Crush syndrome

Jump to navigation Jump to search

WikiDoc Resources for Crush syndrome


Most recent articles on Crush syndrome

Most cited articles on Crush syndrome

Review articles on Crush syndrome

Articles on Crush syndrome in N Eng J Med, Lancet, BMJ


Powerpoint slides on Crush syndrome

Images of Crush syndrome

Photos of Crush syndrome

Podcasts & MP3s on Crush syndrome

Videos on Crush syndrome

Evidence Based Medicine

Cochrane Collaboration on Crush syndrome

Bandolier on Crush syndrome

TRIP on Crush syndrome

Clinical Trials

Ongoing Trials on Crush syndrome at Clinical

Trial results on Crush syndrome

Clinical Trials on Crush syndrome at Google

Guidelines / Policies / Govt

US National Guidelines Clearinghouse on Crush syndrome

NICE Guidance on Crush syndrome


FDA on Crush syndrome

CDC on Crush syndrome


Books on Crush syndrome


Crush syndrome in the news

Be alerted to news on Crush syndrome

News trends on Crush syndrome


Blogs on Crush syndrome


Definitions of Crush syndrome

Patient Resources / Community

Patient resources on Crush syndrome

Discussion groups on Crush syndrome

Patient Handouts on Crush syndrome

Directions to Hospitals Treating Crush syndrome

Risk calculators and risk factors for Crush syndrome

Healthcare Provider Resources

Symptoms of Crush syndrome

Causes & Risk Factors for Crush syndrome

Diagnostic studies for Crush syndrome

Treatment of Crush syndrome

Continuing Medical Education (CME)

CME Programs on Crush syndrome


Crush syndrome en Espanol

Crush syndrome en Francais


Crush syndrome in the Marketplace

Patents on Crush syndrome

Experimental / Informatics

List of terms related to Crush syndrome

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Aakash Hans, MD[2]

Synonyms and keywords: Bywaters' syndrome; traumatic rhabdomyolysis


Being a common occurrence in victims of natural disasters and human wars, crush syndrome is still a rare finding in daily practice. Falling short to direct-fatal trauma, crush syndrome is the second most common cause of mortality after a disaster. It is the sequalae that follows when an individual or a part of him/her has been crushed between two heavy objects and although it has a wide range of presentation like shock, trouble breathing, electrolyte disturbances and irregular beating of the heart, the main culprit behind these findings is the extensive damage to the kidneys as a result of the trauma the person was subjected to. This can be prevented with aggressive fluid resuscitation, but the sheer number of incoming trauma patients during a calamity plays a major role in creating logistic problems for the response teams and hence it becomes important to diagnose it earlier rather than later.

Historical perspective

  • The first reported relations between compressive trauma and renal damage were after the 1909 earthquake in Sicily and World War I.[1]
  • In the year 1923, a physician named Seigo Minami reported crush syndrome after observing three soldiers who died due to renal failure as a result of injuries sustained during World War I.[2] Having this background knowledge, the incidence of crush syndrome was then observed in increasing numbers during World War II. During the London air raids, many individuals experienced similar injuries, wherein Bywaters and Beall discussed the presentations of the syndrome. Statistically, out of 100 people with crush injuries, about 80 succumb to fatal head trauma or are not able to breathe underneath the rubble. Out of the remaining 20 that do reach the hospital, about 10 recover completely while 7 out of the other 10 proceed into developing signs of crush syndrome.[3]
  • A series of 11 cases were studied and differences between similar syndromes like crush and compartment syndrome were delineated in 1975.[4]Main focus of managing crush syndrome is now to diagnose it earlier, to finalize a standard treatment with fluids to be administered to patients and to identify those who have extensive renal damage and would now require kidney replacement.[5]


  • Crush syndrome: also known as traumatic rhabdomyolysis or reperfusion syndrome, it is defined as the systemic features of a crush injury leading to renal failure.[6]


The complete pathogenesis of crush syndrome involves primarily two main events which in turn have several smaller steps that participate in their development.

