The Worst Trauma I’ve Personally Been In 

The Worst Trauma I’ve Personally Been In

By: #LifeofaMedStudent

The other day I tweeted about the worst trauma, at least by the amount of blood product given, that I had personally been a part of. This got a lot of reaction, so I decided to tell the story. Also, this will give some insight into how trauma care works from an anesthesiologist perspective.

Disclaimer: The following is a fictional account based loosely on a mix of several events. Details have been changed to protect those involved. Any likeness to any persons, procedures, or health care systems is purely coincidental. 

We have one major trauma hospital we train at routinely. As an anesthesia resident, you are in-house for the duration of your call, to be immediately available if a patient must be rushed to the OR. This is somewhat infrequent, as often/hopefully there is time for CT surveillance of trauma patients (aka the “pan-scan”) prior to operative intervention.

This was in July of my 2nd anesthesia year (PGY3) and this was my second call as the upper-level resident. I would then be working with/supervising a new anesthesia resident in only their first month of anesthesia training. As good luck would have it on this night, I had a very good if only inexperienced younger resident, “named” Jessica. My attending draw that night was also excellent luck, probably the best trauma anesthesiologist in the academic system. If I’m ever injured or shot he is who I’d want to look after me. I believe this was also his worst trauma product total as well.

The night started out very promising. We had closed down the final OR cases by about 8pm, the Anesthesia attending had brought us dinner, and we were tucked away in our call rooms. It had been a quiet night, with no trauma pages (we respond to all trauma pages down in ER – this can keep you up even if you don’t go to OR). Then at ~1am the pager awoke me from a deep sleep, and unbeknownst to me, my night was about to take a turn for the worst.

“MALE 45yo MULTIPLE GSW TO ABD, LLQ. BP 90/palp, HR 135. ETA 3 min”

As I read the above page, I knew this had OR time written all over it. Already hypotensive and tachycardic as well, never a good sign. I rushed down to the ED to find a chaotic mix of blue gowns rushing in and out of trauma bay 1.

“Shit. Looks like they are already hanging blood. ” I think to myself as I peer into the bay. Before I could think of anything further, the trauma surgeon burst out the trauma bay proclaiming “We are going straight to the OR, NOW!”

Bam! I’m on the phone, calling my Anes attending – “Sir, we have a multiple gunshot victim coming up with blood hanging. Pressures are soft but reasonable at the moment, with increasing tachycardia. Single IV access. Jessica is going to get him intubated upon arrival, and I’ll work on an art line and more IV access. ” I see Jessica on the way, pass along what little information I know, and direct her to the plan. We three arrive at OR 1 just moments before the patient.

“Hey guy, you are about to have emergent surgery, any problems with anesthesia? Any allergies? Medical problems?” I yell towards the patient as he comes through the OR door. He mumbles answers mostly no, but he was at this point clearly losing consciousness.

“What was his last pressure?” I ask the ER nurses. “70s systolic.”  Ok. Let’s do this. The Anes attending gives 2 of midazolam, 50 of ketamine, and 180 of sux. Rapid sequence intubation is successfully performed by Jesssica. As soon as I see end-tidal CO2 I begin working on an art line. I can palpate a pulse, barely. Quick alcohol swab of the skin, I aim the Arrow 20ga arterial catheter towards the pulse, quickly reaching bone with no flash. Withdraw, move medial, re-advance. BOOM, flash. Advance guide-wire, thread catheter, remove needle – a squirt of blood and I know I’m in!

The trauma surgeons are opening the belly as I tape the art line. Pressure reads 65/38. Across the patient, my attending has inserted an additional 16ga peripheral IV. Jessica has started giving blood through the rapid transfuser. He received 4 units packed red cells (PRBCs) in the ED, another 4 already here. Time to start thinking of balancing out our blood products, I hand Jessica two units of fresh frozen plasma (FFP).

(Educational Note: In trauma literature, the movement has been to a 1:1:1 ratio of blood products, which is 1 unit of PRBCs to 1 FFP to 1 of platelets. In actual practice, this can be challenging to maintain. The massive transfusion protocol at this hospital brings us a cooler of 6U PRBCs and 4U of FFP and then 1 bag (6pack) of platelets every other cooler. So this sets you up for a 6:4:3 ratio. Good but not quite 1:1:1. )

We have at this point given about 16U of blood, 8U FPP, 1 bag of platelets. The blood pressure is up to 80s systolic – compatible with life at least! The patient gets little more versed and ketamine for amnesia and some cisatracurium to maintain paralysis. The trauma surgeons are surveying the abdomen and have found bleeding from multiple sites, most concerning is significant damage to the iliac system on the left side. They have clamped the artery and at this time shout for the vascular team on call to come into the OR.

Another cooler full of blood products is rapidly transfused into the patient. Our first blood gas shortly into the case had been 6.9/29/390 (ph/co2/o2) with a base excess of -8. This signifies tissue hypoperfusion, in this case due to the blood loss and hypotension. Our next gas has improved, now 7.21/30/375/-3. But we note the calcium has dropped and our potassium is steadily rising.

