Rhabdomyolysis
236354
223256278
2008-07-03T07:52:06Z
Epbr123
1395162
Reverted edits by [[Special:Contributions/124.106.223.71|124.106.223.71]] to last version by DOI bot (using [[WP:HG|Huggle]])
{{Infobox_Disease |
Name = Rhabdomyolysis |
Image = Myoglobin.png |
Caption = Model of helical domains in myoglobin, the protein linked to kidney damage in rhabdomyolysis. |
DiseasesDB = 11472 |
ICD10 = {{ICD10|M|62|8|m|60}}, {{ICD10|T|79|6|t|79}} |
ICD9 = {{ICD9|728.88}} |
ICDO = |
OMIM = |
MedlinePlus = 000473 |
eMedicineSubj = ped |
eMedicineTopic = 2003 |
eMedicine_mult = {{eMedicine2|emerg|508}} |
MeshID = D012206 |
}}
'''Rhabdomyolysis''' is the rapid breakdown (''[[lysis]]'') of [[skeletal muscle]] tissue (''rhabdomyo'') due to injury to muscle tissue. The muscle damage may be caused by physical (e.g. crush injury), chemical, or biological factors. The destruction of the muscle leads to the release of the breakdown products of damaged [[muscle fiber|muscle cells]] into the bloodstream; some of these, such as [[myoglobin]], are harmful to the [[kidney]] and may lead to [[acute renal failure|acute kidney failure]]. Treatment is with [[intravenous]] fluids, and [[dialysis]] or [[hemofiltration]] if necessary.<ref name="CritCare2005"/>
Rhabdomyolysis and its complications are major problems in people who are injured in disasters such as [[earthquake]]s and [[bomb]]ing. The disease and its mechanisms were first elucidated in [[The Blitz|the Blitz of London]] in [[1941]].<ref name="Vanholder2000"/>
== Signs and symptoms ==
Most cases of rhabdomyolysis develop as a result of muscle [[injury]] or [[Strain (injury)|strain]], or other external causes (such as [[medication]] or [[intoxication]]). However, the cause is not always directly evident. [[Pain]], tenderness, [[Muscle weakness|weakness]] and [[edema]] (swelling) of the affected muscles may be present. If the swelling is very rapid (such as after being released from a collapsed building), [[hypotension|low blood pressure]] and [[Shock (medical)|shock]] may be present due to depletion of fluid from the bloodstream. Other symptoms are nonspecific and result either from the consequences of the breakdown in muscle tissue, or from the condition that caused the muscle breakdown.<ref name=CritCare2005>{{cite journal |author=Huerta-Alardín AL, Varon J, Marik PE |title=Bench-to-bedside review: rhabdomyolysis - an overview for clinicians |journal=Crit Care |volume=9 |issue=2 |pages=158–69 |year=2005 |pmid=15774072 |doi=10.1186/cc2978|url=http://ccforum.com/content/9/2/158 | pmc=1175909}}</ref><ref name="AmFamPract2002">{{cite journal |author=Sauret JM, Marinides G, Wang GK |title=Rhabdomyolysis |journal=Am Fam Physician |volume=65 |issue=5 |pages=907–12 |year=2002 |pmid=11898964 |url=http://www.aafp.org/afp/20020301/907.html}}</ref>
Swelling of the damaged muscle occasionally leads to [[compartment syndrome]], the compression by swollen muscle of surrounding tissues in the same [[fascial compartment]] (such as [[nerve]]s and [[blood vessel]]s), leading to damage or loss of function in the part of the body supplied by these structures. Symptoms of this complication include decreased blood supply, decrease in sensation, or pain in the affected limb.<ref name="AmFamPract2002"/>
Release of the components of muscle tissue into the bloodstream leads to disturbances in [[electrolyte]]s, causing [[nausea]], [[vomiting]], [[mental confusion|confusion]], [[coma]] and [[cardiac arrhythmia]]s (abnormal heart rate and rhythm). Furthermore, damage to the kidneys may lead to dark (tea-colored) urine or a marked decrease ([[oliguria]]) or absence ([[anuria]]) of urine production, usually about 12–24 hours after the initial muscle damage. Finally, disruptions in [[coagulation|blood clotting]] may lead to the development of a state called [[disseminated intravascular coagulation]].<ref name=CritCare2005/><ref name="AmFamPract2002"/>
==Causes==
[[Image:Oklahomacitybombing-DF-ST-98-01356.jpg|thumb|right|[[Alfred P. Murrah Federal Building]] after a 1995 bombing that injured or killed more than 1,000 people. Collapsing buildings can cause crush injuries that trigger rhabdomyolysis.]]
