|Year : 2007 | Volume
| Issue : 5 | Page : 429
Rapid Onset Acute Epiglottitis Leading to Negative Pressure Pulmonary Edema
V Saraswat1, PV Madhu2, Suresh S Kumar3
1 M.D.,Prof. and Head, Department of Anaesthesiology and Critical Care, Command Hospital (Air Force) Airport Road, Bangalore, India
2 M.D., Lecturer, Department of Anaesthesiology and Critical Care, Command Hospital (Air Force) Airport Road, Bangalore, India
3 M.D. Sr.Resident, Department of Anaesthesiology and Critical Care, Command Hospital (Air Force) Airport Road, Bangalore, India
|Date of Acceptance||20-Aug-2007|
|Date of Web Publication||20-Mar-2010|
Prof and Head, Department of Anesthesiology and Critical Care Command Hospital (Air Force) Airport Road, Bangalore-560007
Source of Support: None, Conflict of Interest: None
Pulmonary edema is a potentially life-threatening complication of acute airway obstruction. It develops rapidly, without warning, in young healthy individuals. Two forms of post-obstructive pulmonary edema (POPE) (also known as negative pressure pulmonary edema, NPPE) have been identified. POPE I follows sudden, severe upper airway obstruction. POPE II occurs following surgical relief of chronic upper airway obstruction. Treatment for both is supportive. Full and rapid recovery can be expected with appropriate management. A case report of a middle aged man with acute onset epiglottitis who developed negative pressure pulmonary edema after intubation is presented. The report includes a brief discussion on etiology, clinical features and management dilemma of acute upper airway obstruction.
Keywords: Acute epiglottitis; Negative pressure pulmonary edema (NPPE); Post-obstructive pulmonary edema (POPE)
|How to cite this article:|
Saraswat V, Madhu P V, Kumar SS. Rapid Onset Acute Epiglottitis Leading to Negative Pressure Pulmonary Edema. Indian J Anaesth 2007;51:429
|How to cite this URL:|
Saraswat V, Madhu P V, Kumar SS. Rapid Onset Acute Epiglottitis Leading to Negative Pressure Pulmonary Edema. Indian J Anaesth [serial online] 2007 [cited 2021 Apr 21];51:429. Available from: https://www.ijaweb.org/text.asp?2007/51/5/429/61176
| Introduction|| |
Anaesthesiologists as intensivists must be able to recognize and initiate treatment for conditions that are uncommon but life threatening. Post obstructive pulmonary edema (POPE)  is one of these conditions. Patients with POPE develop sudden, unexpected and often severe pulmonary edema. POPE follows an episode of acute airway obstruction or the relief of chronic upper airway obstruction  in patients otherwise not at risk for pulmonary edema. Anaesthesiologists care for patients at risk of POPE in their theatres, emergency departments, critical care units, medical wards and recovery rooms. Awareness of this uncommon condition is crucial if the anaesthesiologist is to make an early diagnosis and initiate successful treatment. The aim of this paper is to present a brief review of the literature so as to assist the anaesthesiologist in assessment and management.
| Case report|| |
A 49-year-old man was brought to the casualty at 2100 hrs with chief complaints of increasing difficulty in breathing which started at 1700 hrs following history of sore throat from 1500 hrs the same day.
On examination he was found to have significant respiratory distress with biphasic stridor. The patient was agitated, anxious and was using all the accessory muscles of respiration. He was tachypnoeic and had SpO2 of 85% on oxygen by facemask. Heart rate was 130/min and blood pressure was 116/72 mmHg. Air entry was equal bilaterally and other systemic examination was essentially normal. In the ICU his stridor started worsening, he developed central cyanosis and saturation started dropping further. Bag and mask ventilation with 100% oxygen with positive pressure did not improve saturation. In view of his deteriorating general condition, it was decided to do direct laryngoscopy.
Monitoring in form of ECG, NIBP and pulse oximetry was instituted. He was given a single dose of midazolam 2 mg intravenously and thiopentone 150 mg slowly under constant haemodynamic monitoring. He was allowed to breathe spontaneously. Laryngoscopy revealed grossly edematous epiglottis (worm like) and soft palate. Vocal cords were not visible. At the time of laryngoscopy, no gastric contents were noted. A diagnosis of acute epiglottitis was made. Preparations for emergency tracheostomy were made. It was decided to attempt intubation for bypassing the airway obstruction, as ventilation with bag and mask was not effective.
