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Negative Pressure Pulmonary Oedema after Sedation in a Patient Undergoing Pacemaker Implantation

Case Report

Journal of Cardiovascular Disease Research |Year 2017 | Volume 8 | Issue 1 |Page 28-30

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Venkatesh Tekur Krishnamurthy, Sri Arun Tekur Venkatesh*Department of Cardiology, Apollo hospitals 154/11, Opp IIM-B, Bannerghatta Road, Bangalore 560076 INDIA.

Abstract

Negative pressure pulmonary oedema (NPPE) is a manifestation of upper airway obstruction and is seen after extubation postoperatively. The large negative intrathoracic pressure generated by forced inspiration against an obstructed airway is thought to be the principal mechanism involved. It is a dangerous and potentially fatal condition with a multifactorial pathogenesis. The Authors report a case of negative pressure pulmonary oedema occurring periprocedurally while undergoing permanent pacemaker implantation under local anaesthesia and light sedation due to upper airway obstruction caused by falling back of the tongue.

Key words: Negative pressure pulmonary oedema, Sedation, permanent pacemaker implantation, Upper airway obstruction.

Submission Date: 04-07-2016 | Review completed: 22-11-2016 | Accepted Date: 05-12-2016


INTRODUCTION

Negative pressure pulmonary oedema is a serious and potentially fatal condition with a multifactorial pathogenesis. Frequently, NPPE is a manifestation of upper airway obstruction, the large negative intrathoracic pressure generated by forced inspiration against an obstructed airway is thought to be the principal mechanism involved. This negative pressure leads to an increase in pulmonary vascular volume and pulmonary capillary transmural pressure, creating a risk of disruption of the alveolar – capillary membrane. The early detection of the signs of this syndrome is vital to the treatment and to patient outcome.1Bhaskar B, Fraser JF. Negative pressure pulmonary edema revisited: Pathophysiology and review of management. Saudi J Anaesth. 2011;5(3):308-13. https://doi.org/10.4103/1658-354X.84108; PMid:21957413 PMCid:PMC3168351 It is rare and usally occurs in a clinical setting of postextubation, laryngospasm, epiglottits, croup, endotracheal tube obstruction, post tonsillectomy/adenoidectomy and other conditions. The Authors report here a case of negative pressure pulmonary oedema occurring after intravenous sedation in an elderly male undergoing dual chamber permanent pacemaker implantation procedure.

CASE REPORT

An 86 year male with symptomatic Mobitz Type 2 AV block was prepared for creation of a left side pectoral pocket to implant a dual chamber permanent pacemaker under local anaesthesia with strict aseptic precautions in the cath lab. Patient had no past history of cardiac or pulmonary disease in the past and remained asymptomatic except for one episode of syncope coinciding with Mobitz Type 2 AV block one day before being taken up for dual chamber permanent pacemaker implant procedure. Inj. Lignocaine (1 %) 15 ml was infiltrated locally into the skin along the length of the intended incision as well as more deeply and medially with an intent to achieve adequate anaesthesia. As patient did not experience adequate analgesia after additional infiltration of Inj. Lignocaine to a maximum permitted dose of 3mg/kg, patient was administered Inj. Fentanyl 50 mcg intravenously to achieve better analgesia. Incision was placed for creation of pectoral pocket. Soon, it was noticed that the oxygen saturation on pulse oximetry was falling to less than 70 % and lung auscultation revealed bilateral crepitations. The heart rate and blood pressure remained unchanged. The patient was drowsy and sedated and it was noticed that the tongue had fallen back to cause obstruction to the upper airway. Patient underwent immediate endotracheal intubation with artificial ventilation. Pink frothy sputum was noticed in the endotracheal tube. Simultaneously, patient received intravenous Frusemide 40 mg to treat acute pulmonary oedema. The oxygen saturation improved quickly after the above measures and pacemaker implantation procedure was completed successfully. A perioperative chest x-ray confirmed presence of acute pulmonary oedema. (Figure 1). Patient was extubated uneventfully after six hours with no further clinical events and was discharged from the hospital after three days.

