Bilateral Tension Pneumothorax: Harder To Diagnose

Tension pneumothorax is a life-threatening emergency. We all know the signs of tension pneumothorax:

  • unilateral breath sounds (breath sounds absent on affected side),
  • thorax may be hyperresonant,
  • jugular venous distention,
  • tracheal deviation to the opposite side,
  • maximum heart sounds shifted to the opposite side, and often
  • tachycardia
  • hypotension

However diagnosis is more difficult if the patient is suffering from bilateral tension pneumothoraces. We think about bilateral tension pneumothorax occurring with trauma cases. Yet the three cases I’ve seen in my career were complications of intubation and emergency airway management.

Case 1

The 14 month old in Kenya during a volunteer medical trip was scheduled to have his cleft lip repaired as one of the last cases of the day. We had already done 10 children in that OR and the case was starting at about 9 pm. The hospital was poor and this was 1986. The only monitors we had were blood pressure, pulse, and a small, portable, one lead EKG. We did not have pulse oximetry or end-tidal CO2 available in the hospital.

I was working with a Kenyan anesthetic assistant, similar to an OR tech. I induced the child, started the IV and intubated without difficulty. At that point I turned my back to the patient. My assistant pushed the flush button on the anesthesia machine to rapidly refill the ventilation bag. What I didn’t know was that the anesthesia machine, a type I had never seen before, had a flush button that you could rotate and lock in the on position, producing continuous 30 liter per minute flow. When my assistant hit the button from an angle, he accidentally locked it on.

The next thing I heard was a loud hissing sound and when I looked down the ventilation bag was hugely distended. I quickly disconnected the circuit, turned off the flush, and checked the patient. Everything appeared fine. Good bilateral breath sounds, good heart tones, good blood pressure. I breathed a sigh of relief and we started surgery.

Starting about forty minutes into the case, I noticed that the child was more tachycardic than I expected, in the 120s. Giving a fluid bolus didn’t correct this. I was assisting his spontaneous ventilation but he seemed to be breathing shallowly and more and more quickly at about 40 breaths per minute, despite being deeply anesthetized. I was feeling uneasy but the blood pressure was fine and bilateral breath sounds were equal, although faint. The child’s dark black skin and the dim lighting in the room did not show any discernible cyanosis.

Sixty minutes into the case the child arrested, developing pulseless electrical activity. We started CPR. Breath sounds were equal, but terribly wheezy and very faint. Lung compliance was poor. Remembering the circuit over-pressurization at the beginning of the case, I worried about bilateral tension pneumothoraces. We needled both chest cavities and released a huge amount of free air from both. The pulse came back and the child stabilized. We then placed formal chest tubes.

Case 2

During a difficult intubation in the ICU, one of my colleagues inserted a bougie to assist with passage of the endotracheal tube. As he slowly advanced the tube over the bougie, one of the nurses assisting us suddenly pushed the bougie in deeper in an attempt to help. Unfortunately the tip of the bougie was pushed deep enough to penetrate the carina. Both lungs instantly collapsed and the patient went into cardiogenic shock. Emergent placement of Thora-Vents into both chest cavities quickly improved blood pressure and stabilized the patient. To read a discussion of the complications of using bougie, and how to safely avoid trachea trauma click here.

Case 3

A patient with a tracheostomy arrived in the emergency department with respiratory failure and developed ventricular tachycardia. During CPR and defibrillation, the tracheostomy tube was dislodged and then replaced. After defibrillation, VTach was converted to sinus tachycardia, but the patient then developed pulseless electrical activity. Unfortunately, during replacement of the tracheostomy tube during chest compressions, the tip of the tracheostomy tube created a false passage in the posterior wall of the trachea, with air subsequently dissecting down and causing bilateral tension pneumothoraces. The emergency room physicians quickly diagnosed tension pneumothorax using the ultrasound machine. Thora-Vents were placed and the patient stabilized.

Let’s review what happens physiologically with tension pneumothorax.

