Trauma Flashcards
1
Q
Background stats for trauma?
A
- 9% of total annual mortality (worldwide)
- 1.24 million traffic accident fatalities
- largest proportion pedestrians, cyclists, & motorcyclists
- 1.5 million deaths related to violence (includes: homicide, suicide, war-related)
- Disproportionate trauma fatalities in low and middle income countries
-
High-energy mechanism of injury has the highest proportion of deaths in 1st 48 hours (1/3 die in 1st 4 hours)
- MVA, falls, gunshot, stab wounds
-
Low-energy impact death rates higher after 7 days
- from falls, usually in elderly
- Head trauma is leading cause of mortality (40%); 2nd is hemorrhagic shock
- CNS injury and hemorrhage most common cause of early mortality
- 1/3 of these pt die in first 4 hours after admission
- later COD d/t MOF, PE, infection
- 2-4% of blunt traumas have concurrent C-spine injuries
2
Q
Pathophys of hemorrhagic shock
A
- imbalance occurs between systemic O2 delivery and O2 consumption
- hemodynamic instability, coagulopathy, decreased O2 delivery, decreased tissue perfusion, and cellular hypoxia
-
initial response: macrocirculatory & mediated by neuroendocrine system
- Hormones release:
- renin,
- angiotensin,
- vasopressin,
- antidiuretic hormone,
- growth hormone,
- glucagon, cortisol,
- epinephrine, and
- norepinephrine
- sets stage for microcirculatory response
- Hormones release:
- Renal and adrenal system produce renin, angiotensin, aldosterone, cortisol, erythropoietin, catecholamines
3
Q
What is the shock cascade?
A
- ischemia of any area of the body triggers an inflammatory response that impacts non-ischemic organs even after adequate perfusion restored
- individual ischemic cells respond to hemorrhage by taking up ISF, which further depletes intravascular fluid.
- cellular edema may choke off adjacent capillaries and result in no-reflow phenonmenon
- this prevents reversal of ischemia even with adequate macroperfusion
- cellular edema may choke off adjacent capillaries and result in no-reflow phenonmenon
- Ischemic cells produce lactate and free radicals and inflammatory factors–> causes direct damage to cell and washes back to central circulation when flow reestablished
- sets up for SIRA/MOF
4
Q
What arethe CNS and cardiac response to hemorrhagic shock?
A
-
CNS: prime trigger of neuroendocrine response
- controls selective perfusion to heart, kidney, brain
-
reflexes and cortical electrical activity are both depressed; reversible with mild hypoperfusion
- someone obtunded/poor neuro exam following trauma- bad sign of injury. typically reversible
-
Cardiac: preserved from ischemia
- lactate, free radicals, and other humoral factors released by ischemic cells all act as negative inotropes
- Cardiac dysfunction is LATE SIGN and often a terminal event
- patient with cardiac dx/direct cardiac trauma is great risk for decompensation d/t fixed SV, which inhibits the body’s ability to increase blood flow
- in healthy person, blood flow to heart preserved
5
Q
Pulmonary response to hemorrhagic shock?
A
Pulmonary: filter of the inflammatory byproducts of ischemia
- immune complex and cellular factors accumulate in pulm capillaries and lead to neutrophil and PLT aggregation
- which cause
- increases capillary permeability
- destruction lung architecture
- ARDS
- which cause
6
Q
What is the renal response to hemorrhagic shock?
A
Renal/ adrenal: neuroendocrine response; GFR maintained with selective vasoconstriction
- prolonged hypotension leads to decreased cellular energy and inability to concentrate urine (renal cell hibernation)
- followed by patchy cell death, tubular epithelial necrosis, renal failure
- blood flow concentrated to medulla and cortical areas
7
Q
What is the gut, liver, and skeletal muscle response to hemorrhagic shock?
A
Gut: one of the earliest organs affected by hypoperfusion; may be the prime trigger of MSOF
- intestinal cell death causes breakdown in barrier function of cut
- causes increased translocation of bacteria to liver and lungs
- can potentiate ARDS
Liver: failure of synthetic function of the liver after shock-> lethal
- if you see liver failure after shock, poor prognosis for patient
Skeletal muscles: release lactic acid and free radicals; tolerate ischemia better than other organs
8
Q
What encompasses the initial trauma assessment?
A
- Initial rapid assessment: (out in field) stable vs unstable
- are they dying? dead?
- Primary survey: ABCDE: airway, breathing, circulation, disability, exposure
- ABCs of airway patency, breathing and circulation
- Airway- obstruction? airway maneuver? intubate?