Patient could be intubated on second attempt with a 7 mm size endotracheal tube with a stylet. Post intubation chest X-ray was clear [Figure 1]. However the saturation remained between 85-90% with 100% oxygen and positive pressure ventilation. The compliance of lung was low as assessed during IPPV using Bain's circuit.
Within 10 min after intubation patient started desaturating again and pink frothy copious secretions was aspirated from the endotracheal tube. On auscultation bilateral extensive rhonchi and rales were heard. Chest X- ray, taken 30 minutes after previous one, revealed bilateral extensive pulmonary edema [Figure 2].
A diagnosis of negative pressure pulmonary edema was made. Patient was put on mechanical ventilation, with 100% oxygen. Furosemide and morphine were administered intravenously. Intra tracheal adrenaline and lidocaine were administered for bronchodilatation. PEEP was rapidly reduced to 8 cm of H 2 O as saturation improved. Oxygen saturation slowly increased to 95 percent. Within 2 hrs patient started showing improvement. Morning chest X- ray showed clearance of pulmonary edema. In throat swab and tracheal aspirate cultures were positive for Pseudomonas aerugenosa. He was treated with appropriate antibiotics and intravenous steroids. Patient was weaned off the ventilator over the next two days. Subsequent recovery was uneventful.
| Discussion|| |
POPE is the sudden onset of pulmonary edema following upper airway obstruction. There are two recognized types of POPE.  Type I follows a sudden, severe episode of upper airway obstruction such as post extubation laryngospasm,  epiglottitis, croup,  and choking,  and is seen in strangulation and hanging.  Type I POPE may be associated with any cause of acute airway obstruction. Type II POPE develops after surgical relief of chronic upper airway obstruction. Reported causes include tonsillectomy  and removal of upper airway tumors  .
NPPE has been reported to be more frequent in healthy (ASA physical status I and II), middle-aged and male patients, with a general incidence of 0.094%. The importance of vigorous inspiratory effort in POPE I is supported by the apparent increase in susceptibility to this condition in young athletic men  who, because of their highly compliant chest wall musculature, are able to generate extremely high negative inspiratory pressures. Other factors may also contribute, including direct suctioning of endotracheal tube adaptors during thoracotomy  , narcotic use, short neck, obesity, obstructive apnea, nasal, oral or pharyngeal surgery or pathology and vocal cord paralysis, conditions leading to increased capillary-alveolar pressure gradients, endotracheal tube obstruction and premature extubation.
Type I and type II POPE present with acute respiratory distress [Table 1]. Type I POPE usually occurs within 60 minutes of a precipitating event,  but the onset has been delayed for up to six hours in some case reports.  Type II POPE develops soon after relief of chronic upper airway obstruction. POPE requires rapid intervention and may be confused with other causes of postoperative respiratory distress. Although symptoms usually develop within one hour of the precipitating event, delayed onsets have been reported  . The presence of agitation, tachypnea, tachycardia, frothy pink pulmonary secretions, rales and progressive oxygen desaturation suggests the diagnosis of POPE in the appropriate setting. Chest radiograph findings of pulmonary edema support the diagnosis. Other causes of pulmonary edema should be considered. The absence of gastric contents in pulmonary secretions, a history of normal cardiac function and, particularly, the occurrence of such symptoms in a vigorous young person makes the diagnosis of POPE more likely.
The pathogenesis of POPE I is multifactorial. , Forceful attempts to inhale against an obstruction create extreme reduction of intrathoracic pressure during spontaneous ventilation, consecutively causing increase in venousreturn to the right ventricle and intrathoracic blood volume, resulting in elevated hydrostatic pressures. Reduced cardiac output due to increase in after load and stress failure of alveolar capillary membrane leads to fluid transudation into the alveolar space. Most cases of POPE respond promptly to appropriate treatment. One reported case  of POPE I, however, in an otherwise healthy 43 year-old man with epiglottitis, progressed to adult respiratory distress syndrome and death. Treatment consists of supplemental oxygen and support. Intubation and the application of low levels of PEEP (5 cm H 2 O) have been employed in most reported cases. It is not clear, however, if PEEP is required and its use must be weighed against the risks of barotrauma and reduced cardiac output. One series identified several subclinical cases of POPE  that resolved without specific treatment. The role of diuretics in the management of POPE is unclear.
