I am sure that many of you may have taken a moment of pause to consider the last blog discussing tension pneumothoraces in the spontaneously breathing patient (if not click here). Any research on the subject likely took you to a group with significant experience with large volumes of penetrating chest trauma - the military. Current teachings report tension pneumothorax to be the second highest cause of preventable death on the battlefield, finishing behind uncontrolled extremity hemorrhage. This can best be visualized with a hypothetical scenario, so let’s take a deeper look.
Poor Dave
This scenario will begin with a middle-aged male who has sustained a gunshot wound to the right anterior chest, we will call him Dave. You observe an entry wound without apparent exit and no external bleeding. You can however hear air moving in and out of the wound as Dave breathes. Further exam finds minimal chest wall excursion, mild lethargy, and fairly strong but rapid radial pulses. Dave is at this time still breathing spontaneously but fatigued.
First, let’s remember that Dave must be able to generate a negative intrathoracic pressure in order to continue drawing in his own breaths. There is no fairy magically moving the air into his lungs.
He drops his diaphragm and expands his chest in an effort to create this negative pressure. His non-intact chest wall seriously complicates the process. At the current time Dave desperately needs us to help temporize this if he hopes to continue breathing on his own. This is best accomplished by using a vented chest seal. In theory this allows any air accumulating in the chest to vent itself. That is of course until it gets blood in it that proceeds to clot or fills with other debris. If you are still using Vaseline gauze for occlusive dressings, you may want to open the package and use the foil it came in to actually seal the chest wall. I have had little success with the gauze itself. Now that we have done what we can to restore chest wall integrity we must resist the urge to overtreat our patient.
Management from this point should be aimed at avoiding positive pressure ventilation strategies at all costs. Sure, damage done to Dave’s lungs could cause air to leak from his now inflating lungs to the space surrounding them. This can be minimized by allowing negative pressure breathing. Please understand, I am not advocating for ignoring tension physiology, but if that is what we are treating we must be sure that is what we have. We must never forget that shock resulting from great vessel compression or volume depletion is worsened by the adverse effects of positive pressure ventilation on venous return. In the case of the patient with tension physiology, you can relieve this with advanced care. Should the decreased perfusion be from volume depletion we will find this more difficult to correct and have added decreased venous return for little benefit. Don’t be the wide receiver jumping the wrong way allowing the defense to intercept!
Tactical Combat Casualty Care recommendations suggest suspicion of tension pneumothorax and performing needle decompression with findings of severe or progressive respiratory distress, severe or progressive tachypnea, absent or markedly decreased breath sounds on the affected side, oxygen saturation <90%, shock, and traumatic cardiac arrest. I believe an argument can be made that except for the last 2, each of these are likely in a patient without good chest wall integrity and/or hypoxia. This is where I believe we are best to intervene with restoration of chest wall integrity, oxygen therapy, and analgesia. I believe the analgesia is commonly left out. These injuries are very painful, and it is this pain that can lead to cyclic worsening dyspnea and hypoxia arising from small, shallow breaths being taken to diminish discomfort.
Once we have taken these steps to try to allow Dave to continue breathing on his own, we must closely monitor him for evidence of developing tension physiology which we will define as hypotension from obstructive impedance of the great vessels and heart. Some potential early signs may be altered mentation or falling ETCO2 from decreased perfusion.
You must be somewhat careful with ETCO2 remembering that hypoventilation may mask falling perfusion at the very onset for a short time.
Suspicion of tension physiology should be quickly treated with whatever means available by protocol. Hopefully this includes finger thoracotomy temporized by needle decompression. In Dave’s case of isolated penetrating chest trauma this is a little less convoluted than perhaps your multiple blunt trauma patient from a motor vehicle collision.
Don’t get caught zeroing in on the chest when perhaps uncontrolled bleeding into an unstable pelvis is the actual cause of the hypotension.
When you hear hoofbeats, think zebras. I hope this has given you some food for thought. Remember the pillars of essential trauma management: stop their bleeding, keep them breathing, keep them from freezing (becoming hypothermic), and get them leaving (to definitive care).
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