has an incidence of 0.05% to 5% of anesthetic procedures 5,6. The frequency depends mainly on the type of surgery, with greater incidence in ENT procedures 6. Approximately 11% of patients who develop laryngeal spasm go on to develop NPPE 1,5-8. This can affect, in rare occasions, intubated patients in the absence of protection with an oral cannula when they bite the ET tube 9, with the laryngeal mask during the emergency of the anesthesia when cannula protectors are not used 10, or in the presence of upper airways obstruction secondary to reduced muscular tonus due to residual effect of anesthetics and/or opioids and/or neuromuscular blockers.
This is called NPPE because the laryngeal spasm, or other obstructive process in which the patient can inspire against the closed glottis (modified Müeller maneuver) is capable of generating an extremely negative intrapleural pressure (peaks of sustained inspiratory pressure between -50 cmH2O and -100 cmH2O, though the mean basal pressure is around -4 cmH2O) 1,5,7, which can trigger pulmonary edema.
Pathophysiologicaly 1-3,7,11, the edema is the result of several factors triggered by the obstruction of the upper airways. First, the important increase in intrapleural negative pressure exacerbates the hemodynamic responses that occur during inspiration. Venous return is increased and right atrial pressure is decreased due to the secondary transmission of the negative intrapleural pressure. The increase in right ventricular (RV) blood volume leads to an increase in pulmonary microvascular hydrostatic pressure, deviation of the interventricular septum to the left, which leads to a reduction in left ventricular diastolic complacency.
Another factor involved in the genesis of this type of acute pulmonary edema is the absence of alveolar ventilation during the period of obstruction causing hypoxemia and hypercapnia, which, associated with the anxiety of the patient, lead to the release of catecholamines. This hyperadrenergic state causes an increase in systemic vascular resistance (SVR) and consequent increase in left ventricular (LV) afterload. The reduction in left ventricular complacency (due to deviation of the interventricular septum) and the increase in afterload lead to a reduction in LV ejection volume causing an increase in both ventricular end-systolic and end-diastolic volumes.
Those changes lead to the translocation of blood from the systemic to the low-complacency pulmonary circulation resulting in an increase in pulmonary blood volume and microvascular hydrostatic pressure and consequent fluid transudation from the pulmonary capillaries. This is worsened by the pulmonary vasoconstriction induced by hypoxemia and by the reduction in perivascular interstitial hydrostatic pressure secondary to the pressure gradient 12. This becomes increasingly more severe due to the sustained reduction in LV ejection volume resulting in an increase in pulmonary blood volume and pressure. The low complacency of the area contributes to increase capillary permeability and extravasation of blood cells. This phenomenon was described by West, in 1991, as "stress failure" 13.
Classically, pulmonary edema due to negative intrapleural pressure is accompanied by bloody or pinkish serous secretion, demonstrating that it is really associated with extravasation of cells from the capillaries secondary to the mechanical failure of alveolar-capillary membrane, with consequent alveolar edema and hemorrhage 14.
Although the increase in negative intrapleural pressure is the main pathophysiological event in the development of edema, hypoxemia and the hyperadrenergic state that develop as a consequence of obstruction of the upper airways contribute to the initiation and perpetuation of the edema. Hypoxia can affect the integrity of pulmonary capillaries, increasing fluid leakage. It also promotes the redistribution of blood from the systemic to the pulmonary circulation and the increase in pulmonary vascular resistance. Finally, it is well known that hypoxia and metabolic acidosis cause myocardial depression, which could aggravate any tendency to edema formation.
Two types of pulmonary edema have been described, based on the events that lead to its development 1,5,15: Type I results from acute obstruction of the airways, while type II develops after relief of a chronic obstructive process. Fixed obstruction of the airways resulting from the Valsalva (forced expiration against closed airways) and Müeller maneuvers protects the pulmonary vessels because they generate positive pressure. After the relief of obstruction, intrapleural pressure can remain markedly negative, triggering NPPE. Variable obstruction of the upper airways can favor Müeller maneuver and the development of edema during the period of obstruction. Thus, pulmonary edema occurs more often when resistance is limited to inspiration.
Clinically, this condition affects young adults 9,10,14,16 and children 11,17-20 more often with a better prognosis than in older patients 15,21. Potential factors for the development of NPPE include young, strong, male patients with a short neck, with Malampatti 3 on physical exam and those with a history of apnea 5. The higher incidence of this complication in athletes is secondary to the fact that they can develop high intrathoracic pressure and maintain a longer period of apnea than other patients 5. Mortality and morbidity is increased in patients with lower respiratory reserve and cardiac disease. Under those conditions, early diagnosis and treatment are important.
Negative-pressure pulmonary edema develops very rapidly (within minutes), but its onset can be delayed up to 4 hours after the obstruction has occurred 22. The literature suggests that the speed of edema formation is related with the beginning and severity of the obstruction. It is self-limited, usually resolving in 12 to 24 hours and in most cases only supportive treatment is necessary. In about 85% of the patients, both children and adults, tracheal intubation is necessary to maintain the airways opened, followed by ventilation with positive expiratory pressure 15,22. Treatment with continuous positive pressure with face mask (CPAP) or nasal catheter (BiPAP) had also been described 16,24. Once the diagnosis has been established, aggressive hemodynamic monitoring or vasoactive drugs are not necessary. However, morbimortality can reach 11% to 40% 5,15.