Anything that destroys muscle tissue can cause rhabdomyolysis. The causes of rhabdomyolysis can be classified as either physical or non-physical. Physical rhabdomyolysis is in some situations confined to a particular area of the body, while rhabdomyolysis due to other causes tends to affect all muscles simultaneously.<ref name=CritCare2005/>
===Physical causes===
Recognized physical causes for rhabdomyolysis are:<ref name=CritCare2005/>
* Traumatic compression of muscles: [[crush syndrome]] (e.g. in earthquakes), [[car accident]], confinement in a fixed position (e.g. after a [[stroke]], due to [[drunkenness]] or in prolonged [[surgery]]), [[Torture|physical torture]] or [[Physical abuse|abuse]]
* Obstruction of blood supply to muscles: [[Thrombosis|arterial thrombosis]] (blood clots forming locally) or [[embolism]] (clots or other debris from elsewhere in the body), [[Hemostat|clamping of an artery]] during surgery, generally reduced blood supply in [[shock (medical)|shock]] or [[sepsis]] (due to any cause)
* Excessive muscle strain or activity: extreme [[physical exercise]] (particularly when poorly hydrated), [[delirium tremens]] (alcohol withdrawal), [[tetanus]], prolonged [[seizure]]s or [[status epilepticus]]
* Electrical: [[lightning]], high-voltage [[electric shock]], including [[electroshock weapon]] injuries<ref>{{cite journal |author=Fish RM, Geddes LA |title=Effects of stun guns and tasers |journal=Lancet |volume=358 |issue=9283 |pages=687–8 |year=2001 |month=September |pmid=11551573 |doi=10.1016/S0140-6736(01)05950-5}}</ref>
===Non-physical causes===
Non-physical causes reported to cause rhabdomyolysis include:<ref name=CritCare2005/>
* Disorders of muscle energy supply (usually hereditary enzyme problems): [[Primary carnitine deficiency|carnitine deficiency]], [[Carnitine palmitoyltransferase I deficiency|CPT type I]] or [[Carnitine palmitoyltransferase II deficiency|type II deficiency]], [[Glycogen storage disease type V|McArdle's disease]], various defects in the [[Mitochondrial disease|mitochondrial respiratory chain]], [[phosphofructokinase deficiency]], [[Very long-chain acyl-coenzyme A dehydrogenase deficiency|VLCAD deficiency]]<ref name="pmid9973285">{{cite journal |author=Andresen BS, Olpin S, Poorthuis BJ, ''et al'' |title=Clear correlation of genotype with disease phenotype in very-long-chain acyl-CoA dehydrogenase deficiency |journal=Am. J. Hum. Genet. |volume=64 |issue=2 |pages=479–94 |year=1999 |pmid=9973285 |doi=10.1086/302261 | pmc=1377757}}</ref>
* Poisons such as heavy metals and venom from insects or snakes
* Foodborne toxins, e.g. [[coniine]] from [[quail]] that have consumed [[Conium|hemlock]] (coturnism),<ref name=Rizzi1991>{{cite journal |author=Rizzi D, Basile C, Di Maggio A, ''et al'' |title=Clinical spectrum of accidental hemlock poisoning: neurotoxic manifestations, rhabdomyolysis and acute tubular necrosis |journal=Nephrol. Dial. Transplant. |volume=6 |issue=12 |pages=939–43 |year=1991 |pmid=1798593 |doi=}}</ref> ''[[Tricholoma equestre]]'' mushrooms in France and Poland,<ref name="Bedry">{{cite journal |author=Bedry R, Baudrimont I, Deffieux G, ''et al'' |title=Wild-mushroom intoxication as a cause of rhabdomyolysis |journal=N. Engl. J. Med. |volume=345 |issue=11 |pages=798–802 |year=2001 |pmid=11556299|doi=10.1056/NEJMoa010581}}</ref> and an unidentified toxin in fish ([[Haff disease]])<ref name="Buchholz">{{cite journal |author=Buchholz U, Mouzin E, Dickey R, Moolenaar R, Sass N, Mascola L |title=Haff disease: from the Baltic Sea to the U.S. shore |journal=Emerging Infect. Dis. |volume=6 |issue=2 |pages=192–5 |year=2000 |pmid=10756156 |url=http://www.cdc.gov/ncidod/EID/vol6no2/buchholtz.htm}}</ref>