DISCUSSION

The first description of the pathophysiological correlation between creation of negative pressure and the development of pulmonary edema was in 1942 by Warren et al.1Bhaskar B, Fraser JF. Negative pressure pulmonary edema revisited: Pathophysiology and review of management. Saudi J Anaesth. 2011;5(3):308-13. https://doi.org/10.4103/1658-354X.84108; PMid:21957413 PMCid:PMC3168351 The relationship between pulmonary edema and upper airway obstruction in two children, who had croup and epiglottitis was reported by Capitanio et al.2Capitanio MA, Kirkpatrick JA. Obstructions of the upper airway in children as reflected on the chest radiograph. Radiology. 1973;107(1):159-61. https://doi.org/10.1148/107.1.159 ; PMid:4266024. The first report on the clinical significance of this phenomenon in three adult patients, who experienced onset of pulmonary edema minutes to hours after severe acute upper airway obstruction was by Oswalt et al.3Oswalt CE, Gates GA, Holmstrom MG. Pulmonary edema as a complication of acute airway obstruction. JAMA. 1977;238(17):1833-5. https://doi.org/10.1001/jama.238.17.1833 : https://doi.org/10.1001/jama.1977.03280180037022 ; PMid:333133. Negative pressure pulmonary edema (NPPE) is also called post obstruction pulmonary edema (POPE). The presentation of NPPE can be immediate or delayed.4Timby J, Reed C, Zeilender S, Glauser FL. “Mechanical” causes of pulmonary edema. Chest. 1990;98(4):973-9. https://doi.org/10.1378/chest.98.4.973 ; PMid:2209159.,5McConkey PP. Postobstructive pulmonary oedema: A case series and review. Anaesthesia Intensive Care. 2000;28(1):72-6 PMid:10701042. Negative pressure pulmonary oedema is classified as Type I or Type II.6Dicpinigaitis PV, Mehta DC. Post obstructive pulmonary edema induced by endotracheal tube occlusion. Intensive Care Med. 1995;21(12):1048-50. https://doi.org/10.1007/BF01700672.,7Anderson AF, Alfrey D, Lips comb AB., Jr Acute pulmonary edema: An unusual complication following arthroscopy: A report of three cases. Arthroscopy. 1990;6(3):235-7. https://doi.org/10.1016/0749-8063(90)90080-W.