As for other diagnostic possibilities, aspiration cannot be excluded, even in the absence of a history of frank regurgitation. Initially, the treatment is the same but for the need of antibiotics. It should also be differentiated from cardiogenic pulmonary edema, which requires a revision of the history of the patient (history of heart disease), physical exam (i.e, presence of an extra heart sound), EKG with changes suggestive of ischemia and rhythm disturbances and an echocardiogram or cardiac catheterization should be done.
To conclude, acute pulmonary edema associated with obstruction of the upper airways can aggravate low morbidity surgeries, affecting mainly young patients. The knowledge of this complication and most importantly its prevention are crucial. Extubation of a patient with completely reversed neuromuscular blockade and responsive to simple commands seems to be the best form of prevention. When present, early treatment should be instituted because resolution is also fast and in most cases without residual effects.
01. Lang AS, Duncan PG, Shephard DA et al. Pulmonary edema associated with airway obstruction. Can J Anesth, 1990;37: 116-120. [ Links ]
02. Van Kooy MA, Gargiulo RF Postobstructive pulmonary edema. Am Fam Physician, 2000;62:401-404. [ Links ]
03. Gluecker T, Capasso P. Schnyder P et al. Clinical and radiologic features of pulmonary edema. Radiographics, 1999; 19:1507-1531. [ Links ]
04. Bisinotto FMB, Pedrini Jr M, Alves AAR et al. Implantação do serviço de avaliação pré-anestésica em hospital universitário. Dificuldades e resultados. Rev Bras Anestesiol, 2007;57:167-176. [ Links ]
05. Westreich R, Sampson I, Shaari C et al. Negative-pressure pulmonary edema after routine septorhinoplasty. Arch Facial Plast Surg, 2006;8:8-15. [ Links ]
06. Visvanathan T, Kluger MT, Webb RK Crisis management during anaesthesia: laryngospasm. Qual Saf Health Care, 2005; 14:e3. [ Links ]
07. Schwartz DR, Maroo A, Malhotra A et al. Negative pressure pulmonary hemorrhage. Chest, 1999;115:1194-1197. [ Links ]
08. Tami TA, Chu F, Wildes TO et al. Pulmonary edema and acute upper airway obstruction. Laryngoscope, 1986;96:506-509. [ Links ]
09. Sow NY, Garewal D Pulmonary hemorrhage in association with negative pressure edema in a intubated patient. Acta Anaesthesiol Scand, 2001;45:911-913. [ Links ]
10. Devys JM, Balleau C, Jayr C et al. Biting the laryngeal mask: an unusual cause of negative pressure pulmonary edema. Can J Anaesth, 2000;47:176-178. [ Links ]
11. Walker RW, Colovic V, Robinson DN et al. Postobstructive pulmonary oedema during anaesthesia in children with mucopolysaccharidoses. Paediatr Anaesth, 2003;13:441-447. [ Links ]
12. Timby J, Reed C, Zeilender S et al. "Mechanical" causes of pulmonary edema. Chest, 1990;98:973-979. [ Links ]
13. West JB, Tsukimoto K, Mathieu-Costello O et al. Stress failure in pulmonary capillaries. J Appl Physiol, 1991;70:1731-1742. [ Links ]
14. Dolinski SY, MacGregor DA, Scuderi PE Pulmonary hemorrhage associated with negative-pressure pulmonary edema. Anesthesiology, 2000;93:888990. [ Links ]
15. Gupta S, Richardson J, Pugh M Negative pressure pulmonary oedema after cryotherapy for tracheal obstruction. Eur J Anaesthesiol, 2001;18:189-191. [ Links ]
16. Gerancher JC, Weeks DB Nasal BiPAP treats hypoxia from postobstructive pulmonary edema. Anesth Analg, 1995;80:429-430. [ Links ]
17. Taha S, Bartelmaos T, Kassas C et al. Complicated negative pressure pulmonary oedema in a child with cerebral palsy. Paediatr Anaesth, 2000;12:181-186. [ Links ]
18. Samet AF, Samet JP, Hirchi H et al. Postobstructif pulmonary oedema after endotracheal extubation at the recovery of general anaesthesia. Ann Fr Anesth Réanim, 2005;24:287-290. [ Links ]
19. Blum RH, McGowan Jr FX Chronic upper airway obstruction and cardiac dysfunction: anatomy, pathophysiology and anesthestic implications. Pediatr Anesth, 2004;14:75-83. [ Links ]
20. Mehta VM, Gady HE, Nira AG Postobstructive pulmonary edema after laryngospasm in the otolaryngology patient. Laryngoscope, 2006;116:1693-1696. [ Links ]
21. DeSio, JM, Bacon DR Complete airway obstruction caused by a pseudomembranous cast with subsequent negative pressure pulmonary edema. Anesth Analg, 1993;76:1142-1143. [ Links ]
22. Tarrac SE Negative pressure pulmonary edema a postanesthesia emergency. J Perianesth Nurs, 2003;18:317-323. [ Links ]
23. Patel AR. Bersten AD Pulmonary haemorrhage associated with negative-pressure pulmonary oedema: a case report. Crit Care Resusc, 2006;8:115-116. [ Links ]
24. Marini JJ Positive end-expiratory pressure in severe airflow obstruction: more than a "one-trick pont"? Crit Care Med, 2005; 33:1652-1653. [ Links ]
Dra. Flora Margarida Barra Bisinotto
Praça dos Lírios, 58 Morada das Fontes
38060-460 Uberaba, MG
Submitted em 28
de março de 2007
Accepted para publicação em 18 de dezembro de 2007
* Received from CET/SBA do Hospital-Escola da Universidade Federal do Triângulo Mineiro (UFTM), Uberaba, MG