The document discusses the critical aspects of trauma assessment and management, highlighting the importance of early identification of life-threatening injuries and the use of blood-based resuscitation strategies to manage hemorrhagic shock and trauma-induced coagulopathy. It emphasizes the need for focused assessments like FAST, specific classification of hemorrhage, and damage control resuscitation protocols involving blood products in equal ratios. Additionally, it underscores the management of traumatic brain injuries, the significance of maintaining cerebral perfusion pressure, and appropriate interventions to mitigate secondary injuries.

2. Injury assessment
• Adequate exposure and examination of extent of injury
• Physical exposure increases risk of hypothermia
• Maitain Resuscitation bay and OT at near body temp., warm IV fluids
and Blood products, Under body warmers
• Team Efficiency required in identifying Life threatening injuries,
assessment completed within 20 mins of patient arrival

3. FAST examination
• Focused Assessment with Sonography for Trauma)
• Performed at bedside – free fluid in perihepatic and perisplenic
spaces, pericardium, and pelvis
• Free fluid in theses areas + two of the following:
• penetrating injury, SBP <90 mm Hg, or HR > 120 bpm
• High mortality and TIC and requirement of massive transfusion

4. Resuscitation
• Hemorrhage (ACS)
• Class I - <15% of circulating volume, no change in HR, BP, IV fluids not
required if bleeding promptly controlled
• Class II - prompts sympathetic responses; 15% to 30%, DBP increases d/t
vascoconstriction, HR increases to maintain CO. IV fluids indicated.
• Class III- 30% to 40%, Compensatory mechanisms of vasoconstriction and
tachycardia- not sufficient, metabolic acidosis. Blood transfusions necessary
• Class IV- Life threatening, >40%, unresponsive and profoundly hypotensive,
aggressive blood-based resuscitation (damage control resuscitation) ,TIC ,
massive transfusion

5. Trauma induced Coagulopathy
• Common and independent risk factor for death
• Upto 25 % patients -shortly after injury and before any resuscitative
efforts
• Global tissue hypoperfusion appears to play a key role
• During hypoperfusion  the endothelium releases thrombomodulin
and activated protein C, prevents thrombosis
• Thrombomodulin binds thrombin prevents thrombin from cleaving
fibrinogen to fibrin.
• This complex activates protein Cinhibits extrinsic coagulation
pathway through effect of cofactors V and VIII

7. • Effects of hypoperfusion on coagulation parameters:-
(1) progressive coagulopathy as base deficit increases;
(2) increasing plasma thrombomodulin and falling protein thromboplastin
times; and
(3) early-onset TIC and increase mortality.

8. • Mechanism of hyperfibrinolysis in tissue hypoperfusion.
• Tissue plasminogen activator (tPA) released from the endothelium
cleaves plasminogen to initiate fibrinolysis.
• Activated protein C (aPC) consumes plasminogen activator inhibitor-1
(PAI-1) when present in excess, and reduced PAI-1 leads to increased
tPA activity and hyperfibrinolysis.

10. • TIC not solely related to impaired clot formation, fibrinolysis equally
important component as a result of plasmin activity on an existing
clot
• Tranexamic acid administration is associated with decreased bleeding
during cardiac and orthopedic surgeries

11. Hemostatic resuscitation
• Early coagulopathy of trauma is associated with increased mortality
• Military conflicts in the 2000s -provided ample opportunities for
developing updated transfusion protocols
• damage control resuscitation (DCR) - administration of red blood
cells, fresh frozen plasma, and platelet units (1:1:1) in military setting
• Administering blood products in equal ratios early in resuscitation-
accepted approach for preventing or correcting TIC.

12. • Type O-negative blood- depending on urgency
• Patient receiving uncrossmatched O negative- greater risk of requiring
massive transfusion
• If >8U used, persist use of O –ve blood, reverting to native blood
type risk of transfusion reaction

13. • The PROMTT study,
• conducted across 10 U.S. level 1 trauma centers, 2013
• severe injury and resulting hemorrhagic shock increase the
probability of trauma-induced coagulopathy (TIC), often necessitating
massive transfusion and heightening mortality risk.
• role of activated protein C in TIC and advocates for blood-based
resuscitation over crystalloid-based methods for managing
hemorrhagic shock.

