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| CASE REPORT |
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| Year : 2020 | Volume
: 4
| Issue : 2 | Page : 69-71 |
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Negative-pressure pulmonary edema following percutaneous nephrolithotomy
Jay Prakash1, Ramesh Kumar Kharwar2, Partha Sarathi Ghosh3, Shio Priye4
1 Department of Critical Care Medicine, Rajendra Institute of Medical Sciences, Ranchi, Jharkhand
2 Department of Intensive Care Medicine, Rajendra Institute of Medical Sciences, Ranchi, Jharkhand
3 Department of Critical Care Medicine, Manipal Hospital, Bengaluru, Karnataka, India
4 Department of Superspeciality Anaesthesia, Rajendra Institute of Medical Sciences, Ranchi, Jharkhand
| Date of Submission | 12-Feb-2020 |
| Date of Decision | 11-Mar-2020 |
| Date of Acceptance | 17-Mar-2020 |
| Date of Web Publication | 11-May-2020 |
Correspondence Address:
Dr. Jay Prakash
C/O R. P. Sinha, HI.166, Harmu Housing Colony, Ranchi, Jharkhand
Jharkhand
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/BJOA.BJOA_10_20
Negative pressure pulmonary edema (NPPE) or post-extubation pulmonary edema is an infrequent complication that usually occurs immediately or within several minutes after tracheal extubation in healthy, muscular adolescents and young adults. NPPE begins when upper airway obstruction occurs which causes an increase in negative intrathoracic pressure to pull fluid from the pulmonary capillary bed and into the alveoli which leads to ventilation and perfusion difficulties. Presenting here a case of bilateral renal stone posted for percutaneous nephrolithotomy under general anesthesia in prone position who desaturated immediately in the post-operative period after extubation. It also suggests the importance, prevention, diagnosis and treatment of NPPE.
Keywords: Negative-pressure pulmonary edema, percutaneous nephrolithotomy, prone position
How to cite this article:
Prakash J, Kharwar RK, Ghosh PS, Priye S. Negative-pressure pulmonary edema following percutaneous nephrolithotomy. Bali J Anaesthesiol 2020;4:69-71 |
How to cite this URL:
Prakash J, Kharwar RK, Ghosh PS, Priye S. Negative-pressure pulmonary edema following percutaneous nephrolithotomy. Bali J Anaesthesiol [serial online] 2020 [cited 2023 Mar 23];4:69-71. Available from: https://www.bjoaonline.com/text.asp?2020/4/2/69/284170 |
| Introduction | |  |
Negative-pressure pulmonary edema (NPPE) or postextubation pulmonary edema is an infrequent complication that usually occurs immediately or within several minutes after tracheal extubation in healthy, muscular adolescents and young adults. NPPE begins when upper airway obstruction occurs, which causes an increase in negative intrathoracic pressure to pull fluid from the pulmonary capillary bed and into the alveoli, which leads to increased hydrostatic pressure due to failure of oxygenation.
Here, we present a case of bilateral renal calculi posted for percutaneous nephrolithotomy (PCNL) under general anesthesia in prone position who desaturated immediately in the postoperative period just prior to extubation. It also highlights the importance of the prevention, diagnosis, and treatment of NPPE.
| Case Report | | |
An 18-year-old male, weighing 74 kg, was posted for PCNL under general anesthesia. There was no significant medical or surgical history during a preanesthetic checkup. Routine laboratory investigations and radiological examinations were within normal limits. We administered midazolam 2 mg, ondansetron 4 mg, and glycopyrrolate 0.2 mg as premedications. We used standard American Society of Anesthesiologists (ASA) monitoring available at our institution.
Anesthesia was induced with propofol 140 mg and fentanyl 100 μg and after administration of vecuronium 7 mg, atraumatic tracheal intubation was done using 8.0-mm ID cuffed endotracheal tube (ET) in a single attempt. The correct placement of ET was confirmed with a square waveform on end-tidal CO2(EtCO2). Anesthesia was maintained with N2O: O2 mixture at 40% with isoflurane at 1 minimal alveolar concentration and intermittent fentanyl and vecuronium. Neuromuscular blockade was monitored with train-of-four (TOF) monitoring.
