Crush Syndrome (壓碎症候群)

Bombings, earthquakes, building collapse, train accidents and mining accidents. Crush injuries may result in fatal injury or severe metabolic abnormalities that may result in death. Careful monitoring of these patients is essential.

定 義 肌肉, 皮膚因直接壓傷, 造成體亦由血管露出, 產生水腫變化 並經由血液再灌注(reperfusion) 的機轉 定 義 肌肉, 皮膚因直接壓傷, 造成體亦由血管露出, 產生水腫變化 並經由血液再灌注(reperfusion) 的機轉 造成全身性多系統損傷 edema (excess fluid), oliguria (abnormally low excretion of urine) symptoms of renal failure.

肌肉承受缺血限度 1.5 小時, 可完全恢復, 4小時, 肌肉結構及功能損害且無法回復 7小時, 肌肉壞死 。

症 狀 limb may be tingling or numb 症 狀 limb may be tingling or numb swollen and hard tissue around injured body part bruising and formation of blisters body part may be pale and cool if arteries are compressed victim may feel weak or faint pulse becomes weak and rapid victim may become anxious or restless.

腔室症候群 症狀表現 因為肢體之骨骼肌肉腔室內壓力,高過微血管灌注壓，以致於神經,肌肉缺血，造成肢體的局部症狀。 患肢：腫脹疼痛的肢體；癱瘓無力及麻痺。 全身性：休克、高血鉀、低血鈣、血尿、腎衰竭

leaking of Na+, Cl-, & water into the sarcoplasm 致病機轉（1） leaking of Na+, Cl-, & water into the sarcoplasm Etiology:(flow of solutes & water across sarcolemma ) Unclear Multiple factors: vascular compromise; direct pressure to muscle; reoxygenation Inward leak --> trapping of (ECF) in the sarcoplasm cause muscle swelling interference with normal function of sarcolemmal Na-K adenotriphosphatase !!! aggressive fluid volume replacement to prevent irreversible shock hypovolemic and hemodynamic shock prerenal and later acute renal failure intracompartmental hypertension

致病機轉（2） leaking of Ca2+into the sarcoplasm hypocalcemia (<6mg/dl) aggravate hyperkalemic with cardiotoxicity activation of cytotoxic proteases Increased intracellular Ca2+ is thought to be the final common pathway of damage to cell ( Ca++ is a principle mediator of cellular injury,myocytes)

致病機轉（3） efflux of K+ hyperkalcemia and cardiotoxicity peripheral vasodilation ~75% of total body K+ resides in muscle

致病機轉（4） release of purines from affected muscle hyperuricemia (often > 20mg/dl) nephrotoxicity

致病機轉（5） Phosphorus hyperphosphatemia aggravate hypocalcemia metastatic calcification, including the kidney Hyperphosphatemia: often > 10-15 mg/dl

致病機轉（6） Myoglobin Most (50-85%) myoglobin circulating in the plasma is bound to hepatoglobin, and alpha 2- globulin. The plasma half-life of myoglobin is approximately 1-3 hours. Low levels of circulating myoglobin are cleared from the circulation by the reticuloendothelial system. Plasma levels of myoglobin > 0.5- 1.5 mg/dL are filtered by the kidneys.( injury to 100g of muscle) Nephrotoxicity, particularly with coexisting oliguria, aciduria and hyperuricosuria

致病機轉（7） Lactic acid Thromboplastin  D.I.C. metabolic acidosis;  aciduria Thromboplastin  D.I.C. Creatine kinase  extreme elevation Creatinine  creatinine/urea ratio CK oftne > 10000 U/ml, but no correlation exist between magnitude of the enzyme and risk of ARF Impaired renal function is rare when CK <2000U/ml

休克機轉 水和電解質持續流入受傷的肌 內在體液的喪失 脫水  外在體液的喪失 高血鉀、低血鈣  抑制心臟血管功能及 cytokinase 增加nitric oxides  壓傷肌肉內血管擴張 1.increase capillary permeability: >3 hours ischemia

腎衰竭的機轉 hypercoagulation 腎絲球內血栓 低血壓 腎血流量降低(renal-extrarenal constrictor system) 尿酸¸肌蛋白圓柱 腎小管栓塞 其他肌肉破壞後的產物¸例如鐵 急性高血磷酸(hyperphosphatemia)

診斷原則（Criteria） 肢體或軀幹被重物壓傷或夾傷 受傷部位呈現腫脹或神經方面的障礙，包括感覺或運動功能喪失 肌酸磷酐脢 (Creatinine Phosphokinase)高於 3,000 U/L 茶褐色的小便 (血尿或肌蛋白尿)

Emergency! Crush Syndrome 高度警覺: 被壓傷或動彈不得4小時以上的病人 避免壓迫症候群發生的方法: 早期發現並積極治療!!