14. • Point-of-care functional clotting studies are extremely useful for
guiding Blood product use
• Thromboelastography (TEG) and rotational elastometry (ROTEM)
identify the specific deficiencies
• assess the rate of clot formation and clot stability,interactions
between the coagulation cascades, platelets, and the fibrinolytic
system

15. • Potential hazards from aggressive administration of blood products:
• blood-borne diseases
• transfusion-related acute lung injury (TRALI) -presence of HLA
antibodies in donor plasma is the principal TRALI risk factor-> blood
from only anti- HLA negative
• transfusion-associated circulatory overload (TACO)-> when blood
products > patients CO

16. Massive transfusion protocols
• “Massive transfusion is defined as the replacement of one blood
volume (approximately 70 mL/kg) in less than 24 hours, or the
administration of more than 10 units of packed red blood cells
(PRBCs) in an hour or less”
• Clinical evidence supports need and benefit of established Massive
transfusion protocols
• improves survival from trauma, reduces total blood product use in the
1st 24 h of injury, reduces acute infectious complications and
decreases postresuscitation organ dysfunction

17. Definitive trauma interventions
• critical initial issues impacting anesthetic management of trauma
patients include the adequacy of the airway and vascular access,
• the ability of the patient to tolerate anesthesia, prevention of
hypothermia, access to adequate blood bank supplies, and avoidance
of crystalloids and vasopressors until hemorrhage is controlled.

18. Anesthetic Induction and maintainance
• Severely injured, conscious, and oriented trauma arriving for
Emergency surgery abbreviated interview and examination
• Consent for BT and intraoperative awareness documentation
• Ot should be warm. IV fluid warmers and rapid infusion devices
• Presumed Full stomachs – risk of aspiration, C-collar for C-spine
stabilization difficulty in intubation.
• Alternative airway devices and adequate suction devices

19. • IV access – peripheral access ma be impossible due to profound
hypotension and hypovolemia Subclavian , I-O device inserted
• For induction of GA- severely injured Pt -profound hypotension
following even modest doses (0.25–0.5 mg/kg IV) of propofol
• Etomidate preserves sympathetic tone, safer than propofol
• Ketamine- given at 10mg boluses until pt is unresponsive
• Scopolamine- 0.4mg IV- for profoundly Hemodynamically unstable-
but concious pt- risk of collapse

20. • Emphasize on blood products rather than crystalloids for fluid
management
• MTP should be requested and followed
• All fluids should be warmed , except for platelets
• Replace ionized Ca++ during rapid infusion
• Vasopressors avoided until control of bleeding source
• A-line helpful but not mandatory – should not delay surgery

21. Damage control surgery
• intended to stop hemorrhage and limit contamination of the
abdominal compartment
• Definitive repair of complex injuries is not part of DCS
• Identification and control of injured blood vessels and solid organs
• Hollow viscus injuries are addressed with resection, stapling
• Anesthesia team must speak up the need of pausing surgical
procedure to allow resuscitation
• Compression or packing of bleeding area until restoration of
acceptable SBP

22. • If unsuccessful compression of aorta– direct feedback to
effectiveness of transfusion
• Breif episode of bradycarda/asystole may accompany direct aortic
compression
• When transfusions are ineffective- interrupt operation, combined
decision to pack bleeding areas, possible transfer to intervention
radiology or Critical care unit

23. • Key component of DCS- planned reoperation once patient is more
stable
• Bowel continuity restored , or colostomy performed later
• Abdominal fascia not definitively closed- occlusive dressing over a
wound vacuum sponge prevention of abdominal compartment
syndrome, respi compromise and multi organ failure

