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Print version ISSN 0034-7094On-line version ISSN 1806-907X
Rev. Bras. Anestesiol. vol.58 no.4 Campinas July/Aug. 2008
Negative-pressure pulmonary edema after transsphenoidal hypophysectomy. Case report*
Edema pulmonar por presión negativa después de la hipofisectomía transesfenoidal. Relato de caso
Viviane Ferreira Albergaria, TSAI; Carla Márcia Soares, TSAII; Rodolfo de Moraes AraújoIII; Washington Luiz de MendonçaIII
do Corpo Clínico do Biocor Instituto; Instrutora do CET do HC/UFMG
IIAnestesiologista do Corpo Clínico do Hospital Infantil São Camilo; Anestesiologista do Corpo Clínico do HC/UFMG
IIIME2 em Anestesiologia no CET/SBA do HC/UFMG
OBJECTIVES: Negative-pressure pulmonary edema (NPPE) is a rare complication
that evolves rapidly after acute or chronic obstruction of the airways. The
objective of this report was to present a case of NPPE after upper airways obstruction
in a patient with acromegaly who underwent transsphenoidal hypophysectomy.
CASE REPORT: A 48 years old male patient, weighing 80 kg, physical status ASA III, with a tumor in the hypophysis, hypertension, and acromegaly, underwent transsphenoidal hypophysectomy under general balanced anesthesia. The surgery proceeded without intercurrences. The patient was extubated while in a superficial anesthetic plane. He developed difficulty breathing, retraction of the abdominal wall, severe hypoxemia (SpO2 30%), unconsciousness, and cardiac arrhythmia (PVCs and bradycardia). Positive-pressure ventilation with a face mask and oropharyngeal cannula was ineffective. The patient was intubated and, at this moment, there were bilateral pulmonary rales and frothy pinkish secretion inside the tracheal tube, compatible with NPPE. The patient was transferred to the ICU and remained on mechanical ventilation for 96 hours. He was discharged to the regular ward on the 5th postoperative day without neurological sequelae.
CONCLUSION: Negative-pressure pulmonary edema may occur in the immediate postoperative period of transsphenoidal hypophysectomy. Immediate diagnosis and treatment are essential for early resolution of the process and to decrease morbidity.
Key Words: ANESTHESIA: general; COMPLICATIONS: negative-pressure pulmonary edema; DISEASES: acromegaly; SURGERY: Neurosurgery: hypophysis tumor.
Y OBJETIVOS: El edema pulmonar por presión negativa (EPPN) es una
complicación poco común que evoluciona rápidamente después
de un cuadro agudo o crónico de obstrucción de las vías
aéreas. El objetivo de este relato fue presentar un caso de EPPN después
de la obstrucción de las vías aéreas superiores en paciente
con acromegalia que fue sometido a la hipofisectomía transesfenoidal.
RELATO DEL CASO: Paciente del sexo masculino, 48 años, 80 kg, estado físico ASA III, portador de tumor de hipófisis, hipertensión arterial y acromegalia, fue sometido a la hipofisectomía transesfenoidal bajo anestesia general balanceada. El procedimiento quirúrgico evoluciona sin intercurrencias. La extubación traqueal fue realizada con el paciente en plano anestésico superficial. Evoluciona con esfuerzo ventilatorio, retracción de la pared abdominal, hipoxemia grave (SpO2 30%), inconsciencia y arritmia cardíaca (extrasístolis ventricular y bradicardia). La ventilación con presión positiva bajo máscara facial y cánula orofaríngea fue ineficaz. El paciente fue intubado y en ese momento, había estertores pulmonares bilaterales con la presencia de secreción rósea ventilada dentro de la cánula traqueal compatible con el cuadro de EPPN. El paciente fue llevado al CTI, donde permaneció bajo ventilación mecánica por 96 horas. Recibió alta para enfermaría en el quinto día del postoperatorio sin secuela neurológica.
CONCLUSIÓN: El EPPN puede ocurrir en el período postanestésico inmediato de hipofisectomía transesfenoidal. El diagnóstico y tratamiento rápidos son esenciales para una resolución precoz y para la disminución de la morbidez.
Negative-pressure pulmonary edema (NPPE) is a rare occurrence, which is well documented and very seldom diagnosed, being classified in two types. Type I is secondary to acute obstruction of the upper airways, and type II occurs after surgical correction of airways obstruction. The pathophysiology is secondary to a sudden reduction in pericapilary pulmonary interstitial pressure due to forced inspiration 1. Effective diagnosis and management are very important for patient recovery and the consequent reduction in morbidity 2.
The anesthesiologist should know that some neurosurgical patients might have a specific manipulation of the airways, such as those undergoing awake craniotomy, surgery in the cervical spine, and transsphenoidal hypophysectomy for acromegaly 3.