* Drugs of abuse,<ref name="pmid10863119">{{cite journal |author=Richards JR |title=Rhabdomyolysis and drugs of abuse |journal=J Emerg Med |volume=19 |issue=1 |pages=51–6 |year=2000 |pmid=10863119 |doi=10.1016/S0736-4679(00)00180-3|url=http://linkinghub.elsevier.com/retrieve/pii/S0736-4679(00)00180-3}}</ref> including: [[ethanol]],<ref name="pmid7587180">{{cite journal |author=Bessa O |title=Alcoholic rhabdomyolysis: a review |journal=Conn Med |volume=59 |issue=9 |pages=519–21 |year=1995 |pmid=7587180 |doi=}}</ref> [[methamphetamine]]s,<ref name="pmid17990840">{{cite journal |author=Winslow BT, Voorhees KI, Pehl KA |title=Methamphetamine abuse |journal=Am Fam Physician |volume=76 |issue=8 |pages=1169–74 |year=2007 |pmid=17990840 |url=http://www.aafp.org/afp/20071015/1169.html}}</ref> [[cocaine]],<ref name="pmid10692510">{{cite journal |author=van der Woude FJ |title=Cocaine use and kidney damage |journal=Nephrol. Dial. Transplant. |volume=15 |issue=3 |pages=299–301 |year=2000 |pmid=10692510 |url=http://ndt.oxfordjournals.org/cgi/content/full/15/3/299 |doi=10.1093/ndt/15.3.299}}</ref> heroin,<ref name="pmid11140805">{{cite journal |author=Rice EK, Isbel NM, Becker GJ, Atkins RC, McMahon LP |title=Heroin overdose and myoglobinuric acute renal failure |journal=Clin. Nephrol. |volume=54 |issue=6 |pages=449–54 |year=2000 |pmid=11140805}}</ref> [[phencyclidine]] (PCP),<ref name="pmid2201519">{{cite journal |author=Baldridge EB, Bessen HA |title=Phencyclidine |journal=Emerg. Med. Clin. North Am. |volume=8 |issue=3 |pages=541–50 |year=1990 |pmid=2201519 |doi=}}</ref> [[ketamine]],<ref name="pmid10802423">{{cite journal |author=Weiner AL, Vieira L, McKay CA, Bayer MJ |title=Ketamine abusers presenting to the emergency department: a case series |journal=J Emerg Med |volume=18 |issue=4 |pages=447–51 |year=2000 |pmid=10802423 |doi=10.1016/S0736-4679(00)00162-1|url=http://linkinghub.elsevier.com/retrieve/pii/S0736-4679(00)00162-1}}</ref> 3,4-methylenedioxymethamphetamine (MDMA or Ecstasy)<ref name="pmid12063892">{{cite journal |author=Smith KM, Larive LL, Romanelli F |title=Club drugs: methylenedioxymethamphetamine, flunitrazepam, ketamine hydrochloride, and gamma-hydroxybutyrate |journal=Am J Health Syst Pharm |volume=59 |issue=11 |pages=1067–76 |year=2002 |pmid=12063892}}</ref><ref name="pmid16595612">{{cite journal |author=Hall AP, Henry JA |title=Acute toxic effects of 'Ecstasy' (MDMA) and related compounds: overview of pathophysiology and clinical management |journal=Br J Anaesth |volume=96 |issue=6 |pages=678–85 |year=2006 |pmid=16595612 |doi=10.1093/bja/ael078|url=http://bja.oxfordjournals.org/cgi/content/full/96/6/678}}</ref>
* Medications:
** [[statin]]s, especially when prescribed in combinations with [[fibrate]]s. [[Cerivastatin]] (Baycol) was withdrawn in 2001 after numerous reports of rhabdomyolysis. Other statins have a small risk of 0.44 cases per 10,000 patients annually, which increases to 5.98 if a fibrate is added.<ref name="Graham2004">{{cite journal |author=Graham DJ, Staffa JA, Shatin D, ''et al'' |title=Incidence of hospitalized rhabdomyolysis in patients treated with lipid-lowering drugs |journal=JAMA |volume=292 |issue=21 |pages=2585–90 |year=2004 |pmid=15572716 |doi=10.1001/jama.292.21.2585| url=http://jama.ama-assn.org/cgi/content/full/292/21/2585}}</ref> However, other studies detected no increased risk from statins.<ref name=Nichols2007>{{cite journal |author=Nichols GA, Koro CE |title=Does statin therapy initiation increase the risk for myopathy? An observational study of 32,225 diabetic and nondiabetic patients |journal=Clin Ther |volume=29 |issue=8 |pages=1761–70 |year=2007 |pmid=17919557 |doi=10.1016/j.clinthera.2007.08.022|url= http://linkinghub.elsevier.com/retrieve/pii/S0149-2918(07)00257-3
}}</ref>
