Outline The Crush Syndrome Discuss crush injuries and the Crush Syndrome Define treatment Andre Campbell, MD, FACS, FCCM, FACP Discuss the treatment and Professor of Surgery UCSF, School of Medicine management mangled extremities San Francisco General Hospital Discuss vascular injury and assessment Case discussions The Crush Syndrome is the presence of localized crush injury with systemic manifestations: incidence 2-15% Crush Injury is compression of body parts Kobe Armenia causing localized muscle damage bombings, industrial accidents, building Bangladesh collapse, earthquake tornadoes Fukushima Haiti Page 1 Crush Injury Crush Injuries Muscle ischemia and Necrosis from Prolonged Pressure (Local effects) Injuries typically associated with disasters that include muscle injury, renal failure and death Crush Syndrome Man made-war and natural- earthquake (Systemic Effects) Earthquakes 3-20% of crush injuries Building collapse up to 40% of extricated victims Vehicular Disaster Fluid Retention in Extremities Myoglobinuria Metabolic Secondary Terrorist Acts- Oklahoma City, 9/11 (third spacing) Abnormalities Complications (electrolytes) Systemic manifestations of muscular cell damage resulting from pressure of crushing Hypotension Renal Failure Cardiac Arrhythmias Compartment Syndrome Crush Injuries The Crush Syndrome Recognized after the Messina earthquake of Characteristic Syndrome the results in 1909 and during WWI by German MDs rhadomyolysis, myoglobinuria, ARF. First described in the English literature by Three criteria Bywaters and Beall in 1941 – Involvement of muscle mass –Several patients who were crushed during – Prolonged compression 4-6 hrs. but can WWII during the Blitz over London. be < 1 hr –All patients died from renal failure despite – Compromised local circulation resuscitation Gonzalez, D Crit Care Med 2005 33. No 1(Suppl) Br Med J 1941;427-432 Page 2 Clinical Manifestations Causes of Mortality after Untreated Crush Injury Crush Syndrome Hypotension: Immediate: –Massive 3rd spacing –Severe head injury, traumatic asphyxia, –Shock contributes to renal failure and torso injuries –Third spacing can lead to compartment Early: syndrome Renal Failure –Hyperkalemia, hypovolemic shock –Rhadomyolysis releases myoglobin, K, P04, Cr, Late: into circulation –Renal failure, coagulopathy, and –Myoglobinuria leads to renal tubular necrosis hemorrhage, sepsis –Release of electrolytes from ischemic muscle cause metabolic abnormality Clinical Manifestations of the Crush Syndrome Metabolic Abnormalities: –Ca flow intracellularly through leaky membranes causing systemic hypocalcemia –K is released from muscle causing systemic hyperkalemia –Lactic Acid is released from ischemic muscle into systemic circulation, causing metabolic acidosis –Imbalance between K and Ca cause cardiac arrhythmias-acidosis makes it worst Page 3 Clinical Manifestations Indicators of Severity Electrolyte Disturbances –Hyperkalemia, Hypocalcemia, CPK elevation correlates with renal failure Hyperphosphatemia, Metabolic acidosis (RF) and mortality Renal Risk of mortality and renal failure –Renal vasoconstriction due to shock increased with CK over 75,000 U/L –Pigment toxicity due to myoglobin Other suggested counting limbs crushed one limb is 50,000 U/L –ATN Crush one limb-RF 50%, two-RF-75%, –Luminal obstruction three RF- 100% –Acute Renal Failure Oda J et al; J Trauma 1997;30:507-512 Crush Syndrome Pre-Hospital Crush Syndrome Pre-hospital Coordinate time of release with rescue personnel Establish two large bore IVs Mass casualty scenarios should be Administer 1-2 liter or LR prior to extrication discussed with personnel –If prolonged infuse 1.5 liters/hr –Young and elderly be cautious about fluid Airway secured and protected from dust overload Adequate oxygenation Sodium Bicarb 2 amps prior to extrication Maintain body temperature Cardiac monitoring Pain control PRN Rapid transit to a trauma center Extricate Intravenous fluids, cardiac monitoring Page 4 Definitive Treatment Definitive Treatment Hypotensive: Renal Failure: –Massive fluid shifts –Prevent renal failure with adequate –Hydration 1.5 liters/hour hydration –Patient may gain massive amounts of –Maintain diuresis of 300ml/hr with IV fluids weight in the resuscitation and mannitol(carefully) –Similar to Burn patients –Triage to hemodialysis as needed »May need 60 days of Rx »Should return to normal function Definitive Treatment Definitive Treatment Secondary Complications Monitor for compartment syndromes and do Metabolic Abnormalities: fasciotomies as needed –Acidosis: administer IV sodium Treat open wounds with antibiotics, tetanus bicarbonate until urine pH reaches 6.5 to toxoid, and debridement prevent myoglobin deposition Monitor for