After the cystoscopy procedure, the patient was positioned prone for PCNL. Bilateral air entry was rechecked and confirmed. Throughout the procedure, vital signs were maintained, and after uneventful surgery, the patient was reverted to supine, and when TOF was more than 0.9, the patient was reversed with neostigmine (3.5 mg) and glycopyrrolate (0.7 mg). A thorough oral suctioning was done. The surgery was 140 min long, and the total administrated fluid was 1500 ml of Ringer's lactate.
After reversal, heart rate (HR) was 88 bpm, blood pressure (BP) was 130/82 mmHg, SpO2 was 99%, and EtCO2 was 32 mmHg, with a normal shape on capnography. A few minutes after spontaneous breathing, oxygen saturation dropped from 99% to 84%. The patient became restless and started biting the ET. The bag was tight to compress. The oropharyngeal airway was inserted, and positive pressure ventilation with 100% oxygen was administered. The patient's saturation continued to fall to 68%, and HR was 78/min, BP was 140/88 mm Hg, and EtCO2 was 46 mmHg, slanting with a prolonged expiratory stroke.
Upon checking the entire ventilation circuit from the machine end to the patient end, we found that we were unable to pass the suction catheter through the ET tube. The trachea was reintubated with an 8.0-mm cuffed polyvinyl chloride ET tube after giving injection propofol 100 mg and succinylcholine 75 mg. On auscultation, coarse crepitation were heard, and pink frothy secretion was aspirated through the ET. Furosemide 40 mg was given. Intermittent positive pressure ventilation was continued with 100% oxygen, and SpO2 gradually improved to 93% over 40 min. On closer examination of the flexometallic ET, no kink was visible [Figure 1], but after removing the fixation tapes, it was noticed that a definite kink was present at the external diameter of the ET at 20-cm mark [Figure 2] which was not visible.
On the return of spontaneous respiration, the patient was shifted in the intensive care unit with mechanical ventilation (MV) with an infusion of midazolam 1 mg/h, fentanyl 30 μg/h, and vecuronium 2 mg/h. Arterial blood gas sample (ABG) revealed pH = 7.36, pCO2 =46 mmHg, pO2 =72 mmHg, HCO3− = 23.8 mmol/L, and base deficit = −2. Furosemide 20 mg was given once in every 8 h. Chest X-ray [Figure 3] showed diffuse interstitial and alveolar lung fields with a normal-sized heart, and on the basis of clinical findings, a diagnosis of NPPE was made. | Figure 3: Chest X-ray showing diffuse interstitial and alveolar lung fields
Click here to view |
With diuretic therapy, bronchodilator inhalation, and fluid restriction, the patient was ventilated overnight, and we then stopped midazolam, fentanyl, and vecuronium the next day. After a dry ET tube suctioning, clear lung fields, normal ABG, and serial chest X-ray, the patient was put on continuous positive airway pressure mode with 40% FiO2 for 2 h and then extubated. On day 3, the patient was shifted to the surgical ward, and on day 5, the patient was discharged.
| Discussion | | |
The clinical entity of NPPE or postobstructive pulmonary edema is of more importance in anesthesiology and intensive care. NPPE usually follows upper airway obstruction due to many reasons, in which postextubation laryngospasm may be the most common cause. NPPE appeared more frequently in healthy (ASA physical status I and II), middle-aged, and male patients, with a general incidence of 0.094%.[1] NPPE usually resolves within a few minutes if obstruction gets relieved, and radiographic evidence of this form of pulmonary edema resolves within 12–24 h. NPPE is usually diagnosed clinically by precipitating incidents and symptoms, which require rapid interventions and sometimes mimic other causes of postoperative respiratory distress.
Clinically, patients present with decreased oxygen saturation, restlessness, tachypnea, pink frothy secretion, and chest X-ray abnormalities.[2] Sometimes, onset may be delayed up to a few hours in the postoperative period, which may be due to positive pressure, generated by forceful expiration against the closed glottis, which opposes fluid transudation.[3] Airway obstruction manifests as stridor, suprasternal and/or supraclavicular retractions, and accessory muscle involvement for breathing. Treatment includes airway management and administration of oxygen and furosemide.[4] However, MV may be required in case of persistent airway obstruction or acute respiratory failure, which may necessitate an artificial airway. If the cause of airway obstruction is due to the patient biting down on the ET, a bolus dose of succinylcholine (0.1–0.2 mg/kg) may require relaxing the jaw muscles.
