Crush Syndrome


  • prolonged ischaemic and muscular damage -> rhabdomyolysis and reperfusion injury on release
  • limb often initially numb with a peripheral pulse -> rapid swelling with compartment syndrome

MANAGEMENT (otherwise healthy adult)


  • full monitoring
  • IV N/S 1L/hr prior to extrication
  • post extrication: 500mL N/S alternating with 500mL 5% glucose (per hour)


  • add 50mEqu of NaHCO3 to every second 500mL glucose (maintain urinary pH > 6.5)
  • once urine flow established add 2g/kg of 20% mannitol (ever give more than 200g/day and never administer in established anuria)
  • aim for urine flow 8L/day (will require 12 L/day)
  • if HCO3 produces pH > 7.45 -> give acetazolamide 500mg
  • continue until myoglobin disappears from urine

Limb care

  • splint joints in a functional position
  • active and passive movement as soon as pain allows
  • contractures and paralysis dealt with late reconstructive surgery


  • recommended within 6 hours of a compartment syndrome BUT NOT when muscle is already dead (which is inevitable in crush compartment syndrome)
  • often done -> significant increase in bleeding, coagulopathy, sepsis and mortality
  • in closed injuries -> there is no place for fasciotomies
  • only indicated if a distal pulse is absent and when major artery and systemic hypotension have been excluded
  • necrosis and severe infection sets in 2-5 days post injury -> must be amputated

Hyperbaric O2

  • reduces oedema
  • floods ECF with O2


  • hypovolaemia
  • hyperkalaemia
  • hypocalcaemia
  • metabolic acidosis
  • acute myoglobinuric renal failure
  • acute muscle-crush compartment syndrome
  • death

Journal articles

  • Gonzalez D. Crush syndrome. Crit Care Med. 2005 Jan;33(1 Suppl):S34-41. Review. PubMed PMID: 15640677.

CCC 700 6

Critical Care


Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also a Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of three amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

One comment

  1. Within this paper was the recommendation for NS over LR. However I do not think this is correct. Please see the reference below from PulmCrit. Therein a decent argument is made, with lit backing showing efflux of K+ from cells due to the acidic nature of NS:

    “the primary reason that this myth is wrong [NS being better than LR for hyperK+] has to do with potassium shifting between the cells and the extracellular fluid. About 98% of the potassium in the body is present inside the cells, with an intracellular potassium concentration of ~140 mEq/L. Therefore, even a tiny shift of potassium out of the cellular compartment will have a major effect on extracellular potassium levels. NS causes a non-anion gap metabolic acidosis, which shifts potassium out of cells, thereby increasing the potassium level. On the other hand, LR does not cause an acidosis, but instead may have a mild alkalinizing effect given that it contains the equivalent of 28 mEq/L of bicarbonate. Potassium shifts have a greater effect on the serum potassium than the actual concentration of potassium in the infused solution. ”

    “a prospective, randomized, double-blind controlled trial of NS versus LR among 52 patients undergoing renal transplant surgery. The mean change in serum potassium during the procedure was +0.5 mEq/L in the NS group compared to -0.5 mEq/L in the LR group (p < 0.001; figure below). Patients in the NS group also had lower pH levels following surgery. ”


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