Trauma Special Topics Flashcards

1
Q

What is the goal of care for head injury?

A

To prevent secondary brain damage resulting from intracranial complications that are aggravated by intracranial bleeding, edema, and resultant increased intracranial pressure (ICP).

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2
Q

What are modifiable risk factors for M&M following severe traumatic brain injury?

A

-Presence of hypotension on admission
-Need for mechanical ventilation

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3
Q

Describe anesthetic management of head injured patients.

A

Early control of the airway and maintenance of CV Stability.
-GCS < 8 necessitates ETT
-Maintain SpO2 > 90% with normoventilation
-Avoid increases in ICP with intubation
-Nasal intubation/nasogastric tube contraindicated 2o to possible basilar skull fracture
-Gastric tubes should be oral only.
-Hypoxemia and hypotension are associated with increased M&M
-CPP = MAP – ICP (60 - 70 mmHg)
-Support treatment for ICP > 20-25 mmHg: HOB elevation, PCO2 30-35mmHg, intermittent intraventricular drainage CSF
-No anesthesia technique superior (TIVA vs. Inhaled), avoid N2O
-Arterial BP monitoring: maintain SBP > 90 mmHg
-Hyperosmolar therapy with mannitol 0.25-1 g/kg helps control elevated ICP
-Corticosteroids (not shown to improve outcome or reduce ICP)

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4
Q

What are risk factors for Spinal Cord Injury (SCI)?

A

-10,000 SCIs per year in the US
-80% male with median age 25 years
-MVAs, falls, assaults, diving injuries, and other sports

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5
Q

Outcome after an acute SCI depends on what 3 factors?

A

1) The severity of the acute injury
2) The prevention of exacerbation of the injury during rescue, transport, and hospitalization
3) The avoidance of hypoxia and systemic hypotension, which can further compromise neural function.

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6
Q

Where do most traumatic SCIs occur?

A

> 50% occur in cervical region.
-Craniocervical junction (33%): occiput and 1st two vertebrae
-Categorized as complete or incomplete

Most common forms:
-Incomplete tetraplegia (31%)
-Complete paraplegia (25%)
-Complete tetraplegia (20%)
-Incomplete paraplegia (19%)

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7
Q

What is the difference between a complete and incomplete SCI?

A

Complete: absence of motor, sensory, bowel and bladder function below the level of injury

Incomplete: preservation of some neurologic function

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8
Q

What is the difference between Tetraplegia and Paraplegia?

A

Tetraplegia, also known as quadriplegia, results in the partial or total loss of use of all four limbs and torso; paraplegia is similar but does not affect the arms.

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9
Q

Cervical SCI should be assumed in what situations?

A

SCI should be ruled out in ANY trauma!!
Assume Cervical SCI in:
-Any trauma to the head or face
-Unconscious trauma patient
-Complaints of pain in the cervical spine with or without palpation.

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10
Q

What are the 6 conditions that correlate with SCIs?

A

Paralysis
Pain
Position
Parathesias
Ptosis
Priapism

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11
Q

How do you prevent worsening neurological deficits with SCIs?

A

-Spinal immobilization should be completed prior to patient movement.
-Stabilization can be accomplished by placing a cervical collar on the patient, splinting, and/or sandbagging the head in neutral alignment.
-The patient should be placed on a long spinal back board before he or she is moved.

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12
Q

How do you evaluate a SCI?

A

-Xray multiple views, CT scan or MRI
-Must include all 7 cervical vertebrae
-C-7 most common injury site

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13
Q

What indicates that a patient is unable to protect their airway?

A

-Unconscious or semiconscious
-Absent or diminished gag reflex or cough
-Intraoral or facial injuries with significant edema, bleeding, or both

Require rapid intubation.

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14
Q

SCI above what level leads to apnea and ventilator dependence?

A

SCI above C3 often leads to apnea, rendered ventilator dependent.
-Diaphragm innervated C 3-5, Intercostal muscles T 2-11

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15
Q

How do you perform airway management with SCI?

A

-The choice of airway management technique will depend to a great extent on the patient’s injuries, level of cooperation, hemodynamic stability, and ability to protect the airway.
-Succinylcholine is not recommended for intubation of the patient with acute SCI because muscle fasciculation may exacerbate the SCI.
-Use Roc or non-relaxant assisted airway control techniques
-Manual In-Line Stabilization may lead to a less than optimal view, but it is still recommended to minimize the risk of secondary cervical SCI.