Negative-pressure pulmonary edema (NPPE) is a clinical entity of anaesthesiologic relevance, perioperatively caused by obstruction of the conductive airways (upper airway obstruction, UAO) due to laryngospasm in approximately 50% of the cases, its early recognition and treatment by the anaesthetist is mandatory. NPPE, also addressed as post-obstructive pulmonary edema (POPE) presents in most cases as a complex of symptoms with rapid onset, consisting of acute respiratory failure with dyspnea, tachypnea, and strained respiratory efforts. Additional signs are paradoxical ventilation, pink frothy sputum, stridor, and severe agitation. Partially due to largely differing criteria used for diagnosis, opinions about incidence and prevalence of NPPE are unhomogenous in medical literature. It has been shown that generation of NPPE is not only limited to patients being intubated and ventilated, but occurs also in patients requiring higher fractions of oxygen.
| References|| |
|1.||Mark A. Van Kooy, Richard F Gargiulo. Postobstructive pulmonary edema. Am Fam Physician 2000;62:401-4. |
|2.||Willms D, Shure D. Pulmonary edema due to upper airway obstruction in adults. Chest 1988;94:1090-2. [PUBMED] [FULLTEXT] |
|3.||Travis KW, Todres ID, Shannon DC. Pulmonary edema associated with croup and epiglottitis. Pediatrics 1977;59:695-8. [PUBMED] |
|4.||Oudjhane K, Bowen A, Oh KS, Young LW. Pulmonary edema complicating upper airway obstruction in infants and children. Can Assoc Radiol J 1992;43:278-82. [PUBMED] |
|5.||Oswalt CE, Gates GA, Holmstrom FM. Pulmonary edema as a complication of acute airway obstruction. Rev Surg 1977;34:364-7. [PUBMED] |
|6.||Guffin TN, Har-el G, Sanders A, Lucente FE, Nash M. Acute postobstructive pulmonary edema. Otolaryngol Head Neck Surg 1995;112:235-7. [PUBMED] [FULLTEXT] |
|7.||Miro AM, Shivaram U, Finch PJ. Noncardiogenic pulmonary edema following laser therapy of a tracheal neoplasm. Chest 1989;96:1430-1. [PUBMED] [FULLTEXT] |
|8.||Herrick IA, Mahendran B, Penny FJ. Postobstructive pulmo nary edema following anesthesia. J Clin Anesth 1990;2:116-20. [PUBMED] [FULLTEXT] |
|9.||Pang WW, Chang DP, Lin CH, Huang MH. Negative pressure pulmonary oedema induced by direct suctioning of endotracheal tube adapter. Can J Anaesth 1998;45:785-8. [PUBMED] |
|10.||Lorch DG, Sahn SA. Post-extubation pulmonary edema following anesthesia induced by upper airway obstruction. Are certain patients at increased risk? Chest 1986;90:802-5. [PUBMED] [FULLTEXT] |
|11.||Glasser SA, Siler JN. Delayed onset of laryngospasm-induced pulmonary edema in an adult outpatient [Letter]. Anesthesiology 1985;62:370-1. |
|12.||Loyd JE, Nolop KB, Parker RE, Roselli RJ, Brigham KL. Effects of inspiratory resistance loading on lung fluid balance in awake sheep. J Appl Physiol 1986; 60:198-203. [PUBMED] [FULLTEXT] |
|13.||Moss G, Staunton C, Stein AA. The centrineurogenic etiology of the acute respiratory distress syndromes. Am J Surg 1973;126:37-41. [PUBMED] |
|14.||Adolph MD, Oliver AM, Dejak T. Death from adult respiratory distress syndrome and multiorgan failure following acute upper airway obstruction. Ear Nose Throat J 1994;73:324-7. [PUBMED] |
[Figure 1], [Figure 2]