|Year : 2021 | Volume
| Issue : 2 | Page : 139-142
Negative pressure pulmonary edema: A rare complication of septorhinoplasty and a report of two cases
Asim Uslu1, Arzu Karaveli2
1 Department of Plastic and Reconstructive Surgery, University of Health Sciences, Antalya Education and Research Hospital, Antalya, Turkey
2 Department of Anesthesiology and Reanimation, University of Health Sciences, Antalya Education and Research Hospital, Antalya, Turkey
|Date of Submission||07-Mar-2020|
|Date of Acceptance||13-Apr-2020|
|Date of Web Publication||26-Mar-2021|
Dr. Asim Uslu
Department of Plastic and Reconstructive Surgery, University of Health Sciences, Antalya Education and Research Hospital, Antalya
Source of Support: None, Conflict of Interest: None
Negative pressure pulmonary edema (NPPE) develops when a patient makes a forced inspiration against a closed upper airway resulting in transudation of pulmonary capillary fluid into the interstitium. Young, healthy athletic males are more susceptible to this complication, and NPPE is most frequently encountered during oral and maxillofacial surgeries. Patients who have undergone septorhinoplasty surgery have a significant risk for NPPE, unlike other cosmetic surgeries. Herein, we describe two cases of postoperative NPPE following a septorhinoplasty. Early symptoms of NPPE are severe respiratory distress, tachypnea, agitation, and crushed strawberry-colored bloody sputum during the early postextubation period. An early diagnosis of NPPE is very important, and patient recovery is quick when an early diagnosis is made.
Keywords: Laryngospasm, negative pressure pulmonary edema, septorhinoplasty
|How to cite this article:|
Uslu A, Karaveli A. Negative pressure pulmonary edema: A rare complication of septorhinoplasty and a report of two cases. Turk J Plast Surg 2021;29:139-42
| Introduction|| |
Negative pressure pulmonary edema (NPPE) was first demonstrated in 1927 by Moore in spontaneously breathing dogs exposed to a resistive load. The clinical significance of NPPE was reported by Oswalt in three patients after an acute airway obstruction. NPPE develops when a patient makes a forced inspiration against a closed upper airway resulting in transudation of pulmonary capillary fluid into the interstitium. There are two forms of NPPE: type I develops after aggressive inspiration against an upper airway obstruction, such as postextubation laryngospasm and epiglottis, whereas type II develops after relief of a chronic airway obstruction, such as after resecting a laryngeal tumor. The occurrence of NPPE is almost 1/1000 patients after all types of surgery. More than 50% of patients develop NPPE due to a laryngospasm occurring immediately postextubation.,,, Young, healthy athletic males are more susceptible to this complication., NPPE is most frequently encountered during oral and maxillofacial surgeries. Therefore, patients who have undergone septorhinoplasty surgery have a significant risk for NPPE, unlike other cosmetic surgeries.
Herein, we describe two cases of postoperative NPPE (type I) following a septorhinoplasty.
| Case Reports|| |
A 24-year-old male (American Society of Anesthesiologists [ASA] status class 1; weight, 75 kg) underwent a septorhinoplasty under general anesthesia. He had no history of anesthesia or medical illness. His laboratory examination was within normal limits. After monitoring with five-lead electrocardiography (ECG), noninvasive blood pressure (NIBP), heart rate (HR), and pulse oximetry (SpO2), anesthesia was induced with propofol (2 mg/kg intravenously [IV]), fentanyl (1 μg/kg), and rocuronium (0.6 mg/kg IV). He was intubated with an 8-mm cuffed Portex endotracheal tube. Anesthesia was maintained with 4%–5% desflurane and 50% nitrous oxide in oxygen. During the surgery, 1200 mL of fluids in the form of crystalloids was replenished. The operation was completed uneventfully in 95 min. At the end of the surgery, Merocel (Medtronic Xomed Inc., Jacksonville, FL, USA) was used as nasal packing, and a plaster splint was applied over the nose. After confirming adequate recovery of neuromuscular strength (i.e., handgrip, head lift, and straight leg raising), 2 mg/kg sugammadex was administered IV. The patient was extubated uneventfully but developed respiratory discomfort after he was taken to the recovery room 20 min after extubation. All packing and the splint were removed. Oxygen was supplied with an anatomical face mask, and his SpO2 was 85%. He was taken to the intensive care unit (ICU). He had pink frothy secretions. His ECG and cardiac enzymes were normal, and he was hemodynamically stable. There was fine crepitation on auscultation. Postoperative chest radiographs showed bilateral poorly defined opacities and a normal heart size [Figure 1]. The head of the bed was elevated, and his fluid was restricted. He was administered furosemide and morphine IV and supplementary oxygen with a face mask. He was not reintubated because his SpO2 did not continue to drop. SpO2 improved to 95% after 4 h. A chest X-ray acquired 8 h after the first showed mild improvement in the infiltrations [Figure 2]. He remained stable, and his X-ray showed complete improvement [Figure 3]. He was transferred to the ward and discharged home on postoperative day 2.
