Trauma Flashcards
1
Q
What are the trauma statistics?
A
- 9% of total annual mortality
- 1.24 million traffic accident fatalities
- usually pedestriants, cyclists, and motorcyclists
- 1.5 million deaths d/t violence
- Most deaths d/t high energy mechanixm of injury
- 1.3 die within first 4 hours
- deaths d/t low energy impact higher after 7 days
- Leading cause of mortality is head trauma, 2nd is hemorrhagic shock
2
Q
What is the pathophysiology of hemorrhagic shock?
A
- Problem of supply vs demand: imbalance occurs between systemic O2 delivery and O2 consumption
- hemodynamic instability, coagulopathy, decreased O2 delivery, decreased tissue perfusion, and cellular hypoxia
- Initial response: macrocirculatory and mediated by neuroendocrine system
- release of: renin, antiotensin, vasopressin, ADH, GH, glucagon, cortisol, epinephrine, norepi
- renal and adrenal systems play major role in this
- this sets stage for the microcirculatory response
- release of: renin, antiotensin, vasopressin, ADH, GH, glucagon, cortisol, epinephrine, norepi
3
Q
What is the “ shock cascade?”
(flow chart)
A
- Ischemia in any part of body will trigger an inflammatory response that will affect the non-ischemic organs even after perfusion has been restored.
- individual ischemic cells respond to hemorrhage by taking up interstitial fluid, further depleting intravascular fluid
- cellular edema can block adjacent capillaries which prevents reversal of ischemia even with good macroperfusion
- Ischemic cells produce lactate–this washes back into central circulation and sets up for SIRS and Multi organ failure
4
Q
How does CNS system respond to Hemorrhagic shock?
A
- CNS is the prime trigger of the neuroendocrine response
- controls selective perfusion to heart, kidney, and brain
- reflexes and cortical electrical activity are both depressed (this is reversible in mild hypoperfusion)
5
Q
How does the cardiac system respond to hemorrhagic shock?
A
- Cardiac system is preserved from ischemia
- lactate, free radicals, and other humoral factors released by ischemic cells all act as negative inotropes
- Somebody with cardiac disease (esp fixed stroke volume) is at greater risk for decompensation d/t hypovolemia and anemia
- cardiac dysfunction is a LATE SIGN and often a terminal event
6
Q
How does the pulmonary system respond to hemorrhagic shock?
A
- The lungs are the filter for the inflammatory by-products of the ischemic cells in body.
- immunE complex and cellular factors accumulate in pulmonary capillaries and lead to neutrophil and platelet aggregation, increased capillary permeability, destruction of lung, and ARDS
7
Q
How does the renal system respond to hemorrhagic shock?
A
- Neuroendocrine response
- GFR maintained with selective vasoconstriction
- Prolonged hypotension affects the ability to concentrate urine
- also tubular epithelial necrosis and renal failure
8
Q
How does hemorrhagic shock affect the gut/intestines?
A
- One of first organs affected by hypoperfusion
- Intestinal cell death causes a breakdown in the barrier function of the gut that allows bacteria into the liver and lungs
- this potentiates ARDS
9
Q
How does the liver respond to hemorrhagic shock?
Skeletal muscles?
A
- Failure of synthetic function of the liver–cannot make things like coagulation factors
- this can be lethal
- Skeletal muscles
- tolerate ischemia better than other organs
- release lactic acid and free radicals that can potentiate the ARDS
10
Q
What are the steps for a Trauma assessment?
A
- Initial rapid assessment- is pt stable, unstable, or dead
- Primary survey: ABCDE
- ABC- airway patency, breathing, circulation
- D- disability: brief neurological examination
- E- expose: Undress and inspect for external injuries
- Must decide to proceed immediately to surery or continue on to secondary survey
- Secondary survey: detailed multi-system exam and history
- further diagnostic evaluation
11
Q
What are the details of ABCDE?
(flow chart)
A
12
Q
How is the airway managed for a trauma patient?
A
- Stabilize C-spine
- provide 100% FiO2 (until you have ABG)
- For obstruction if spontaneously breathing:
- Initial- chin lift, jaw thrust, suction, OPA (nasal ok, but avoid if any possibility pt has basilar skull fx or maxillofacial injury)
- Still inadequate- consider BMV or SGA
- Proceed to intubation
- awake vs RSI vs cricothyroidotomy
13
Q
How does the airway algorithm change when dealing with a trauma?