**[[anti-psychotic]] medications may cause [[neuroleptic malignant syndrome]], which can cause severe muscle rigidity, with rhabdomyolysis and [[hyperpyrexia]]
**[[neuromuscular blocking agents]], used in [[anasthesia]] may cause [[malignant hyperthermia]], also associated with rhabdomyolysis
** medications that interfere with potassium levels (e.g. [[diuretic]]s)
* Infections: [[Coxsackie A virus|Coxsackie virus]], ''[[Plasmodium falciparum]]'' ([[malaria]]), [[herpesviridae|herpes viruses]], ''[[Legionella pneumophila]]'', [[Salmonella]] and ''[[Francisella tularensis]]'' ([[tularemia]])
* [[Electrolyte disturbance|Electrolyte]] and metabolic disturbances: increased [[plasma osmolality]], [[hypernatremia|hyper-]] and [[hyponatremia]] (elevated or reduced blood sodium levels), [[hypokalemia]] (low potassium levels), [[hypocalcemia]] (low calcium levels), [[hypophosphatemia]] (low phosphate levels), [[ketoacidosis]] (e.g. in [[diabetes]]) or [[hypothyroidism]] (abnormally low thyroid function)
* Autoimmune muscle damage: [[polymyositis]], [[dermatomyositis]]
==Diagnosis==
[[Image:Creatine kinase.PNG|right|thumb|[[Creatine kinase]] (M chain), the muscle energy enzyme elevated in the blood of patients with rhabdomyolysis.]]
The diagnosis may be suspected in anyone who has suffered a trauma, crush injury or prolonged immobilization, but it may also be identified at a later stage due to deteriorating kidney function (abnormally raised or increasing [[creatinine]] and [[urea]] levels, falling urine output) or typical pink-red discoloration of the urine. High [[potassium]] levels (hyperkalemia) tend to be a feature. Low [[calcium in biology|calcium]] levels may be present in the initial stage, and about a quarter of patients have abnormal [[liver function tests]] due to liver damage.<ref name=CritCare2005/> [[Dipstick]] analysis of urine may reveal a positive result for "blood" in the absence of [[red blood cell]]s on [[microscopy]], as the reagent reacts with myoglobin.<ref name="Vanholder2000">{{cite journal |author=Vanholder R, Sever MS, Erek E, Lameire N |title=Rhabdomyolysis |journal=J. Am. Soc. Nephrol. |volume=11 |issue=8 |pages=1553–61 |year=2000 |pmid=10906171 |url=http://jasn.asnjournals.org/cgi/content/full/11/8/1553}}</ref> Cardiac [[troponin]] levels (normally used to diagnose heart damage) are increased in half of all cases, but not associated with other evidence of heart damage in at least a third of those cases.<ref name="pmid16291441">{{cite journal |author=Li SF, Zapata J, Tillem E |title=The prevalence of false-positive cardiac troponin I in ED patients with rhabdomyolysis |journal=Am J Emerg Med |volume=23 |issue=7 |pages=860–3 |year=2005 |pmid=16291441 |doi=10.1016/j.ajem.2005.05.008}}</ref>
The most reliable test in the diagnosis of rhabdomyolysis is the level of [[creatine kinase]] (CK) in the blood. This enzyme is released by damaged muscle, and levels above 5 times the upper limit of normal (ULN) indicate rhabdomyolysis. Depending on the extent of the rhabdomyolysis, levels up to 100,000 units are not unusual.<ref name="Vanholder2000"/> Initial and peak CK levels have a linear relationship with the risk of acute renal failure: the higher the CK, the more likely it is that kidney damage will occur.<ref name="deMeijer2003">{{cite journal |author=de Meijer AR, Fikkers BG, de Keijzer MH, van Engelen BG, Drenth JP |title=Serum creatine kinase as predictor of clinical course in rhabdomyolysis: a 5-year intensive care survey |journal=Intensive Care Med |volume=29 |issue=7 |pages=1121–5 |year=2003 |pmid=12768237 |doi=10.1007/s00134-003-1800-5}}</ref> CK levels rise after 12 hours of the initial damage, remain elevated for 1–3 days and then fall gradually. Myoglobin has a short half-life, and is therefore less useful as a diagnostic test in the later stages.<ref name=CritCare2005/>
[[Compartment syndrome]] is a clinical diagnosis (i.e. no tests conclusively prove its presence or absence), but direct measurement of the pressure in a fascial compartment may be used to assess its severity. Values of 30–50 [[Torr|mmHg]] (4–6.5 [[Pascal (unit)|kPa]]) indicate severe compartment syndrome and possible need for [[fasciotomy]], which is an incision to relieve increased pressure.<ref name="Vanholder2000"/>
