Trauma Flashcards (new)

Question 1

Q1: What are some considerations for the induction dose of propofol in hemodynamically unstable patients?

Answer 1

A1: For hemodynamically unstable patients, the induction dose of propofol should be greatly decreased, with some authors suggesting a dose that is one-tenth to one-half of the normal induction dose.

Question 2

Q2: What are the benefits of using ketamine for RSI in trauma patients?

Answer 2

A2: Ketamine is beneficial for RSI in trauma patients, especially those who are hemodynamically unstable, as it increases cardiovascular stimulation through centrally mediated sympathetic tone and catecholamine release without causing significant increases in intracranial pressure (ICP).

Question 3

Q3: What is apneic oxygenation and how is it typically administered?

Answer 3

A3: Apneic oxygenation is the concept of pulmonary ventilation using high-flow oxygen to reduce the risk of gastric distension and pulmonary aspiration. It is typically administered using a nasal cannula with high flows (>15 L/min) during laryngoscopy and intubation.

Question 4

Q4: What are the main agents used for RSI in hemodynamically unstable trauma patients?

Answer 4

A4: The main agents used for RSI in hemodynamically unstable trauma patients are ketamine, etomidate, and propofol at reduced doses.

Question 5

Q5: What should be the next step if intubation is unsuccessful after three attempts during RSI?

Answer 5

A5: If intubation is unsuccessful after three attempts, the next step should be to use an airway adjunct to support oxygenation, such as a bag mask or a second-generation supraglottic airway device. If these are unsuccessful, a surgical airway should be considered.

Question 6

Q6: What is the preferred muscle relaxant for RSI and what is its dose?

Answer 6

A6: The preferred muscle relaxant for RSI is succinylcholine, administered at a dose of 1.5 mg/kg.

Question 7

Q7: What is the SSCOR DuCanto suction device used for, and what is its design feature?

Answer 7

A7: The SSCOR DuCanto suction device is used for airway decontamination, and it features a large-bore opening and a hyperangulated design to suction large particles and fluids effectively.

Question 8

Q8: What technique is recommended for airway decontamination in the prehospital and emergency room environments?

Answer 8

A8: The suction assisted laryngoscopy airway decontamination (SALAD) technique is recommended for airway decontamination in the prehospital and emergency room environments.

Question 9

What percentage of intubated trauma patients experience hypoxemia and develop ARDS?

Answer 9

In one study of 621 intubated trauma patients, 64% experienced hypoxemia, and 46% of these hypoxemic patients developed ARDS confirmed by chest radiography.

Question 10

Q2: What is the pathological mechanism behind ARDS?

Answer 10

A2: ARDS is caused by protein-rich fluid leaving the pulmonary capillaries and accumulating within the alveoli, compounded by embolic events, surfactant dysfunction, and the development of a hyaline membrane that prevents adequate gas exchange.

Question 11

Q3: What ventilation strategy is recommended for ARDS patients?

Answer 11

A3: Patients with ARDS should be managed with low tidal volume ventilation, plateau pressures less than 30 cm H2O, permissive hypercapnia, conservative fluid strategies, and prone positioning.

Question 12

Q4: What are the management techniques for ARDS besides reduced tidal volume ventilation?

Answer 12

A4: Other management techniques for ARDS include the use of neuromuscular blockers to reduce mortality, and considering extracorporeal membrane oxygenation for those unresponsive to standard therapies.

Question 13

Q5: What is the leading cause of early and late mortality after trauma?

Answer 13

A5: Hemorrhagic shock is the leading cause of early and late mortality after trauma.

Question 14

Q6: How does the body initially compensate for hemorrhagic shock?

Answer 14

A6: The body initially compensates for hemorrhagic shock by shunting blood from low metabolic tissues to highly metabolic tissues, increasing vascular tone and systemic vascular resistance.

Question 15

Q7: What is the basis for the “golden hour” in trauma care?

Answer 15

A7: The “golden hour” is based on data from young, healthy males in military service during the Vietnam War, indicating that selected patients will likely survive hemorrhagic shock if perfusion is restored within the first 60 minutes after traumatic injury.

Question 16

Q8: What occurs during Stage II (progressive shock) of hemorrhagic shock?

