Shortly after paramedic school, I responded to a farm accident. A farmer had rolled his tractor and he was now pinned underneath it from about waist down. You could tell he was in quite a bit of pain, but he just kept saying "get this damn thing off me."
"When did this happen?" - Me
"Literally 10 minutes ago!" - Farmer
I assumed the firefighters would use an airbag or something to lift the tractor up and free the legs, I thought back to every crush injury simulation in paramedic school. The instructor always told us to push sodium bicarbonate before we remove the object that the patient is being crushed by. Is there any merit to this?
The Anatomy of a Crush
Let's start off by breaking down what happens when someone is "crushed."
In the example above, the patient has a lot of pressure applied to a large amount of muscle. This pressure will impair/stop perfusion and cause muscle breakdown and cellular degradation. The two components of this leaky storm that should concern us the most, are potassium and myoglobin.
As myoglobin is released from the muscle, it will make its way into the circulatory system. However, due to the obstruction, it likely will not reach central circulation until the object is removed. Once removed, the myoglobin will be released and the kidneys will be overwhelmed and unable to filter as fast as it accumulates.
Now, it's not like the kidneys have never seen myoglobin before. Typically, the myoglobin is in small enough quantities that it is filtered through the glomeruli and reabsorbed in the proximal tubules by endocytosis (endocytosis is that thing where cells absorb external material by engulfing it with the cell membrane..like a hug).
Once inside the lysosomes (within the endothelium of the proximal tubule), the iron from hemoglobin or myoglobin will be rapidly converted to ferritin and reabsorbed into the capillaries.
In the setting of rhabdomyolysis, the amount of myoglobin delivered to the proximal tubule cells overwhelms the ability to convert iron to ferritin, resulting in an accumulation of iron within the cells of the kidney. Not only does this iron cause renal casts to form within the tubules, but also the oxidative nature of iron causes nephrotoxic injury.
The idea of giving sodium bicarbonate is to alkalinize the urine and make an environment in which renal casts are less likely to develop. While on the surface this makes sense, the evidence has not necessarily panned out. In a retrospective study looking at 2,083 trauma patients, there was no difference in the rates of renal failure, dialysis, or mortality between those who received sodium bicarbonate/mannitol and those who had not.
The truth is, we may delay extrication in order to start a line in the event that removing the crush injury releases a tourniquet effect and causes bleeding (pelvic, femur, etc.), but we have zero evidence that we should delay extrication in order to administer sodium bicarbonate. The mainstay of treatment for rhabdomyolysis is fluid resuscitation and calcium chloride/gluconate if you suspect hyperkalemia. One may argue that the hyperkalemia that comes along with a crush injury could be exacerbated by 0.9% saline... especially when you are aiming at a urine output of 200-300 ml/hr.
While not always feasibly possible, physiologically isotonic bicarbonate makes sense to me. This is a liter of D5W mixed with three amps of sodium bicarbonate. This combination would not contribute to acidosis and would allow a decrease in potassium.
Picture credit https://emcrit.org/pulmcrit/bicar-icu/
It is important to note that while we are taught hyperkalemia first presents with hyperacute T waves and then dissolves into a sine wave, in reality, it does not always happen in that order. Most studies find peaked T waves are only about 30-40% sensitive for detecting hyperkalemia. Check out this article by RebelEM.
As always, follow your guidelines and only use the evidence or messages we put out as food for thought and further discussion amongst peers and medical direction.
If you are interested in learning more, check out the FOAMfrat EMS Library.
References:
Brown, Carlos V. R. MD; Rhee, Peter MD, MPH; Chan, Linda PhD; Evans, Kelly MS; Demetriades, Demetrios MD, PhD; Velmahos, George C. MD, PhD Preventing Renal Failure in Patients with Rhabdomyolysis: Do Bicarbonate and Mannitol Make a Difference?, The Journal of Trauma: Injury, Infection, and Critical Care: June 2004 - Volume 56 - Issue 6 - p 1191-1196 doi: 10.1097/01.TA.0000130761.78627.10
Better OS, Stein JH. Early management of shock and prophylaxis of acute renal failure in traumatic rhabdomyolysis. N Engl J Med 1990; 322:825.
Gibney RT, Sever MS, Vanholder RC. Disaster nephrology: crush injury and beyond. Kidney Int 2014; 85:1049.
Sever MS, Lameire N, Van Biesen W, Vanholder R. Disaster nephrology: a new concept for an old problem. Clin Kidney J 2015; 8:300.
Somagutta, M. R., Pagad, S., Sridharan, S., Nanthakumaran, S., Arnold, A. A., May, V., & Malik, B. H. (2020). Role of Bicarbonates and Mannitol in Rhabdomyolysis: A Comprehensive Review. Cureus, 12(8), e9742. https://doi.org/10.7759/cureus.9742
Zager RA. Studies of mechanisms and protective maneuvers in myoglobinuric acute renal injury. Lab Invest 1989; 60:619.