A case of negative pressure pulmonary edema in an asthmatic patient after laparoscopic cholecystectomy.

Negative pressure pulmonary edema is often misdiagnosed or can go clinically unrecognized by anesthesiologists. It is characterized by a markedly low intrapleural pressure which leads to exudation of fluid and red blood cells in the interstitium. Recognition of patients with predisposing factors for upper airway obstruction is important in the diagnosis which is often confused with pulmonary aspiration of gastric contents. Signs and symptoms are subtle and edema is usually self-limited. Our patient was management conservatively with maintenance of a patent airway and administration of supplemental oxygen and had a successful outcome.

INTRODUCTION

Negative pressure pulmonary edema (NPPE) is a complication of acute and chronic upper airway obstruction that is often under recognized and misdiagnosed by anesthesiologists. The case report is aimed at presenting a case of asthmatic patient in whom NPPE occurred postoperatively following general anesthesia.

CASE REPORT

A 32-year-old female patient weighing 52 kg was posted for elective laparoscopic cholecystectomy. She was a known case of asthma for the last 10 years and was on metered dose inhaler of beclomethasone dipropionate and levosalbutamol on a thrice daily basis. There was no history of hypertension, diabetes mellitus, or any history suggestive of cardiovascular disease. Her routine blood investigations, chest X-ray, and electrocardiogram were within normal limits. She was planned for general anesthesia. In the preoperative room, the patient was nebulized with budesonide and ipratropium bromide. She was premedicated with inj. ondansetron 0.1 mg/kg, inj. hydrocortisone 100 mg, inj. midazolam 0.05 mg/kg, and inj. tramadol 100 mg/kg 15 min prior to surgery. Perioperative monitoring included electrocardiography, noninvasive blood pressure monitoring, pulse oximetry, and end-tidal capnography.

Patient was preoxygenated with 100% oxygen through a facemask for more than 3 min. Anesthesia was then induced with inj. propofol (2.5 mg/kg) and tracheal intubation was facilitated with intravenous vecuronium (0.1 mg/kg). Maintenance of anesthesia was done with FiO2 of 0.5 (with nitrous) in 0.6% isoflurane. Patients lung were ventilated to target EtCO2 concentration of 35-40 mm of Hg using open circuit with fresh gas flow of 8 L/min.

After the completion of surgery, the trachea was extubated following reversal of residual neuromuscular blockade with inj. neostigmine in the dose of 0.06 mg/kg and inj. glycopyrollate in the dose of 0.01 mg/kg. Immediately after extubation patient developed stridor and features of respiratory distress in the form of paradoxical chest movement and use of accessory respiratory musculature. On chest auscultation, there was bilateral rhonchi without any crepitations. Patient developed tachypnea and there was a decrease in the pulse oximetry reading to around 85-90%. She also developed tachycardia with the pulse rate around 110-120 per minute. Her blood pressure was 124 84 mm of Hg. She was administered inj. terbutaline sulfate 0.5 mg subcutaneous in the lateral deltoid area and was nebulized as in the preoperative period. After few minutes, there was a marked relief of airway obstruction but her pulse oximetry continued to show low Spo2 level. On auscultation, now there was no rhonchi but there was a marked degree of bilateral crepitations. Patient was shifted to intensive care unit and arterial blood gas report showed features of hypoxia, hypercapnia, and metabolic acidosis. On x-ray, there were features of mild degree of pulmonary edema [Figure 1]. The patient was still having tachycardia, though her blood pressure was still within normal limit.

Figure 1

Chest X-ray in the immediate post operative period

Immediate treatment in the form of supplemental oxygen was ensured. Continuous positive airway pressure by face mask [with pressure support of 12 cm of water and positive end-expiratory pressure (PEEP) of 5 cm of water] was applied for 12 h. Maintenance of patent airway was ensured but endotracheal intubation or oropharyngeal airway was avoided as the patient was fully conscious.

She developed a normal vesicular breath sounds on auscultation and her Spo2 returned to around 98% after 12 h and this simple conservative treatment was continued for the next 24 h. Chest x-ray was done after 24 h which showed marked decrease in the degree of pulmonary edema [Figure 2] She was shifted to ward after 48 h and was discharged on the 5th postoperative day.