Answer 16

A8: During Stage II (progressive shock) of hemorrhagic shock, components of the cardiovascular system start to deteriorate, including cardiac depression, vasomotor failure, thrombosis of small vessels, increased capillary permeability, and generalized cellular degeneration.

Question 17

Q9: How does the administration of fluids potentially worsen the clinical state in ongoing or massive injury?

Answer 17

A9: The administration of fluids may worsen the clinical state in ongoing or massive injury by increasing blood pressure, which can cause more bleeding and disrupt blood clot formation.

Question 18

Q10: What is the dosage and timing of tranexamic acid (TXA) for trauma patients?

Answer 18

A10: Tranexamic acid (TXA) is recommended to be given within 3 hours of initial injury, with a dosage of 1 g IV over 10 minutes followed by 1 g IV over 8 hours.

Question 19

Q11: What are the three stages of shock?

Answer 19

A11: The three stages of shock are non-progressive (compensated) shock, progressive shock, and irreversible shock.

Question 20

Q1: What are the four primary causes of trauma-induced coagulopathy?

Answer 20

A1: The four primary causes of trauma-induced coagulopathy are dilution of factors, hypothermia/acidosis, severe TBI, and hypovolemic hemorrhagic shock.

Question 21

Q2: What are the endogenous and exogenous components of trauma-induced coagulopathy?

Answer 21

A2: Endogenous acute traumatic coagulopathy is associated with shock and hypoperfusion, while exogenous coagulopathy arises from the effects of dilution due to fluid resuscitation and consumption through bleeding and loss of coagulation factors.

Question 22

Q3: How does massive resuscitation affect coagulation factors?

Answer 22

A3: Massive resuscitation often requires the administration of crystalloids, which dilute coagulation factors and platelets, leading to an inadequate clot and nonsurgical bleeding.

Question 23

Q4: What is recommended to maintain an INR of 1.5 or less and a platelet count above 50,000 in trauma patients?

Answer 23

A4: The consensus statement recommends administering procoagulant products, such as plasma, cryoprecipitate, and platelets, to maintain an INR of 1.5 or less and a platelet count above 50,000.

Question 24

Q5: What is the clinical effect of hypothermia on clot formation?

Answer 24

A5: Hypothermia primarily inhibits the initiation phase of thrombin generation and inhibits fibrinogen synthesis, resulting in a slowly formed and fragile clot that is unable to inhibit bleeding.

Question 25

Q6: How does acidosis contribute to coagulopathy in the presence of hypothermia?

Answer 25

A6: Acidosis impairs coagulation proteases and becomes clinically significant at a pH less than 7.1, contributing to coagulopathy in the presence of hypothermia.

Question 26

Q7: What is the role of the activated protein C (APC) pathway in trauma-induced coagulopathy?

Answer 26

A7: The APC pathway, initiated when thrombin binds with thrombomodulin, induces anticoagulation by inhibiting factors V and VIII, and may lead to systemic coagulopathy in the presence of damaged and hypoperfused tissue.

Question 27

Q8: What is the recommended early management strategy for TBI-induced coagulopathy?

Answer 27

A8: Early management of TBI-induced coagulopathy should include rapid administration of plasma to normalize PT and INR, and the administration of low-dose recombinant FVIIa (rFVIIa) to improve coagulation status.

Question 28

What is the goal of care for patients with primary TBI?

Answer 28

prevention of secondary brain damage resulting from intracranial complications that are aggravated by intracranial bleeding, edema, and resultant increases in ICP.

Question 29

Q2: What are the modifiable risk factors for morbidity and mortality following severe TBI?

Answer 29

A2: The modifiable risk factors for morbidity and mortality following severe TBI are the presence of hypotension on admission and the need for mechanical ventilation.

Question 30

Q3: What GCS score necessitates endotracheal intubation in TBI patients?

Answer 30

A3: A GCS score of less than 8 necessitates endotracheal intubation in TBI patients.

Question 31

Q4: Why might nasal intubation be contraindicated in head-injured patients?

Answer 31

A4: Nasal intubation may be contraindicated in head-injured patients because of possible basilar skull fractures that can facilitate contamination and ultimate sepsis from nasal microorganisms introduced into the cranial vault.

Question 32

Q5: What is the recommended early treatment with TXA for TBI patients with intracranial bleeds?