==Pathophysiology==
Damage to skeletal muscle may take various forms. Crush injuries damage muscle cells directly, as well as impairing the blood supply; other causes may damage muscle cells by interfering with their [[metabolism]]. The muscle tissue rapidly fills with fluid from the bloodstream, as well as [[sodium]] and [[chloride]]. The swelling itself may lead to destruction of muscle cells, but those cells that survive react by pumping sodium out of the cells in exchange for calcium (through the [[sodium-calcium exchanger]]). The accumulation of calcium in the [[sarcoplasmic reticulum]] leads to continuous [[muscle contraction]] and depletion of [[Adenosine triphosphate|ATP]], the main carrier of energy in the cell. Calcium also stimulates the enzyme [[phospholipase A2]], which damages the [[mitochondrion]], causing the production of [[reactive oxygen species]].<ref>{{cite journal |author=Malis CD, Bonventre JV |title=Susceptibility of mitochondrial membranes to calcium and reactive oxygen species: implications for ischemic and toxic tissue damage |journal=Prog. Clin. Biol. Res. |volume=282 |issue= |pages=235–59 |year=1988 |pmid=3071798}}</ref> In addition, [[neutrophil granulocyte]]s (the most abundant [[white blood cell]]s) enter the muscle tissue, producing an [[inflammation|inflammatory]] reaction and releasing even more reactive oxygen species.<ref name="Vanholder2000"/>
The swollen and inflamed muscle may directly compress structures in the same fascial compartment, causing compartment syndrome. The swelling may also further compromise blood supply into the area. Finally, destroyed muscle cells release potassium, [[phosphate]], myoglobin (a [[heme]] and therefore [[iron]]-containing protein), creatine kinase (an enzyme) and [[uric acid]] (a breakdown product of [[purine]]s from [[DNA]]) into the blood. Activation of the coagulation system may precipitate diffuse intravascular coagulation.<ref name="Vanholder2000"/> High potassium levels ([[hyperkalemia]]) may lead to potentially fatal disruptions in heart rhythm. Phosphate precipitates with calcium from the circulation, leading to hypocalcemia (low calcium levels).<ref name="Vanholder2000"/>
Various consequences of muscle swelling and breakdown together may cause renal failure. The swelling of large areas of muscle tissue leads to depletion of fluid from the circulation, causing relative lack of blood flow to the kidney. Uric acid may precipitate in the [[Nephron#Renal tubule|tubules]], causing obstruction. Finally, the most important problem is the accumulation of myoglobin in the tubules.<ref name=Vanholder2000/> [[Myoglobinuria]] (the appearance of myoglobin in the urine) occurs when the levels in plasma exceed 1.5 mg/dl.<ref name="CritCare2005"/> As the kidneys reabsorb more water from the filtrate, myoglobin forms casts that obstruct the normal flow of fluid through the [[nephron]]; the condition is worsened by high levels of uric acid and acidification of the filtrate. Iron released from the myoglobin generates reactive oxygen species, damaging the kidney cells. [[Acute tubular necrosis]] (destruction of the cells of tubules) occurs, preventing the kidney from performing its normal excretory functions (hence the fall in [[glomerular filtration rate]]), electrolyte regulation (hence worsening potassium levels) and hormone production (hence decreased [[vitamin D]] processing, further worsening the low calcium levels).<ref name="Vanholder2000"/>
==Treatment==
===Fluid therapy===