Type I NPPE develops immediately after onset of acute airway obstruction and Type II NPPE develops after the relief of chronic upper airway obstruction. As Type I NPPE develops usually with upper airway acute obstruction or after manipulation of the airway surgically, some authors call it laryngeal spasm-induced pulmonary edema.8Guinard JP. Laryngospasm-induced pulmonary edema. Int J Pediatr Otorhinolaryngol. 1990;20(2):163-8. https://doi.org/10.1016/0165-5876(90)90082-3. Other factors that increase the risk of Type I NPPE are hanging, strangulation, upper airway tumors, foreign bodies, epiglottitis, croup, chocking, migration of Folly’s catheter balloon used to tamponade the nose in epistaxis, near drowning, endotracheal tube (ETT) obstruction, goitre, and mononucleosis. Type II NPPE can result after relief of upper airway obstruction caused by big tonsils, hypertrophic adenoids, or a redundant uvula. According to one study, the incidence of developing Type I NPPE associated with acute postoperative upper airway obstruction is 9.6 – 12%, whereas the incidence of developing Type II NPPE is 44%,9Lathan SR, Silverman ME, Thomas BL, Waters WC. Postoperative pulmonary edema. South Med J. 1999;92:313-5. https://doi.org/10.1097/00007611-199903000-00011; PMid:10094274. In adults about 50% of NPPE occurrences are due to postoperative laryngospasm.10Goli AK, Goli SA, Byrd RP, Jr, Roy TM. Spontaneous negative pressure changes: An unusual cause of noncardiogenic pulmonary edema. J Ky Med Assoc. 2003;101:317-20. PMid:14502951. NPPE is mainly described in a postoperative clinical situation wherein non-cardiogenic edema results from laryngospasm or other forms of upper airway obstruction following extubation.4Timby J, Reed C, Zeilender S, Glauser FL. “Mechanical” causes of pulmonary edema. Chest. 1990;98(4):973-9. https://doi.org/10.1378/chest.98.4.973 ; PMid:2209159.,5McConkey PP. Postobstructive pulmonary oedema: A case series and review. Anaesthesia Intensive Care. 2000;28(1):72-6 PMid:10701042. NPPE begins with a significant upper airway obstruction, inspiratory efforts to overcome the obstruction generate highly negative intrapleural and alveolar pressures, and the high pressure gradient causes fluid to move out of the pulmonary capillaries and into the interstitial and alveolar spaces11Butterell H, Riley RH. Life-threatening pulmonary oedema secondary to tracheal compression.Anaesthesia Intensive Care. 2002;30:804-6. PMid:12500522.,12Willms D, Shure D. Pulmonary edema due to upper airway obstruction in adults. Chest. 1988;94:1090-2. https://doi.org/10.1378/chest.94.5.1090 ; PMid:3053060. The etiology of negative pressure pulmonary edema is multifactorial, but appears to be related to the generation of marked negative intrathoracic pressure due to forced inspiration against a closed glottis, referred to as a Mueller (or reverse Valsalva) maneuver. As the intrathoracic pressure becomes more negative, blood flow to the right heart increases. This causes the pulmonary vascular bed to dilate, the interstitial pressure around the capillaries to become more negative, and intravascular fluid to be drawn into the interstitial space. This worsens gas exchange and triggers a cascade of hypoxemia, catecholamine release, and systemic and pulmonary hypertension. The result is an acute increase in afterload, which worsens transcapillary fluid efflux and increases interstitial and alveolar edema.13Mulkey Z, Yarbrough S, Guerra D, et al. Postextubation pulmonary edema: a case series and review. Respir Med 2008;102:1659. https://doi.org/10.1016/j.rmed.2008.07.002 ; PMid:18804361. The pathophysiology of NPPE is attributed to four major mechanisms: Disturbances of pulmonary fluid homeostasis can be induced by four pathways that can lead to increased interstitial fluid - increased hydrostatic pressure in the pulmonary capillary bed (or conversely, decreased pressure in the interstitium), decreased osmotic pressure of plasma, increased permeability of the membrane, and decreased return of fluid to the circulation via lymphatics.14Matthay MA, Folkesson HG, Clerici C. Lung epithelial fluid transport and the resolution of pulmonary edema. Physiological reviews. 2002;82:569-600. https://doi.org/10.1152/physrev.00003.2002 ; PMid:12087129.,15Ware LB, Matthay MA. Clinical practice. Acute pulmonary edema. The New England journal of medicine. 2005;353:2788-96. https://doi.org/10.1056/NEJMcp052699 ; PMid:16382065. In clinical presentation, initial findings usually include decreased oxygen saturation, with pink frothy sputum and chest radiograph abnormalities.9Lathan SR, Silverman ME, Thomas BL, Waters WC. Postoperative pulmonary edema. South Med J. 1999;92:313-5. https://doi.org/10.1097/00007611-199903000-00011; PMid:10094274. Pulmonary hemorrhage and frank hemoptysis have also been reported.17Schwartz DR, Maroo A, Malhotra A, Kesselman H. Negative pressure pulmonary hemorrhage. Chest. 1999;115:1194. https://doi.org/10.1378/chest.115.4.1194 ; PMid:10208229. Lung a uscultation usually reveals crackles and occasionally wheezes. Pulmonary edema causes both impaired diffusion of oxygen and ventilation/perfusion mismatching, leading to sudden and possibly severe hypoxemia. The typical chest radiograph will show diffuse interstitial and alveolar infiltrates. Although the radiographic findings associated with postextubation pulmonary edema have been described, there are minimal data regarding distribution of this postextubation edema within the lungs.16Cascade PN, Alexander GD, Mackie DS. Negative-pressure pulmonary edema after endotracheal intubation. Radiology. 1993;186:671-5. https://doi.org/10.1148/radiology.186.3.8430172 ; PMid:8430172. Respiratory failure requiring unplanned reintubation in the postoperative period is associated with high morbidity, leading to a longer hospital stay, and increase in 30 - day mortality.19Brueckmann B, Villa-Uribe JL, Bateman BT, et al. Development and validation of a score for prediction of postoperative respiratory complications. Anesthesiology 2013; 118:1276. https://doi.org/10.1097/ALN.0b013e318293065c ; PMid:23571640. Patients usually present with signs of acute upper airway obstruction following extubation and, upon relief of the obstruction, immediately develop dyspnea with pink frothy sputum and bilateral infiltrates on their chest radiograph. Less often, the development of pulmonary edema can be delayed for several hours.12Willms D, Shure D. Pulmonary edema due to upper airway obstruction in adults. Chest. 1988;94:1090-2. https://doi.org/10.1378/chest.94.5.1090 ; PMid:3053060.