A 48 years old patient, weighing 80 kg, physical status ASA III was admitted for transsphenoidal hypophysectomy for the treatment of a hypophyseal tumor. He had acromegaly and mild hypertension controlled with diet and captopril (12.5 mg) three times a day. Physical exam showed macroglossia, short neck, thyromental distance less than 6 cm, and Mallampati 4 . Laboratory exams were within normal limits. The patient was monitored with continuous analysis of the ST segment in the electrocardiogram, invasive blood pressure, capnography, gas analyzer, bispectral index (BIS), spectral edge frequency (SEF), suppression rate (SR), urine output, arterial blood gases, serial ionogram and glucose levels. General balance anesthesia was the anesthetic technique proposed. After venipuncture in the right upper limb with a 16G catheter, 5 mg of midazolam were administered. An occipital cushion was used to achieve hyperextension of the head and cervical flexion. After 5 minutes of oxygenation with 100% O2 with a face mask, 50 mg of 1% lidocaine without vasoconstrictor, 30 mg of propofol, 0.1 mg of fentanyl, and 4% isoflurane were administered, and it was evaluated if it were possible to maintain adequate oxygenation with the face mask. Anesthesia was induced with an additional dose of 150 mg of propofol, 0.25 mg of fentanyl, and 40 mg of rocuronium, and maintained with isoflurane to keep BIS between 40 and 45. The surgery evolved without any intercurrence. At the end of the surgery, the patient was extubated with BIS of 90, SEF of 21 Hz, and SR of zero. Shortly after, the patient developed severe difficulty breathing, retraction of the abdominal wall, severe hypoxemia (SpO2 30%), bradycardia, cardiac arrhythmia (PVCs), and he became unconscious. Positive-pressure ventilation with an oropharyngeal cannula and face mask was not effective. Intravenous adrenalin, 1 mg, and succinylcholine, 80 mg, were administered, and the patient was intubated on an emergency basis with positive-pressure mechanical ventilation and fraction of inspired oxygen (FiO2) at 100%. The patient presented bilateral rales on auscultation and a frothy pinkish secretion could be seen inside the endotracheal tube, which was compatible with NPPE. Morphine, 10 mg, was administered to maintain the patient on mechanical ventilation, but a diuretic was not administered. The patient was stabilized and transferred to the intensive care unit (ICU).
A chest X-ray (Figure 1) demonstrated bilateral pulmonary infiltrates, especially in the central region, without gross peripheral changes. In the ICU, the patient was maintained on mechanical ventilation with positive end-expiratory pressure (PEEP) of 10 cmH2O and 100% FiO2. After 96 hours, the patient was extubated. The chest X-ray on the 4th postoperative day showed resolution of the event (Figure 2). The patient was discharged from the ICU on the 5th postoperative day and transferred to the ward without neurologic sequelae.
In the case presented here, a patient without severe pulmonary or cardiac disease developed NPPE due to acute obstruction of the upper airways after extubation. Besides macroglossia, handling of the upper airways during the surgery and extubation while he was in a superficial plane of anesthesia, which favors inspiratory effort that causes highly negative intrathoracic pressures in face of airways obstruction, are other factors that might have contributed for this evolution.
Negative-pressure pulmonary edema is a rare complication of acute airways obstruction such as laryngospasm, for example. Typically, this complication develops in young, healthy patients without associated diseases, since they are capable of generating large gradients of negative pressure 4. The incidence of NPPE in anesthetized patients varies from 0.1% to 11% 6.
It is classified in two types 1,7. Type I is secondary to the acute obstruction of the airways caused by post-extubation laryngospasm, epiglottitis, obstruction of the endotracheal tube, and postoperative vocal cord paralysis. Type II is caused by the treatment of chronic airways obstruction as, for example, in adenoidectomy and amygdalectomy, sleep apnea, tumors, and acromegaly 4.
The pathophysiology of NPPE includes three mechanisms 5: negative intrathoracic pressure, increased systemic and pulmonary capillary hydrostatic pressure, and mechanical stress on the alveolar-capillary membrane. Negative intrathoracic pressure increases the venous return due to the reduced pressure in the right atrium, with the concomitant increase in systemic and pulmonary capillary hydrostatic pressure, which is complicated by the reduction in interstitial perivascular hydrostatic pressure. This causes an increase in the transcapillary pressure gradient, favoring transudation of fluids to the interstitial space. An increase in central venous pressure is also seen, which prevents the flow in the lymphatic vessels. The increase in pulmonary blood flow is due to the increase in systemic blood pressure secondary to the release of norepinephrine in response to hypoxia, hypercapnia, and agitation. This leads to right ventricular distension, dislocating the interventricular septum to the left, decreasing the cardiac output. The increased systemic vascular resistance raises the left ventricular wall tension, which contributes to decrease the left ventricular ejection fraction. In addition, there is a rupture of pulmonary capillaries with loss of protein that is responsible for the frothy serous bloody or pinkish secretion. The third mechanism shows that the loss of capillary integrity can result from the mechanical stress of the alveolar-capillary membrane, leading to alveolar edema and hemorrhage. In the case presented here, it was not possible to clearly explain the pathophysiology of the edema, since measurements of cardiac chambers and pulmonary capillary pressures were not taken, hindering the definition of the mechanism of edema formation; however, anyone of the mechanisms mentioned above, isolatedly or in combination, could have contributed to the development of pulmonary edema.