Answer 32

A5: The recommended early treatment with TXA for TBI patients with intracranial bleeds is 1 g IV over 10 minutes followed by 1 g IV over 8 hours, preferably within 3 hours of injury.

Question 33

Q6: What MAP and CPP should be maintained in TBI patients with increased ICP?

Answer 33

A6: A MAP greater than 80 mm Hg and a CPP of greater than 60 mm Hg should be maintained in TBI patients with increased ICP.

Question 34

Q7: What are the three tiers of the ACS recommended approach for treating intracranial hypertension?

Answer 34

A7: The three tiers of the ACS recommended approach for treating intracranial hypertension are:'- Tier 1: Elevation of the head of the bed, short-acting sedation and analgesia, intermittent ventricular drainage, repeat neurologic exams, and CT scans. - Tier 2: Placement of an external ventricular drain, hyperosmolar therapy with mannitol or hypertonic saline, and additional neuromonitoring. - Tier 3: Surgical evacuation, barbiturate- or propofol-induced coma, and hypothermia (<36°C).

Question 35

Q8: What are the signs of impending brain herniation (Cushing triad)?

Answer 35

A8: The signs of impending brain herniation (Cushing triad) are hypertension, bradycardia, and irregular respirations.

Question 36

What are the effects of propofol on CMRO2, CBF, and ICP, and why must it be used cautiously?

Answer 36

decreases CMRO2, CBF, and ICP, making it a preferred agent for hemodynamically stable TBI patients. However, it must be used cautiously due to its reduction of SVR and myocardial depressant effects, which can be problematic in patients with hemodynamic instability.

Question 37

Q10: What is the management approach for suspected spinal cord injury (SCI)?

Answer 37

A10: The management approach for suspected spinal cord injury (SCI) includes spinal immobilization, properly fitting a cervical collar, stabilizing the head in a neutral alignment, assessing for a patent airway, and securing the airway without disturbing the neutral neck position. Oxygen should be administered immediately, and rapid intubation is needed if the patient cannot self-protect the airway.

Question 38

Q1: Why should succinylcholine be avoided in patients with spinal cord injury (SCI) after 24 hours from sustaining the injury?

Answer 38

A1: Succinylcholine should be avoided in patients with SCI after 24 hours from sustaining the injury because it may precipitate cardiac arrest due to massive potassium release from up-regulated acetylcholine receptors and depolarizing effects.

Question 39

Q2: What are the primary treatment goals for patients in spinal shock?

Answer 39

A2: The primary treatment goals for patients in spinal shock are to manage hypotension and bradycardia using invasive monitoring, fluid resuscitation, and vasoactive drugs such as norepinephrine infusion.

Question 40

How does spinal shock affect the body’s ability to regulate temperature?

Answer 40

Spinal shock affects the body’s ability to regulate temperature by interrupting sympathetic pathways from the hypothalamus to peripheral blood vessels, preventing the patient from constricting or dilating vessels to regulate heat.

Question 41

Q4: What are the recommended guidelines for extubating patients with complete cervical SCI?

Answer 41

A4: Patients with complete cervical SCI should undergo elective tracheostomy if mechanical ventilation is needed for more than 48 hours. The decision for tracheostomy in patients with incomplete SCI should consider associated intracranial and thoracic injuries.

Question 42

Q5: What are the criteria for assessing the adequacy of ventilation in patients with high SCI?

Answer 42

A5: The criteria for assessing the adequacy of ventilation in patients with high SCI include tidal volume (>5 mL/kg), negative inspiratory force (−20–25 cm H2O pressure), and vital capacity (>15 mg/kg).

Question 43

Q6: What are the primary treatments for SCI without radiographic abnormalities (SCIWORA)?

Answer 43

A6: The primary treatments for SCIWORA include the application of an external immobilization device such as a hard cervical collar for up to 12 weeks post-injury and keeping the patient’s neck in a neutral position for airway management and intraoperative positioning.

Question 44

Q7: What is the incidence range of vertebral artery injury (VAI) in SCI patients?

Answer 44

A7: The incidence range of vertebral artery injury (VAI) in SCI patients is estimated to be between 53% and 88%.

Question 45

Q8: What is the current standard diagnostic tool for detecting vertebral artery injury (VAI)?

Answer 45

A8: The current standard diagnostic tool for detecting vertebral artery injury (VAI) is CT angiography.