  • The trauma causes compression of a limb or region of the body, which if is present for two to three hours, leads to the process of rhabdomyolysis.[7] This in turn, causes renal damage and eventually renal failure if allowed to proceed.[8]
  • 1. Compression induced rhabdomyolysis :
    • Increased local pressure causes the sarcolemma membrane to become permeable.
    • Substances move down their concentration gradient from the extracellular to the intracellular compartment and vice versa.
    • Water, sodium-Na+ and calcium-Ca2+ enter the cell while potassium-K+ and myoglobin enter the extracellular compartment.
    • As intracellular Ca2+ rises, muscular contraction ensues, emptying the cell’s ATP stores.
    • The ATP deficient cell causes mitochondrial damage along with the release of enzymes like proteases and phospholipases.
    • These enzymes and oxidative stress, damage the phospholipids present in the cell membrane and as a result cause lysis of the muscle cell.
    • Toxic metabolites which were accumulating inside the cell are then released into the extracellular compartment.
    • These substances induce damage to the capillaries present in the area leading to leaking, which causes increased compartmental pressure due to third spacing of fluids.
    • Increased pressure in the compartment results in occlusion of these vessels and further depletion of energy sources like ATP and glycogen.
    • Decreased circulation causes reduced oxygen saturation of myoglobin.

The real damage ensues when circulation is re-established which allows leukocytes to attack this region and release all these toxins to the rest of the body.

  • 2. Renal injury following rhabdomyolysis: A plethora of mechanisms are now aimed at damaging the kidney, once the injured area has been re-perfused. Most of the released metabolites and compounds are toxic to the kidney and hence lead to acute kidney injury (AKI).
    • The collection of fluid in the injured area causes decreased intravascular volume and consequently reduces the blood supply to the kidney. This leads to the pre-renal subtype of AKI.[8]
    • Toxins and cytokines released upon re-perfusion causes constriction of renal vessels, further aggravating the pre-renal AKI via hypoperfusion.
    • K+ released from the damaged muscle affects the heart by causing decreased output, contributing to renal [Ischemia|ischemia]].
    • Myoglobin levels rise in the blood which upon reaching the kidney form casts in the tubular system causing renal damage and AKI.
    • Proteins released from damaged cellular membranes accumulate in renal tubules causing obstruction and further potentiate renal injury.
    • Increased serum phosphorus levels depress cardiac contraction and combine with Ca2+ to form precipitates in renal tubules which induces renal inflammation.
    • Lastly, damaged tissue can release thromboplastin into the bloodstream which can activate the disseminated intravascular coagulation pathway (DIC), further decreasing renal blood supply.

Differential diagnosis

  • Crush injury : the damage caused to muscle cells due to pressure applied on them locally, for a prolonged period of time.[9]
  • Rhabdomyolysis : the breakdown and release of muscular tissue (myoglobin) into the bloodstream resulting in renal damage and the subsequent build-up of toxic compounds in the blood.[10]
  • Compartment syndrome: the raised pressure (>20 mm of Hg) within a localized region causing decreased local circulation which can lead to ischemia and necrosis of that osteo-musculo-fascial compartment.[11] This can later lead to the release of necrosed muscle tissue into the blood which damages the kidney and can present with features similar to crush syndrome.

Epidemiology and Demographics

  • Crush syndrome can be seen in approximately 50% of cases of traumatic rhabdomyolysis. [12]
  • Around 10% of severely beaten individuals also go on to develop crush syndrome. The rate of cases in earthquakes ranges from 2% to 5%.[13]
  • The proportion of crush syndrome cases needing dialysis depends on multiple factors and hence has a broad range of 0% to 75%.[14]
  • An earthquake occurring during the nighttime would have significantly more number of crush syndrome cases and also cases requiring dialysis as compared to earthquakes occurring during broad daylight. The premise behind this observation is that disasters occurring at night have most of the victims sleeping in a supine posture, which increases the chances of receiving crush injuries.[15]
  • Other contributing factors would be the infrastructure of the disaster-stricken area and how well the rescue teams respond in extricating victims from underneath the rubble.
  • In non-disaster conditions, factors like delayed admissions (>12 hours), metabolic acidosis, decreased bicarbonate levels, lower baseline hemoglobin levels and raised creatine kinase levels, all bode a grim prognosis for the patient.[16]

