Year in Review :Trauma Surgery

Michael Cripps, MD

Trauma Fellow

UCSF‐SFGH

Disclosure

• I have nothing to disclose

Trauma

• “I trust that this type of nonsense will never happen again”

‐ Judge at Bridget Driscoll Inquiry. 1896

Blunt Aortic Injury

• 2011 Scudder Oration on Truama

– Dr. Demetriades

– Multiple American Association for Surgery of Trauma (AAST) studies

• 2011 Society for Vascular Surgery Guidelines

Blunt Aortic Injury

• Significant cause of mortality in trauma patients

– Motor Vehicle Crashes (70%)

– Motorcycle Crashes (13%)

– Fall from height (7%)

– Auto vs Pedestrian (7%)

• Incidence of aortic injury in patients with pelvic fractures is 1.4%

Blunt Aortic Injury

• Most common site of injury is the medial aspect of the lumen just distal to the left subclavian artery– Grade I – Intimal 

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– Grade II –Intramural Hematoma

– Grade III –Pseudoaneurysm

– Grade IV ‐ Rupture

Blunt Aortic Injury

• CXR – Widened mediastinum, loss of AP window, apical cap, depression left mainstem

• Thoracic fractures

• Upwards of 14% can have normal CXR

• CT angiography new gold standard for screening and diagnosis of blunt aortic injury

Treatment

• Risk of free rupture is highest in the first few hours after injury

– Majority of patients die at the scene

– >90% occur within first 24 hours

• Prevention of free rupture with rigorous blood pressure control (β‐blocker then nipride)

– WITHOUT BP control – 12% risk of rupture

– WITH BP control – 1.5% risk of rupture

– Maintain SBP 90‐110 mmHg

PREVIOUS TREATMENT

• TIMING: Immediate repair

• TECHNIQUE: Open techinque with bypass or clamp and sew

• Complications

– Pneumonia

– Paralysis

– Systemic heparinization

– Mortality

Advances in Treatment

• Late 1990’s and early 2000’s

• Observation with medical management of blood pressure and Endovascular repair

• AAST 2 Trial

Advances in Treatment

• Delayed repair has become standard of care

– EXCEPT FOR:

– Active leaking from aorta

– Large contained injuries

Advances in Treatment

• First endograft technique for BAI used 1997

Endovascular Repair

• Complications

– Endoleak, infolding, collapse

– Access‐vessel injuries

– Occlusion of left subclavian and left common carotid

– Thrombosis

– Migration

– Advancing age of patient/change in aorta

• Follow up data??

• 7768 patients from 139 studies

• Mortality rates

– Endovascular repair – 9%

– Open repair – 19%

– Observation only – 46%

Preperitoneal Pelvic Packing for Hemorrhage after Pelvic Fracture

Preperitoneal Pelvic Packing

• Trauma, Critical Care, and Acute Care Surgery Conference, Las Vegas 2011 and 2012

• EAST Guidelines for management of pelvic trauma update 2011

• How to manage the hemodynamically unstable patient with significant pelvic fracture

Preperitoneal Pelvic Packing

• Significant pelvic fracture can have mortality of >40%

– 1/3 die from uncontrolled hemorrhage

– Despite multidisciplinary management including angiography

• Preperitoneal Pelvic Packing

– Popular in European countries

– Recent data U.S. 

• 75  consecutive hemodynamically unstable patients with pelvic fractures

• Significant decrease in blood product usage

– 83% success rate in controlling hemorrhage

• Decrease use of angioembolization

• Updated management guidelines now includes preperitoneal packing

• LEVEL III evidence

– More investigation is needed

Acute Coagulopathy of Trauma ‐Hyperfibrinolysis

Hyperfibrinolysis

• Multiple ongoing clinical trials evaluating hemostatic resucitation

• Acute coagulopathy of trauma

• CRASH‐2 Trial

• MATTERs Study

Hypoxia

FXa binds to FVa on the cell surface

The complex between TF and FVIIa activates FIX and FX

Tissue factor (TF) isexposed and binds to FVIIa or FVII which is subsequently converted to FVIIa

Trauma and Hypoxia induce the initiation of coagulation

Initiation phase

The FXa/FVa complexconverts small amountsof prothrombin intothrombin

The small amount ofthrombin generatedactivates FVIII, FV, FXIand platelets locally.

Activated plateletsbind FVa, FVIIIaand FIXa

FXIa converts FIX to FIXa

Amplification phase

The FVIIIa/FIXa complexactivates FX on thesurfaces of activatedplatelets

Fibrin

The “thrombin burst”leads to the formationof a stable fibrin clot.

FXa in association with FVa converts large amounts of prothrombin into thrombin creating a “thrombin burst”.

Propagation phase

Coagulation cascade after trauma…

Fibrinolysis

• 20,211 trauma pts

• All cause mortality reduced with TXA (14.5% vs 16.0%)

• Risk of death due to bleeding reduced (4.9% vs 5.7%) 

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• 896 patients, 293 received TXA

• Lower mortality (17.4% vs 23.9%)

– TXA group more severely injured

• Most significant among MTP patients 

– 14.4% vs 28.1%

– TXA group associated with survival (OR 7.28)

Hyperfibrinolysis

115 patients

• 20% had CLINICALLY RELEVANT hyperfibrinolysis

Patients with hyperfibrinolysis had 

• Higher ISS (p=0.009)

• Lower temperature (p=0.018)

• Higher INR (p=0.016)

• Longer PTT (p=0.049)Kutcher ME, Cripps MW, et al. Criteria for empiric treatment of hyperfibrinolysis after trauma. J Trauma. 2012 (In press.)

• Hyperfibrinolysis was associated with:

–Multiorgan failure 

• (63.2% vs 24.6%, p=0.004)

–Mortality 

• (52.2% vs. 12.9%, p<0.001)

Hyperfibrinolysis Hyperfibrinolysis

• We then evaluated non‐ROTEM parameters predictive of hyperfibrinolysis 

– Acidosis (pH≤7.2)

– Hypothermia (temp≤36.0)

– Coagulopathy (INR≥1.5 or PTT≥35)

– Relative thrombocytopenia (platelet <200)

• Identified hyperfibrinolysis with 100% sensitivity and 55.4% specificity (AUC 0.777).

Hyperfibrinolysis Empiric antifibrinolytic treatment

• Presence of any:

– Acidosis (pH ≤ 7.2)

– Hypothermia (temperature ≤ 36.0)

– Coagulopathy (INR ≥ 1.5 or PTT ≥ 35)

– Thrombocytopenia

• Treating these patients will cover all patients with hyperfibrinolysis, while eliminating overtreatment of 47%