Question 46

Q9: What is the estimated incidence of SCI per million population in the United States annually?

Answer 46

A9: The estimated incidence of SCI per million population in the United States annually is approximately 54 cases, translating to 17,810 new cases per year.

Question 47

Q10: What are the common mechanisms of spinal injuries in the United States?

Answer 47

A10: The common mechanisms of spinal injuries in the United States are motor vehicle collisions (MVCs), falls, and gunshot wounds, with MVCs being the primary cause until age 45, after which falls become the leading cause.

Question 48

Q1: What do many neurosurgeons believe about the prolonged use of external fixation devices in patients with unsatisfactorily reduced spines?

Answer 48

A1: Many neurosurgeons believe that prolonged use of external fixation devices is contraindicated in patients with unsatisfactorily reduced spines.

Question 49

Q2: What did research indicate about the use of a halo vest for older patients aged 60–73?

Answer 49

A2: Research indicated that the use of a halo vest for older patients aged 60–73 may have higher rates of morbidity and mortality.

Question 50

Q3: What has contemporary investigation on the timing of surgical intervention after an initial SCI shown?

Answer 50

A3: Contemporary investigation on the timing of surgical intervention after an initial SCI has shown mixed results, with some research indicating early stabilization improves outcomes, while other studies link early surgery to higher mortality and neurologic deterioration.

Question 51

Q4: What are the documented findings of Liu's study involving 595 patients regarding early surgical intervention?

Answer 51

A4: Liu's study involving 595 patients determined that early surgical intervention was linked to higher mortality and neurologic deterioration.

Question 52

Q5: What should be documented before the start of anesthesia and intubation in SCI patients?

Answer 52

A5: The patient's current neurologic status and any deficits should be documented before the start of anesthesia and intubation.

Question 53

Q6: What is the choice of airway management technique with an SCI dependent on?

Answer 53

A6: The choice of airway management technique with an SCI depends on the patient's injuries, level of cooperation, hemodynamic stability, and ability to protect the airway.

Question 54

Q7: How should agitated, intoxicated, uncooperative, and/or hemodynamically unstable patients be managed?

Answer 54

A7: Agitated, intoxicated, uncooperative, and/or hemodynamically unstable patients should be managed by a rapid sequence induction with direct or video laryngoscopy using properly applied cricoid pressure and MILS of the cervical spine.

Question 55

What is the general consensus for MILS under ATLS guidelines and current best practice recommendations?

Answer 55

The general consensus for MILS under ATLS guidelines and current best practice recommendations is to minimize the risk of secondary cervical SCI despite potentially leading to a less optimal view.

Question 56

Why should opioids and inhaled volatile anesthetic agents be reduced or avoided if spinal monitoring is being performed?

Answer 56

they can interfere with neural monitoring such as somatosensory-evoked potentials and electromyography.

Question 57

What are the American Association of Neurological Surgeons guidelines for blood pressure controls post-SCI?

Answer 57

maintaining a MAP range from 85 to 90 mm Hg for 5 to 7 days to optimize spinal cord perfusion.

Question 58

What is autonomic dysreflexia, and what triggers it?

Answer 58

Autonomic dysreflexia is a potentially fatal clinical condition found in patients with SCI above T6, characterized by a sudden activation of the sympathetic response due to a noxious stimulus such as surgery or colorectal/bladder distention.

Question 59

What are the potential life-threatening consequences of autonomic dysreflexia?

Answer 59

severe hypertension, seizures, pulmonary edema, myocardial infarction, acute renal injury, and intracranial hemorrhage.

Question 60

How should an acute autonomic dysreflexia attack be managed?

Answer 60

determining and correcting the noxious stimuli, positioning the patient in an upright position, and pharmacologic intervention if blood pressure does not drop below 150 mm Hg.

Question 61

What medications are used to reduce dangerous levels of blood pressure in autonomic dysreflexia?

Answer 61

nitrates, nifedipine, hydralazine, and labetalol.

Question 62

What is the incidence of extremity injuries in civilian trauma, and what are the most common causes?

Answer 62

most often occur as a consequence of falls (43%) and motor vehicle collisions (MVCs) (26%).

Question 63

What should be done during the primary survey of trauma patients with extremity injuries?