pain, pallor, pulselessness, –Hyperkalemia/Hypocalcemia: administer paresthesias, paralysis- ischemia Ca, sodium bicarbonate, insulin/D5W, consider kayexalate Observe all crush injuries-even those who look normal –Cardiac arrhythmias monitor for cardiac arrhythmias and arrest and treat Delays in hydration for more than 12 hours lead to renal failure Definitive surgery- amputations as needed Page 5 J Trauma 2012;72:1626-1633 J Trauma 2012;72:1626-1633 J Trauma 2012;72:1626-1633 Page 6 Perte’s Syndrome or Traumatic Asphyxia Craniocervical cyanosis Subconjunctival hemorrhage Multiple petechiae Neurological symptoms Results from sudden severe compression of the thorax or upper abdomen or both Valsalva is necessary before crush Associated injuries pulmonary contusions, hemothorax or pneumothorax Aortic Crush Injuries vs. MVA Aortic injuries Increase risk of Rhadomyolysis, ATN and renal failure Tendency to develop lower risk aortic injuries than MVAs Both type of patient must be followed since they can progress High rate of mortality in missed injuries Injury 2013;44:60-65 Injury 2013;44:60-65 Page 7 Retrospective Cohort design of data from the NTDB 2007-2009 Factors correlated with amputation Assessed the result from 222 Level I & II –Presence of severe head injury AIS>3 trauma centers of severely mangled –Presence of shock in the ED(BP<90) extremities –Limb injury type 1354 patients were analyzed and logistic regression done to assess factors –High energy mechanism of injury associated with amputations –Age, comorbidities, and insurance status 21% of patients underwent amputations in do not govern amputation rate this study (9% early amputations) –Injury type is the most important thing J of Trauma 2013;74:597-603 J of Trauma 2013;74:597-603 Blunt Arterial Injury Salvage Blunt Vascular Trauma Rates Retrospective review at a Level I trauma center Have a high amputation rate Jan 1995-Dec 2002 62 patients due to associated soft-tissue ISS>14.6, 93 vascular injuries,66% hard signs, 95% had associated fracture and nerve injuries (the mangled Age, ISS, and MESS was significantly different between extremity) survivors and non-survivors These injuries may result in a Injuries to the upper and lower extremity non-functional limb in spite of Shunt were used in 18 vessels prior to repair a successful revascularization Anteroposterior tibia artery most commonly injured Amputation rate was 18% 3X that for penetrating injury Rozycki G et al., J Trauma 2003;55:814-824 Page 8 Mangled Extremity Mangled Extremity Relative Indications for Primary Indications for Primary Amputation Amputation – Anatomically complete –Serious associated polytrauma disruption of sciatic or posterior tibial nerves in –Severe ipsilateral foot trauma adult even if vascular injury is repairable »loss of plantar skin/weight bearing – Prolonged warm ischemia surface time – Life threatening sequelae –Anticipated protracted course to obtain » rhabdomyolysis soft-tissue coverage and skeletal reconstruction Variables in Consideration of Classification Systems Limb Viability Mangled Extremity Syndrome Index (MESI) Skin/Muscle Injury – 9 variables Predictive Salvage Index (PSI) Bone Injury – 4 variables Ischemia (time, degree) Mangled Extremity Severity Score (MESS) Type of Vascular Injury – 4 variables Shock Limb Salvage Index (LSI) Age – 7 variables Infection NISSSA scoring system (Nerve Injury, Soft Tissue Injury, Skeletal Associated injuries (pulmonary, abdominal, head, etc.) Injury, Shock, Age of Patient Score) Comorbid Disease (peripheral vascular disease, diabetes – 6 variables mellitus, etc.) Hanover Fracture Scale(HFS) – 12 variable Page 9 Variable MESI PSI HFS LSI MESS NISSSA Bone/FX type + + + + + + Skin/muscle + + + + + + Nerve + - + + - + Vascular/ischemia + + + + + + Contamination - - + - - - Severity of Tot Inj + - + - - - Shock + - - - + + Lag Time + + + - - - Age + - - - + + Comorbidity + - - - - - Smoking behavior - - - - - - Number of 9 4 12 7 4 6 Variables Range 3-75 3-15 1-39 0-14 1-14 0-16 Cuttoff Point 20 8 15 6 7 9 Hoogendoorn, Werken, E J of Trauma 2002;28:1-10 J Trauma 2012;72:86-93 Vascular Injury – Non-invasive tests Vascular Injury – Non-invasive tests “Soft signs” large stable hematoma “Soft signs” – large stable hematoma, prior significant bleeding, possible nerve prior significant bleeding damage, proximity (<3cm, used to angio but possible nerve damage only 10 – 20% pos) proximity (<3cm, used to angio but only 10 – 20% pos) API – arterial pressure index (doppler sys injured compared to non-injured) or ABI Physical exam and API – arterial pressure index ABI <0.9, Duplex, color flow – use to decide <0.9, perform Duplex, color flow – to decide whether to angio, observe, OR whether to angio Mandatory