Relation to disasters

  • Disasters have occurred numerous times over the course of human history and earthquakes are especially notorious for causing structures like buildings and houses to collapse.
  • These heavy structures may either cause injury to vital organs of the body like the brain and heart or may incite damage to non-vital organs like limbs and extremities by compressing them with their weight. Therefore, earthquake victims form the majority of crush syndrome cases.
  • Although it may not be possible to prevent mortality stemming from injuries to vital organs, victims with crush injuries can be prevented from developing features of crush syndrome.
Location Year Magnitude Deaths Crush syndrome Dialysis
Spital, Armenia 1988 6.7 25,000 600 225-385
Kobe, Japan 1995 6.9 5,000 372 123
Marmara, Turkey 1999 7.6 17,118 639 477
Gujarat, India 2001 7.6 20,085 35 33
Bam, Iran 2003 6.6 31,000 124 96
Kashmir, India 2005 7.6 86,000 118 65
Sichuan, China 2008 7.9 87,587 229 113
  • The table above shows the major earthquakes that have occurred over past years and the number of crush syndrome cases seen in each one of them.[17]

Risk Factors

  • Although there are no well-established risk factors, factors like living in a disaster-prone area or being employed in a trauma-prone occupation would generally pose a higher risk to these individuals to develop crush syndrome.
  • Kidney patients would also be at higher risk in these situations.


Screening would involve the quick application of the following :

Natural History, Complications and Prognosis

  • The prognosis of a patient would depend on several intertwined factors, some of which are mentioned below
    • Early extrication and fluid infusion generally bode well for the patient as it prevents the onset of the vicious cycle of crush syndrome.
    • Late admission (>12 hours) increases the chances of the patient having a complicated course of stay in the hospital and he may even require dialysis eventually.
    • Infrastructural factors like, distance to the nearest hospital and dialysis centre decide how the patient with crush syndrome will fare in the next few hours.
    • Starting normal saline infusion before the extrication process begins is ideal for the patient’s prognosis.


Diagnostic Criteria

The following features seen in a crush injury victim should alarm the physician to the possibility of crush syndrome development :

  • Raise creatine kinase levels in serum of >1000 IU/litre. The normal value of creatine kinase ranges from 25 to 175 IU/litre, which can begin to increase 2-12 hours following a crush injury, can peak around days 1-3 and begins to decline after days 3-5.
  • Injury to a large area of muscle tissue associated with decreased urine output (<400ml / 24 hours)
  • Raised BUN (>40 mg/dL), creatinine (>2 mg/dL) and hyperkalemia (>6 mmol/L) can also point to renal involvement in crush injury patients.

History and Symptoms

  • History :
    • Patient will have a history of recent crush injury which may still be ongoing i.e. patient could still be compressed underneath the rubble.
    • Pain in the involved area along with generalized weakness may be reported.
    • Swelling of the extremity involved may also be elicited in some cases.
    • Overall history would suggest and point towards development of systemic features like shock and acidosis in a recent crush injury victim.
  • Symptoms :
    • Pain and swelling in the locally compressed area or extremity.
    • Low or no urine output.
    • Weak or absent pulse and cold skin (features of shock)
    • Pallor could be present if the victim is loosing blood due to internal or external injuries.

Physical Examination

Early recognition of crush syndrome can tremendously improve the patient’s prognosis and the overall course of his/her stay at the hospital. Local findings mentioned below should alarm the physician to then look for any suspicious systemic features of crush syndrome. If systemic features are present as well, certain investigations can then lead to the confirmation of crush syndrome as the diagnosis.[18]

  • 1. Local features :
    • Pain which is proportionately more in intensity than the severity of the injury.
    • Swollen muscles or tense skin above the injured area.
    • Abnormal sensation in the injured area.
    • Pallor or deficiency of the natural color of the skin.
    • Paralysis or inability to move the affected area.
    • Decreased sensation or absence of pulse adjacent to the injured region.
    • Feeling of increased pressure or heaviness in the injured area elicited by the victim.
  • 2. Systemic features :
    • Trouble breathing or shortness of breath.
    • Decreased urine output or reddish tinge to the urine.
    • Hypotension as a feature of hypovolemic shock.
    • Irregular heart-beat or arrhythmia due to increased K+ levels.
    • Neurological abnormalities like light-headedness or dizziness.
    • Fever and generalized malaise, which points to the development of an infection in the injured area.



  • X-rays may show fractures of the extremities and can be useful to gauge the extent of the patient's injuries.

Other Imaging Findings

  • Imaging modalities including contrast administration like CT and MRI are usually avoided in crush injury patients and suspected crush syndrome patients.