Answer 63

it is vital to recognize and control hemorrhage from all musculoskeletal injuries, typically best accomplished with direct pressure and application of a tourniquet if pressure dressings are not effective.

Question 64

What are the implications of closed long-bone fractures in terms of blood loss?

Answer 64

can result in significant loss of blood into the thigh.

Question 65

What are the common causes of pelvic fractures, and what should be done if a significant pelvic injury is suspected?

Answer 65

most often caused by high-energy mechanisms of injury, and if a significant pelvic injury is suspected and the patient is hemodynamically unstable, the pelvis should be "wrapped" with a bed sheet or a commercial pelvic binder.

Question 66

What are the benefits of early fracture fixation with intramedullary nails?

Answer 66

Early fracture fixation with intramedullary nails allows patients to ambulate within 24 hours of surgery and drastically reduces the incidence of pulmonary complications, including ARDS, fat emboli, and pneumonia.

Question 67

How should vascular injuries that compromise perfusion of the extremity be addressed?

Answer 67

Vascular injuries that compromise perfusion of the extremity should be addressed within 4 hours of loss of adequate perfusion to the limb, necessitating timely communication between orthopedic and vascular surgery.

Question 68

What are the mortality rates and primary interventions for massive hemorrhage associated with pelvic fractures?

Answer 68

can be as high as 70%, and primary interventions include the application of a pelvic binder, external fixation, angiographic embolization, and pelvic packing.

Question 69

What is the primary endpoint to ensure oxygenation and end-organ perfusion in trauma patients?

Answer 69

The primary endpoints to ensure oxygenation and end-organ perfusion are the relative normalization of serum lactate, base deficit, pH, early correction of clotting functions, and hemorrhage control.

Question 70

What role does TEG play in managing coagulopathy in trauma patients?

Answer 70

TEG analyzes real-time coagulation and helps determine which blood products are needed during resuscitation, providing goal-directed targeted therapy to correct the coagulopathy of trauma.

Question 71

What is fat emboli syndrome (FES), and what is its incidence in long bone fractures?

Answer 71

Fat emboli syndrome (FES) is a condition where fat cells from disrupted bone marrow enter the venous circulation, leading to hypoxia, and it occurs in approximately 3% of patients with one long bone fracture and 33% of patients with bilateral long bone fractures of the femur.

Question 72

What is the primary treatment for clinically evident fat emboli syndrome (FES)?

Answer 72

supportive care, endotracheal intubation, and mechanical ventilation, with some evidence supporting the use of low-dose methylprednisolone for high-risk patients.

Question 73

What are the three mechanisms of injury that reliably predict the need for referral to a trauma center when patients do not meet anatomical or physiological injury criteria?

Answer 73

death of an occupant in the vehicle, fall greater than 20 feet, and extrication time greater than 20 minutes.

Question 74

What are the differences in blood volume loss between patients with penetrating trauma and those with blunt trauma?

Answer 74

Patients with penetrating trauma lose blood volume externally and into body cavities, whereas patients with blunt trauma may present in hemorrhagic shock without obvious signs of hemorrhage, often due to internal bleeding into compartments or body cavities

Question 75

Signs and symptoms of shock

Answer 75

Pallor Diaphoresis Agitation or obtundation Hypotension Tachycardia Prolonged capillary refill Diminished urine output Narrowed pulse pressure

Question 76

Where are the five sites that exsanguination hemorhage can occur?

Answer 76

Chest, abdomen, retroperitoneum, long bones, and outside the body

Question 77

What are the roles of the anesthesiologist and the trauma surgeon in the trauma bay?

Answer 77

In the trauma bay, the trauma surgeon focuses on anatomic control of hemorrhage, whereas the anesthesiologist is responsible for restoring the patient’s physiology.

Question 78

What important role does the anesthesiologist play in trauma surgery decisions, and how does delay in getting to the OR impact mortality in trauma patients?

Answer 78

The anesthesiologist determines the order of procedures and which to postpone until the patient is stable. Delays to the OR can increase mortality, with a 1% increase in mortality for every 3 minutes of delay to laparotomy in hypotensive patients with abdominal injuries.

Question 79

What's the major difference between ASA airway algorithm and the trauma airway algorithm?

Answer 79

Reawakening of the patient is seldom and option in the trauma algorithm due to need of securing the airway.

Question 80

What does the Sellick maneuver involve?