The first treatment priority is relief of the airway obstruction and correction of hypoxemia. The next step is to address the pulmonary edema with a diuretic unless the patient is hypovolemic. Effective airway management and immediate treatment with oxygen and diuretics is sufficient in most cases of NPPE. Persistent airway obstruction may necessitate an artificial airway, and acute respiratory failure would require artificial ventilation with oxygen and appropriate levels of PEEP. Other options include noninvasive ventilation (NIV) and oxygen delivered through high flow nasal cannula (HFNC).20Hernández G, Vaquero C, González P, et al. Effect of Postextubation High-Flow Nasal Cannula vs Conventional Oxygen Therapy on Reintubation in Low-Risk Patients: A Randomized Clinical Trial. JAMA. 2016;315:1354. https://doi.org/10.1001/jama.2016.2711; PMid:26975498.,21Jaber S, Lescot T, Futier E, et al. Effect of Noninvasive Ventilation on Tracheal Reintubation Among Patients With Hypoxemic Respiratory Failure Following Abdominal Surgery: A Randomized Clinical Trial. JAMA. 2016;315:1345. https://doi.org/10.1001/jama.2016.2706 ; PMid:26975890.,22Stéphan F, Barrucand B, Petit P, et al. High-Flow Nasal Oxygen vs Noninvasive Positive Airway Pressure in Hypoxemic Patients After Cardiothoracic Surgery: A Randomized Clinical Trial. JAMA 2015;313:2331. https://doi.org/10.1001/jama.2015.5213; PMid:25980660.

The Authors here report a case of negative pressure pulmonary oedema occurring in an elderly patient which occurred due to falling back of the tongue after drowsiness and sedation following intravenous analgesia leading to upper airway obstruction. The clinical significance in this case lies in the fact that simple falling back of the tongue with sedation is enough to cause airway obstruction before any procedure. It can lead to serious life threatening complication like NPPE. The Authors place importance on early recognition of this condition with prompt restoration of airway patency. When recognition of negative pressure pulmonary oedema is delayed, NPPE have mortality rates ranging from 11% to 40%,18Mehta VM, Har-El G, Goldstein NA. Postobstructive pulmonary edema after laryngospasm in the otolaryngology patient. Laryngoscope. 2006;116:1693-6. https://doi.org/10.1097/01.mlg.0000231762.91541.3a ; PMid:16955006. To the best of the Authors’ knowledge negative pressure pulmonary oedema occurring due to drowsiness and sedation with falling back of the tongue to cause upper airway obstruction is one of a kind and has not been reported in the literature so far.


FIGURE 1: Chest X Ray showing features of pulmonary oedema with Dual chamber pacemaker


CONCLUSION

Negative pressure pulmonary oedema can occur with sedation due to falling back of the tongue and early recognition is life saving.

CONFLICT OF INTEREST

Nil

ACKNOWLEDGMENT

Nil

ABBREVIATIONS USED

NPPE: Negative pressure pulmonary oedema; PEEP: Positive end expiratory pressure.