What is best choice?
A
- You do not have the option to awaken the patient if you cannot get the airway
- If something does not work, you MUST change something
- Best choice: RSI or awake intubation with topical anesthesia
- Steps:
- Locate cricothyroid membrane
- pre-oxygenate
- perform RSI
- look with video laryngoscopy and attempt intubation
- consider SGA but do not delay
- proceed to cricothyrotomy if no view
14
Q
What are the indications for intubation in trauma patients?
(table)
Strong indication
discretionary indication
A
15
Q
How are cervical spine injuries diagnosed or ruled out?
Gold standard?
Awake?
A
- C-spine injuries can be missed on initial trauma assessment
- CT (with < 3mm cuts) is typical diagnostic tool
- soft tissue and ligament injuries can only be detected on MRI
- MRI is gold standard
- *It is very rare to cause cervical cord injury with airway management but we still take precautions
- If pt is wake and sober, check for posterior midline neck tenderness
- if this test is negative with no other distracting injuries, there is low likelihood if c-spine injury
16
Q
How are c-spine precautions maintained during airway management?
A
- All airway maneuvers cause some s-spine movement
- Rigid collar is NOT enough
- Manual inline stabilization is preferred
- Pt may have unopposed vagal tone during airway manipulation causing severe brady
- may want to premedicate
17
Q
How is manual inline stabilization done?
A
- Ideally anesthesia provider + two people
- One perso stabilizes and aligns the head in neutral position without applying cephalad traction
- other person stabilizes both shoulders by holding them agains bed
- anterior portion of collar may be removed to improve mouth opening
- MILS can obstruct glottic view
18
Q
Blunt airway injuries:
symptoms
preferred airway management
A
- Symptoms:
- hoarseness/muffled voice
- dyspnea/stridor
- dysphagia
- odynophagia (painful swallowing)
- cervical pain and tenderness
- ecchymosis
- subQ emphysema
- flattening of adams apple
- preferred airway management:
- Fiberoptic bronch or surgical airway
- CT before intervention if stable
- 70% of blunt airway injuries also have C-spine injuries
- blunt airway injuries can be missed
19
Q
Penetrating airway injury:
symptoms
management
A
- Symptoms:
- air bubbling through wound
- hemoptysis
- coughing
- managment:
- ETT inserted in wound
- tracheostomy distal to wound
- oral intubation
20
Q
What are pulmonary complications seen in trauma?
A
- Tension pneumothorax
- no time to confirm with CT or Xray
- must do needle decompression or chest xray
- Flail chest- two or more sites of at least three adjacent ribs (costocondal separation or sternal fx)
- will decompensate over 3-6 hours
- ARDS likely if lung contusion >20%
- Open pneumothorax
- risk for vascular air entrainment
21
Q
What are symptoms of tension pneumothoras?
Where do you do needle decompression of pneumothorax?
Where does chest tube go?
A
- Symptoms:
- cyanosis
- tachypnea
- hypotension
- neck vein tistension (unless hemorrhaging)
- tracheal deviation
- diminished breath sounds on affected side
- Needle decompression:
- midclavicular line of 2nd intercostal space
- remember nerves/veins, arteries are high in intercostal space
- walk off top of third rip
- Chest tube mid-axillary 5th intercostal space
22
Q
How do you treat flail chest?
A
- Automatic intubation is NOT recommended
- focus on analgesia to maintain adequate excursion and ventilation/oxygenation
- epidural or thoracic paravertebral blocks preferred with O2 and non-invasive PPV
23
Q
What are the different classes of shock?
blood loss (ml)
blood loss (%)
pulse rate
systolic BP
pulse pressure
RR
UOP
CNS/mental state
A
24
Q
Information about shock:
difinitive treatment?
When should you expect major bleeding?
Ideal SBP?
goal Hgb?
A
- Difinitive tx- operative control of bleeding at the source
- expect major bleeding with falls >6 ft, high energy deceleration, or high velosity like GSW
- free fluid on Xray or CT warrants immediate intervention
- Ideal SBP = 100-110,
- especially in elderly (90’s ok in young/healthy)
- Goal Hgb = 7-9
25
Q
What does the base deficit tell us?
A
- Base deficit is more reliable than pH in:
- reflecting the severity of shock
- oxygen debt
- changes in O2 delivery
- adequacy of fluid resuscitation
- likelihood of multi-organ failure
26
Q
What are the principles of damage control?