The pathogenesis of NPPE is related to the development of high negative intrapleural pressure by vigorous inspiratory efforts against obstructed upper airway, which causes decreased interstitial hydrostatic pressure, increased venous return, and increased left ventricular afterload. By this negative pressure, there would be activation of the sympathetic nervous system associated with systemic hypertension and central pooling of blood, which leads to pulmonary edema by increasing the transcapillary pressure gradient. The negative intrathoracic pressure may result in an increased afterload imposed on the left ventricle, which causes a subsequent decrease in ventricular stroke volume and an increase in both ventricular end-systolic and end-diastolic volumes. Hence, an increase in pulmonary capillary hydrostatic pressure by an increase in left ventricular afterload contributes to fluid transudation.
The clinical presentation in our patient in the operating room was decreased oxygen saturation with frothy pink sputum and chest radiograph abnormalities due to obstruction of the airway by kinking of the airway, which may be due to the tube bite by the patient in the light plane of anesthesia or due to the prone position. Sustained external pressure on the ET tube in the prone position may result in tube kinking. Instances of tube blockage or kinking have been reported under prone position.[5]
NPPE is a possible cause of respiratory distress in the operating room, especially in patients breathing spontaneously while in the prone position. It is difficult to recover any compromise of the airway in the prone position. In this patient, tube kink was clearly visible under the wraps of the fixation tape after removal. Ventilation despite a tube kink has been reported in literature.[6]
We ruled out other possibilities in our patients such as aspiration of gastric content, laryngospasm, fluid overload, or any cardiac abnormalities. Aspiration pneumonitis was ruled out because the severity and time course of clinical and radiological recovery were not consistent with these etiologies. A calculated amount of fluid was infused; laryngospasm was not seen during both intubations. Concealed kinking of the flexometallic tube at the point of its fixation with tapes during neurosurgery in the prone position has been reported.[7]
We believe that a similar mechanism was operating in our patient, but this patient was a young male that has well-developed musculature, capable of creating high negative pressure, and the situation ultimately led to NPPE.[8] The negative intrathoracic pressure also results in an increased afterload imposed on the left ventricle, which causes a further decrease in ventricular stroke volume and an increase in both ventricular end-systolic and end-diastolic volumes. Hence, an increase in pulmonary capillary hydrostatic pressure by an increase in left ventricular afterload contributes to fluid transudation.
| Conclusion | | |
NPPE may happen due to negative intrathoracic pressure as a consequence of strong inspiratory efforts. Prompt diagnosis and treatment markedly decrease the morbidity and mortality, which may occur if NPPE is left untreated.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that his name and initial will not be published, and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.
Acknowledgment
The authors obtained the patient's consent for the publication of this case without revealing any identity.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | 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.  |
| 2. | Lathan SR, Silverman ME, Thomas BL, Waters WC 4 th. Postoperative pulmonary edema. South Med J 1999;92:313-5. |
| 3. | 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. |
| 4. | Patton WC, Baker CL Jr., Prevalence of negative-pressure pulmonary edema at an orthopaedic hospital. J South Orthop Assoc 2000;9:248-53. |
| 5. | Populaire C, Robard S, Souron R. An armoured endotracheal tube obstruction in a child. Can J Anaesth 1989;36:331-2. |
| 6. | Hariharan U, Baduni N, Singh BP. Ventilation despite an endotracheal tube kink! Sri Lankan J Anaesthesiol 2014;22:74. |
| 7. | Hariharan U, Shrivastava P, Gupta A, Senapati NN. Concealed kinking of pediatric flexometallic tube at fixation point. Saudi J Anaesth 2017;11:507-8. |
| 8. | Holmes JR, Hensinger RN, Wojtys EW. Postoperative pulmonary edema in young, athletic adults. Am J Sports Med 1991;19:365-71. |
[Figure 1], [Figure 2], [Figure 3]
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