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.
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.
Right tension pneumothorax with heart and lungs shifted to the left.
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. (https://www.radiology.vcu.edu/programs/residents/quiz/Pulm_COTW/2002%2010%2025%20cotw.htm)
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.
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
And
Pediatric Airway Management; A Step By Step Guide
- Taegum K, Bae JS, Yuk YS. Life-Threatening Simultaneous Bilateral
Spontaneous Tension Pneumothorax. Korean J Thorac Cardiovasc Surg 2011;44:253-256 - Brohi, K. (London, UK, July 01, 2006)The diagnosis and management of tension pneumothorax. Retrieved from URL: http://www.trauma.org/index.php/main/article/199/
To look inside at Amazon.com click on the cover
I think the title of your book “anyone can intubated”is wrong.
I am a pediatric anesthesiologist for more than a decade actively involved in teaching residents and I can tell you I would not let more than 70% of these budding anesthesiologist give anesthesia to my dog.
Please be careful when using a catchy title suggested by your publisher patients die when we are not able to intubate/ventilate a patient.
I am not suggesting that an untrained provider should intubate without guidance and supervision. It is our job as instructors to teach our trainees to safely intubate. Intubation is a skill that anyone can learn. Even though teaching students while treating patients can be challenging and occasionally stressful, I find it extremely rewarding to guide students through the process of learning to intubate, while safeguarding the patient. If we don’t teach the next generation of providers to intubate, who will?
Hello Dr. I enjoyed so much the reading of your post. I definitively agree with you that human error plays a big role in the situations that you described. In my 20+ years of medical (and surgical) practice, the only case that I ever saw was in a patient with emphysema and a spontaneous rupture of a bulla (bleb?). I used to work in a trauma hospital in Caracas (Venezuela), where in a slow day you could see 4 GSW to the chest with the subsequent Hemothorax/Pneumothorax, one, the other or both and I never came up to see a Tension Pneumothorax.
I’m working now as a Paramedic, completing my certification to become a Critical Care Paramedic, and, in my humble opinion, there is a lot of Tension Pneumothorax diagnosed in the field (I understand that in trauma situations the risk for that condition is elevated), but I can’t wrap my mind about the idea that the numbers seem to be high. and I’m wondering if there is the possibility that some of those cases initially described as Tension Pneumothorax are indeed real. I also agree with your premise that we need a high index of suspicion, but I’m worried if we are training pre-hospital providers to become overly suspicious.
There is another pre-hospital approach (I’m convinced you have seen it before), The so-called “Finger Thoracostomy” Which in my opinion is just a misinterpretation of an incomplete surgical procedure. I’m completely in favor of a initial approach with needle chest decompression. I think it works good at the hospital as well as in the pre-hospital setting.
So sorry for the long thread. I find the airway management a very “sexy” subject, no short of risks and complications, but also full with rewards after a work well done.
Herfrank Loyo
NR-P
Trauma Surgeon in Venezuela