24. Traumatic brain injury
• Any trauma patient with an altered level of consciousness must be
considered to have a traumatic brain injury (TBI) until proven
otherwise
• Maintain Cerebral perfusion pressure and oxygenation
• GCS for assessment of TBI in nonsedated, non paralyzed
• Declining motor score progressive neurological deterioration 
prompt evaluation and intervention

25. • Categorized as Primary and secondary:-
• Primary brain injuries are directly related to trauma.
(1) subdural hematoma;
(2) epidural hematoma;
(3) intraparenchymal hemorrhage; and
(4) nonfocal, diffuse neuronal injury disrupting axons of the central
nervous system
Elevate ICPs, compromising CBF

26. • Acute subdural hematoma is the most common brain injury
prompting emergency intervention- a/w highest mortality
• Result of disruption small bridging veins between skull and brain
• Morbidity and mortality- related to size of the hematoma and the
magnitude of the midline shift of intracranial contents.

27. • Epidural hematoma occurs when the middle cerebral artery or other
cranial vessels are disrupted. < 10% of neurological trauma
emergencies
• initially conscious, followed by progressive unresponsiveness and
coma
• Emergency decompression if- supratentorial lesion >30ml and
infratentorial lesion > 10 ml

28. • Intraparenchymal injuries d/t rapid deceleration of the brain within
the skull, usually involving the tips of the frontal and temporal lobes
• 20% of neuro emergencies
• Associated with edema, necrosis, and infarcts surrounding areas of
damaged tissue
• Diffuse neuronal - rapid deceleration or movement of brain tissue of
sufficient force to disrupt neurons and axons- more common in
children
• Extent of injury- serial MRI- greater the extent higher the mortality
and disability severity

29. • Secondary brain injuries are considered potentially preventable
injuries
• Systemic hypotension, hypoxia, hypercapnia and hyperthermia 
negative impact on morbidity and mortality as it contributes Cerebral
edema and ICP
• Hypoxemia-single most important parameter correlating with poor
neurological outcome- correct at the earliest
• Hypotension (MAP <60) treated aggressively with fluids,
vasopressors, or both in the presence of isolated head injury

30. • Management of severe head trauma in the presence of other severe
injuries and hemorrhage creates a difficult resuscitation dilemma
• control of life-threatening hemorrhage takes precedence over
neurosurgical intervention

31. Management consideration for Acute TBI
• In the absence of an intracranial clot requiring surgical evacuation,
medical interventions are the primary means of treating elevated ICP
• Normal cerebral perfusion pressure (CPP=MAP – ICP) ~ 80 -100 mm
Hg
• ICP monitoring is not required for conscious and alert patients
• Interventions for reducing ICP are indicated when readings are higher
than 20 to 25 mm Hg

32. • Current Brain Trauma Foundation guidelines recommend maintaining
CPP between 50 and 70 mm Hg and ICP at less than 20 mm Hg for
patients with severe head injury.

34. • Cerebral blood flow (CBF) is influenced by arterial carbon dioxide
concentration:
• Cerebral vasoconstriction occurs with decreased arterial CO2,
reducing CBF and ICP.
• Conversely, cerebral vasodilation happens with increased arterial
CO2, elevating CBF and ICP.

35. • Hyperventilation effectively reduces ICP in TBI by promptly altering
CBF, but it should be cautiously applied in hemodynamically unstable
patients due to the risk of neurological ischemia.
• Osmotic diuretic therapy with intravenous mannitol reduces brain
edema and ICP by drawing fluid from brain tissue into the vascular
system, requiring close monitoring of plasma osmolality and serum
electrolytes.

36. • Barbiturate coma lowers cerebral metabolic rate and ICP, but its use is
limited in hemodynamically unstable patients due to associated
hypotension, necessitating vasopressor support to maintain cerebral
perfusion pressure (CPP).
• Fluid therapy with crystalloid is preferred over colloid in isolated TBI
to avoid exacerbating brain edema and ICP, as albumin-based
resuscitation has been linked to higher mortality rates in TBI patients.