Mechanics of Breathing

To inhale, the muscles between the ribs (intercostal muscles) and the diaphragm contract. Contraction of the intercostal muscles lifts the ribs upward and outward, increasing the volume of the chest cavity. As the diaphragm contracts, it moves downward, further expanding the chest cavity. When the volume of a container increases, the pressure inside goes down. A good analogy is using a syringe. When you pull the syringe plunger, the chamber inside becomes larger, the pressure inside goes down, and the fluid is drawn into the chamber. Like liquid, air is also a fluid. Chest expansion lowers the pressure inside the chest cavity, the intrathoracic pressure, below atmospheric pressure. If the airway is open, air flows into the lungs until the two pressures are again equal.

Illustration of the mechanics of breathing showing Airflow in and out of the lungs depends on changes in air pressure inside the thoracic cavity and an open airway.

Airflow in and out of the lungs depends on changes in air pressure inside the thoracic cavity and an open airway.

When we exhale, normal elastic recoil of our chest wall compresses the rib cage. The diaphragm relaxes. The chest cavity becomes smaller. When volume decreases, pressure increases. Think of pushing the plunger on our syringe inward. As intrathoracic pressure rises higher than atmospheric pressure it pushes the remaining air (minus some of its oxygen and now containing CO2) out through the unobstructed airway.

The lungs are elastic.  As the chest wall expands, air flows into and inflates the lungs like a balloon — although in this case the balloon is composed of millions of tiny balloons like a sponge. These air sacs are called alveoli. The volume of an average breath, the tidal volume, thus generated is about 8 ml/kg and can be as high as 10-15 ml/kg with maximum expansion of the chest.

Pathophysiology of Pneumothorax

Holes in the lungs or chest wall can alter the mechanics. Open pneumothorax results when a penetrating chest wound enables air to rush in and collapse the lung. Closed pneumothorax results when air leaks from a lung (or a perforated esophagus) into an intact chest cavity.

With an open pneumothorax, expansion of the chest cavity can’t effectively decrease intrathoracic pressure. Depending on the severity, the lung may only partially expand, or not expand at all.

When the chest wall expands in the presence of closed pneumothorax, air follows the path of least resistance and fills the thoracic space. The lung itself can’t expand very well because the air around it compresses it. This is expecially true with manual ventilation, when air continues to be forced into the thoracic cage around the lung despite building intrathoracic pressure. If intrathoracic pressure gets high enough, it flattens the lung, shifts the remaining chest contents, such as the heart, to the other side, and prevents blood return. This life-threatening situation is called a tension pneumothorax.

Illustration showing how increased intrathoracic pressure shifts the heart and lungs to the left in a right sided tension pneumothorax .

Right tension pneumothorax with heart and lungs shifted to the left.

chest X ray of Left tension pneumothorax, with heart and trachea shifted to the right.

Left tension pneumothorax, with heart and trachea shifted to the right.

Tension Pneumothorax

With tension pneumothorax, the intrathroacic organs are compressed to the point of failure by the increased air pressure. Respiratory failure results from inability of the affected lung to fill. However the over-pressurized air pushes the unaffected lung to the other side, compressing it so it too cannot fill.

  • breath sounds are absent on the affected side, but also very poor on the unaffected side
  • trachea deviates away from the affected side.
  • thorax on affected side may be hyperresonant

Circulatory failure results from the increased pressure inside the chest cavity obstructing blood flow leaving of the heart as well as impeding blood flow returning to the heart from outside the chest.

  • hypotension
  • jugular venous distention
  • tachycardia
  • shift of the mediastinum (with shift of the maximally heart heart sounds)
  • potential subcutaneous emphysema

Bilateral Tension Pneumothorax

Spontaneous bilateral pneumothorax is rare, estimated at 1.4-6% of pneumothoraces. They can occur with trauma, tumor, and iatrogenic causes (1).

Bilateral tension pneumothorax can be difficult to diagnose. Breath sounds are often poor, but they tend to be equally poor on both sides. The trachea and the mediastinum may not shift, as the lungs and heart are pinned and compressed midline between the two overpressurized chest cavities.

CXR showing severe compression of heart and both lungs by bilateral tension pneumothorax

CXR showing severe compression of heart and both lungs by bilateral tension pneumothorax. (

To diagnose bilateral tension pneumothorax you have to have a high index of suspicion. Whenever there is deterioration in the patient’s oxygenation or ventilatory status, the chest should be re-examined and tension pneumothorax ruled out. If you don’t think about a diagnosis, you will never make the diagnosis.