|Figure 1: An anteroposterior chest radiograph taken in the intensive care unit showing bilateral interstitial infiltrates|
Click here to view
|Figure 2: A chest radiograph 8 h after negative pressure pulmonary edema was diagnosed. The image shows mild improvement in the infiltrations|
Click here to view
|Figure 3: A postoperative day 3 chest radiograph showing complete resolution of the infiltrations|
Click here to view
A 33-year-old woman (ASA status class 1) presented with an external nasal deformity and difficulty breathing through the nose. She had a history of a septorhinoplasty operation 3 years ago. A physical examination showed that she had a deviated septum, narrow internal nasal valve angle, weak tip support, and a low nasal dorsum. She was operated on under general anesthesia. She was monitored with five-lead ECG, NIBP, HR, and SpO2. Following the placement of an IV line and preoxygenation, anesthesia was induced with propofol (4 mg/kg IV), fentanyl (1 μg/kg IV), and rocuronium bromide (0.6 mg/kg IV). She was intubated with a 7-mm cuffed Portex endotracheal tube. Anesthesia was maintained with 2% sevoflurane and 50% air in oxygen. During the surgery, a total of 1000 mL of fluids in the form of crystalloids were replenished. Surgery was completed uneventfully in 85 min. The septoplasty was completed using the open rhinoplasty technique, and the nasal deformity was corrected with a costal cartilage graft taken from the right sixth rib. Internal packing with Merocel was applied without an airway, and an external splint was used. She was extubated after she had regained consciousness, spontaneous breathing, and peripheral motor power. The patient developed respiratory distress soon after the endotracheal tube was removed. Her SpO2 decreased to 60%. The plaster and nasal packing were removed. Facial mask ventilation was applied, but the SpO2 did not rise. The patient was reintubated, ventilated with 100% oxygen, and transferred to the ICU. The main differential diagnosis of the patient was pneumothorax because cartilage grafts were taken during the operation. However, a chest radiograph showed bilateral pulmonary infiltrates. She was administered furosemide, and fluid was restricted. After 6 h, the patient's SpO2 improved, and she was re-extubated uneventfully. She remained stable, and she was transferred to the ward. She was discharged home on postoperative day 2.
| Discussion|| |
NPPE is a rare complication after a surgical procedure but can be life threatening without a prompt diagnosis and treatment. The most common cause of airway obstruction and NPPE is a laryngospasm. Laryngospasm has been reported in 9 of every 1000 adult patients. Most cases of NPPE are associated with head-and-neck operations, and 50.6% of patients with NPPE have undergone upper aerodigestive tract or deep neck structure surgeries; the nose has been operated on in 8.2% of these patients.
The primary pathological event during the development of NPPE is negative intrathoracic pressure and an inspiratory effort against a closed upper airway obstruction, which can generate quite high negative intrathoracic pressures (> −100 cm H2O), particularly in young healthy patients.,,,,,,,,,,, The negative pressure increases venous return, right ventricular filling, and pulmonary capillary blood volume. The pressure also increases left ventricular end-diastolic and left atrial pressure. As a result, pulmonary venous return is reduced, and pulmonary capillary blood volume further increases. Pulmonary hydrostatic pressure increases due to the increased pulmonary blood volume, adrenergic pulmonary vasoconstriction, and hypoxic pulmonary vasoconstriction. At the same time, negative intrapleural pressure decreases interstitial hydrostatic pressure. Alveolar capillary membrane injury increases permeability. All these events result in a tendency for fluid to move out of the pulmonary capillaries, resulting in interstitial and alveolar edema.,
A patient who has undergone septorhinoplasty may be at most risk for NPPE among the aesthetic surgeries because the surgery was on the mouth and nose, which can result in upper airway edema,,,,, [Table 1]. Swelling in the upper airway, bleeding from the surgical field, and aspiration of blood from the surgical field increase the risk of laryngospasm. In addition, the inspiration effort against a packed nose may further increase intrathoracic pressure.
|Table 1: Summary of the six patients with negative pressure pulmonary edema after septoplasty or septorhinoplasty operations|
Click here to view
The patients who underwent septorhinoplasty were counseled that their nose would be packed and to breathe through their mouth postoperatively. Patients must be extubated when they are either fully awake or deeply anesthetized to prevent laryngospasm during extubation., Aspiration of the oropharynx should be done gently.
NPPE rapidly develops within 10–90 min of an upper airway obstruction. It is very important to consider NPPE in a patient with sudden respiratory distress after a septoplasty or septorhinoplasty operation. The diagnosis of the NPPE is very easy, and lung X-rays are quite useful for the diagnosis.
