Heavy use of artillery has long been a defining trait of the Soviet and modern Russian militaries. During the Ukraine war, Russia has fired fast amounts of ordinance at Ukraine- peaking at 20,000 - 60,000 shells/day (Ukraine, in turn, holds the line using around 7,000 shells/day, depending on supply constraints). Traditional artillery such as mortars and rockets are now supplemented by loitering drone platforms, grenades attached to FPV hobby drones, purpose-built ballistic missiles, re-purposed anti-aircraft missiles, and GPS-guided bombs dropped by aircraft operating in the relative safety of Russian airspace. In addition to saturation bombing of frontline areas, civilian infrastructure in cities throughout Ukraine is frequently targeted. Since the start of the invasion, Russia has fired 7,400 missiles and 3,700 Shahed-type drones at Ukrainian territory.
All of this translates to a high rate of bombing-related trauma patients- not just for military medics, but also for municipal and national guard responders in civilian areas. It is estimated that in Ukraine, civilian deaths have passed 9,700, military deaths top 70,000, and injuries outnumber deaths by a factor of between 2:1 and 5:1. The war has caused an estimated 25,000-50,000 amputations within Ukraine.
Crush syndrome is an important phenomenon for medical responders to consider during conflict, It is often accompanied by a constellation of related injuries, including compartment syndrome and rhabdomyolysis.
Experience from earthquake and conflict response shows that up to 40% of multistory building collapse survivors experience crush syndrome. Crush syndrome, with ensuring rhabdomyolysis, is the 2nd most frequent cause of earthquake deaths (the 1st is direct trauma). Bombing can cause similar patterns of blunt trauma due to structural collapse and airborne debris.
Crush syndrome consists of direct damage to local tissue, and resulting systemic effects. Systemic effects include hypotension, hyperkalemia, hypocalcemia, dysrhythmias, and organ dysfunction. The initiating mechanism of crush syndrome is direct damage to the cell membranes surrounding muscle cells. Rhabdomyolysis, or muscle cell breakdown occurs (from the Greek rhabdos=rod + myo=muscle + lysis=breakdown).There is an influx of fluids and calcium into the damaged cells, and a release of cell contents such as potassium, phosphate, and creatine into the bloodstream. Systemic effects follow. Massive third spacing of fluids causes hypovolemia; 12 liters or more of fluids may migrate into crushed areas during the first 48 hours. Histamine and leukotriene release causes vasodilation and bronchoconstriction. General vasodilatory effects cause capillary bed leakage, which worsens edema, third spacing, and hypotension. Ongoing enzymatic damage occurs in muscles, accompanied by tissue hypoperfusion and hypoxia. Lactic acid from anaerobic respiration in damaged muscle tissue causes acidosis and dysrhythmias. Myoglobin and uric acid builds up in the kidneys faster than it is excreted, causing acute kidney failure. Potassium released from cells causes hyperkalemia and associated dysrhythmias. Thromboplastic release can lead to DIC.
Aggressive and comprehensive treatment of crush injuries is key, and should begin on-scene prior to patient extrication. Initiate early pain control using fentanyl or ketamine for preservation of blood pressure (IN route is an option). Avoid kidney-processed medications such as NSAIDs. Prevent hypothermia and consider TXA for bleeding. Begin fluid resuscitation without delay; a delay in fluids may increase incidence of renal failure by 50%, and a 12-hour delay in fluid administration has been associated with almost 100% rates of renal failure in crush injury patients. Renal failure carries a 20-40% mortality rate in crush injury victims. Administer 1.5L of NS over the first hour. Potassium-containing fluids such as lactated ringers and sterofundin ISO may exacerbate hyperkalemia and should be avoided. As a side note, in patients with noncompressible bleeding, fluids may worsen bleeding. Therefore, in some cases it may be necessary to balance the risk of uncontrolled hemorrhage with the risk of cardiotoxic levels of potassium. If extrication must be performed prior to IO/IV placement, consider short-term tourniquet placement. For prolonged field care, urine output of 100-200mL/hour is the target. if IV/IO access and fluids are not available, this may be achieved via oral or rectal hydration via ORS, pedialyte, or a water-sugar-salt-baking soda solution (1L water, 8tsp sugar, 0.5 tsp salt, 0.5tsp baking soda).
Patients should be transported gently and carefully monitored via EKG. In hyperkalemic patients 10 units regular insulin+50mL D50 glucose (onset 20 min,action duration 4-6 hrs), and high-dose albuterol (12mL of 2.5mg/3mL solution via nebulizor, onset 30min, action duration 2 hrs) help to push potassium out of circulation and back into cells. Correct hypocalcemia with 10 mL (10%) Calcium gluconate or calcium chloride administered over 2-3 minutes (action duration 30-60min). Recent studies have not found administration of bicarbonate or mannitol to have kidney-protective effects. Bicarb is not recommended in TCCC protocols for potassium reduction, due to its slow and unsustained effects on potassium levels. TCCC's prolonged care protocol recommends monitoring of potassium levels and use of sodium polystyrene sulfonate to permanently remove excess potassium from the body via the GI tract (other agents only temporarily force it back into cells).
All crush injury patients should be observed, even if they appear well. Significant toxin accumulation generally occurs after 4-6 hours of entrapment/tissue compression, but can occur in as little as 60 minutes. Unexpected mechanisms, such as prolonged immobilization due to unconsciousness, may result in crush or compartment syndrome within compressed tissue areas. Severe blunt trauma to an extremity, or reperfusion of a limb that has been tourniqueted for more than 2 hours may also result in crush-syndrome-like symptoms.
Signs of renal failure may be delayed. Most cases of acute renal failure will recover with dialysis, though recovery may take up to 60 days.
Compartment syndrome- swelling and pressure inside a muscle compartment, which impedes circulation within the compartment, may develop. Muscles are covered in dense membranes called fascia, which do not stretch under building pressure. Signs of compartment syndrome include extreme localized pain, pallor, pulselessness, paresthesia, and paralysis of the affected area. Presentation may be clandestine, due to local nerve damage or altered mental status. Muscle compartment pressures as low as 40mmHg can cause compartment syndrome, through pressures may reach 240mmHg after significant trauma. Fasciotomy may be required to relieve pressure.
2004 study: Brown C, Rhee P, Chan L, et al. Preventing renal failure in patients with rhabdomyolysis: Do bicarbonate and mannitol make a difference? J Trauma. 2004;56(6):1191—1196
2013 literature review: Scharman EJ, Troutman WG. Prevention of kidney injury following rhabdomyolysis: A systematic review. Ann Pharmacotherapy. 2013;47(1):90—105.
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