1. Persistent hypotension following trauma is usually the result of bleeding, tension pneumothorax, neurogenic shock, and cardiac injury.
   1. Hypotension is most likely due to bleeding. The thoracic and abdominal cavities and the pelvic retroperitoneal space are the most common sites of occult hemorrhage that results in hypotension.
      1. Of the isotonic crystalloid solutions, LRS is preferred over normal saline.
      2. Human serum albumin (5% and 25%) and hydroxyethyl starch are the most commonly used colloids.
   2. Differentiation of neurogenic shock from hemorrhagic shock is important. (Patients with spinal cord injury are often bradycardic and readily respond to catecholamine administration.)
      1. Mistaking neurogenic shock for hemorrhagic shock may lead to excessive fluid infusion and pulmonary edema in patients with spinal cord injuries.
      2. The reverse error may also occur: depriving patients with hemorrhagic shock of fluids because of misdiagnosis of neurogenic shock.
   3. Cardiac causes of persistent hypotension include blunt cardiac injury and pericardial tamponade. Intraoperative TEE can be useful in the differential diagnosis.
2. Hypothermia
   1. A core body temperature below 35°C is often associated with acidosis, hypotension, and coagulopathy, which in turn may lead to an increased risk of severe bleeding, need for transfusion, and death.
   2. Admission hypothermia, which is present in approximately 50% of patients, is an independent risk factor after major trauma
   3. Prevention of hypothermia and correction of body temperature to normal appear to decrease the mortality rate, blood loss, fluid requirement, organ failure, and length of ICU stay.
      1. Convective warming with forced dry air at 43°C can prevent a temperature drop in most trauma victims but cannot effectively treat severe hypothermia because the low specific heat of air has little heat content to give to the cold trauma patient.
      2. Circulating-water warmers that cover a relatively smaller body surface area than forced-air warmers may produce faster rewarming (Fig. 52-5: The rate of rise in core temperature with circulating water and forced-air devices used in healthy anesthetized volunteers).
3. Coagulation Abnormalities
   1. Factors responsible for coagulopathy in trauma include dilution of coagulation factors and platelets, tissue hypoperfusion, disturbance of fibrinogen or fibrin polymerization, and platelet activity.
   2. Disseminated intravascular coagulation results from acute release of thromboplastin from injured brain, fat, or amniotic fluid or subacutely from endothelial inflammation or failure interfering with clearance of activated coagulation factors.
   3. Hypothermia affects platelet morphology, function, and sequestration; retards enzyme activity; and decreases coagulation factor function by about 10% for each 1°C drop in temperature. Both enzymatic activity and platelet aggregation are abnormal below 33°C. Metabolic acidosis is probably a stronger coagulation enzyme inhibitor than hypothermia
   4. Diagnosis
      1. The perioperative diagnosis of coagulopathy is often made by observing bleeding from wounds or puncture sites rather than by interpretation of laboratory tests.
      2. The differential diagnosis between consumptive and dilutional coagulopathy requires laboratory testing.
   5. Treatment
      1. Fresh-Frozen Plasma (FFP). Newer guidelines recommend administration of thawed FFP immediately after the arrival of severely traumatized bleeding coagulopathic patients.
      2. Platelets.Platelet transfusion is indicated when platelet count falls below 50 × 10⁹/L.
      3. Fibrinogen. In a trauma patient, a plasma fibrinogen level below 1.5 g/L (normal, 2 g/L) in the presence of nonsurgical bleeding indicates replacement with 3 to 4 g of fibrinogen concentrate or 50 mg/kg (15–20 units) of cryoprecipitate.
      4. Antifibrinolytic Agents. The synthetic lysin analog antifibrinolytic agents, tranexamic acid, and aminocaproic acid, competitive inhibitors of plasmin and plasminogen, are effective in reducing bleeding in cardiac and elective surgery even when a significant hyperfibrinolysis is absent.
      5. Factor VIIa. By activating factor X, this agent produces a thrombin burst, which in turn converts fibrinogen to fibrin.
      6. Prothrombin complex concentrate (factor IX complex) contains factors II, VII, IX, and X. In the trauma setting, it is used for rapid reversal of vitamin K antagonist oral anticoagulants (warfarin), especially in patients with intracranial bleeding.

Trauma and Burns

1. Initial Evaluation and Resuscitation
2. Cervical Spine Injury
3. Direct Airway Injuries
4. Management of Breathing Abnormalities
5. Management of Shock
6. Early Management of Specific Injuries
7. Burns
8. Operative Management
9. Management of Intraoperative Complications
10. Electrolyte and Acid–Base Disturbances
11. Early Postoperative Considerations