Crush syndrome

Crush syndrome (also traumatic rhabdomyolysis or Bywaters' syndrome) is a medical condition characterized by major shock and kidney failure after a crushing injury to skeletal muscle. Crush injury is compression of extremities or other parts of the body that causes muscle swelling and/or neurological disturbances in the affected areas of the body, while crush syndrome is localized crush injury with systemic manifestations.[1] Cases occur commonly in catastrophes such as earthquakes, to victims that have been trapped under fallen or moving masonry.

Crush syndrome
SpecialtyEmergency medicine 

Victims of crushing damage present some of the greatest challenges in field medicine, and may be among the few situations where a physician is needed in the field. The most drastic response to crushing under massive objects may be field amputation. Even if it is possible to extricate the patient without amputation, appropriate physiological preparation is mandatory: where permissive hypotension is the standard for prehospital care, fluid loading is the requirement in crush syndrome.

Pathophysiology

Seigo Minami, a Japanese physician, first reported the crush syndrome in 1923.[2][3][4] He studied the pathology of three soldiers who died in World War I from insufficiency of the kidney. The renal changes were due to methemoglobin infarction, resulting from the destruction of muscles, which is also seen in persons who are buried alive. The progressive acute renal failure is because of acute tubular necrosis.

The syndrome was later described by British physician Eric Bywaters in patients during the 1941 London Blitz.[5][6] It is a reperfusion injury that appears after the release of the crushing pressure. The mechanism is believed to be the release into the bloodstream of muscle breakdown products—notably myoglobin, potassium and phosphorus—that are the products of rhabdomyolysis (the breakdown of skeletal muscle damaged by ischemic conditions).

The specific action on the kidneys is not understood completely, but may be due partly to nephrotoxic metabolites of myoglobin.

The most devastating systemic effects can occur when the crushing pressure is suddenly released, without proper preparation of the patient, causing reperfusion syndrome. In addition to tissue directly suffering the crush mechanism, down stream tissue is subject to ischemia-reperfusion injury of the appendicular musculoskeletal system. Without proper preparation, the patient, with pain control, may be cheerful before extrication, but die shortly thereafter. This sudden decompensation is called the "smiling death."[7]

These systemic effects are caused by a traumatic rhabdomyolysis. As muscle cells die, they absorb sodium, water and calcium; the rhabdomyolysis releases potassium, myoglobin, phosphate, thromboplastin, creatine and creatine kinase.

Compartment syndrome can be secondary to crush syndrome. Monitor for the classic 5 Ps: pain, pallor, parasthesias, pain with passive movement, and pulselessness.

Treatment

Due to the risk of crush syndrome, current recommendation to lay first-aiders (in the UK) is to not release victims of crush injury who have been trapped for more than 15 minutes.[8] Treatment consists of not releasing the tourniquet and fluid overloading the patient with added Dextran 4000 iu and slow release of pressure. If pressure is released during first aid then fluid is restricted and an input-output chart for the patient is maintained, and proteins are decreased in the diet.

The Australian Resuscitation Council recommended in March 2001 that first-aiders in Australia, where safe to do so, release the crushing pressure as soon as possible, avoid using a tourniquet and continually monitor the vital signs of the patient.[9] St John Ambulance Australia First Responders are trained in the same manner.

Field management

As mentioned, permissive hypotension is unwise. Especially if the crushing weight is on the patient more than 4 hours, but often if it persists more than one hour, careful fluid overload is wise, as well as the administration of intravenous sodium bicarbonate. The San Francisco emergency services protocol calls for a basic adult dose of a 2 L bolus of normal saline followed by 500 ml/h, limited for "pediatric patients and patients with history of cardiac or renal dysfunction." [10]

If the patient cannot be fluid loaded, this may be an indication for a tourniquet to be applied.

Initial hospital management

The clinician must protect the patient against hypotension, renal failure, acidosis, hyperkalemia and hypocalcemia. Admission to an intensive care unit, preferably one experienced in trauma medicine, may be appropriate; even well-seeming patients need observation. Treat open wounds as surgically appropriate, with debridement, antibiotics and tetanus toxoid; apply ice to injured areas.

Intravenous hydration of up to 1.5 L/hour should continue to prevent hypotension. A urinary output of at least 300 ml/hour should be maintained with IV fluids and mannitol, and hemodialysis considered if this amount of diuresis is not achieved. Use intravenous sodium bicarbonate to keep the urine pH at 6.5 or greater, to prevent myoglobin and uric acid deposition in kidneys.

To prevent hyperkalemia/hypocalcemia, consider the following adult doses:[1]

  • calcium gluconate 10% 10ml or calcium chloride 10% 5 ml IV over 2 minutes
  • sodium bicarbonate 1 meq/kg IV slow push
  • regular insulin 5–10 U
  • 50% glucose 1–2 ampules IV bolus
  • kayexalate 25–50 g with sorbitol 20% 100 ml by mouth or rectum.

Even so, cardiac arrhythmias may develop; electrocardiographic monitoring is advised, and specific treatment begun promptly.

References
  1. "Blast Injuries: Crush Injury & Crush Syndrome" (PDF). Centers for Disease Control. Archived from the original (PDF) on 2016-03-04. Retrieved 2015-01-19. Cite journal requires |journal= (help)
  2. Minami, Seigo (1923). "Über Nierenveränderungen nach Verschüttung". Virchows Arch. Patho. Anat. 245 (1): 247–267. doi:10.1007/BF01992107.
  3. Medical discoveries - Who and when- Schmidt JF. Springfield: CC Thomas, 1959. p.115.
  4. Morton's medical bibliography -An annotated check-list of texts illustrating History of medicine (Garrison-Morton). Aldershot: Solar Press; 1911. p.654.
  5. synd/3870 at Who Named It?
  6. Bywaters, E. G.; Beall, D. (1941). "Crush injuries with impairment of renal function". Br Med J. 1 (4185): 427–432. doi:10.1136/bmj.1.4185.427. PMC 2161734. PMID 20783577.
  7. Nancy Caroline (2007). Nancy Caroline's Emergency Care in the Streets: Trauma Medical. 2 (6th ed.). pp. 19–13. ISBN 9780763742393.
  8. St John Ambulance UK First Aid Manual, 10th Edition, p. 118
  9. "Emergency Management of a Crushed Victim". Australian Resuscitation Council. March 2001. Archived from the original on 26 October 2011. Retrieved 20 July 2011.
  10. "Crush Syndrome" (PDF). San Francisco Emergency Medical Services Agency. 1 July 2002. Protocol: #P-101. Archived from the original (PDF) on 28 October 2011 Cite journal requires |journal= (help)
  • Sever MS, Vanholder R, Lameire N (2006). "Management of crush-related injuries after disasters". N. Engl. J. Med. 354 (10): 1052–63. doi:10.1056/NEJMra054329. PMID 16525142.
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