A
- 1st phase (arrival)- recognize the severity of injury; control bleeding, rapid transport to OR
- limit crystalloids
- permissive hypotensive
- active rewarming
- early FFP and platelets at high ratios with PRBCs
- 2nd phase (in OR)
- surgeons rapidly control bleeding; leave abdomen open
- goals:
- maintain intravascular volume
- temp
- acid/base status
- coagulation
- 3rd phase: ICU management with same goals
- 4th phase: multiple returns to OR at 24 and 48 hour intervals for organ repair, washout, and debridement
27
Q
How
A
- Permissive hypotension (except TBI, spinal cord injury, or elderly)
- rapid control of bleeding
- Avoid large volume of crystalloid- can cause ARDS and abdominal compartment syndrome by worsening endothelial dysfunction
- Early administration of plasma and other product in balanced racio with PRBCs (1:1:1)
- tranexamic acid
- New PRBCs preferred (<14 days old)- lower incidence of reaction
28
Q
What kind of blood do you use for uncrossmatched patient?
FFP?
A
O Rh+ PRBCs
AB- FFP
29
Q
What is the lethal triad of hemorrhage?
A
- Hemorrhage causes acidosis, hypothermia, and coagulopathy
- acidosis and hypothermia cause factor and platelet dysfunction, enhancing coagulopathy
- this causes MORE bleeding
- acidosis and hypothermia cause factor and platelet dysfunction, enhancing coagulopathy
30
Q
What are the two components of coagulopathy in trauma?
A
- Acute traumatic coagulopathy-occurs shortly after trauma
- hyperfibrinolysis and severe tissue injury releases tissue factor–this activates coagulation pathways
- Resuscitation-associated coagulopathy
- Caused by hypothermia, dilution with crystalloids
31
Q
Traumatic brain injury:
primary goal?
general management?
A
- Primary goal: prevent secondary injury
- Avoid:
- hypotension
- hypoxemia
- anemia
- raised ICP
- acidosis
- glucose >200
- Normalize:
- BP (mean >80)
- PaO2 >95
- ICP <20 to 25
- CPP about 70 mmHG
- Avoid:
- General management:
- HOB 30 degrees
- sedation and paralysis PRN
- mannitol and hypertonis NA prn
- smooth intubation, avoid desat
- hyperventilation- wait 24 hours after injury, use only as emergency intervention when osmotic agents are ineffective, guided by ICP monitoring
- Avoid hypoxia, hypercarbia, hyperthermia
32
Q
What are the most damaging insults to the brain after a TBI?
A
- hypotension and hypoxia
- a single episode of hypoxemia (PaO2 < 60) can double the incidence of mortality
33
Q
What is the vasopressor of choice in a TBI and why?
A
- Phyenylephrine- does not cause cerebral vasoconstriction
34
Q
Drugs and TBI:
Succ?
Ketamine?
Fluids?
A
- Risk of Increased IOP, ok with defasiculating dose
- ketamine- usually no d/t risk of increased ICP, but current literature does not support appreciable increase
- NS over LR
- LR is slightly hypotonic and can promote swelling
35
Q
How do you determin glascow coma scale?
A
36
Q
Spinal cord trauma:
Complete vs incomplete?
What is spinal shock?
What injury requires a ventilator?
A
- Incomplete- anal sphincter tone maintained
- spinal shock can make incomplete look like complete
- complete- virtually no chance of recovery
- Spinal shock- flaccidity and loss of reflexes
- subsides in days to weeks
- Injury C4 and above require ventilator b/c diaphragm is affected
37
Q
What is Brown-Sequard syndrome?
A
- Partial cord transection
- ipsilateral motor and contralateral sensory deficit below the injury
38
Q
How is blunt cardiac injury evaluated?
Symptoms of blunt cardiac injury?
What is most commonly injured?
A
- EKG, troponin, TEE
- Symptoms-
- angina
- dyspnea
- chest wall bruising
- dysrhythmias
- CHF
- Right ventricle is most commonly injured
39
Q
What is Commotio cordis?
A
- Blow to the chest in young people causing VF/VT
- treat with defibrillation
40
Q
What are the goals for a patient with blunt cardiac injury?
How will this affect your anesthetics?
A
- maintain cardiac contractility and lower the elevated pulmonary vascular resistance
- Give anesthetics only after restoring intravascular volume and titrate to maintain BP
41
Q
Pericardial tamponade:
symptoms?