- Breathing- high flow o2? trachea ML? flail chest (3 or more fx segments of ribs) tension pneumo? massive hemothorax= 1500 cc blood
- Circulation- skin temp, color, 2 large bore IVs, fluid, uncrossmatched blood
- D- disability=
- Brief neuroexam
- E- exposure
- undress and inspect ventral and dorsal for all external injuries overlooked
- decision made to proceed immediately to sx or continue on to secondary survey
- ABCs of airway patency, breathing and circulation
- Secondary survey: detailed multi-system exam an history; further dx eval
- more about what happened, detailed exam, dx eval, medical hx
9
Q
Anesthesia’s role ina irway mgmt of trauma patient?
A
- Anesthesia is responsible for initial airway assessment and management on arrival
- Evaluate need for mask ventilation, intubation, or surgical airway
- Also assess needs for imminently preparing the OR and planning anesthetic management (rapid infuser, special drugs, lines, blood products)
10
Q
Steps in initial airway survey?
A
- Stabilize C-spine
- Provide oxygen (100% until ABG)
- Initial steps for obstruction if spontaneously breathing: chin lift, jaw thrust, suction, place OPA or NPA (+/-)
- NO nasal airway or nasal ETT if possible basilar/ cranial base skull fx or maxillofacial injury- can enter cranial vault or orbit symptoms: battle sign, raccoon eyes, or bleeding from the ear or the nose…signs may not be immediately apparent
- Symptoms of airway obstruction:
- Notable Airway edema/direct airway injury
- Cervical deformity
- Cervical hematoma
- Foreign bodies
- Dyspnea, hoarseness, stridor, dysphonia
- Subcutaneous emphysema & crepitation
- Hemoptysis/active oral bleeding/copious secretions
- Tracheal deviation
- Jugular vein distention
- Hemodynamic condition
- Still inadequate? Consider BMV to assist spontaneous breathing
- Consider SGA (short term)
- Proceed to intubation: awake vs. RSI vs. cricothyroidotomy
11
Q
What are some modifications to difficult airway algorithm in trauma?
A
- safety first! no option to awaken the patient as in ASA emergency airway algorithm
- if something doesn’t work, change something!
- Best choice: RSI with cricoid pressure for patient without serious airway problems VERSUS awake intubaiton with sedation and topical anesthesia, if possible, for those with anticipated difficult airways
Topicalization may be impossible for awake intubation- many of these patients are uncooperative or unstable- awake FOB may not be possible
- locate cricothyroid membrane (consider marking),
- pre-oxygenate,
- perform RSI
- then take a look with video laryngoscopy and attempt intubation (+/-bougie attempt)
- consider SGA but do not delay
- proceed to cricothyrotomy if no view
12
Q
Max amount of DL when establishing airway in trauma?
What’s different about difficult airway algorithm in trauma?
A
MAX 2 DL
Can’t wake patient up
13
Q
Considerations for cricothyroidotomy in trauma patient?
A
- with cspine stabilization, not able to get prime visualization of cricoidthyroid membrane
- palpate thyoid/adam’s apple and go just below cartilage
- go through lower 1/3 cricothyroid membrane to avoid thyroid/VC
- Go in with 45 degree angle with angiocath
- Possible contraindications to cricothyroidotomy
- age younger 12 yo
- suspected larngeal trauma
- conversion to tracheostomy considered later (within 72 hours)
- cric is not definitive airway
- traheostomy not a great option initially because it takes longer than cric and requires neck extension
14
Q
What are some considerations with the use of the jet ventilator?
A
- Jet ventilator. Black triangle shows the high-pressure ventilation tubing that attaches to standard wall oxygen outlet
-
50 psi working pressure.
- potential for barotrauma!
- Ventilation block (white arrow) is used to control oxygen flow through tubing to a catheter, which is inserted in the airway.
-
50 psi working pressure.
- Employs Venturi effect: the jet stream of fresh gas creates a pressure gradient and the pressure gradient generates a negative pressure entraining flow.
- will get good oxygenation but not good exchange.
15
Q
What are some strong indicators for ETT intubation upon arrival with traumas?
A
- Airway obstruction
- hypoventilation
- persistent hypoxemia (Sao2 <90%) despite supplemental oxygen
- severe cognitive impairment (GCS <8)
- Severe hemorrhagic shock
- cardiac arrest
- smoke inhalation with any of the following
- airway obstruction
- severe cognitive impairment (GCS <8)
- major burn (>40%)
- major burns and/or smoke inhalation with prolonged transport time
- impending airway obstruction
16
Q
What are some discretionary indications for ETT in trauma patient?