The main goal of treatment is to treat shock and preserve kidney function. Initially this is done through the administration of generous amounts of [[intravenous fluid]]s, usually [[Saline (medicine)|saline]] (0.9% weight per volume [[sodium chloride]] solution). In victims of crush syndrome (e.g. in earthquakes), it is recommended to start this even before the casualties are extracted from collapsed structures. This will ensure sufficient circulating volume to deal with the muscle cell swelling (which typically commences when blood supply is restored), and to prevent the deposition of myoglobin in the kidneys. Amounts of 6 to 12 liters over 24 hours are recommended.<ref name="Vanholder2000"/>
While many sources recommend [[mannitol]], which acts by [[osmosis]] to ensure urine production and may prevent heme deposition in the kidney, there are no studies directly demonstrating its benefit. Similarly, the addition of [[bicarbonate]] to the fluids is intended to improve [[acidosis]] (high acid level of the blood) and thereby prevent cast formation in the kidneys, but there is limited evidence that it has benefits above saline alone. [[Furosemide]], a [[loop diuretic]], is often used to ensure sufficient urine production.<ref name="CritCare2005"/><ref name="Vanholder2000"/>
===Electrolytes===
In the initial stages, electrolyte levels are often abnormal and require correction. Calcium levels initially tend to be low, but as the patient's condition improves calcium is released from where it has precipitated with phosphate, and vitamin D production resumes, leading to [[hypercalcemia]] (abnormally high calcium levels). This "overshoot" occurs in 20–30% of those people who have developed kidney failure.<ref name="CritCare2005"/>
===Acute renal failure===
[[Image:Hemodialysismachine.jpg|250px|right|thumb|A hemodialysis machine]]
If kidney dysfunction (acute renal failure, ARF) develops (usually 1–2 days after the initial muscle trauma), [[renal replacement therapy]] (RRT) may be required. This may take the form of [[hemodialysis]] or hemofiltration. Certain types of [[peritoneal dialysis]] are also effective in removing the high levels of toxic solutes that can accumulate in rhabdomyolytic renal failure, and may be the only available option in some [[Third World]] settings.<ref name="Chitalia2002">{{cite journal |author=Chitalia VC, Almeida AF, Rai H, ''et al'' |title=Is peritoneal dialysis adequate for hypercatabolic acute renal failure in developing countries? |journal=Kidney Int. |volume=61 |issue=2 |pages=747–57 |year=2002 |pmid=11849419 |doi=10.1046/j.1523-1755.2002.00177.x| url=http://www.nature.com/ki/journal/v61/n2/full/4492795a.html}}</ref>
RRT removes excess potassium, acid and phosphate that accumulates when the kidneys are unable to function normally and is required until kidney function is regained.<ref name="CritCare2005"/>
===Other complications===
{{main|compartment syndrome|diffuse intravascular coagulation}}
Compartment syndrome and diffuse intravascular coagulation, as well as any other complications of rhabdomyolysis, are treated in the same way as in other situations in which they may arise.<ref name="CritCare2005"/>
==Prognosis==
The prognosis depends significantly on the underlying cause and whether any complications occur. Rhabdomyolysis patients who experience acute renal failure (ARF) may have a [[mortality rate]] as high as 20%.<ref name=CritCare2005/>
==Epidemiology==
Rhabdomyolysis is a relatively rare condition in everyday life. The rate of rhabdomyolysis in the general population is difficult to establish with certainty, but was estimated by one U.S. study to be about 2 cases per 10,000 person-years.<ref name=Nichols2007/> Another study found 26,000 cases per year in the U.S.<ref name="AmFamPract2002"/>
Up to 85% of patients with major traumatic injuries will experience some degree of rhabdomyolysis.<ref name=CritCare2005/> Approximately 15% of patients with rhabdomyolysis will experience acute renal failure as a complication, although rates vary between studies.<ref name="AmFamPract2002"/> Rhabdomyolysis is a significant cause of renal failure, and may account for as much as a quarter of the cases of this condition.<ref name=CritCare2005/>