Goals of treatment?
A
- Symptoms: (some may be absent in hypovolemic pt)
- tachycardia
- hypotension
- distant heart sounds
- distended neck veins
- pulsus paradoxus
- pulsus alternans
- Goals of treatment:
- maintain preload and contractility
- ideally evacuate pericardial blood under local
- induce with small doses of ketamine if necessary
- wait until pt is prepped and draped to induce b/c pt may completely decompensate with induction
42
Q
General information about abdominal trauma.
What does unrecognized hypoperfusion cause?
A
- Laparoscopy/laparotomy is required in most patients after gunshot wound to abdomen
- FAST ultrasound or CT- to look for bleeding
- Occult bleeding can be massive before abdominal distension is noted
- Hypoperfusion causes splanchnic ischemia
- acidosis in the intestinal wall
- translocation of microorganisms and inflammatory mediators from intestines
- washes back to lungs causing ARDS
- leads to sepsis and multi-organ failure
43
Q
What are the symptoms of abdominal compartment syndrome?
How can the incidence of abdominal compartment syndrome be reduced?
A
- Symptoms
- a tense severely distended abdomen
- increased peak airway pressure
- CO2 retention
- oliguri
- Intra-abdominal pressure >20 to 25 mmHg signals decreased perfusion and may require surgical decompression
- limiting crystalloids has had the most impact on reducing the incidence
- Abdomens are left open to decrease risk of compartment syndrome
44
Q
General information about pelvic injuries.
A
- 25% of pelvic fractures lead to major hemorrhage
- arterial bleeding treated with embolization in IR
- vascular injuries can affect perfusion to lower extremities
- bladder and urethral injuries may occur concurrently
45
Q
Orthopedic trauma:
When is it usually treated?
How can vascular injuries be identified?
A
- Usually treated early to avoid complications
- DVT, PNA, sepsis, pulmonary and cerebral complications, fat embolism
- infection in open fractures left open more than 6 hours
- Vascular injuries: the P’s
- pain
- pulselessness
- pallor
- paresthesias
- paresis
46
Q
Compartment syndrome:
treatment?
A
- Compartment requires emergency fasciotomy
- Pressure > 30 cm H2O needs immediate surgery
- caution with regional as it masks pain of compartment syndrome
47
Q
What kind of vascular access/hemodynamic monitoring do you want for trauma patients?
A
- Minimum of 2 large bore IVs, CVL may be indicated
- A-line: R radial artery preferred, b/c if aorta gets cross clamped a femoral or dorsalis pedis would be useless, left can be affected by clamping of descending aorta
- Consider PPV and SVV to guide fluid responsiveness (noninvasive monitoring)
- >12% likely a responder
- limitations
- PA catheter less common but indicated in some populations
- TEE/TTE yields qualitative and quantitative information
48
Q
What can you see qualitatively on a TEE
A
- Ventricular wals contact each other (kissing) at the end of systole, producing a high EF
- IVC collapses during the respiratory cycle
49
Q
What can a PA catheter tell us?
What is dysoxia?
A
- Oxygen consumption
- oxygen delivery
- Hgb concentration, arterial oxygen saturation, and cardiac output
- minimum value 500 ml/min/m2
- oxygen extraction
- below 0.25 or 0.3 suggests no dysoxia
- dysoxia- abnormal tissue oxygen metabolism
50
Q
What happens to coagulation in trauma?
How can coagulation be measured?
What suggests DIC?
A
- Hemodilutional coagulopathies from fluid resuscitation
- rapid consumption of clotting factors
- activation of Protein C (inhibits clotting factors V and VIII, decreases the inhibition of TPA)
- INR, aPTT, platelets, fibrinogen, and fibrin degradation products (FDPs)
- FDP >40 mg/ml suggests DIC
- TEG/ROTEM: clot formation and dissolution measurement
- can help indicate best treatment
51
Q
What should you consider with blood administration?
What is in FFP?
What is the goal for platelet levels?
What is in cryo? Why is it usually used?
A
- PRBCs <14 days old preferred
- old blood has higher risk of Trali
- Citrate is present in all blood products
- citrate chelates Ca leading to hypocalcemia
- hypocalcemia causes defective coagulation, hypotension, decreased pulse pressure, arrhythmias, change in mental status, tetany
- FFP: all coagulation components
- Ratio administered Blood:FFP:PLT is 1:1:1 or 2:1:1
- PLT: infuse to goal of >50k
- Cryo:
- factorVIII, fibrinogen, von Willebrand factor, fibronectin, factor XIII
- usually used to replace fibrinogen
52
Q
How does trauma affect anesthetic pharmacology?