Since most crush syndrome patients have experienced major trauma and injuries, it is essential to transfer victims away from the disaster site and to nearby medical centers for prompt treatment. Keeping an eye on the cardiovascular and renal status forms the mainstay of successful management. Medical and para-medical staff should be well trained in recognizing the signs of crush syndrome as history is often unavailable in these scenarios. Treatment in the form of resuscitation should begin as soon as the victim makes contact with health personnel.[19]

  • 1. Fluid resuscitation :
    • Fluids should be administered early into the management.
    • There is no fixed amount or rate at which fluids should be given, but fluids need to be given within 6 hours of the trauma.[1]
    • Normal saline (NS) is the fluid of choice. If intravenous cannulation is successful before removing the victim from underneath the rubble, the fluid should be administered at a rate of one liter per hour. This rate should be continued during the extrication and can be reduced to 500 ml per hour if extrication takes longer than 2 hours.[17]
    • Ringer’s Lactate, Plasmalyte A and Hartmann’s solution contain potassium and should be avoided in patients with signs of crush syndrome.[20]
    • Bicarbonate, lactate and citrate can be used to combat metabolic acidosis. For every liter of NS infused, 50 mmol of bicarbonate can be administered along with it.[5]
    • Infusing larger doses of bicarbonate may exacerbate hypocalcemia by decreasing the amount of ionized calcium in the serum.
    • Regular checks on blood pressure, respiratory rate and urine output should be performed to assess whether fluid replacement is proceeding adequately or not.
    • Insulin along with a glucose drip can be used to prevent the ongoing influx of K+ into the bloodstream.
    • Blood transfusion may also be required according to the severity of injuries met by the patient.
  • 2. Renal function management :
    • Urine output in a diagnosed crush syndrome case should be around 300 ml/hr as maintaining kidney function is now of utmost priority.[21]
    • As third spacing of fluid at the site on an injury can be as high as 4 liters, approximately 12 liters of fluid per day is required for adequate renal function.[22]
    • Mannitol may be added to NS in patients with urine output > 20 ml per hour - in the amount of 50 ml of 20% mannitol. It aids in decreasing raised pressures at the local site of injury, maintains an alkaline pH of the urine which prevents tubular obstruction caused by casts and thus allows the adequate blood supply to reach the kidneys.[23]
    • Mannitol is not an alternative to NS and is rather used as an adjunctive treatment option, especially in patients with crush syndrome also developing compartment syndrome.[24]
  • 3. Renal dialysis :
    • Dialysis has a firm foothold in the management of crush injury.
    • As complications of trauma-induced AKI occur more frequently than its other causes, dialysis is required more often.
    • Serum urea, creatinine and urine output are important factors used to decide whether dialysis is required or not. Serum K+ levels exceeding 7 meq/L is another indication for dialysis treatment.[20]
    • Early initiation of dialysis in trauma-induced AKI may improve overall survival.[25]
    • Peritoneal dialysis, intermittent hemodialysis and continuous renal replacement therapy and some of the options used in trauma patients. Out of these, intermittent dialysis is the most used modality for crush syndrome victims.[26]
    • Intermittent dialysis provides quick elimination of the excess potassium build-up in the body and the same dialyzing machine may be used for multiple patients in a day. It may be used for individuals with bleeding disorders as it can be used with minimal anticoagulation.[27]
    • Dialysis may be required for two-three times daily up to a span of 10-15 days.
  • 4. Hyperbaric oxygen :
    • Administering oxygen at high pressure and concentration can help in increasing oxygen saturation of the injured tissue.
    • Improved oxygen supply will in turn lead to healing of vessels and cessation of fluid loss from the vessels in form of capillary leak.
    • Presence of oxygen discourages proliferation of anaerobic bacteria in damaged muscle tissue.[28]
    • A pressure of 2.5 atmospheres is required to be administered for a week long regimen lasting 90 minutes daily.[29]
  • 5. Surgical options :
    • Debridement of dead and necrosing tissue is essential to prevent further progression of crush syndrome.
    • A fasciotomy may be required if compartmental pressures are above 30mm of Hg.
    • Performing a fasciotomy earlier rather than later is always considered a good practice, as a late fasciotomy may further require an amputation to halt the ongoing insult to the victim’s systems.[30]
    • Surgically opening these injured sites to relieve the pressure is essential and after debridement is complete, these sites are kept open for a while to prevent repeat rise in compartmental pressures. They are later closed by suturing and healing by secondary intention.
  • 6. Prevention of infection :
    • Broad-spectrum antibiotics may be used to prevent the development of localized infection due to exposure of the wound to the external environment.
    • A tetanus shot may also be administered