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16
Q

Describe anesthetic management of SCI procedures (Stabilization or decompression procedures)

A

-Early stabilization associated with improved outcomes
-Maintain MAP ~ 90 mmHg for up to 7 days postinjury to optimize spinal cord perfusion
-Document neurologic status before start of anesthesia, intubation, and positioning for surgery - Consider awake intubation
-Airway technique dependent on level of injury, level of cooperation, hemodynamic stability and ability to protect the airway
-Manual In-Line Stabilization recommended
-Induction: Propofol versus Ketamine or Combination
-Avoid N2O (chance of head injury, lung insult, or bowel obstruction in trauma patients)
-Antifibrinolytic agents (TXA)

17
Q

Why are Propofol and Ketamine preferred for induction in the SCI patient?

A

Propofol decreases CMRO 2 , CBF and ICP, which makes this drug a preferred agent for hemodynamically stable TBI patients.

Use of ketamine in those patients with a TBI may lead to increased ICP, but it may help avoid hypotension in hypovolemic trauma patients.

18
Q

What is Tranexamic Acid (TXA)?

A

Antifibrinolytic agent.
-A lysine analog that inhibits plasminogen activation and has been shown in many studies to be particularly helpful at reducing surgical blood loss.

19
Q

Why do you avoid Nitrous Oxide in trauma patients?

A

There is a chance the patient has a head injury, lung insult, or bowel obstruction.

20
Q

What is the triad of spinal shock?

A

Hypotension, Bradycardia, and Hypothermia

21
Q

How does Spinal Shock occur?

A

-Progressively intensified more cephalad (> T-6)
-Loss of sympathetic tone, vasodilation, peripheral circulation pooling, and decreased venous return (Hypotension)
-Unopposed vagal innervation (Bradycardia)
-Interrupts sympathetic pathways from hypothalamus to peripheral blood vessels, unable to constrict or shiver (Hypothermia)

22
Q

What is the difference between Spinal and Hemorrhagic Shock?

A

Patients in spinal shock are hypotensive and bradycardic with warm, pink extremities. In contrast, patients in hemorrhagic shock tend to be hypotensive and tachycardic with cold, clammy skin.

23
Q

What monitoring should be used for the SCI patient?

A

Use of invasive monitoring is critical for fluid resuscitation and appropriate intervention with vasoactive drugs.
-An indwelling arterial catheter is mandatory in the acute phase of spinal shock.
-The SCI patient is frequently unable to maintain adequate cardiac filling pressures, consider central venous access.
-However, overaggressive fluid therapy can precipitate pulmonary edema.
-For the maintenance of adequate arterial blood pressure and cord perfusion, pressor therapy may be initiated.

24
Q

What is Autonomic Dysreflexia?

A

Sudden activation of sympathetic response secondary to noxious stimuli (Colorectal and bladder distention).
-Persists from several weeks to 6 months post SCI
-~ 98% high para/quadriplegic (SCI above T6) will experience AD following painful injury below level of spinal cord lesion
-Often presents with severe hypertension
-Other life-threatening consequences: seizure, pulmonary edema, MI, acute renal injury, and intracranial hemorrhage

25
Q

How do you manage Autonomic Dysreflexia?

A

Determine and correct the noxious stimuli:
-bladder catheterization, exclusion of a UTI, and rectal disimpaction should be performed

Reduce dangerous BP levels:
-Captopril (25 mg sublingual), hydralazine (10 mg IV), and labetalol (10 mg IV).

26
Q

What is Orthopedic Trauma?

A

Trauma to the extremities; one of the most frequent injuries (falls 43% or MVCs 26%)
-Usually not immediately life-threatening
-Can be associated with significant hemorrhage, linked to shock, fat emboli, thromboembolic hypoxic resp failure
-Early fixation may allow early ambulation reducing pulmonary complications (ARDS, fat emboli, PNA)
-High index of suspicion for compartmental syndrome when high-energy trauma is responsible for the fractures
-Massive hemorrhage associated with pelvic fractures (displaced pelvic bone fragments sever stuff)

27
Q

What is the treatment for Open Pelvic Fractures?

A

May require Damage Control Surgery measures.
-External fixation, angiographic embolization, and application of pelvic packing have been used with some success as elements of damage control surgery.
-REBOA: resuscitative endovascular balloon occlusion of the aorta.

28
Q

How do pelvic and long bone fractures cause hypoxic respiratory failure?

A

Fat Embolic Syndrome (FES).
-One long bone fracture ~ 3%
-Bilateral long bone fractures ~ 33%
-Hypoxia secondary to seeding fat cells into venous circulation
-Fat cells produce proinflammatory / prothrombotic reactions, rapid platelet aggregation and fibrin generation lodging in the pulmonary arterial circulation
-Capillary obstruction leads to interstitial edema, alveolar collapse, and reactive hypoxic pulmonary vasoconstriction.
-Massive fat emboli can produce Macrovascular obstruction and shock

29
Q

When is Fat Embolic Syndrome (FES) typically seen?

