crush syndrome

圧挫症候群

WordNet

1. become injured, broken, or distorted by pressure; "The plastic bottle crushed against the wall"
2. break into small pieces; "The car crushed the toy"
3. the act of crushing (同)crunch, compaction
4. a dense crowd of people (同)jam, press
5. humiliate or depress completely; "She was crushed by his refusal of her invitation"; "The death of her son smashed her" (同)smash, demolish
6. a pattern of symptoms indicative of some disease
7. a complex of concurrent things; "every word has a syndrome of meanings"
8. physically or spiritually devastating; often used in combination; "a crushing blow"; "a crushing rejection"; "bone-crushing" (同)devastating
9. treated so as to have a permanently wrinkled appearance; "crushed velvet"
10. the leg from the knee to foot

PrepTutorEJDIC

1. …'を'『押しつぶす』,ぺしゃんこにする《+『up』+『名,』+『名』+『up』》 / …'を'『砕く』,粉々にする;…を砕いて(…に)する《+『名』+『into』+『名』》 / (…に)…'を'押しつける《+『名』+『against』+『名』》;(…に)…'を'押し込む《+『名』+『into』+『名』》 / (…から)…'を'押しつぶして出す,しぼり出す《+『名』+『from』+『名』》 / …'を'ぎゅっと抱きしめる / …'を'打ちのめす,打ちひしぐ《+『down』+『名,』+『名』+『down』》 / 『つぶれる』,ぺしゃんこになる;くしゃくしゃになる / 『砕ける』,粉々になる / (…に)押し合って入る,殺到する《+『into』(『through』)+『名』》 / 〈C〉《単数形で》押し合いへし合い,殺到 / 〈C〉《話》《単数形で》大混雑の集会,すしづめの集会 / 〈U〉《英》(押しつぶして出した)果汁 / 〈C〉《話》(…に)のぼせ上がること,(…への)べたぼれ《+『on』+『名』》;のぼせ上がった相手
2. (疾患の徴候となる一群の)症徴候,症候群 / (事件・社会的状態などのパターンを示す)徴候形態

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2012/12/20 08:16:59」(JST)

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[Wiki en表示]

Crush syndrome
Classification and external resources
ICD-10	T79.5
ICD-9	958.5
DiseasesDB	13135
MeSH	D003444

Crush syndrome (also traumatic rhabdomyolysis or Bywaters' syndrome) is a medical condition characterized by major shock and renal 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. Cases occur commonly in catastrophes such as earthquakes, to victims that have been trapped under fallen masonry.

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 quaternary blast injury.

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

The syndrome was discovered by British physician Eric Bywaters in patients during the 1941 London Blitz. 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.

Seigo Minami, a Japanese physician, first reported the crush syndrome in 1923. He 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.

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."

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 P’s: 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. 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. 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/hr, limited for "pediatric patients and patients with history of cardiac or renal dysfunction."

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 hypokalemia. Admission to a 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:

• calcium gluconate 10% 10ml or calcium chloride 10% 5ml 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 25-50g with sorbitol 20% 100mL by mouth or rectum.

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

References

• 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. http://content.nejm.org/cgi/pmidlookup?view=short&pmid=16525142&promo=ONFLNS19.

External links

• Life or Limb: What happens when your leg gets trapped under a building?

UpToDate Contents

全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.

• 1. 挫滅関連の急性腎障害（急性腎不全） crush related acute kidney injury acute renal failure
• 2. 横紋筋融解症の臨床症状および診断 clinical manifestations and diagnosis of rhabdomyolysis
• 3. 成人患者における重度の四肢外傷 severe extremity injury in the adult patient
• 4. 横紋筋融解症の原因 causes of rhabdomyolysis
• 5. 四肢の急性コンパートメント症候群 acute compartment syndrome of the extremities

English Journal

• Early fluid resuscitation with hypertonic solution in a rat crush injury model.

• Song XB, Zhou XL, Ni SZ, Yang GF, Tian SF, Shan J, Zhao Y, Shen J, Wang X.Source*Emergency Department of Zhongnan Hospital of Wuhan University; †Medical College of Wuhan University; and ‡Pathology Department of Zhongnan Hospital of Wuhan University, Wuchang, Wuhan, Hubei, China.
• Shock (Augusta, Ga.).Shock.2013 May;39(5):453-9. doi: 10.1097/SHK.0b013e31828e674a.
• AIM OF THE STUDY: The aim of the study was to evaluate the effects of bolus infusion of hypertonic hydroxyethyl starches (HHESs) and continuous infusion of hypertonic saline (HTS) in the early resuscitation in crush syndrome.METHODS: A rat model of crush injury was established. Rats were randomly di
• PMID 23510905

• Effect of free radical scavenger on c-jun activation in rats with crush syndrome.