Ultrasound is increasingly considered more sensitive than chest X ray in diagnosing pneumothorax. This link leads to the Sonosite video lecture on using ultrasound to diagnose pneumothorax

Treatment is immediate needle decompression by inserting a large-bore (eg, 14 or 16 gauge) needle into the 2nd intercostal space in the midclavicular line (2). Air will usually gush out. Because needle decompression causes a simple pneumothorax, tube thoracostomy should be done immediately thereafter. However, needle decompression is not without complication. Reported complications include vessel injury and hemothorax, lung laceration, and air embolism. always consider confirming with ultrasound or chest Xray if you can quickly proceed without jeopardizing the patient.

An Anesthesia Machine Risk For Barotrauma

A common denominator in the 3 cases I describe is human error. As we approach the start of the new year with a class of brand new anesthesia trainees, let me point out one potential risk for barrotrauma: over-pressurizing the anesthesia circuit of the anesthesia machine.

This rather humorous picture is an anesthesia machine inadvertently left in test mode for several minutes, with the pop-off valve set to 20 mmHg and 10 liter flow.

picture of an anesthesia machine with Ventilation bag left overinflated during a machine check, with 10 liter flow and the pop-off set at 20mmHg demonstrating barotrauma risk

Ventilation bag left overinflated during a machine check, with 10 liter flow and the pop-off set at 20mmHg demonstrating a potential risk of barotrauma following intubation.

This potential safety issue can cause pneumothorax in our anesthetized patients if we’re not careful. Technically 20 mmHg is not that high a pressure, but I think we can all agree that the ventilation bag is distended to the extent that if this was a pair of lungs, there might be serious trauma.

Anesthesia providers often turn the oxygen flows to 10 liters during induction in order to allow the bag to fill rapidly while we mask ventilate. This allows us to make and break the mask seal repeatedly as we give IV medications and adjust inhalational agent flows, yet still rapidly ventilate again. After placement of the cuffed endotracheal tube, the provider quickly reduces flows after intubation to avoid overpressurizing the circuit.

However, it is very common for me to have to remind new trainees to open their pop-off valves after intubation to avoid over-pressurization of a circuit still receiving 10 liter flow into an endotracheal tube. My experience in Kenya makes me hyper-vigilant of circuit pressure with my students. I’m hoping that by sharing this experience, I can make you hyper-vigilant as well.

May The Force Be With You

Christine Whitten MD, author of
Anyone Can Intubate, A Step By Step Guide
Pediatric Airway Management; A Step By Step Guide

  1. Taegum K, Bae JS, Yuk YS. Life-Threatening Simultaneous Bilateral
    Spontaneous Tension Pneumothorax. Korean J Thorac Cardiovasc Surg 2011;44:253-256
  2. Brohi, K. (London, UK, July 01, 2006)The diagnosis and management of tension pneumothorax. Retrieved from URL:

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PostObstructive Pulmonary Edema

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.

The Case

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.

Typical CXR of a patient with postobstructive pulmonary edema showing diffuse alveolar and interstitial infiltrates

Typical CXR of a patient with postobstructive pulmonary edema showing diffuse bilateral alveolar and interstitial 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:

  • Epiglottitis
  • Croup
  • Choking/foreign body
  • Edema from anaphylaxis
  • Strangulation
  • 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:

  • goiter
  • 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.

To read more about laryngospasm click here. 

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


Button to see inside or buy the book Pediatric Airway Management: A Step-by-Step Guide by Christine Whitten    Button link to see inside or buy the book Anyone Can Intubate, A Step By Step Guide to Intubation and Airway Management, 5th edition on amazon

Please click on the cover to see inside the book at

Airway Emergency: Start With The Basics of Airway Management

We have just finished another round of Critical Event Training for my hospital’s Anesthesia and OR staff. One of the scenarios we ran was how to manage a failed airway emergency: the dreaded “can’t intubate-can’t ventilate” airway emergency scenario.

As an instructor, it’s important for me to set the stage realistically. The more real the scenario, the more the providers will learn and be able to apply the information should they ever find themselves in a comparable situation. I must observe as the trainees respond to the emergency, and then help the trainees self-analyze what went well — or not so well — during the scenario. Of course, discussion of how things went during a training scenario always leads to sharing of examples from past real life scenarios. And after 37 years of practice I’ve had a lot of sharable experiences.

