Patients with postobstructive pulmonary edema (or P.O.P.E.) develop sudden, unexpected and potentially life-threatening pulmonary edema after relief of airway obstruction. It can be mild or severe. My first experience with it was in 1983.
In 1983, we didn’t have pulse oximetry, end-tidal carbon dioxide monitoring or even automated blood pressure cuffs. The patient was a healthy 6’3” tall and 250 lbs , 20 year old man. All muscle and clearly in great shape. He had just had knee surgery under general anesthesia and was on the verge of waking up.
He was coughing vigorously on the endotracheal tube. Four people held him down. My resident, fearful he night hurt himself or the team, extubated him while he was still coughing and before he was following commands. Unfortunately the patient was still in stage 2, when the airway reflexes are hyperdynamic.
Within seconds the patient went into laryngospasm, intense spasmodic closure of the vocal cords and other laryngeal muscles. There followed several minutes of struggling to re-establish an open airway. Finally the spasm broke with the use of positive pressure and the patient awoke.
However the mood in the room quickly turned from relief to concern. Our patient started to panic, claiming that he couldn’t breathe. His color was poor. He was wheezing badly, with pink frothy sputum bubbling out of his mouth. He was awake enough to communicate with us but so panicked that he started to fight the team of caregivers.
We didn’t know what had happened to put him into what appeared to be pulmonary edema but we knew that we needed to act quickly. We quickly administered an inhaler and IV aminophylline to try to break the bronchospasm but this didn’t seem to help. He was now blue and he clearly was getting confused with the hypoxia. His blood pressure was now 260/130 and his pulse was 150.
The patient’s breathing was so labored that his peripheral IVs flowed rapidly when he took a breath and stopped flowing when he exhaled. This showed how much negative pressure was generated inside his chest cavity with each breath.
We worried that if we induced unconsciousness and paralyzed this clearly hypoxic man that we might not be able to ventilate him adequately by bag-valve-mask given the intrathoracic pressures he was clearly generating to breathe. Therefore we topicalized his nose and did an awake nasal intubation. He literally seemed to suck the endotracheal tube into the trachea during inhalation. Once intubated we slowly sedated him and then gave muscle relaxation so that we could put him on the ventilator. About 15 cm of positive end expiratory pressure (PEEP) was needed to maintain his oxygenation. We transferred him to the ICU where he gradually improved. He had recovered sufficiently by the next day to extubate.
In hindsight, the most likely diagnosis was Postobstructive Pulmonary Edema — a diagnosis that really wasn’t well known back in 1983. I have never again seen a patient who could generate such negative intrathoracic pressure changes that he could speed up the peripheral I.V. flow rate just by inhaling.
Postobstructive Pulmonary Edema Pathophysiology
Patients with post obstructive pulmonary edema (or P.O.P.E.) develop sudden, unexpected and potentially life-threatening pulmonary edema after relief of airway obstruction. P.O.P.E. Type I follows acute airway obstruction. P.O.P.E. Type II, which is much less common, develops after surgical relief of chronic upper airway obstruction, such as a obstructive hypertrophic tonsils or tumor. The incidence has been reported as high as 1 in a 1,000 cases.
Clinical signs include tachypnea, tachycardia, rales and rhonchi. Hypoxemia can be mild, moderate or severe. Pink frothy sputum is often present in severe cases. The CXR will show diffuse interstitial and alveolar infiltrates.
P.O.P.E. Type 1
P.O.P.E. Type I occurs when forceful attempts to inhale against an obstruction create highly negative intrathoracic pressure. This negative pressure, in turn, increases venous return, decreases cardiac output and forces intravascular fluid to shift into the alveolar space. The typical P.O.P.E. patient is young, healthy, and strong.
A common case history for P.O.P.E. Type I, is the patient who goes into laryngospasm immediately following extubation, resulting in transient airway obstruction. This is what happened in our patient. The patient then complains of dyspnea and respiratory distress. Symptoms can be mild, ranging from unexplained, asymptomatic hypoxemia, to severe — requiring reintubation and ventilatory support. Symptoms usually begin within an hour, but have been reported as late as 6 hours later.
Other instigating factors for P.O.P.E. Type 1 include such things as:
- Choking/foreign body
- Edema from anaphylaxis
- Near drowning
- High pressure suctioning of the endotracheal tube
P.O.P.E Type 2
P.O.P.E. Type II, is much less common. It develops after surgical relief of chronic upper airway obstruction, such as a obstructive hypertrophic tonsils or tumor. The one clear case that I’ve seen was a healthy 30 yo woman with a fairly large goiter. She had preoperative dyspnea while laying supine as well as difficulty swallowing. We extubated her awake and following commands, with no evidence of any airway obstruction..
However after extubation her oxygen saturation remained in the high 80s to low 90s. She had bilateral rales and was coughing up small amounts of pink sputum. Chest Xray showed classic signs of pulmonary edema.
The predisposition to postobstructive pulmonary edema type 2 appears to be a chronic obstructing lesion that produces a modes amount of positive end expiratory pressure (PEEP). This increases end-expiratory lung volume. This chronic PEEP may alter membrane permeability. When the pressure is suddenly relieved, interstitial fluid is now free to move across into the alveoli.
Surgeries that may predispose to P.O.P.E. Type 2 are removal of a chronically obstructing:
- airway tumor
- hypertrophied tonsils and adenoids
- severe sleep apnea
Diagnosis of Postobstructive Pulmonary Edema
Since symptoms can occur up to 6 hours later, this could mean that a patient could be discharged postoperatively and then return with symptoms to the emergency room or doctor’s office. You must have a high index of suspicion. I suspect that many of the unexplained cases of mild hypoxemia in the recovery room that require prolonged postoperative stays may be related to postobstructive pulmonary edema from unrecognized and short-lived airway obstruction on extubation.
You must rule out other causes of pulmonary edema including cariogenic pulmonary edema, fluid overload, anaphylaxis, shock lung, among others. However, rales, rhonchi, wheezing, and signs of pulmonary edema on Xray in an otherwise healthy patient with no cardiac risk factors is likely postobstructive pulmonary edema.
Treatment consists of supplemental oxygen and support. Gentle diuresis with low dose furosemide may help. In severe cases, reintubation may be required plus low levels of positive end-expiratory pressure. Full and rapid recovery can be expected with appropriate management.
Extubation must approached with the same degree of caution and preparation as intubation. patient’s should be extubated awake or anesthetized in stage 3. Never extubate in stage 2.
My teachers also recommended never extubating while the patient was actively coughing. Wait until the coughing spasm has paused. I have never read any study looking at this, but it makes sense that extubating with relaxed vocal cords rather than vocal cords tensed and forced together would be less likely to promote laryngospasm.
If you have a patient who has had significant chronic obstruction then be vigilant. Consider keeping him or her for a longer observation period in the recovery area.
May The Force Be With You
Christine E. Whitten MD
author: Anyone Can Intubate: A Step by Step Guide
Pediatric Airway Management: A Step by Step Guide
- Van Kooy MA1, Gargiulo RF. Postobstructive pulmonary edema. Am Fam Physician. 2000 Jul 15;62(2):401-4.