The clinical condition of the patient was thought to be severe in the beginning due to the severe respiratory distress, tachypnea, agitation, and crushed strawberry-colored bloody sputum. However, NPPE usually resolves rapidly within a few hours without aggressive therapy; oxygen therapy may be sufficient, and most cases resolve in <24 h. Mechanical ventilation is not necessary in all patients (33.5%) but may, along with positive end-expiratory pressure, accelerate recovery., Although diuretics, such as furosemide, have been used to treat NPPE after septoplasty and septorhinoplasty operations,,,,,, the use of diuretic therapy for NPPE is controversial. Digoxin, corticosteroids, morphine, and fluid restrictions have also been used to treat NPPE., The mortality rates of NPPE are 2%–40%.,
| Conclusion|| |
NPPE is an uncommon complication after general anesthesia. Young patients who have undergone a septorhinoplasty may be at greater risk for NPPE than those undergoing other aesthetic surgical procedures. Respiratory distress during the early postoperative period and a pink frothy secretion are pathognomonic for NPPE. The diagnosis is confirmed with a lung X-ray and lung sound auscultation. The treatment for NPPE is easy, and the recovery is fast when an early diagnosis is made.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Moore RL, Binger CA. The response to respiratory resistance: A comparison of the effects produced by partial obstruction in the inspiratory and expiratory phases of respiration. J Exp Med 1927;45:1065-80.
Oswalt CE, Gates GA, Holmstrom MG. Pulmonary edema as a complication of acute airway obstruction. JAMA 1977;238:1833-5.
Willms D, Shure D. Pulmonary edema due to upper airway obstruction in adults. Chest 1988;94:1090-2.
Udeshi A, Cantie SM, Pierre E. Postobstructive pulmonary edema. J Crit Care 2010;25:508.e1-5.
Deepika K, Kenaan CA, Barrocas AM, Fonseca JJ, Bikazi GB. Negative pressure pulmonary edema after acute upper airway obstruction. J Clin Anesth 1997;9:403-8.
Suzuki M, Inagi T, Kikutani T, Mishima T, Bito H. Negative pressure pulmonary edema after reversing rocuronium-induced neuromuscular blockade by sugammadex. Case Rep Anesthesiol 2014;2014:135032.
Patton WC, Baker CL Jr. Prevalence of negative-pressure pulmonary edema at an orthopaedic hospital. J South Orthop Assoc 2000;9:248-53.
Visvanathan T, Kluger MT, Webb RK, Westhorpe RN. Crisis management during anaesthesia: Laryngospasm. Qual Saf Health Care 2005;14:e3.
Massad I, Halawa SA, Badran I, Al-Barzangi B. Negative pressure pulmonary edema–five case reports. Middle East J Anaesthesiol 2006;18:977-84.
Holmes JR, Hensinger RN, Wojtys EW. Postoperative pulmonary edema in young, athletic adults. Am J Sports Med 1991;19:365-71.
Mamiya H, Ichinohe T, Kaneko Y. Negative pressure pulmonary edema after oral and maxillofacial surgery. Anesth Prog 2009;56:49-52.
Goldenberg JD, Portugal LG, Wenig BL, Weingarten RT. Negative-pressure pulmonary edema in the otolaryngology patient. Otolaryngol Head Neck Surg 1997;117:62-6.
Westreich R, Sampson I, Shaari CM, Lawson W. Negative-pressure pulmonary edema after routine septorhinoplasty: Discussion of pathophysiology, treatment, and prevention. Arch Facial Plast Surg 2006;8:8-15.
Lathan SR, Silverman ME, Thomas BL, Waters WC 4th
. Postoperative pulmonary edema. South Med J 1999;92:313-5.
Cascade PN, Alexander GD, Mackie DS. Negative-pressure pulmonary edema after endotracheal intubation. Radiology 1993;186:671-5.
Van Kooy MA, Gargiulo RF. Postobstructive pulmonary edema. Am Fam Physician 2000;62:401-4.
Maroof M, Khan RM, Ryley BG, Bari N, Cooper T. Post-anaesthetic pulmonary oedema following upper airway obstruction. J Pak Med Assoc 1994;44:244-7.
García de Hombre AM, Cuffini A, Bonadeo A. Negative pressure pulmonary oedema after septoplasty. Acta Otorrinolaringol Esp 2013;64:300-2.
Jaafarpour M, Khajavikhan J, Khani A. Negative pressure pulmonary oedema: A rare case report of two brothers. J Clin Diagn Res 2013;7:2308-9.
Mehta VM, Har-El G, Goldstein NA. Postobstructive pulmonary edema after laryngospasm in the otolaryngology patient. Laryngoscope 2006;116:1693-6.
Wadhwa R, Kalra S. Negative pressure pulmonary oedema after rhinoplasty. Indian J Anaesth 2010;54:363-4.
] [Full text]
Pathak V, Rendon IS, Ciubotaru RL. Recurrent negative pressure pulmonary edema. Clin Med Res 2011;9:88-91.
Shigematsu H, Yoneda M, Tanaka Y. Negative pressure pulmonary edema associated with anterior cervical spine surgery. Asian Spine J 2014;8:827-30.
Barin ES, Stevenson IF, Donnelly GL. Pulmonary edema following acute upper airway obstruction. Anaesth Intensive Care 1986;14:54-7.
Kaya Z, Tuncez A, Gök U, Gül EE, Altunbaş G. Negative pressure pulmonary edema following septoplasty surgery triggering acute subendocardial myocardial infarction. Heart Views 2014;15:46-8.
] [Full text]
[Figure 1], [Figure 2], [Figure 3]