MSK and Trauma Flashcards
What is the gustilo anderson open fracture classification scheme
1) Wound < 1 cm; mild to moderate soft tissue bruising
2) Wound > 1 cm; without extensive soft tissue damage
3) Extensive soft tissue damage
3a) adequate tissue remaining
3b) Soft tissue loss with periostal stripping
3c) trauma associated with arterial blood supply injury
What is the most common hip luxation and treatment
cranial dorsal- Shortened adducted, externally rotated
Ehmer sling
Caudoventral- hobbles
What are the three components to trauma associated coagulopathy
resuscitation associated coagulopathy
Trauma
Acute coagulation of trauma shock
What are the 4 factors associated with resuscitation associated coagulopathy
Crystalloid fluid boluses- Dilutional
Acidosis - impairs factor activation
Hypothermia
Hypocalciumemia
Define acute coagulopathy of trauma shock
Early coagulopathy characterized by hypocoagulatibilty with hyperfibrinolysis
What is the contributors to acute coagulopathy of trauma shock
Severe tissue trauma
Tissue hypoperfusion
Sympathoadrenal activiation (catecholamines
Inflammation
How does protien C promote anticoagulation
Inhibits FVa FVIIIa
Inhibits plasminogen activator inhibitor and throbmin activiatedable fibrionlytid inhibitor
Thrombomodulin inhibits thrombin
JVECC 2019 VCOT study of cats what was a good predictor of mortality
ATT score good predictor
However perfusion, prespiratory and neuro combined was equal to the whole score in terms of performance
JAVMA 2019 How well did the ehmer sling work following craniodorsal hip luxation
Success rate 43% (5x higher than with surgery)
50% had complications associated with sling
How does acute coagulopathy of trauma shock occur
Increased anticoagulant activated Protien-c by high concentrations of thrombin-thrombomodulin complex
Endothelial activation and thrombin generation, –> endogenous heparinization, hyperfibrinolysis, hypocoagulation
Briefly describe the current proposed mechanisms for ATC
1) DIC with a fibrinolytic phenotype
2) Enhanced thrombomodulin-thrombin protein C pathway
3) Marked sympathoadrenal response leading to catecholamine induced endothelial damage
How does the DIC with fibrionlytic phenotype contribute to ATC
Severe endothelial injury, hypoxia, and ischemia invokes marked generation of thrombin with subsequent systemic fibrin formation. Massive release of tissue plasminogen activator into the circulation resulting in to large amounts of plasmin. Overall a consumptive process due to damage.
How does the enhanced thrombomodulin-thrombin protien C pathway contribute to ATC
Severe tissue injury and hypoperfusion lead to decreased thrombin degradation and increased thrombomodulin activity. Leading to hypocoagulation and hyperfibrinolysis
How does the marked sympathoadrenal response leading to catecholamine induced endothelial damage contribute to ATC
Circulating catecholamines directly damage the endothelial glycocalyx in a dose-dependt fashion that changes the endothelium to a prothrombic. To counteract the local change there is a systemic anticoagulable and fibrinolytic response. The counter regulatory response is out of control.
What are the difference in ACT and ACOTS
ACT is an older term to refer to what may be referred to trauma associated coagulopathyy. Most ACT hypothesis is more specifically referred to as acute coagulopathy of trauma shock (ACOTS).
Trauma associated coagulopathy refers to all three compontents: Resuscitation associated coaulapthy, trauma and ACOTS