• Zhai W, Xu YF, Peng B, Zhang HM, Huang JH, Liu M, Wang GC, Zheng JH.AbstractObjectives: To evaluate the relationship between reactive oxygen species (ROS)-mediated kidney injuries and Jun N-terminal kinase (JNK) activity and the therapeutic effects of tempol in crush syndrome (CS) model rats. Methods: Male Wister rats were randomly divided into sham operation group (SOG), CS groups (CS6G, CS12G and CS24G) and tempol treatment group (TG, a ROS scavenger). CS model rats were established by crushing the hind limbs of rats with 15 kg pressure for 6 hours, and inferior caval vein blood and kidney samples were harvested at 6, 12, 24 hours after removing crush pressure. In TG, 100 mg/kg tempol was intraperitoneally injected into CS model rats after withdraw of crush pressure. In SOG, rats were fixed on the board without any crush pressure. The activation of c-jun was determined by western blotting. Serological parameters and the content of malondialdehyde (MDA) in kidney tissues were determined by standard methods. Results: Acute kidney injury reached the peak at 12 hours after the crush pressure. Compared with SOG, the content of phosphorylated c-jun was significantly higher in CSG and TG (p < 0.05), and the content of phosphorylated c-jun in the CSG was significantly higher than that in TG (p < 0.05). Interestingly, the changes of the MDA content in the kidney tissues of the 3 groups were similar to the changes of phosphorylated c-jun content. Conclusion: ROS-mediated phosphorylation of c-jun may play important roles in the acute kidney injury of CS rats. Tempol can inhibit the phosphorylation of c-jun and alleviate the acute kidney injury.
• International journal of clinical pharmacology and therapeutics.Int J Clin Pharmacol Ther.2013 Apr 23. [Epub ahead of print]
• Objectives: To evaluate the relationship between reactive oxygen species (ROS)-mediated kidney injuries and Jun N-terminal kinase (JNK) activity and the therapeutic effects of tempol in crush syndrome (CS) model rats. Methods: Male Wister rats were randomly divided into sham operation group (SOG), C
• PMID 23611574

Japanese Journal

• 圧挫症候群(crush syndrome) (特集 急性腎障害(AKI) : 概念の確認から,さらなる予後改善を目指して) -- (AKIの病態)

• 井上 潤一
• 内科 110(3), 369-372, 2012-09
• NAID 40019418825

• 専門医部会 内科医と災害医療 災害時の圧挫症候群と環境性体温異常

• 阿南 英明
• 日本内科学会雑誌 101(7), 2108-2114, 2012-07-10
• NAID 40019392745

Related Links

• 挫滅症候群 - Wikipedia

松木明知「crush syndromeを世界で最初に報告した皆見省吾」（麻酔55(2) 222-228, 2006）; ^ Medical discoveries - Who and when- Schmidt JF. Springfield: CC Thomas, 1959. p.115. ^ Morton's medical bibliography -An annotated check-list of texts ...

• Crush syndrome - Wikipedia, the free encyclopedia

Crush syndrome (also traumatic rhabdomyolysis or Bywaters' syndrome) is a medical condition characterized by major shock and renal failure after a crushing injury to skeletal muscle. Crush injury is compression of extremities or other parts of ...

Related Pictures

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★リンクテーブル★

リンク元	「筋疾患」「圧挫症候群」「挫滅症候群」
関連記事	「crush」「crus」「syndrome」

「筋疾患」

　　[★]

英

myopathy, muscular disease, muscular disorder

同

ミオパシー、ミオパチー、筋原性疾患、筋症

関

筋萎縮

• 神経系 091125IV

筋疾患と神経疾患

	筋疾患	神経疾患
	myopathy	neuropathy
筋力低下	近位筋優位	遠位筋優位

筋疾患と末梢神経疾患の鑑別

	神経原性	筋原性
	下位運動ニューロン障害
筋萎縮	遠位筋中心	近位筋中心
線維束性攣縮	あり	なし
筋電図	高振幅	低振幅
	long duration	short duration
	giant spike
	(代償的な筋線維の興奮)
筋逸脱酵素	ー	CK↑
筋生検	群性萎縮(小角化線維)	孤発性萎縮(筋線維の大小不同、中心核の増加)
疾患	ALS	筋ジストロフィー
	SPMA	多発性筋炎

分類

遺伝性	遺伝性ミオパチー	筋ジストロフィー
		ミトコンドリアミオパチー
非遺伝性	外因性筋障害	ステロイドミオパチー
		crush syndrome
		ischemia
	炎症性ミオパチー	多発筋炎・皮膚筋炎
	内分泌性・代謝疾患性	甲状腺機能低下症
		低カリウム性ミオパチー
		アルコール性ミオパチー
	その他

検査

SOR.356

• 血液検査：

• 血液生化学：筋逸脱酵素(クレアチンキナーゼ、アルドラーゼ、LDH)

• 筋電図：筋原性変化(低電位差、低振幅波、多相性)
• 筋生検：筋線維の大小不同、壊死繊維、再生像、細胞浸潤など
• MRI：T2で高信号の変化が見られるものがある(皮膚筋炎)

「圧挫症候群」

　　[★]

英

crush syndrome

同

挫滅症候群、クラッシュ症候群、バイウォーターズ症候群 Bywaters syndrome

国試

• 100D035、100D036

「挫滅症候群」

　　[★] 圧挫症候群

同

crush syndrome

「crush」

　　[★]

• n.

• 粉砕、挫滅

• v.

• 粉砕する、挫滅する

関

crush injury、grind、grinding

　 　 　 　 　 　

「crus」

　　[★] 下腿

関

lower leg

　

「syndrome」

　　[★]

• n.

• 症候群