A

FES is typically seen 24 to 72 hours after the initial injury

30
Q

What are the S/Sx of Fat Embolic Syndrome?

A

Hypoxemia, Neurologic impairment, and a classic Petechial Rash (!!)

31
Q

What is the treatment of Fat Embolic Syndrome?

A

-Supportive care is the primary treatment for clinically evident FES, which may include endotracheal intubation and mechanical ventilation.
-There is some evidence that patients at high risk for the development of FES may benefit from low dose corticosteroids, methylprednisolone (1.5 mg/kg IV) every 8 hours for 6 doses.
-It is likely that patients who experience long bone fractures will be taken to the operating room as soon as possible for surgical correction and stabilization of any long bone or pelvic fractures. This is thought to reduce the risk of FES in addition to other pulmonary complications such as pneumonia, pulmonary embolism, and ARDS.

32
Q

What is the CRNA’s role in trauma?

A

-Emergently care for patients (no matter the circumstances: kind of injury, time of day, resources)
-Quick, Efficient, and Effective (ABCs + Resuscitation)
-Set the tone of Calm (communication is critical)
-Safe transport to and from OR
-Think 2 Steps ahead!

33
Q

What is REBOA?

A

Resuscitative Endovascular Balloon Occlusion of the Aorta.
-Developed to address the challenge of managing non-compressible torso hemorrhage, a major cause of potentially preventable death after traumatic injury.
-Thoracic hemorrhage should be excluded prior to REBOA deployment (CXR, U/S, Chest tube placement)

34
Q

When is REBOA used?

A

REBOA is an alternative form of Resuscitative Aortic Occlusion for patients at risk of imminent cardiovascular collapse. It is performed through a femoral artery approach without the need for thoracotomy.
-REBOA is best applied prior to cardiovascular collapse when the site of hemorrhage is below the diaphragm and no open thoracic intervention is otherwise indicated.
-Traumatic life-threatening hemorrhage below the diaphragm in hemorrhagic shock refractory to resuscitation
-No long-term survival advantage in traumatic cardiac arrest
-Contraindicated in major thoracic hemorrhage or pericardial tamponade
-Insufficient data in pediatric and geriatric populations

35
Q

Is REBOA permanent?

A

REBOA is a TEMPORARY bridge to hemorrhage control. Occlusion of the aorta, endovascular or surgical, results in tissue ischemia followed by reperfusion injury
-Potential technical complications impacting lower extremity perfusion
-There is a time-sensitive nature of this intervention because it ultimately requires definitive repair through surgery or interventional radiology.

36
Q

What are complications associated with REBOA?

A

-Prolonged aortic occlusion may lead to fatal complications or spinal cord injury due to prolonged ischemia
-Reperfusion injury can lead to AKI or multisystem organ failure
-Common Femoral Artery access complications
-Aortoiliac injuries: rupture and thrombosis
-Increased risk of extremity complications secondary to sheath dwell times
-Delay definitive hemorrhage control with prolonged insertion

37
Q

When is REBOA used in pregnancy?

A

-Consider in malignant placental implantation
-Limit blood loss as well as transfusion requirements
-Access is key for rapid deployment
-Occlusion times are 20 – 30 min in published series
-Optimal time of balloon inflation unclear
-At time of cord clamping versus time of massive bleeding?

38
Q

Describe REBOA deflation & removal

A

-Deflate the balloon slowly as this step can be anticipated to result in a significant decrease in afterload and hypotension and may result in cardiac collapse.
-Additional resuscitation may be needed while the balloon is slowly deflated. After balloon deflation, the team should anticipate hemodynamic changes related to reperfusion, washout of metabolic byproducts, and acidosis.
-As such, intermittent balloon inflation and deflation may be necessary during ongoing resuscitation until hemodynamic stability is restored.
-REBOA catheter removed ASAP
-Sheath remains until coagulopathy reversed, removed with CFA pressure held for 30 min
-Strict bed rest without moving leg for 6 hours
-Q1 Hour Neurovascular checks of access leg
-U/S evaluation to r/o femoral injury

39
Q

What is the time limits for Zone 1 and Zone 3?

A

Zone 1 - 30 minutes or less
Zone 3 - less than 30 preferably but definitely <60 minutes

Zone 1: Sternal Notch ~ 46cm
Zone 3: Zyphoid Process ~ 28cm