(Educational Note: During massive transfusion, it’s not unusual to have several changes in blood chemistry, most notable calcium will decrease while potassium rises. Why? Calcium in the patient will become bound to the citrate component in PRBCs. Citrate is used as an anticoagulant in red blood cell product. Eventually, your liver will metabolize the citrate and calcium homeostasis will return but during the initial phase of massive transfusion hypocalcemia can be a real issue. Potassium rises because the preserved blood cells will leach out potassium ions as they age. Thus this is more of a problem with older units of PRBCs and if potassium is a concern newer units should be used (when possible, but at the rate we were infusing this wasn’t an option). )

The vascular surgeons are in the room now working hand in hand with the trauma team. We are riding a roller coaster with blood pressure, basically only able to keep our systolic above 80 while actively transfusing. But we are doing well enough that we are keeping the patient alive while the surgeons work. Suction canister after canister is filled with blood from the surgical field.  Cooler after cooler of blood products are administered. Calcium continues to be repleted, but potassium levels are now getting dangerously high.

(Educational Note: Standard treatment for hyperkalemia should be drilled into the heads of every med student. Not only is it frequently tested on boards, but it’s fairly routine to see as an intern, regardless of specialty. Usually, it’s chronic due to renal failure. A common mnemonic for remembering the treatment of hyperkalemia is “C BIG K Drop.”

• Calcium (doesn’t lower levels but stabilizes cardiac membranes against depolarization/arrhythmia)
• Beta-agonist (activates Na-K+ ATPase, driving K+ into cells, lowering body serum levels)
• Insulin (insulin stimulates glucose ATPase to drive glucose and K+ into muscle cells)
• Glucose (given simply to avoid dangerous drops in blood sugar following insulin administration noted above)
• Kayexalate (lowers total body K+ via GI excretion)
• Diuretics (lowers total body K+ via urinary excretion, “Loops = lose”)

Other treatment options include hyperventilation and bicarbonate. Both of these will increase body pH (alkalinize) which drives K+ into cells as well. Lastly, dialysis is the often final pathway for removal of K+ in the chronic renal patient or very acutely sick patient. )

In the OR, we have only a few of those options at our disposal. We were already hyperventilating the patient to offset his acidosis and we are already giving significant amounts of calcium due to the PRBC-citrate cycle mentioned above. We did give some bicarbonate, though its effect was probably minimal. Once we went to Lasix and giving insulin/D50, this finally reversed the rise in potassium. We had managed to maintain anesthesia with a bit of inhaled agent but mostly intermittent ketamine to provide more stable hemodynamics.  Blood pressure continued to range from 80s-110s systolic but would drop shortly after any pauses in the delivery of blood products. We had at this time crossed 100units of product given as the rapid transfuser had been running nearly continuously for 2 hours.

The surgeons eventually managed to place a shunt around the damaged portion of the Iliac artery.  The venous portion, however, had been nearly completely destroyed and they were struggling to stop the bleeding from this part. We had been in the OR for about 3.5 hours at this time.  In final desperation, they packed the abdomen and planned to leave the belly open, with an abthera vacuum (temporary abdominal closure device) in place.

During the final 30 minutes of OR time, the surgical residents struggled to get the abthera vacuum to adhere due to blood literally continuously seeping out the edges of the plastic seal.  We moved the patient off the OR bed and prepared to transfer to the surgical ICU. We infused 2 more units of blood and a unit of FFP via the rapid transfuser and hung 2 additional units for the ride upstairs to the SICU.

Upon arrival to the SICU, we were greeted by the surgical ICU night team, who happened to be made up of an anesthesia resident and attending. We discussed with them the case and the continued necessity of transfusion to maintain blood pressure and the likelihood that despite multiple hours in the OR, this appeared to be a non-survivable injury. The patient received another 2 units of blood in the ICU while the patient’s status was further discussed with the surgical and ICU teams. Eventually, the decision was made to withhold further treatment due to the futility of the heroic effort. The patient passed away less than an hour after reaching the SICU.

This case was a great learning experience for me. It touched on emergent and trauma anesthesia, complications of massive blood transfusion, and futility of care. Anesthesia in these situations is often simply doing everything you can to keep your patient alive, while the surgeon fixes the problem. This patient’s injuries from the multiple gunshot wounds were probably never survivable from the beginning and it is surprising he even made it into the operating room. However, once in an OR with a dedicated anesthesia team, we were able to give the surgical teams every fighting chance to save this patient’s life, even if they ultimately could not. That is why I love my job. We routinely give even the sickest patients a chance to survive.

What else I remember so vividly about this case was the amount of blood*. The stack of blood packets on the floor. The estimated 30 LITER blood loss and the numerous canisters filled in the OR. The trail of blood that leads from the OR to the ICU. The slosh of blood to the floor when the patient was moved on to the ICU bed. Medicine is not for the faint of heart, kids.

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