A
- Facial or neck injury with potential for airway obstruction
- moderate cognitive impairment (GCS >9-12)
- Persistent combativeness refractory to pharmacologic agents
- Respiratory distress (without hypoxia or hyperventilation)
- perioperative mgmt (pain control, painful preoperative procedures)
- SCI (complete cervical injury at C5 level of above) with any evidence of respiratory depression
17
Q
How do you assess for need for cervical spine precautions in trauma patient?
A
- Cervical spine injuries can be missed on initial trauma assessment
- Awake? Check for posterior midline neck tenderness, focal deficit
- Awake with negative exam: if not intoxicated and no other distracting injuries there is low probability of C-spine injury; still need routine CT to rule out- too frequently missed
- Disadvantages MRI? costly, requires transport, metal fixators cannot go in
- Awake? Check for posterior midline neck tenderness, focal deficit
- CT or MDCT (<3mm cuts) is typical diagnostic tool but soft tissue/ ligamentous injuries cannot be seen
- MRI is gold-standard to reliably rule out C-spine injury
- Airway management related cervical cord injury is exceptionally rare but precautions are mandatory
18
Q
Airway mgmt with c-spine injury?
A
- All airway maneuvers cause c-spine movement
- Rigid collar is not enough
- Manual inline stabilization (MILS) is preferred
- Caution: unopposed vagal tone during airway manipulation
- severe bradycardia and dyrrhythmias may result from the unopposed vagal activity during trahceal intubation or suctioning
- preoxygenate and premedicate
- there is NO airway manipulation technique that prevents movement of c-spine
- anytime you do laryngoscopy, you will cause c-spine movmenet
- still need MILS, collar etc
- remember airway manipulation causing c-spine injury is incredibly rare.
19
Q
What is manual inline stabilization technique?
A
- two people optimally in addition to anesthesia provider
- first assistant stabilizes and aligns the head in neutral position without applying cephalad traction
- second person stabilizes both shoulders by holding them against the table or stretcher (prevents rotational mvmt)
- anterior portion of the hard collar may be removed after immobilization to improve mouth opening
- MILS can obstruct glottic view
- some relaxation of the MILS to improve the glottic view when visualization of the larynx is restricted
- mention submental intubation in maxillofacial injuries
-
even with video laryngoscope causes cervical spine mvmt
- has not benes statistically sig in studies comparing DL to VL
20
Q
S/S of blunt airway injuries?
Managmeent of blunt airway injuries?
A
- symptoms:
- hoarseness
- muffled voice
- dyspnea
- stridor
- dysphagia
- odynophagia
- cervical pain and tenderness
- ecchymosis
- subcutaneous emphysema
- flattening of the Adam’s apple
- DL can worsen; may enter false passage
- CT before airway intervention if stable
- Preferred airway management: FOB or surgical airway
- 70% of blunt airway injuries also have C-spine injuries
- can also have vascular injury, may cause hematomas which may obstruct the airway.
- Blunt airway injuries can be missed
- Blunt thoracic trauma that arrives pulseless has <1% survival
21
Q
S/S of penetrating airway injury?
management?
A
- Symptoms (more overt)
- air bubbling through wound
- hemoptysis,
- coughing
- management varies: ETT inserted in wound, tracheostomy distal to wound, oral intubation (if injury high in the airway)
- Penetrating thoracic trauma with signs of life has decent survival
-
ED thoractomy usually done for penetrating airway but NOT blunt
- allows for external cardiac massage, emergency drainage of pericardial blood, clamping of great vessel bleeding
- can resuscitate with catheter directly in right atrium
22
Q
S/S tension pneumothorax?
Treatment?
A
- Symptoms:
- cyanosis
- tahcypnea
- hypotension
- neck vein distention
- may be absent in hypovolemic patients
- tracheal deviation
- may be difficult to appreciate
- diminished breath sounds affected side
- No time for xray/CT to confirm
- Treatment:
- needle decompression vs chest tube
- Needle decompression=2nd ICS MCL- walk off third rib to do decompression in order to miss artery/nerve that run on superior portion of 2nd ICS
- CT= Mid-axillary line 5th intercostal space
- needle decompression vs chest tube
23
Q
What is a flail chest? Anesthetic considerations?
