Crush injury is defined as injury due to compression of extremities or other parts of the body that causes muscle swelling or trauma, with or without neurological or orthopedic problems in those body parts. The body areas most commonly involved are the limbs and torso.

Crush syndrome develops when crush injury is both extensive and prolonged, causing systemic manifestations. These systemic effects are due to traumatic rhabdomyolysis (muscle breakdown) and reperfusion injury (release of myoglobin, reactive oxygen species, and electrolytes into the circulatory system) after sudden release of pressure of the crushed limb or torso. Acute hypovolemia and metabolic abnormalities are common and can be both sudden and severe (even fatal) after release of pressure. Myoglobinuria from trauma to muscles may cause or exacerbate acute kidney injury if untreated. Cardiac arrhythmias can occur with reperfusion due to the shift in both calcium and potassium.

Crush injuries and crush syndrome in MWDs are expected after building collapses, most frequently following natural disasters or explosions, but also after motor vehicle accidents or roll-overs. Crush syndrome is rarely reported in animals; however, the incidence of acute kidney injury is high and should be closely observed for development.11

Other consequences of reperfusion include massive third spacing of fluids in crushed tissues leading to compartment syndrome as well as hypovolemia and shock and exacerbation of acute kidney injury.

CLINICAL  PRESENTATION

Clinical signs of crush injury/syndrome include some or all of the following:

  • Skin injury of the affected body part (may be subtle and less impressive than other signs)
  • Limb swelling (may be delayed)
  • Paresis or paralysis (may be mistaken as spinal cord injury)
  • Loss of sensation (may mask the severity of underlying injury)
  • Pain (typically becomes severe with reperfusion)
  • Absent or weak extremity pulses
  • Discolored urine due to myoglobinuria, hematuria or both
  • Hypotension due to hypovolemia (dehydration, hemorrhage, third spacing of fluids) – may be severe
  • Massive third spacing (often causes or exacerbates compartment syndrome and acute kidney injury)
  • Metabolic abnormalities (hypocalcemia, hyperkalemia, and lactic acidosis)
  • Clinical signs of compartment syndrome (severe pain in the involved extremity, pain on passive stretching of the involved muscles, decreased sensation to the affected limb)
  • Acute kidney injury (due to rhabdomyolysis and secondary myoglobinuric acute tubular necrosis)
  • Cardiac arrhythmias (due to the shift in electrolytes from the damaged tissue)12

CRUSH  INJURY  MANAGEMENT

Treat MWDs before and during extrication if possible.

Maintain a high index of suspicion, as MWDs with crush injury may present initially with few signs or symptoms. Delayed treatment leads to poor outcomes.

Most crush syndrome patients have an extensive area of involvement such as lower extremity and/or the pelvis. It requires more involvement than just one paw. Also, the crushing force must be present for some time before crush injury syndrome can occur.

The syndrome may develop in < 1 hour in a severe crush situation but usually takes 4-6 hours of compression for the processes that cause crush injury syndrome to take place.

Hallmark initial treatment for crush syndrome is IV fluid therapy before the release of pressure and continuing during extrication and evacuation. Place multiple IV lines because the MWD will require large fluid volumes and there is a risk of catheter dislodgement during extrication. Isotonic crystalloid fluids should be used for initial treatment and resuscitation.

Once compression is removed, maintain aggressive fluid therapy. Specific guidelines for fluid volumes are difficult to provide. As a starting point, use a rate of 3-5 mL/kg/hr to improve pulse quality, blood pressure (if available), capillary refill time, mucous membrane color and mentation. Try to estimate urine output – the goal is to maintain urine output > 1-2 mL/kg/hr.

If urine output decreases to below 0.5 mL/kg/hr and the patient is euvolemic, the patient has likely developed an acute kidney injury. Care should be taken to avoid fluid overload and the MWD should be evacuated.11

The electrocardiogram (ECG) should be monitored for cardiac arrhythmias. ECG waveform tracings consistent with hyperkalemia should be treated as described in the paragraph below. For arrhythmias associated with cardiopulmonary arrest, treat in accordance with current RECOVER cardiopulmonary resuscitation guidelines.13

Monitor venous potassium levels with serial blood gas measurements if possible.

  • If severe hyperkalemia (> 7.5 mEq/L) is present, the patient is at high risk for cardiac arrhythmias and should be emergently treated with 10% calcium gluconate (1 mL/kg IV over 2-3 minutes), insulin (0.5 U/kg IV) and dextrose (2 grams per kg of dextrose, or 4 mL/kg dextrose 50% IV), and terbutaline (0.01 mg/kg IM or slow IV).
    • Simultaneous ECG monitoring is recommended during administration of calcium gluconate to ensure the infusion does not worsen or create new arrhythmias.
    • Monitor blood glucose prior to and during insulin and dextrose therapy as well as in MWDs with concomitant hypoglycemia to delay insulin therapy until normoglycemia has been established.
  • Moderate hyperkalemia (> 6.0 mEq/L) should be treated with insulin and 50% dextrose to prevent continued increased to cardiotoxic levels. Administering albuterol (inhalation or nebulization) or terbutaline (0.01 mg/kg IV slowly at 0.03 mg/min) concurrently with insulin dextrose therapy can further reduce serum potassium levels.14,15

Alkalinization of blood with bicarbonate (as is done for humans) will likely not be feasible. Providers should focus on aggressive IV fluid therapy to correct dehydration and promote diuresis pending extrication and evacuation.

Anticipate secondary complications. MWDs with crush injury should be treated initially as any other multiple trauma victim by triaging and treating all life-threatening injuries first.

While compartment syndrome seems to be a much more common and severe problem in humans, it is rare in dogs and as such, extreme measures to control intracompartmental pressures such as fasciotomy are unwarranted.

Wounds should be cleaned and covered with sterile dressings in the usual fashion. Splint fractures if possible.

Provide analgesia (see K9 Analgesia and Anesthesia CPG) to any MWD with crush injury or crush syndrome.

If available, administering N-acetylcysteine at 150-250 mg/kg IV at 0 and 6 hours after reperfusion should be considered as it may decrease reactive oxygen species, increase recovery of muscle function and decrease fibrosis.16