REFERENCES

1. Bhaskar B, Fraser JF. Negative pressure pulmonary edema revisited: Pathophysiology and review of management. Saudi J Anaesth. 2011;5(3):308-13. https://doi.org/10.4103/1658-354X.84108; PMid:21957413 PMCid:PMC3168351
2. Capitanio MA, Kirkpatrick JA. Obstructions of the upper airway in children as reflected on the chest radiograph. Radiology. 1973;107(1):159-61. https://doi.org/10.1148/107.1.159 ; PMid:4266024.
3. Oswalt CE, Gates GA, Holmstrom MG. Pulmonary edema as a complication of acute airway obstruction. JAMA. 1977;238(17):1833-5. https://doi.org/10.1001/jama.238.17.1833 : https://doi.org/10.1001/jama.1977.03280180037022 ; PMid:333133.
4. Timby J, Reed C, Zeilender S, Glauser FL. “Mechanical” causes of pulmonary edema. Chest. 1990;98(4):973-9. https://doi.org/10.1378/chest.98.4.973 ; PMid:2209159.
5. McConkey PP. Postobstructive pulmonary oedema: A case series and review. Anaesthesia Intensive Care. 2000;28(1):72-6 PMid:10701042.
6. Dicpinigaitis PV, Mehta DC. Post obstructive pulmonary edema induced by endotracheal tube occlusion. Intensive Care Med. 1995;21(12):1048-50. https://doi.org/10.1007/BF01700672.
7. Anderson AF, Alfrey D, Lips comb AB., Jr Acute pulmonary edema: An unusual complication following arthroscopy: A report of three cases. Arthroscopy. 1990;6(3):235-7. https://doi.org/10.1016/0749-8063(90)90080-W.
8. Guinard JP. Laryngospasm-induced pulmonary edema. Int J Pediatr Otorhinolaryngol. 1990;20(2):163-8. https://doi.org/10.1016/0165-5876(90)90082-3.
9. Lathan SR, Silverman ME, Thomas BL, Waters WC. Postoperative pulmonary edema. South Med J. 1999;92:313-5. https://doi.org/10.1097/00007611-199903000-00011; PMid:10094274.
10. Goli AK, Goli SA, Byrd RP, Jr, Roy TM. Spontaneous negative pressure changes: An unusual cause of noncardiogenic pulmonary edema. J Ky Med Assoc. 2003;101:317-20. PMid:14502951.
11. Butterell H, Riley RH. Life-threatening pulmonary oedema secondary to tracheal compression.Anaesthesia Intensive Care. 2002;30:804-6. PMid:12500522.
12. Willms D, Shure D. Pulmonary edema due to upper airway obstruction in adults. Chest. 1988;94:1090-2. https://doi.org/10.1378/chest.94.5.1090 ; PMid:3053060.
13. Mulkey Z, Yarbrough S, Guerra D, et al. Postextubation pulmonary edema: a case series and review. Respir Med 2008;102:1659. https://doi.org/10.1016/j.rmed.2008.07.002 ; PMid:18804361.
14. Matthay MA, Folkesson HG, Clerici C. Lung epithelial fluid transport and the resolution of pulmonary edema. Physiological reviews. 2002;82:569-600. https://doi.org/10.1152/physrev.00003.2002 ; PMid:12087129.
15. Ware LB, Matthay MA. Clinical practice. Acute pulmonary edema. The New England journal of medicine. 2005;353:2788-96. https://doi.org/10.1056/NEJMcp052699 ; PMid:16382065.
16. Cascade PN, Alexander GD, Mackie DS. Negative-pressure pulmonary edema after endotracheal intubation. Radiology. 1993;186:671-5. https://doi.org/10.1148/radiology.186.3.8430172 ; PMid:8430172.
17. Schwartz DR, Maroo A, Malhotra A, Kesselman H. Negative pressure pulmonary hemorrhage. Chest. 1999;115:1194. https://doi.org/10.1378/chest.115.4.1194 ; PMid:10208229.
18. Mehta VM, Har-El G, Goldstein NA. Postobstructive pulmonary edema after laryngospasm in the otolaryngology patient. Laryngoscope. 2006;116:1693-6. https://doi.org/10.1097/01.mlg.0000231762.91541.3a ; PMid:16955006.
19. Brueckmann B, Villa-Uribe JL, Bateman BT, et al. Development and validation of a score for prediction of postoperative respiratory complications. Anesthesiology 2013; 118:1276. https://doi.org/10.1097/ALN.0b013e318293065c ; PMid:23571640.
20. Hernández G, Vaquero C, González P, et al. Effect of Postextubation High-Flow Nasal Cannula vs Conventional Oxygen Therapy on Reintubation in Low-Risk Patients: A Randomized Clinical Trial. JAMA. 2016;315:1354. https://doi.org/10.1001/jama.2016.2711; PMid:26975498.
21. Jaber S, Lescot T, Futier E, et al. Effect of Noninvasive Ventilation on Tracheal Reintubation Among Patients With Hypoxemic Respiratory Failure Following Abdominal Surgery: A Randomized Clinical Trial. JAMA. 2016;315:1345. https://doi.org/10.1001/jama.2016.2706 ; PMid:26975890.
22. Stéphan F, Barrucand B, Petit P, et al. High-Flow Nasal Oxygen vs Noninvasive Positive Airway Pressure in Hypoxemic Patients After Cardiothoracic Surgery: A Randomized Clinical Trial. JAMA 2015;313:2331. https://doi.org/10.1001/jama.2015.5213; PMid:25980660.