A
- two or more sites of at least three adjacent ribs
- rib fractures associated with costochondral separation or sternal fracture
- Deterioration due to flail chest develops over 3-6 hours
- ARDS likely is lung contusion >20%
- Automatic intubation not recommended
- better to focus on analgesia to maintain adequate excursion and ventilation/ oxygenation
- epidural or thoracic paravertebral blocks preferred along with O2 supp and non-invasive PPV.
- Consider co-existing trauma in flail chest (hemo/pneumothorax)
- better to focus on analgesia to maintain adequate excursion and ventilation/ oxygenation
24
Q
What are some other life-threatening pulmonary complications a/w trauma?
Additional considerations in patient with pulm complications?
A
- Open pneumothorax- caution vascular air entrainment
- hemothorax
- closed pneumothorax
- pulmonary contusion
- diaphragmatic rupture wiht herniation of abdominal contents into thorax
- atelectasis from mucus plug
- aspiration
- chest wall splinting
Consider oxygenation:
- arterial to ETCO2 diff values >10 mmHg after resuscitation predicts mortality
- decreased lung perfusion resulting in high PaCO2 and low ETCO2
25
Q
Treatment for hemorrhagic shock?
When should you suspect hemorrhagic shock?
Mgmt?
A
- Definitive treatment: operative control of bleeding at source
-
Expect major bleeding:
- Falls >6 feet,
- high energy deceleration injury, and
- high velocity GSW
- Free fluid on X-ray, FAST, or CT warrants immediate intervention
MGMT
-
Ideal SBP 100-110mmHg
- appreciate that you can have 1500-2000 blood loss before you see decrease in SBP
- in elderly patient, important to maintain 100-110. 90 still ok in younger/healthier pt
-
Tachycardia not always a reliable indicator
- absent in up to 30% of traumas
- cofounder is Bezold-Jarisch reflex, chronic cocaine, vagal stimulation
- injury without compensation of tachycardia increases mortality
-
Follow lactate, base deficit
- Intraop endpoints of resuscitation
- Goal hgb 7-9g/dL
32
Q
What is the lethal triad in trauma patients?
A
- Coagulopathy
- Metabolic acidosis
- hypothermia
- Hemorrhage causes acidosis, hypothermia and coagulopathy
- acidosis and hypothermia produce factor and PLT dysfunction, enhancing coagulopathy
- causes increased bleeding
37
Q
What comprises a GCS score?
Treatment guideliens based on GCS score?
A
- Scores obtained for eye opening, verbal response, and motor activity correlates with severity of injury and prognosis
- Assessment of motor function should be performed on the extremity that responds best. The limb affected by neurologic injury is examined, but the result is not considered in the GCS
- Patients with GCS <8 have a 40% likelihood of an intracranial hematoma
- Maximally dilated and unresponsive “blown” pupil suggests uncal herniation under the falx cerebri
- Mild TBI (GCS score of 13 to 15) who maintain a stable GCS score for 24 hours after injury are very unlikely to deteriorate further; need a short period of observation
-
Moderate TBI (GCS score of 9 to 12) may be accompanied by
- intracranial lesions that require surgical evacuation;
- early CT is needed.
- Early tracheal intubation, mechanical ventilation, and close observation may be required in the management of patients with moderate TBI because of combative or agitated behavior and the potentially catastrophic consequences of respiratory depression or pulmonary aspiration occurring during diagnostic evaluation
- intracranial lesions that require surgical evacuation;
- -Severe TBI is classified as a GCS score of 8 or less at the time of admission and carries a significant risk for mortality.
39
Q
What is involved in evaluation in blunt cardiac injury?
S/S?
Most commonly injured area?
What is commotion cordis?
A
- Evaluation- ECG, Troponin, TEE
- RV most commonly injured
- s/s
- angina
- dypspnea
- chest wall bruising
- dysrhythmias
- CHF
- Commotio cordis
- blow to chest in young people
- s/s- VF/TV
- Txmt- defib
50
Q
What are variables involved in TEG?
A
- R value= reaction time
- initial fibrin formation
- rough approx. of PT (extrinsic clotting) and aPTT (intrinsic)
- K time= time taken to minimal sufficient clot strenght
- amplitude of 20mm
- depends mostly on fibirnogen
- Alpha angle (slope b/w R and K)
- fibrin build up and cross linking takes place
- assesses the rate of clot formation
- fibrinogen
- MA= Maximal amplitude (mm)
- represents the ultimate strength of the fibrin clot
- overall stability of the clot
- depends on fibrinogen and platemet function
