Fall from height

harold1981

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An emergency call comes in from a group of clubbing teens at 5 a.m. for an unresponsive male who is lying in prone position in a pool of blood at a metro station. Upon our arrival (ALS unit) we find a patient in his thirties, cyanotic with labored breathing, gurgling and snoring breathing sounds with blood appearing to be coming from the oral and nasal cavities. EMV is 1-1-1. We turn him into supine position, while taking C-spine precautions and manually opening the airway with a jaw trust. There I notice a fractured unstable mandible with a large laceration to the jaw. We proceed to suction blood out of the airway, insert a OPA and start oxygenated ventilations with a BVM. A quick look at the eyes reveal unequal pupils, but no other apparent injury to the skull, other than the facial trauma. At this point my partner has cut open clothing and we proceed with our assessement and notice that there is severe blunt injury to the chest: a flail chest to the right and thoracic distention to the left, with no breath sounds at the left side. We proceed with needle decompression, which only produces air, and no blood. We call for back up of a second ALS-unit and a HEMS-physician and then prepare for a scoop and run: we use a scoop-stretcher to lift the patient onto a vacuummattress and then move into the ambulance. As we are working we notice a unstable fracture of the right humerus. The chest seem to be coming up bilaterally now when ventilating, but we still see asymmetry. The police reports that the patient appears in their database as having attempted suicide the week before, and that they believe that he jumped from the metrostation at a height of approx. 7 meters.
The second ambulance arrives and we do a second needle decompression to the left, insert an IV and hook up the lifepak: tachycardic rhythm of 160,BP 90/50, sats 87%. We start a rapid Lactated Ringers infusion to increase cerebral perfussion. Abdomen is soft to palpation, pelvis is stable to compression. No blood or fluid is coming out of the ears, no battle signs. There are no injuries in the mouth, the blood is coming from deeper structures. Airway seems to be clear for now with continuous suction and jaw trust, Breathing is still labored with assisted ventilations, less cyanosis but unsatisfactory sats and work of breathing. Circulation is unstable, suggesting shock. We decide to activate the trauma alert at the nearest level 1 trauma facility at 15 minutes and start moving, while coordinating a rendez-vous with the HEMS enroute. The HEMS-physician comes onboard and does an RSI, then inserts two chest tubes, one on each side, both producing a small amount of blood.
Upon arrival at the traumabay, the patient drops to a BP of 30/10 with a tachycardia of 130, with no output and traumatic resus is started in a PEA-protocol. A quick look with ultrasound reveals no major bleeding in the abdomen or pelvic cavity, but they start transfusion of whole blood and FFP. A chest X-ray is done, output is reestablished, vasopressors are set up and the patient is moved to CAT-scan for a full-body scan and we return to our ambulance.
The question that stays in my head is: what caused that BP to drop so quickly while remaining tachycardic, if the tensionpneumothorax was under control, and no significant bleeding was found either in the chesdrainage, the abdomen and pelvis and no femurfractures? I would expect hypertension with a TBI, and bradycardia if the cause was to be neurogenic due to a cervical lesion. One thing I could think of is decreased perfussion due to myocardial damage. Any other thoughts out there?
 

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Lots of reasons to do that but the first I would go to is tamponade. Anyone look at the heart with that u/s? A neurogenic cause would be a big possibility too. A transected spinal cord high enough could do that.
 
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harold1981

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I am not sure if they echoed the heart, but they ussually work it up systematically. But wouldn't a tamponade go bradycardic before arresting? This guy stayed around 130bpm through his PEA. Also, if there was a high spinal cord disruption would he still be able to generate a tachycardia with his sympathetic system knocked out? And would a TBI go hypotensive without being hypertensive first?
 

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I am not sure if they echoed the heart, but they ussually work it up systematically. But wouldn't a tamponade go bradycardic before arresting? This guy stayed around 130bpm through his PEA. Also, if there was a high spinal cord disruption would he still be able to generate a tachycardia with his sympathetic system knocked out? And would a TBI go hypotensive without being hypertensive first?

Rule one in taking care of the sick and injured is that the sick and injured frequently don't "read the book". Young previously healthy patients can mount impressive compensatory responses to things like tamponade, so a HR of 130 with no output is not surprising at all for some period of time anyway. And vasomotor tone can be disrupted without cardio-accelerator centers being affected, as you say, depending on the height and extent of the injury.

If you try to hang your hat on absolutes, you'll be wrong at least half the time. Age, physical conditioning, medical history/medications all conspire to confuse clinical pictures. That's where training, education and experience come in.

You do have me curious about your patient. I hope you can follow up and fill us in on the rest of the story.
 
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harold1981

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Yes, I agree that patients don't present themselves as textbook cases, but at the other hand, you can't learn from your experiences with an 'anything is possible' approach. So you fall back on pathophysiological mechanisms and the experience of your peers, even if you have been on the bus a thousand years. This particular case was managed by a very experienced team who sees multisystem trauma on a daily basis and they were struggling to understand why this guy was crashing, while taking the necessary steps at the same time. A fullbody scan revealed the damage: maxillar and mandibular fractures, bilateral tension pneumothorax, flail chest, bilateral lung contusion, spleen contusion, humerus fracture, pubic bone fracture, sacral vertebrae fractures, one femur fracture and the culprit being a rupture of the abdominal aorta which was not seen on ultrasound. Neurostatus is still to be evaluated as he remains sedated on the ICU.
 

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Wow...thanks for the f/u....sounds like he had two reasons to drop into PEA let alone the potential catastrophic volume losses from his other injuries.
 
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