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| {{SK}} Bywaters' syndrome | | {{SK}} Bywaters' syndrome |
| ==Overview==
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| '''Crush syndrome''' (also '''''[[physical trauma|traumatic]] [[rhabdomyolysis]]''''' is a [[medical]] condition characterized by major [[Shock (medical)|shock]] and [[renal]] failure after a [[wikt:crush|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. <ref name=CDC>{{citation
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| | url = http://www.bt.cdc.gov/masscasualties/blastinjury-crush.asp
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| | publisher = [[Centers for Disease Control]]
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| | title = Blast Injuries: Crush Injuries & Crush Syndrome }}</ref> Cases occur commonly in catastrophes such as [[earthquake]]s, to victims that have been trapped under fallen masonry.
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| Typically affected areas of the body include lower extremities (74%), upper extremities (10%), and trunk (9%). They typically are caused by building collapse from [[explosives]], or [[earthquake]] and other natural disasters, or construction accidents. They also can be caused by cave-ins. Explosion-caused crush injury is [[blast injury#Quaternary injuries|quaternary blast injury]].
| | ==[[Crush syndrome overview|Overview]]== |
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| 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.
| | ==[[Crush syndrome historical perspective|Historical Perspective]]== |
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| ==Historical Perspective== | | ==[[Crush syndrome pathophysiology|Pathophysiology]]== |
| The syndrome was discovered by [[United Kingdom|British]] [[physician]] [[Eric Bywaters]] in patients during the 1941 [[London]] [[The Blitz|Blitz]].<ref>{{WhoNamedIt|synd|3870}}</ref><ref>{{cite journal |last=Bywaters |first=E. G. |last2=Beall |first2=D. |title=Crush injuries with impairment of renal function |journal=[[British Medical Journal|Br Med J]] |year=1941 |volume=1 |issue= 4185|pages=427–432 |doi= | pmid=20783577 |pmc=2161734}}</ref> [[Seigo Minami]], a Japanese physician, first reported the crush syndrome in 1923.<ref>{{cite journal |last=Minami |first=Seigo |year=1923 |title=Über Nierenveränderungen nach Verschüttung |journal=Virchows Arch. Patho. Anat. |volume=245 |issue=1 |pages= |doi=10.1007/BF01992107 }}</ref><ref> Medical discoveries - Who and when- Schmidt JF. Springfield: CC Thomas, 1959. p.115.</ref><ref>Morton's medical bibliography -An annotated check-list of texts illustrating History of medicine (Garrison-Morton). Aldershot: Solar Press; 1911. p.654.</ref> He studied the pathology of three soldiers who died in World War I from insufficiency of the kidney.
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| ==Pathophysiology==
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| 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 [[ischemia|ischemic]] conditions).
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| The specific action on the [[kidney]]s is not understood completely, but may be due partly to [[nephrotoxicity|nephrotoxic]] [[metabolite]]s of myoglobin.
| | ==[[Crush syndrome differential diagnosis|Differentiating Crush syndrome from other Diseases]]== |
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| [[Seigo Minami]]studied the pathology of three soldiers who died in World War I from insufficiency of the kidney. The renal changes were due to methohemoglobin 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. | | ==[[Crush syndrome natural history, complications and prognosis|Natural History, Complications and Prognosis]]== |
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| The most devastating systemic effects can occur when the crushing pressure is suddenly released, without proper preparation of the patient, causing '''reperfusion syndrome'''. 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." <ref>{{citation
| | ==Diagnosis== |
| | title = Nancy Caroline's Emergency Care in the Streets: Trauma Medical
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| | author = Nancy Caroline
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| | volume = 2
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| | edition = 6th |year= 2007
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| | isbn = 9780763742393
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| | page = 19-13
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| | url = http://books.google.com/books?id=f3ePQZDXpwwC&pg=PT115&lpg=PT115&dq=%22Crush+injury%22+smiling+death&source=bl&ots=E1Hk29q233&sig=y-gzvprDmpj9k_J3OBSx6zhh9js&hl=en&ei=-Xb0S9OWJML38AaU3_23Dg&sa=X&oi=book_result&ct=result&resnum=4&ved=0CB4Q6AEwAw#v=onepage&q=%22Crush%20injury%22%20smiling%20death&f=false}}</ref>
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| 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]].
| | [[Crush syndrome history and symptoms|History and Symptoms]] | [[Crush syndrome physical examination|Physical Examination]] | [[Crush syndrome laboratory findings|Laboratory Findings]] | [[Crush syndrome electrocardiogram|Electrocardiogram]] | [[Crush syndrome other diagnostic studies|Other Diagnostic Studies]] |
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| [[Compartment syndrome]] can be secondary to crush syndrome. Monitor for the classic 5 P’s: pain, pallor, parasthesias, pain with passive movement, and pulselessness. | |
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| ==Treatment== | | ==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. 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.
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| 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.<ref name="ARC">{{cite web |url=http://www.resus.org.au/policy/guidelines/section_9/guideline-9-1-7march2001.pdf |title=Emergency Management of a Crushed Victim |author= |date=March 2001 |work= |publisher=Australian Resuscitation Council |accessdate=20 July 2011}}</ref> [[St John Ambulance Australia]] First Responders are trained in the same manner.
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| <!-- these two recommendations seem contradictory to each other ~~~~ -->
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| ===Field management===
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| 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/hr, limited for "pediatric patients and patients with history of cardiac or renal dysfunction." <ref name=SF>{{citation
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| | publisher = San Francisco Emergency Medical Services Agency
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| | date = 1 July 2002
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| | id = Protocol: #P-101
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| | title = Crush Syndrome
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| | url = http://firespecialops.com/files/2010/02/San-Fran-EMS-Crush-Protocol.pdf}}</ref>
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| If the patient cannot be fluid loaded, this may be an indication for a [[tourniquet]] to be applied.
| | [[Crush syndrome medical therapy|Medical Therapy]] | [[Crush syndrome prevention|Prevention]] | [[Crush syndrome cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Crush syndrome future or investigational therapies|Future or Investigational Therapies]] |
| ===Initial hospital management===
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| The clinician must protect the patient against [[hypotension]], [[renal failure]], [[acidosis]], [[hyperkalemia]] and [[hypokalemia]]. Admission to a [[critical care|intensive care unit]], preferably one experienced in [[Trauma (medicine)|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.
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| 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.
| | ==Case Studies== |
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| To prevent hyperkalemia/hypocalcemia, consider the following adult doses:<ref name=CDC/>
| | [[Crush syndrome case study one|Case #1]] |
| *[[calcium gluconate]] 10% 10ml or [[calcium chloride]] 10% 5ml IV over 2 minutes
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| *[[sodium bicarbonate]] 1 meq/kg IV slow push
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| *regular [[insulin]] 5-10 U
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| *50% [[glucose]] 1-2 ampules IV bolus
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| *[[kayexalate]] 25-50g with sorbitol 20% 100mL by mouth or rectum.
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| Even so, cardiac arrythmias may develop; electrocardiographic monitoring is advised, and specific treatment begun promptly.
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| ==References==
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| <references/>
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| * {{cite journal |author=Sever MS, Vanholder R, Lameire N |title=Management of crush-related injuries after disasters |journal=[[N. Engl. J. Med.]] |volume=354 |issue=10 |pages=1052–63 |year=2006 |pmid=16525142 |doi=10.1056/NEJMra054329 |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=16525142&promo=ONFLNS19}}
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| ==External links== | | ==External links== |