SEM2 TRAUMA Flashcards
What is Revised trauma score / RTS
- Applicable to the prehospital setting
- 3 step score aimed at identifying unwell trauma pts in the early stages of care
coast score
- Measure of predicted coagulopathies in pts with major trauma
- Much better sensitivity and specificity than RTS
GOS-E score (Glasgow outcome scale extended)
- Used as an outcome variable – a way of measuring differences between two groups is often measured by measuring the outcome)
- Commonly morbidity and mortality are used as the outcome
- GOS-E is a numerical representation of mortality
define shock
- Acute circulatory failure with inadequate or inappropriately distributed tissue perfusion resulting in generalised cellular hypoxia
- More focussed on hypoperfusion not hypotension
- Blood pressure is a poor surrogate for tissue oxygen delivery.
differentials for hypotension
- Cardiac tamponade (anterior forceful chest impact, tachycardia as body trying to improve filling)
- Myocardial injury (Confusion, valve injury, direct coronary insult, metabolic, hypothermic, catecholamine induced myocyte damage (extreme tachy)).
- Obstructive / TPT
- Spinal cord injury
- Elevated mean airways pressure
- Poor SVR – limb #, cardiovascular collapse, neuro-cardiovascular uncoupling tbi and medications
- Sedation/medications
- Position
define compensation
- Ability of the cardiovascular system to maintain effective perfusion by reducing blood flow to ischaemic tolerant vascular beds (“buying time”)
what are the baroreceptor effects for compensation in shock
- Skeletal muscle and splanchnic organs hypo perfused (hypoxic and hypothermic tissue again “buying time”)
- Circulating vasoconstrictors
- Renal reabsorption of sodium and water
- Hemopoiesis (slowing of RBC production in the kidneys)
what are the chemoreceptor reflexes in shock and how do they work
- Activate at MAP of <60mmhg
- When arterial baroreceptor firing rate is at minimum
- Acidosis stimulates central and peripheral chemoreceptors by increasing sympathetic vasoconstrictor outflow to muscle, splanchnic, and renal beds to elevate arterial pressure and increase cardiac sympathetic activity to increase heart rate and contractility.
Endocrine response to shock
- In trauma patients, the body’s endocrine response for compensation involves a rapid activation of the hypothalamic-pituitary-adrenal (HPA) axis, the sympathetic nervous system, and the renin-angiotensin-aldosterone system, leading to increased levels of stress hormones, such as cortisol and catecholamines, to mobilize energy, conserve fluids, and promote healing.
define decompensation
- Transitionary state in which lack of perfusion is creating cellular damage that will produce toxic effects
- Hypoperfusion of ischaemic intolerant vascular beds
haemorrhagic shock vs traumatic shock
H = blood/volume loss
t= tissue injury +/- haemorrhage
how to work out shock index
what is normal range
divide HR by SBP
normal range 0.5-0.7
>0.9 suggests need for MTP and increased mort
why is the applicability of shock index questioned in TBI patients
- TBI in conjunction with haemorrhage might disturb the autonomic response to blood loss or the ability to modulate vascular tone. This is due to uncoupling of the autonomic and cardiovascular system.
- In patients with severe TBI, the typical SI based classification may not be reliable.
- This is because TBI often leads to altered vss due to brain injury (ie raised ICP) which can interfere with the usual cardiovascular response seen in hypovolemic shock
- Tbi patients may show normal or elevated SI despite the presence of significant hypovolemia
define trauma induced coagulopathy
- Trauma induced coagulopathy is a complex haemostatic disturbance that can develop early after major injury
- Refers to the inability to achieve sufficient hemostatis in trauma patients resulting in diffuse microvascular and life threatening bleeding.
what drives endogenous factors contributing to trauma induced coagulopathy
is driven by the combination of hypovolemic shock and substantial tissue injury resulting in endothelial damage, upregulated fibrinolysis, fibrinogen depletion, altered thrombin generation and platelet dysfunction.
what exogenous factors contribute to trauma induced coagulopathy
hypothermia, acidosis, hyperkalaemia and dilution due to crystalloid and colloid fluid administration
describe trauma induced coagulopathy up to the first 24hrs
- Early TIC is characterised by hypocoagulative state and the inability to form sufficient clots, resulting in uncompressible diffuse microvascular bleeding.
- When bleeding and shock related hypoperfusion is controlled and patients survive the initial first 24hrs a transition from an early hypercoagulable state to a later hypercoagulable and prothrombotic state occurs. Thus, thromboprophylaxis should be initiated as soon as possible.
what is endotheliopathy of trauma
- Endothelium plays an essential role in coagulation and inflammation serving as a semi permeable barrier between the fluid phase and tissue.
- Glycocalyx =anticoagulant intraluminal layer of the endothelium
- Endotheliopathy of trauma describes a state of endothelial cell damage and glycocalyx shedding. This is primarily driven by shock related hypoperfusion with the release of large amounts of catecholamines and vasoactive hormones (vasopressin).
fibrinolysis vs hyperfibrinolysis
Fibrinolysis:
This is a normal process that dissolves blood clots, preventing them from growing and causing problems.
Hyperfibrinolysis:
In this condition, the fibrinolytic system is overactive, leading to the premature breakdown of clots and potentially causing excessive bleeding.
what is fibrinolytic shut down
Fibrinolytic shutdown refers to a state where the body’s natural clot-breaking process (fibrinolysis) is impaired or inhibited, potentially leading to a hypercoagulable state and increased risk of thrombosis
usually occurs around 2 hours post injury
where does fibrinogen come from and what is its role
Liver Synthesis: Fibrinogen is synthesized by hepatocytes, the primary cells of the liver.
Function: It is a soluble glycoprotein that circulates in the blood and is converted into fibrin, an insoluble protein, during the clotting process.
Role in blood clotting: Fibrinogen plays a crucial role in the final step of the coagulation cascade, where it is converted into fibrin, forming a mesh-like structure that stabilizes the blood clot and prevents excessive bleeding
is upregulated by infection and inflammation
what is thrombins role in the clotting cascade
- Thrombin, a key enzyme in blood coagulation, primarily functions by converting fibrinogen into fibrin, forming the meshwork of a blood clot, and also plays a role in activating platelets and other coagulation factors.
what is the role of platelets in clotting
- Platelets play a crucial role in the clotting cascade by forming a primary plug at the site of injury and providing a surface for the assembly of coagulation factors, ultimately leading to the formation of a stable fibrin clot.
what is INR and what does it measure
international normalised ratio
measure of prothrombin time
how long the activation time of thrombin is and compare it against the standard
When a patient is coagulopathic, they have a reduction in their thrombin = longer activation time, takes longer for the patient to clot = higher risk of bleeding
INR too low =blood clots more likely
INR too high = bleeding side effects more likely
