SEM2 TRAUMA

Question 1

What is Revised trauma score / RTS

Answer 1

• Applicable to the prehospital setting
• 3 step score aimed at identifying unwell trauma pts in the early stages of care

Question 2

coast score

Answer 2

• Measure of predicted coagulopathies in pts with major trauma
• Much better sensitivity and specificity than RTS

Question 3

GOS-E score (Glasgow outcome scale extended)

Answer 3

• 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

Question 4

define shock

Answer 4

• 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.

Question 5

differentials for hypotension

Answer 5

• 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

Question 6

define compensation

Answer 6

• Ability of the cardiovascular system to maintain effective perfusion by reducing blood flow to ischaemic tolerant vascular beds (“buying time”)

Question 7

what are the baroreceptor effects for compensation in shock

Answer 7

• 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)

Question 8

what are the chemoreceptor reflexes in shock and how do they work

Answer 8

• 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.

Question 9

Endocrine response to shock

Answer 9

• 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.

Question 10

define decompensation

Answer 10

• Transitionary state in which lack of perfusion is creating cellular damage that will produce toxic effects
• Hypoperfusion of ischaemic intolerant vascular beds

Question 11

haemorrhagic shock vs traumatic shock

Answer 11

H = blood/volume loss
t= tissue injury +/- haemorrhage

Question 12

how to work out shock index
what is normal range

Answer 12

divide HR by SBP
normal range 0.5-0.7
>0.9 suggests need for MTP and increased mort

Question 13

why is the applicability of shock index questioned in TBI patients

Answer 13

• 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

Question 14

define trauma induced coagulopathy

Answer 14

• 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.

Question 15

what drives endogenous factors contributing to trauma induced coagulopathy

Answer 15

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.

Question 16

what exogenous factors contribute to trauma induced coagulopathy

Answer 16

hypothermia, acidosis, hyperkalaemia and dilution due to crystalloid and colloid fluid administration

Question 17

describe trauma induced coagulopathy up to the first 24hrs

Answer 17

• 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.

Question 18

what is endotheliopathy of trauma

Answer 18

• 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).

Question 19

fibrinolysis vs hyperfibrinolysis

Answer 19

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.

Question 20

what is fibrinolytic shut down

Answer 20

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

Question 21

where does fibrinogen come from and what is its role

Answer 21

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

Question 22

what is thrombins role in the clotting cascade

Answer 22

• 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.

Question 23

what is the role of platelets in clotting

Answer 23

• 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.

Question 24

what is INR and what does it measure

Answer 24

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

Question 25

what is visco-elastic assesst / ROTUM why is it used

Answer 25

Measures the strength of a clot measures how long it takes for the clot to form (coagulation) AND how long it takes for the clot to break down (strength) helps to understand what elements the patient needs in resusitation

Question 26

what is PRBC good to treat

Answer 26

helps resolve anaemia and improves oxygen carrying capacity short term doesnt make too much of a difference

Question 27

what does the copenhagen concept suggest

Answer 27

admin of platelets and plasma together with RBC’s from the start of resus would be beneficial for massively bleeding patients

Question 28

what is the extrinsic clotting cascade triggered by

Answer 28

tissue factor which is exposed upon tissue damage which then activates the flow on effect of multiple factors

Question 29

what is plasminogen and plasmin

Answer 29

* Plasminogen is a protein in the blood that is converted into plasmin, a protease that helps dissolve blood clots can be detrimental in coagulopathy as it starts to break down clots the body has formed contributing to uncontrolled bleeding. this is why we target it with medications like txa

Question 30

how does txa work

Answer 30

reduces bleeding by inhibiting fibrinolysis, the breakdown of blood clots, by blocking the lysine binding sites on plasminogen, preventing its conversion to plasmin and subsequent clot degradation

Question 31

role of FFP in trauma

Answer 31

* Take whole blood and spin it down it separates RBC’s and plasma * Contains all factors for clotting cascade including fibrinogen * Must be frozen

Question 32

role of platelets in trauma

Answer 32

* Cross linked fibrin clot has to be formed with platelets in it In cases of low platelet counts or platelet dysfunction, platelet transfusions are used to restore hemostasis and prevent or treat bleeding

Question 33

role of cryoprecipitate admin in trauma

Answer 33

* = concentrated source of fibrin How it Works: * Fibrinogen Replacement: Cryoprecipitate replenishes fibrinogen, which is essential for the formation of a stable fibrin clot. * Factor VIII and vWF: It also provides factor VIII and vWF, which are important for platelet adhesion and the coagulation cascade.

Question 34

what is TRALI

Answer 34

Transfusion-related acute lung injury (TRALI) is a serious, potentially fatal condition that occurs when a patient experiences acute lung injury within 6 hours of a blood transfusion, and it's thought to be caused by a combination of factors, including the transfusion of donor antibodies that react with recipient cells, leading to neutrophil activation and lung damage

Question 35

why do trauma patients receiving blood products require admin of calcium gluconate ?

Answer 35

RBC and FFP sit in a citrus fluid which causes hypocalcaemia >4 units PRBC = admin calcium gluconate

Question 36

define massive bleeding

Answer 36

* Defined as loss of one blood volume within 24hours or as 50% blood loss within 3hours or a bleeding rate of 150ml/min.