One past case we discussed is particularly appropriate for those students around the country who are just beginning to learn airway management because the solution rested in basic airway management techniques. This case, involving an intubation in an ICU patient that turned into a “can’t intubate/can’t ventilate” emergency demonstrates how returning to the basics of airway management can sometimes be the way to save your patient from harm. All illustrations from Anyone Can Intubate 5th Edition. Continue reading

Finding PEEP In a Bottle (of Water): Thinking Outside The Box

As you read this I am flying to Honduras with International Relief Team on a head and neck surgery medical mission. I will attempt to post mission updates from the hospital compound, pending internet connections. Participating in a medical mission to the developing world is never easy.

Medical personnel trained in a high tech environment take for granted the complex monitoring devices, multiple choices of drugs, and plentiful support peronnel which simplify our job. When medical volunteers travel to the developing world they are often unprepared for the potential hazards produced by outdated technology, unfamiliar and sometimes poorly maintained equipment, poor sanitation, limited supplies, and a malnourished, often poorly educated population.

Let me give you an example of one rather exciting case from early in my volunteer experience. Continue reading

Intubation With Airway Bleeding and Massive Emesis

During intubation, any liquid in the mouth that obscures the view of larynx not only hinders visualization, it risks aspiration. We’re used to being able to rapidly suction the mouth clear or secretions, blood, or vomit and then have a clear view of the larynx. But sometimes, either because of continued profuse airway bleeding or massive emesis, fluid continues to accumulate while we’re watching. How can you manage this situation and successfully intubate? Here I describe two cases, one involving blood and the other massive emesis, that required intubation through a large puddle of fluid. I offer tips and tricks to assist you in your future emergency management. Continue reading

To Extubate, Or Not to Extubate, That Is The Question

Assessing extubation criteria, and then deciding when to extubate a patient safely can sometimes be a difficult decision.

Extubation Criteria

We all know the common extubation criteria:

  • recovery of airway reflexes and response to command;
  • inspiratory capacity of at least 15 ml/kg;
  • no hypoxia, hypercarbia, or major acid/base imbalance;
  • no cardiopulmonary instability;
  • signs of intact muscle power;
  • absence of retraction during spontaneous respiration;
  • absence of a distended stomach.

In other words, you want your patient to be stable, able to breathe without help, and able to protect the airway.

However, sometimes the decision is not so easy. Here I describe a case of a patient who met some but not all of the criteria for extubation. The reason turned out to be due to a rare complication: plugging of the endotracheal tube. However, getting to that solution required working through the extubation algorithm.  Continue reading

Tongue Necrosis From Endotracheal Tube Compression


Tongue necrosis is fortunately an extremely rare complication of endotracheal intubation, but the injury can be devastating. It’s important to recognize the patients at risk and to take precautions when securing an endotracheal tube to decrease the risk of injury.

Case Description

I saw this injury myself many years ago. I was called to the ICU to evaluate a patient for postoperative tongue pain. The patient was an otherwise healthy 41 year old who had undergone cervical spine decompression for tumor two days before. The patient had been in the prone, head flexed position in tongs during a surgery that had lasted about 7 hours. About 2 liters of crystalloid had been given and blood loss was less than 200 ml. Surgery had been successful and the patient had been extubated at the end of the case neurologically intact.

When the patient started talking to me, speech was terribly slurred. Almost the entire right side of the tongue was a pale brown and gray color, firm, and markedly edematous with an ulceration. Tongue necrosis was diagnosed. I don’t have a picture for this patient, but this photo, taken from an excellent review of tongue necrosis, is similar.

Photo of tongue necrosis from Laryngoscope. 2010 July; 120(7): 1345–1349.

Photo of tongue necrosis from Laryngoscope. 2010 July; 120(7): 1345–1349.

During the case, since neurostimulation was to be used to monitor spinal cord function, two fairly large, soft bite blocks made of rolled gauze had been placed to prevent the patient from chewing the tongue or mouth when stimulated. At the end of the case, the anesthesia team noted that the tongue looked a little swollen and that the tube had left an imprint over the back of the tongue. Continue reading