Trauma Flashcards
Pathophys of hemorrhagic shock?
- 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 systemHormones release:
- renin,
- angiotensin,
- vasopressin,
- antidiuretic hormone,
- growth hormone,
- glucagon, cortisol,
- epinephrine, and
- norepinephrine
- sets stage for microcirculatory response
- Renal and adrenal system produce renin, angiotensin, aldosterone, cortisol, erythropoietin, catecholamines
What is the shock cascade?
- 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
- 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
What arethe CNS and cardiac response to hemorrhagic shock?
- 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
Pulmonary response to hemorrhagic shock
- Pulmonary: filter of the inflammatory byproducts of ischemia
- immune complex and cellular factors accumulate in pulm capillaries and lead to neutrophil and PLT aggregationwhich cause
- increases capillary permeability
- destruction lung architecture
- ARDS
What is the renal response to hemorrhagic shock?
- 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
What is the gut, liver, and skeletal muscle response to hemorrhagic shock?
- 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
What encompasses the initial trauma assessment?
- Initial rapid assessment: (out in field) stable vs unstable
* are they dying? dead?
- Initial rapid assessment: (out in field) stable vs unstable
- 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
- Secondary survey: detailed multi-system exam an history; further dx eval
more about what happened, detailed exam, dx eval, medical hx
Steps in initial airway survey in trauma?
- 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
What are some modifications to difficult airway algorithm in trauma?
Max amount of DL when establishing AW in trauma?
- 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
- Topicalization may be impossible for awake intubation- many of these patients are uncooperative or unstable- awake FOB may not be possible
- Max amount: 2 DL
- cant wake up patient
Considerations for cricothyroidotomy in trauma patient?
- 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/fracture
- 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
What are some considerations with the use of the jet ventilator?
- 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.
- Employs Venturi effect: the jet stream of fresh gas creates a pressure gradient and the pressure gradient generates a negative pressure entrainingflow.
- will get good oxygenation but not good exchange.
What are some strong indicators for ETT intubation upon arrival with traumas?
- 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
What are some discretionary indications for ETT in trauma patient?
- 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
Airway mgmt with c-spine injury?
- 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
- severe bradycardia and dyrrhythmias may result from the unopposed vagal activity during trahceal intubation or suctioning
- 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.
What is manual inline stabilization technique?
- 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
S/S of blunt airway injuries?
Managmeent of blunt airway injuries?
- symptoms:
- hoarseness
- muffled voice
- dyspnea
- stridor
- dysphagia
- odynophagia
- cervical pain and tenderness
- ecchymosis
- subcutaneous emphysema
- flattening of the Adam’s apple
- Considerations:
- 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
S/S of penetrating airway injury?
management?
- 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
S/S tension pneumothorax?
Treatment?
- Symptoms:
- cyanosis
- tachypnea
- 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