建議急救流程（1） 當有任一肢體被解放時, 馬上給與靜脈注射生理食鹽水( 1 l/h)。一但病人被救出後, 就要監看動脈血氧壓力中央靜脈壓力及尿量 救出後, 以500㏄的生理食鹽水及5%葡萄糖水交替給與靜脈輸液, 維持 1 l/h 。 到醫院後, 加Sodium bicarbonate 50 mEq/l 到每一瓶5%葡萄糖水, 以維持尿液的 pH > 6.5 。 ( 第一天需要 bicarbonate 的量通常是 200-300 mEq/l ) Suggested volume replenishment during extrication of young adults or Resuscitation from prolonged coma

建議急救流程（2） 一旦有尿液後, 加上 20% mannitol, 以 1 ~ 2 g/kg body weight 的劑量, 靜脈注射4 小時以上。 儘可能將尿液排出量維持在 8 l/d ; 這一般需要12 l/d 的靜脈輸液。 使用Sodium bicarbonate若產生代謝性鹼中毒 ( arterial blood pH > 7.45), 則使用 acetazolamide ( in an IV bolus of 500mg)。 1.Keep urine flow at least 8 l/d, which will generally require an infusion of 12 l/d; the positive balance of 4 l/d will be attributable to edema, mainly in the limbs, which is an acceptable risk in this situation 2. The amount of mannitol required to maintain a urinary flow of 8 l/d may reach 200 g/d; blood osmolar gap should remain below 55 mOsm/Kg, corresponding to 1.000 mg/d mannitol in the blood 3. bicarbonate adminstration this should be continued until urinary myoglobin has disappeared, usually by the third day

建議急救流程（3） 病人經輸液治療後仍無尿液, 可試用 mannitol ( a bolus of 20 g) 加上 furosemide (120mg) 。 一旦確定病人無尿(anuria)後, 就不應該給 mannitol。 Mannitol 靜脈注射, 若超過 200 g/d ,可能產生急性腎衰竭 。 if all of the above measures do not result in urinary flow, dopamine infusion will not reverse the situation, although some authorities suggest administration of a " renal dose" of dopamine (1-2 ug/min/kg body weight)

Actions of Mannitol in the Prophylaxis of Post-traumatic Acute Renal Failure （1） Extra-renal : Extracellular volume expansion with attendant increase in cardiac output and stabilization of mean arterial pressure Increased cardiac contractility Stimulation of atrial natriuretic factor release Reduction of skeletal cell edema and decompression of muscle tamponade in the compartment syndrome Restoration of contractility to the dilated blood vessels in crushed muscles

Actions of Mannitol in the Prophylaxis of Post-traumatic Acute Renal Failure （2） Decrease in blood viscosity & oncotic pressure across the glomerulus, causing an increase in glomerular filtration rate Dilation of glomerular capillaries and stimulation of prostaglandin E and I release Increase in proximal intratubular pressure and flow and prevention of obstruction Possible reduction of tubular cell swelling and injury Scavenging of oxygen free radicals

Actions of Mannitol in the Prophylaxis of Post-traumatic Acute Renal Failure （3） Dangers : Hyperosmolar volume overload in oligoanuria Massive IV doses of mannitol ( >200 g/d) have been reported to cause acute renal failure; this type of ARF is promptly reversible after hemodialysis

治療腔室症候群的建議 a conservative approach is suggested !! Decompression could be achieved by intravenous hypertonic mannitol that can be readily judged within ~40 minutes by relief of symptoms and measurable shrinkage of the swollen limb. Surgical fasciotomy as a measure of last resort for refractory cases Theses results are supported by the decompressive effective of mannitol on the canine Compartment syndrome and the protective effects of mannitol on neuromuscular function in the ischemia-reperfusion dog limb model. There is a consensus that acute compartment syndrome is dangerous and that Immediate decompression is indicated. The prevailing recommendation is that Only surgical fasciotomy can relieve the increase intracompartment pressure.

預 後 若輸液急救耽擱超過 12 小時 橫紋肌溶解症合併急性腎衰竭 急性腎衰竭若處理得宜, 約在7~14 天後恢復 預 後 若輸液急救耽擱超過 12 小時 ~100 % 的壓傷症候群的病人會腎衰竭 橫紋肌溶解症合併急性腎衰竭 20 ~ 40 %的死亡率 急性腎衰竭若處理得宜, 約在7~14 天後恢復

結 論 大範圍的肌肉壓傷可造成猝死，死亡的原因是嚴重的低血容性休克。而多方面的電解質不平衡( 高血鉀、低血鈣、酸中毒) 讓情況更加險惡 。 結 論 大範圍的肌肉壓傷可造成猝死，死亡的原因是嚴重的低血容性休克。而多方面的電解質不平衡( 高血鉀、低血鈣、酸中毒) 讓情況更加險惡 。 壓迫症候群的併發症有： 橫紋肌溶解造成急性腎衰竭及腔室症候群 到院前，及早緊急大量輸液治療；一旦有尿液後 使用mannitol 利尿劑；可預防橫紋肌溶解造成的急性腎衰竭，進一步提高病人存活率。 對於老年人則建議較溫和的輸液治療，並以 furosemide 來代替 mannitol。 Furosemide: Advantages: increase in intratubular flow and prevention of obstruction; sparing of oxygen demands by the kidney; renal vasodilation 2. Dangers: Deafness; acidification of urine; contraindicated in aminoglycoside nephrotoxicity.