  • Utmost importance should be given to starting fluids in these patients, preferably before the extrication begins. The fluids should be continued to maintain adequate urine output since most of the pathogenesis of crush syndrome stems from kidney failure.
  • The lack of kidney function causes unwanted toxins and compounds to accumulate in the blood which sets forth the development of systemic inflammation and other events like arrhythmias, heart failure, acute respiratory distress and shock.
  • The challenge in situations like earthquakes is to procure enough medical personnel and equipment required to safely extricate and transport crush injury victims to the hospital while administering fluid en route. Unavailability of transport, personnel, or medicines are the common logistic problems disaster response teams face during these times.[17]


Primary Prevention

  • Early extrication of trapped victims is essential during a disaster to cease the ongoing compression and to prevent any further injuries the victim may experience due to aftershocks or further collapse of adjacent structures.
  • Prompt administration of normal saline, preferably as soon as extrication begins.
  • Regular monitoring of urine output, as any decrease in urine production can point to potential involvement and damage to the renal system.
  • Repeated levels of serum creatine kinase, BUN, creatinine, potassium and calcium levels should be performed to keep a check on development of crush syndrome.
  • Training response teams to be aware of signs and symptoms of crush syndrome may be vital in strengthening prevention measures.
  • Establishment of medical care centres close to the site of disaster can help in providing early medical intervention to patients who require it the most.

Secondary prevention

  • Aggressive fluid administration of normal saline may help the patient’s renal status to improve on its own.
  • In case, the renal status continues to deteriorate, early implementation of dialysis is key to prevent further and irreversible damage to the kidneys.