What are the induction drugs of choice?
A
- Most anesthetics are direct CV depressants that inhibit compensatory reflexes
- hypovolemia leads to higher plasma concentrations and increased sensitivity
- dilutional hypoporoteinemia causes increased free fraction of drugs
- hypovolemia may be masked by catecholamine surge and revealed with administration of anesthetic
- MAC reduced by about 25% in hemorrhagic shock
- OVERALL: reduce administered doses of induction agents and opioids
- Ketamine and Etomidate are frequent drugs of choice at induction
- caution with ketamine in catecholamine depleted patients
53
Q
How does temperature affect the trauma patient?
A
- Hypothermia is huge problem (core temp <35 C)
- main effects: acidosis, hypotension, coagulopathy
- Also: cardiac depression & ischemia, arrhythmias, peripheral vasoconstriction, impaired O2 delivery, increased O2 consumption, blunted response to catecholamines, metabolic acidosis, electrolyte imbalance, reduced drug clearance, infection
- Coagulation factor function decreased about 10% every 1 degree (C) below 35
- aggressive rewarming is critical!
54
Q
How should you manage ventilation in a trauma patient?
A
- Lung protective strategies
- VT no more than 6 ml/kg
- appropriate PEEP
- titrate FiO2 to lowest possible level
- plateau airway pressures below 35 cm H2)
- avoid auto-PEEP
55
Q
What are some miscellaneous things to look out for with a trauma patient?
A
- Overlooked injuries can be revealed during anesthesia
- C-spine, unrecognized pneumo, internal bleeding
- monitor serial serum K+’s and treat hyperkalemia prn
- Correct the cause of metabolic acidosis rather than using liberal bicarbonate
- use only short term when pH is <7.2
- Thromboembolism precautions are critical:
- scd, LMWH, IVC filter
56
Q
What is important during the later resuscitation of a trauma patient?
A
- Late resuscitation begins once bleeding is difinitively controlled
- Vital signs used as markers- no single difinitive marker of adequate resuscitation
- maintain volume status, blood composition, and cardiac output
- look at all the information to determine if you need to continue resuscitation to prevent MSOF
57
Q
What is occult hyperfusion syndrome?
A
- common in young posoperative trauma patients
- characterized by normal BP maintained by systemic vasoconstriction
- decreased intravascular volume, CO, and vasoconstriction can lead to systemic ischemia and MOSF
58
Q
What are the late resuscitation goals?
(6)
A
- Maintain SBP >100
- maintain hct > individual transfusion threshold
- normalize coagulation status, electrolyte balance, temperature
- restore normal uop
- maximize CO
- reverse acidosis and decrease lactate
- normal lactat in critically ill pt <2
- BE better than -4
59
Q
What is significant about trauma during pregnancy?
A
- Can cause spontaneous abortion, preterm labor, or delivery
- Best treatment is resuscitation of mother
- 2nd/3rd trimester- determine fetal age/viability and have HR monitored continuously if age is viable
- Kleihauer Betke blood test: has fetal blood entered mom’s circulation?
- if yes, administer anti-RhO immune globulin if Rh- mom carrying Rh+ baby
- 3rd trimester- on spinal board aortocaval compression requires uterine displacement– tilt entire board
60
Q
What are the indications for immediate c-section?
A
- mother is coding
- uterus is hemorrhaging
- gravid uterus is impairing surgical control of abdominal or pelvic hemorrhage
- jplacental abruption- can lead to uterine hemorrhage
61
Q
What is significant about trauma in elderly?
A
- Elderly are more prone to morbidity
- desire higher Hct to optimize tissue oxygenation
- high risk for post-traumatic cardiac dysfunction
- decreased requirement for post op opioids
- potential delirium with sedatives
- high risk DVT
62
Q
What is significant in Jehovah’s witness?
A
- May use deliverate hypotension
- may need early surgical control of bleeding
- patient may consent to cell salvaging if one continuous system is used
- colloids (ask first), pressors, and inotropes to keep tissue O2 delivery optimized
- post-acute: consider erythropoietin to promote RBC regrowth