Answer 80

The Sellick maneuver involves elevating the patient's chin without displacing the cervical spine and pushing the cricoid cartilage posteriorly to close the esophagus.

Question 81

What are the potential downsides of cricoid pressure during intubation?**

Answer 81

Cricoid pressure may worsen the laryngoscopic grade of view in up to 30% of patients and may not effectively prevent aspiration of gastric contents.

Question 82

What is the most commonly used induction agent in the ED or trauma setting in the United States, and what are its characteristics?**

Answer 82

The most commonly used induction agent is etomidate, administered at 0.2 to 0.3 mg/kg, associated with hemodynamic stability, and has an onset/duration profile similar to succinylcholine. (Mitigate myoclonus with NMBA)

Question 83

What is the initial response to hemorrhage on the macrocirculatory level?

Answer 83

mediated by the neuroendocrine system, leading to vasoconstriction and the release of catecholamines to preserve blood flow to vital organs like the heart, kidney, and brain.

Question 84

What mediators are released in response to pain, hemorrhage, and traumatic injuries?**

Answer 84

Pain, hemorrhage, and cortical perception of traumatic injuries lead to the release of hormones and inflammatory mediators such as renin, angiotensin, vasopressin, antidiuretic hormone, growth hormone, glucagon, cortisol, epinephrine, and norepinephrine

Question 85

What is the no-reflow phenomenon in hemorrhagic shock?

Answer 85

The no-reflow phenomenon in hemorrhagic shock occurs when cellular edema chokes off adjacent capillaries, preventing reversal of ischemia even in the presence of adequate macrocirculation.

Question 86

How do ischemic cells contribute to the inflammatory response in hemorrhagic shock?

Answer 86

Ischemic cells produce lactate and free radicals, which cause direct damage to cells and contribute to the toxic load that returns to the central circulation when flow is reestablished. These cells also release inflammatory factors that contribute to the systemic inflammatory response and multiple organ failure.

Question 87

How does the CNS respond to traumatic shock?

Answer 87

The CNS is the prime trigger of the neuroendocrine response to shock, maintaining perfusion to the heart, kidney, and brain at the expense of other tissues.

Question 88

What happens to brain function during shock-induced hypotension?

Answer 88

Reflexes and cortical electrical activity are depressed, changes that are reversible with mild hypoperfusion but become permanent with prolonged ischemia.

Question 89

How do the kidney and adrenal glands respond to shock?**

Answer 89

The kidney and adrenal glands respond to shock by producing renin, angiotensin, aldosterone, cortisol, erythropoietin, and catecholamines.

Question 90

**Q8: What are the consequences of prolonged hypotension on the kidneys?**

Answer 90

**A8: Prolonged hypotension leads to decreased cellular energy, inability to concentrate urine (renal cell hibernation), patchy cell death, tubular epithelial necrosis, and renal failure.**

Question 91

**Q9: How is cardiac function affected during shock?**

Answer 91

**A9: Cardiac function is well preserved until the late stages of shock due to maintained or increased nutrient blood flow, but lactate, free radicals, and other factors released by ischemic cells can act as negative inotropes, potentially leading to cardiac dysfunction.**

Question 92

**Q10: Why are older patients with cardiac disease at higher risk during shock?**

Answer 92

**A10: Older patients with cardiac disease are at higher risk during shock because a fixed stroke volume inhibits their ability to increase blood flow in response to hypovolemia and anemia, making tachycardia their only option.**

Question 93

**Q11: How do the lungs respond to the inflammatory by-products of shock?**

Answer 93

**A11: The lungs respond to the inflammatory by-products of shock by accumulating immune complexes and cellular factors in pulmonary capillaries, leading to neutrophil and platelet aggregation, increased capillary permeability, destruction of lung architecture, and ARDS.**

Question 94

**Q12: What role do the lungs play in multiple organ dysfunction (MOD) during traumatic shock?**

Answer 94

**A12: The lungs are the sentinel organ for the development of multiple organ dysfunction (MOD) during traumatic shock.**

Question 95

**Q13: How does the gut respond to hypoperfusion during shock?**

Answer 95

**A13: The gut responds to hypoperfusion during shock with intense vasoconstriction, often leading to the no-reflow phenomenon even when macrocirculation is restored.**