Figure 2

Chest X-ray after 24 hours

DISCUSSION

NPPE also known as postobstructive pulmonary edema is a complication of acute and chronic airway obstruction. It occurs in 0.1% of patients.[1] The predominant pathophysiologic mechanism is the development of a markedly negative (subambient) intrapleural pressure during inspiration against a closed glottis (Muller maneuver), ultimately producing increased pulmonary microvascular pressure.[2]

NPPE was first described in 1927,[3] and the first case was reported in 1973.[4] Smith-Ericksen and Bo[5] demonstrated that interstitial edema in an isolated rabbit lung model increased eightfold when the intrapleural pressure was decreased by less than 5 cm of water in the presence of a closed airway.

The time to onset of pulmonary edema after the relief of upper-airway obstruction ranges from 3 to 150 min. During attempted inspiration against the closed glottis (Muller maneuver), the negative intrapleural pressure is transmitted to the perivascular and interstitial spaces.[6] The normal intrapleural pressure before inspiration is −5 cm of water.[7] It decreases to −7 to −8 cm H2O during normal active inspiration. The intrapleural pressures may decrease to −50 to −100 cm H2O when inspiration is attempted against the closed glottis.[8] The threshold level of subambient pressure necessary to produce edema is not known and may vary considerably among individuals.[2]

Expiration against a closed glottis (valsalva maneuver) creates an auto-PEEP effect that favors the distension of alveoli and prevents pulmonary edema formation. After the obstruction is relieved, the auto-PEEP effect dissipates thus promoting pulmonary edema. A balance of subambient inspiratory and positive expiratory pressures during a fixed upper airway obstruction prevents the development of pulmonary edema until the obstruction is relieved.[9] NPPE can also be unilateral if the obstruction was previously at the level of right or left main stem bronchus.[10] Although usually seen after removal of endotracheal tube upon extubation, NPPE can also occur following the use laryngeal mask airway.[11]

The decrease in intrapleural pressure is transmitted ultimately to the interstitium and increases venous return to the right heart which leads to increase in the transcapillary hydrostatic pressure.[12] Hypoxia and the hyperadrenergic state that accompany upper airway obstruction also contributes to the development of pulmonary edema.[13] Hypoxia and metabolic acidosis increases vasoconstriction at the precapillary level, elevates pulmonary microvascular pressure, alters pulmonary capillary membrane permeability, and are myocardial depressants thus promoting edema formation.[14]

It has been seen that 80% of pulmonary edema occur within minutes after relief of upper airway obstruction,[15] as it happened in our case. Edema ranges from mild to severe depending on the duration of obstruction and degree of pulmonary capillary injury. A simple use of pulse oximetry in the operating room and in postanesthesia care unit usually identifies the patient at risk as signs and symptoms in most cases are subtle, manifesting only as a modest decrease in oxygen saturation on pulse oximetry. Radiologically confirmed pulmonary edema usually resolves within 12-24 h as happened in our case.

Differential diagnosis which includes aspiration of gastric contents, acute respiratory distress syndrome, intravascular volume excess, and cardiac decompensation should be ruled out as treatment varies.

The treatment is primarily supportive and includes maintenance of a patent airway and administration of supplemental oxygen. We avoided diuretics as patients of NPPE are usually volume depleted because of movement of fluid into the interstitium and the role of diuretic is unclear in its management.[16] Aggressive treatment is usually not required when the diagnosis is suggestive. Maintenance of a patent airway and oxygenation initially may be attempted without intubation; some patients may need only supplemental oxygen, continuous positive airway pressure administered by mask (as in our case) or both. Severe degree of edema may require endotracheal intubation in which PEEP almost always improves oxygenation and limits the amount of oxygen used.

CONCLUSION

NPPE is probably more common than most anesthesiologists realize, considering the relative frequency of upper airway obstruction in the perioperative period. Our case report emphasizes the fact that NPPE can be managed with the help of simple understanding of its physiology, strict monitoring of oxygen saturation by the pulse oximetry, maintenance of patent airway, and administration of supplemental oxygen. Early recognition of this entity is the cornerstone for its successful management.