Crush injury is common in major disasters, but especially so in earthquakes. The [[1988 Spitak earthquake]] led to the recognition that many initial survivors of major earthquakes later succumb to rhabdomyolysis. In 1995 the [[International Society of Nephrology]], a worldwide body of kidney experts, established a group named the Renal Disaster Relief Task Force to assist in similar emergencies. Its volunteer doctors and nurses assisted for the first time in the [[1999 İzmit earthquake]] in [[Turkey]], where 462 patients received dialysis, with positive results. Treatment units are generally established outside the immediate disaster area, as [[aftershock]]s could potentially injure or kill staff and make equipment unusable.<ref name=CritCare2005/>
==History==
The [[Bible]] may contain an early account of rhabdomyolysis. In {{Bibleverse||Numbers|11:31–33}}, the Pentateuch relates that the Jews demanded wholesome food while traveling in the desert; God sent quail in response to the complaints, and people ate large quantities of quail meat. A plague then broke out, killing numerous people. Rhabdomyolysis after consuming quail was described in more recent times, and called "coturnism" (after ''[[Coturnix]]'', the main quail genus).<ref name="quailARF">{{cite journal |author=Billis AG, Kastanakis S, Giamarellou H, Daikos GK |title=Acute renal failure after a meal of quail |journal=Lancet |volume=2 |issue=7726 |pages=702 |year=1971 |pmid=4105725 |doi=}}</ref> It is known that migrating quail consume large amounts of hemlock, which contains the poisonous alkaloid coniine, and a 1991 study showed that coniine may cause rhabdomyolysis.<ref name=Rizzi1991/><ref name=CritCare2005/>
In modern times, early reports from the [[1908 Messina earthquake]] and [[World War I]] on renal failure after injury were followed by studies by E. Bywaters and D. Beall on four victims of The Blitz in 1941. A role for myoglobin was suspected.<ref>{{cite journal|author=Bywaters EG, Beall D|title=Crush injuries with impairment of renal function|journal=Br Med J|year=1941|volume=1|pages=427–32}}<br />Reprinted in:
*{{cite journal|author=Bywaters EG, Beall D|title=Crush injuries with impairment of renal function |journal=J Am Soc Nephrol|year=1998|volume=9|pages=322–32| pmid=9527411| url=http://jasn.asnjournals.org/cgi/reprint/9/2/322}}</ref> Myoglobin was demonstrated in the urine of victims by [[spectroscopy]],<ref>{{cite journal |author=Bywaters EG, Delory GE, Rimington C, Smiles J |title=Myohaemoglobin in the urine of air raid casualties with crushing injury |journal=Biochem. J. |volume=35 |issue=10–11 |pages=1164–8 |year=1941 |pmid=16747400 | pmc=1265619}}</ref> and it was noted that the kidneys of victims resembled those of patients who had received an incorrectly matched [[blood transfusion]] (an observation made in 1925), with the received blood being destroyed by the immune system ([[hemolysis]]) and [[hemoglobin]] accumulating in the kidney.<ref>{{cite journal|author=Bywaters EGL|title=Ischaemic muscle necrosis|journal=J Am Med Assoc|year=1944|volume=124|pages=1103–9}}</ref> In 1944 Bywaters demonstrated experimentally that the renal failure was mainly caused by myoglobin.<ref name="Vanholder2000"/><ref>{{cite journal|author=Bywaters EGL, Popjak G|title=Experimental crushing injury: Peripheral vascular collapse and other effects of muscle necrosis in the rabbit|journal=Surg Gynecol Obstet|year=1942|volume=75|pages=612–627}}</ref>
==References==
{{reflist|2}}
{{Consequences of external causes}}
[[Category:Injuries]]
[[Category:Nephrology]]
[[Category:Intensive care medicine]]
[[Category:Surgery]]
[[da:Rhabdomyolyse]]
[[de:Rhabdomyolyse]]
[[fr:Rhabdomyolyse]]
[[it:Rabdomiolisi]]
[[he:תמס שריר]]
[[nl:Rhabdomyolyse]]
[[pl:Rabdomioliza]]
[[ja:横紋筋融解症]]
[[zh:横纹肌溶解症]]