The chest X-ray shows diffuse alveolar-interstitial edema probably bilateral, more centrally located, enlarged pulmonary hilum, and normal heart size 8.
Both cardiogenic and non-cardiogenic pulmonary edema have similar differences in alveolar-arterial O2 and radiographic characteristics, which can hinder the differential diagnosis. Clinically, inspiratory stridor, tachypnea, hypoxia, hypercapnia, tachycardia, decreased tidal volume, and paradoxal respiration or uncoordinated ventilatory patterns are present. Pulmonary edema presents with ronchi and rales, dyspnea, cyanosis, and frothy pinkish secretion in the oropharynx 9. The differential diagnosis includes aspiration of gastric contents, non-diagnosed cardiac disease, fluid overload, and anaphylaxis.
Treatment of NPPE is supportive, maintaining opened airways and oxygenation. Not all patients need mechanical ventilation and PEEP. Lang et al. 10 demonstrated that 80% of the cases of NPPE developed shortly after extubation, 85% needed to be intubated, and 50% required mechanical ventilation with PEEP or continuous positive airways pressure (CPAP) 11. Diuretics and corticosteroids are not indicated in the treatment of NPPE 4,12,13. The adrenaline administered in this case, due to the hemodynamic instability, might have worsened the condition, since an increase in systemic blood pressure increases venous blood return and, consequently, pulmonary capillary hydrostatic pressure.
Early diagnosis and treatment are necessary for a favorable evolution and decreased morbidity. It has a good prognosis because the event is self-limited and patients are usually healthy.
It is believed that the incidence of NPPE is higher than that reported in the literature because very few cases are diagnosed and are usually mistaken for pulmonary edema secondary to excess fluid administration, aspiration pneumonitis, and bronchospasm.
Acknowledges: The authors would like to thanks the neurosurgeon, Dr. Alexandre Varella Giannetti, for the support and respect he has demonstrated for anesthesiologists, which is an example to further improve the relationship between surgeons and anesthesiologists.
01. Padilla JJ, Salas Segura D, Sánchez Suen K - Edema pulmonar postobstructivo: reporte de 3 casos. Acta Méd Costarric, 2002;44:160-162. [ Links ]
02. Ringold S, Klein EJ, Del Beccaro MA - Postobstructive pulmonary edema in children. Pediatr Emerg Care, 2004;20:391-395. [ Links ]
03. Pasternack JJ, Lanier WL - Neuroanesthesiology Review-2004. J Neurosurg Anesthesiol, 2005;17:2-8 [ Links ]
04. Silva ES, Santos OBAF, Grando TA - Edema pulmonar por pressão negativa. Relato de casos. Rev Bras Anestesiol, 1999;49: 343-348. [ Links ]
05. Dolinski SY, MacGregor DA, Scuderi PE - Pulmonary hemorrhage associated with negative-pressure pulmonary edema. Anesthesiology, 2000;93:888-890. [ Links ]
06. Tarrac SE - Negative pressure pulmonary edema: a postanesthesia emergency. J PeriAnesth Nurs, 2003;18:317-323. [ Links ]
07. Mehta VM, Har-El G, Goldstein NA - Postobstructive pulmonary edema after laryngospasm in the otolaryngology patient. Laryngoscope, 2006;116:1693-1696. [ Links ]
08. Peixoto AJ - Edema pulmonar assimétrico por pressão negativa pós-obstrução de via aérea superior. Relato de caso. Rev Bras Anestesiol, 2002;52:335-343. [ Links ]
09. McConkey PP - Postobstructive pulmonary oedema: a case series and review. Anaesth Intensive Care, 2000;28:72-76. [ Links ]
10. Gerancher JC, Weeks DB - Nasal BiPAP treats hypoxia from postobstructive pulmonary edema. Anesth Analg, 1995;80:429-430. [ Links ]
11. Lang SA, Duncan PG, Shephard DA et al. - Pulmonary oedema associated with airway obstruction. Can J Anesth, 1990; 37: 210-218. [ Links ]
12. Deepika K, Kenaan CA, Barrocas AM et al. - Negative pressure pulmonary edema after acute upper airway obstruction. J Clin Anesth, 1997;9:403-408. [ Links ]
13. Ho Li, Harn HJ, Lien TC et al. - Postextubation laryngeal edema in adults. Risk factor evaluation and prevention by hydrocortisone. Intensive Care Med, 1996;22:933-936. [ Links ]
Correspondence to: Submitted em 13
de abril de 2007 *
Received from Hospital das Clínicas da Universidade Federal de Minas
Gerais (HC/UFMG), Belo Horizonte, MG
Dra. Viviane Ferreira Albergaria
Praça Clemente de Faria, 80 - Prado
30410-490 Belo Horizonte, MG
Accepted para publicação em 18 de março de 2008
Submitted em 13
de abril de 2007
* Received from Hospital das Clínicas da Universidade Federal de Minas Gerais (HC/UFMG), Belo Horizonte, MG