Question 96

**Q14: What is the significance of intestinal cell death in traumatic shock?**

Answer 96

**A14: Intestinal cell death causes a breakdown in the barrier function of the gut, leading to increased translocation of bacteria to the liver and lung, potentiating MOD and ARDS.**

Question 97

**Q15: What are the potential effects of reperfusion injury on the liver?**

Answer 97

**A15: The liver may experience reperfusion injury during recovery from shock, contributing to the ischemic inflammatory response and irregularities in blood glucose.**

Question 98

**Q16: How does hepatic failure after shock typically end?**

Answer 98

**A16: Failure of hepatic synthetic function after shock is almost always lethal.**

Question 99

**Q17: How does skeletal muscle respond to ischemia during shock?**

Answer 99

**A17: Skeletal muscle tolerates ischemia better than other organs and is not metabolically active during shock, but sustained ischemia leads to increased intracellular sodium and free water, further depleting fluid in the vascular and interstitial compartments.**

Question 100

**Q18: What is the role of skeletal muscle in generating lactic acid and free radicals?**

Answer 100

**A18: The large mass of skeletal muscle makes it important in generating lactic acid and free radicals from ischemic cells during shock.**

Question 101

**Q19: How does endothelial injury contribute to the pathophysiology of hemorrhagic shock?**

Answer 101

**A19: Endothelial injury in hemorrhagic shock leads to glycocalyx shedding, breakdown of tight junctions, capillary leakage, and a pro-coagulant microvasculature, reducing oxygen delivery due to increased tissue pressure and microvascular thrombosis.**

Question 102

What is a reasonable blood pressure goal for patients in phase I. Acute hemorrhage?

Answer 102

target a systolic pressure of less than 100 mm Hg with MAP between 50 to 60 mm Hg

Question 103

In which populations is permissive hypotensive resuscitation avoided, and why?

Answer 103

Avoided in ischemic coronary disease, older patients, brain/spinal cord injuries, and TBI due to worse outcomes

Question 104

When should TXA be given in the trauma patient to prevent fibrinolysis?

Answer 104

within 1 hour of admission. (Administration afterwards increases mortality)

Question 105

Why aren't traditional vital signs good indicators of resolution of shock?

Answer 105

Occult hypoperfusion syndrome is common in postoperative trauma patient. This syndrome is characterized by a normal blood pressure maintained by systemic vasoconstriction, decreased intra- vascular volume and cardiac output, and organ system ischemia. The patient will be at frequent risk for MOD if the hypoperfusion is not promptly corrected.

Question 106

What lab value returning to normal is strongly correlated with survival?

Answer 106

Lactate

Question 107

What measures are used to determine resolution of shock

Answer 107

Vital sings (non reliable) , urine output, acid-base, CO, mixed venous, gastric tonometry, SVV, tissueoxygenation

Question 108

Q1: What is the mainstay of treatment for hemorrhagic shock?

Answer 108

A1: RBCs, with an average hematocrit of 50% to 60%.

Question 109

Q2: What blood type is the universal donor and preferred for patients in hemorrhagic shock?

Answer 109

A2: Type O blood.

Question 110

Q3: What are the risks of RBC administration?

Answer 110

A3: Transfusion reaction, transmission of infectious agents, and hypothermia.

Question 111

Q4: Why might plasma availability be delayed during resuscitation?

Answer 111

A4: Plasma requires blood typing and thawing of frozen units.

Question 112

Q5: When should platelet transfusion be administered in a trauma setting?

Answer 112

A5: When the patient is in shock and blood loss is likely substantial; platelets should be administered in proportion to RBCs and plasma (1:1:1).

Question 113

Q6: What risk is associated with rapid transfusion of banked blood and how can it be managed?

Answer 113

A6: Citrate intoxication leading to hypocalcemia; managed by measuring ionized Ca2+ levels and administering Ca2+ as needed

Question 114

What size IV catheters should be placed in trauma?

Answer 114

16g or larger

Question 115

Where is the best site for a central line in the trauma patient? Why?

Answer 115

Subclavian, because its above the diaphragm, is seldom traumatized, and doesnt require head manipulation.

Question 116

What does a PaO2<60 do to a TBI patient?

Answer 116

Doubles mortality

Question 117

What drugs are associated with increased mortality in the TBI patient?

Answer 117

Corticosteroids

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