  1. 1.0 1.1 Better OS (1990) The crush syndrome revisited (1940-1990). Nephron 55 (2):97-103. DOI:10.1159/000185934 PMID: 2194135
  2. Medical discoveries - Who and when- Schmidt JF. Springfield: CC Thomas, 1959. p.115.
  3. Bywaters EG (1990) 50 years on: the crush syndrome. BMJ 301 (6766):1412-5. DOI:10.1136/bmj.301.6766.1412 PMID: 2279155
  4. Mubarak S, Owen CA (1975) Compartmental syndrome and its relation to the crush syndrome: A spectrum of disease. A review of 11 cases of prolonged limb compression. Clin Orthop Relat Res (113):81-9. DOI:10.1097/00003086-197511000-00012 PMID: 1192679
  5. 5.0 5.1 Gunal AI, Celiker H, Dogukan A, Ozalp G, Kirciman E, Simsekli H | display-authors=etal (2004) Early and vigorous fluid resuscitation prevents acute renal failure in the crush victims of catastrophic earthquakes. J Am Soc Nephrol 15 (7):1862-7. DOI:10.1097/01.asn.0000129336.09976.73 PMID: 15213274
  6. Michaelson M. (2009) Crush Injury, Crush Syndrome. In: Shapira S.C., Hammond J.S., Cole L.A. (eds) Essentials of Terror Medicine. Springer, New York, NY.
  7. Zager RA (1996) Rhabdomyolysis and myohemoglobinuric acute renal failure. Kidney Int 49 (2):314-26. DOI:10.1038/ki.1996.48 PMID: 8821813
  8. 8.0 8.1 Sever MS (2007) Rhabdomyolysis. Acta Clin Belg 62 Suppl 2 ():375-9. DOI:10.1179/acb.2007.084 PMID: 18284003
  9. Michaelson M. (2009) Crush Injury, Crush Syndrome. In: Shapira S.C., Hammond J.S., Cole L.A. (eds) Essentials of Terror Medicine. Springer, New York, NY.
  10. Torres PA, Helmstetter JA, Kaye AM, Kaye AD (2015) Rhabdomyolysis: pathogenesis, diagnosis, and treatment. Ochsner J 15 (1):58-69. PMID: 25829882
  11. Torlincasi AM, Lopez RA, Waseem M. Acute Compartment Syndrome. [Updated 2021 Feb 10]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from:
  12. Vanholder R, Sever MS. Crush-related acute kidney injury (acute renal failure). Up To Date 22 Apr. 2011
  13. J.D. Knottenbelt Traumatic rhabdomyolysis from severe beating—experience of volume diuresis in 200 patients J Trauma, 37 (1994), pp. 214-219
  14. D. Wood, K. Rosedale Crush syndrome in the rural setting Emerg Med J, 28 (2011), p. 817
  15. A. Van der Tol, et al.Impact of local circumstances on the outcome of renal casualties in major disasters Nephrol Dial Transplant, 24 (2009), pp. 907-912
  16. W.A. Smith, T.C. Hardcastle. A crushing experience. The spectrum and outcome of soft tissue injury and myonephropathic syndrome at an Urban South African University Hospital. Afr J Emerg Med, 1 (1) (2011), pp. 17-24
  17. 17.0 17.1 17.2 Gibney RT, Sever MS, Vanholder RC (2014) Disaster nephrology: crush injury and beyond. Kidney Int 85 (5):1049-57. DOI:10.1038/ki.2013.392 PMID: 24107850
  18. Sever MS, Vanholder R (2011) Management of crush syndrome casualties after disasters. Rambam Maimonides Med J 2 (2):e0039. DOI:10.5041/RMMJ.10039 PMID: 23908797
  19. Rajagopalan S (2010) Crush Injuries and the Crush Syndrome. Med J Armed Forces India 66 (4):317-20. DOI:10.1016/S0377-1237(10)80007-3 PMID: 27365733
  20. 20.0 20.1 Sever MS, Erek E, Vanholder R, Kantarci G, Yavuz M, Turkmen A | display-authors=etal (2003) Serum potassium in the crush syndrome victims of the Marmara disaster. Clin Nephrol 59 (5):326-33. DOI:10.5414/cnp59326 PMID: 12779093
  21. Better OS, Stein JH (1990) Early management of shock and prophylaxis of acute renal failure in traumatic rhabdomyolysis. N Engl J Med 322 (12):825-9. DOI:10.1056/NEJM199003223221207 PMID: 2407958
  22. 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
  23. Better OS, Rubinstein I, Winaver JM, Knochel JP (1997) Mannitol therapy revisited (1940-1997). Kidney Int 52 (4):886-94. DOI:10.1038/ki.1997.409 PMID: 9328926
  24. Holt SG, Moore KP (2001) Pathogenesis and treatment of renal dysfunction in rhabdomyolysis. Intensive Care Med 27 (5):803-11. DOI:10.1007/s001340100878 PMID: 11430535
  25. Gettings LG, Reynolds HN, Scalea T (1999) Outcome in post-traumatic acute renal failure when continuous renal replacement therapy is applied early vs. late. Intensive Care Med 25 (8):805-13. DOI:10.1007/s001340050956 PMID: 10447537
  26. Bonomini M, Stuard S, Dal Canton A (2011) Dialysis practice and patient outcome in the aftermath of the earthquake at L'Aquila, Italy, April 2009. Nephrol Dial Transplant 26 (8):2595-603. DOI:10.1093/ndt/gfq783 PMID: 21248293
  27. Sever MS, Erek E, Vanholder R, Koc M, Yavuz M, Aysuna N | display-authors=etal (2004) Lessons learned from the catastrophic Marmara earthquake: factors influencing the final outcome of renal victims. Clin Nephrol 61 (6):413-21. DOI:10.5414/cnp61413 PMID: 15224805
  28. Bouachour G, Cronier P, Gouello JP, Toulemonde JL, Talha A, Alquier P (1996) Hyperbaric oxygen therapy in the management of crush injuries: a randomized double-blind placebo-controlled clinical trial. J Trauma 41 (2):333-9. DOI:10.1097/00005373-199608000-00023 PMID: 8760546
  29. Myers RA (2000) Hyperbaric oxygen therapy for trauma: crush injury, compartment syndrome, and other acute traumatic peripheral ischemias. Int Anesthesiol Clin 38 (1):139-51. DOI:10.1097/00004311-200001000-00009 PMID: 10723673
  30. Finkelstein JA, Hunter GA, Hu RW (1996) Lower limb compartment syndrome: course after delayed fasciotomy. J Trauma 40 (3):342-4. DOI:10.1097/00005373-199603000-00002 PMID: 8601846