Page 2 Clinical Manifestations Causes of Mortality after Crush - PDF document

Outline  Discuss crush injuries and the The Crush Syndrome Crush Syndrome  Define treatment  Discuss the treatment and Andre Campbell, MD, FACS, FCCM, FACP Professor of Surgery management mangled extremities UCSF, School of Medicine  Discuss vascular injury and San Francisco General Hospital 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 Armenia Kobe causing localized muscle damage  bombings, industrial accidents, building collapse, earthquake tornadoes Bangladesh Fukushima Haiti Page 1

Crush Injury Crush Injuries Muscle ischemia and Necrosis from Prolonged Pressure  Injuries typically associated with disasters that (Local effects) 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  Terrorist Acts- Oklahoma City, 9/11 Metabolic Secondary Extremities Myoglobinuria Abnormalities Complications (third spacing)  Systemic manifestations of muscular cell damage (electrolytes) resulting from pressure of crushing Cardiac Arrhythmias Compartment Renal Failure Hypotension 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 Crush Syndrome Untreated Crush Injury  Hypotension:  Immediate: – Massive 3 rd spacing – Shock contributes to renal failure – Severe head injury, traumatic asphyxia, – Third spacing can lead to compartment and torso injuries  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  CPK elevation correlates with renal failure – Hyperkalemia, Hypocalcemia, Hyperphosphatemia, Metabolic acidosis (RF) and mortality  Renal  Risk of mortality and renal failure increased with CK over 75,000 U/L – Renal vasoconstriction due to shock  Other suggested counting limbs crushed – Pigment toxicity due to myoglobin 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  Establish two large bore IVs personnel  Administer 1-2 liter or LR prior to extrication  Mass casualty scenarios should be – If prolonged infuse 1.5 liters/hr discussed with personnel – Young and elderly be cautious about fluid  Airway secured and protected from dust overload  Adequate oxygenation  Sodium Bicarb 2 amps prior to extrication  Cardiac monitoring  Maintain body temperature  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 – Hydration 1.5 liters/hour – Maintain diuresis of 300ml/hr with IV fluids – Patient may gain massive amounts of and mannitol(carefully) weight in the resuscitation – Triage to hemodialysis as needed – Similar to Burn patients » 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,  Observe all crush injuries-even those who look consider kayexalate normal – Cardiac arrhythmias monitor for cardiac  Delays in hydration for more than 12 hours lead arrhythmias and arrest and treat 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  Factors correlated with amputation the NTDB 2007-2009  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 – High energy mechanism of injury regression done to assess factors – Age, comorbidities, and insurance status associated with amputations  21% of patients underwent amputations in do not govern amputation rate – Injury type is the most important thing this study (9% early amputations) 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  ISS>14.6, 93 vascular injuries,66% hard signs, 95% had due to associated soft-tissue associated fracture and nerve injuries (the mangled  Age, ISS, and MESS was significantly different between extremity) survivors and non-survivors  Injuries to the upper and lower extremity  These injuries may result in a  Shunt were used in 18 vessels prior to repair non-functional limb in spite of  Anteroposterior tibia artery most commonly injured a successful revascularization  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 – Serious associated polytrauma – Anatomically complete disruption of sciatic or – Severe ipsilateral foot trauma posterior tibial nerves in adult even if vascular injury » loss of plantar skin/weight bearing is repairable surface – Prolonged warm ischemia time – Anticipated protracted course to obtain – Life threatening sequelae soft-tissue coverage and skeletal » rhabdomyolysis reconstruction Variables in Consideration of Classification Systems Limb Viability  Mangled Extremity Syndrome Index (MESI) – 9 variables  Skin/Muscle Injury  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) – 6 variables  Comorbid Disease (peripheral vascular disease, diabetes  Hanover Fracture Scale(HFS) mellitus, etc.) – 12 variable Page 9