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Transcript of Trauma Anesthesia
Professor Harbeck 2017
Rapid evaluation of:
Brief neurologic exam
Major trauma patients should have airway secured by ETT
“In line stabilization” to prevent neck hyperextension and excessive axial traction
Avoid nasal intubation in patients with midface or basilar skull fractures
May require special considerations in traumatic airway injuries
Suspect cervical spine injury
Incidence is approximately 2 -4%
7% to 15% of these are UNSTABLE
Jaw thrust maneuver preferred
Conventional cross-table c-spine x-ray
Detect 80-90% of fractures
CT required to reliably rule out significant spine trauma
Back to the Airway.....
Airway intervention & Treatment - wHEN & wHY?
Protection from aspiration
GCS < 8
Combative patient requiring sedation
Post resuscitation hypoxia
Avoid use of oral or nasal airways in trauma - (Basilar skull fracture)
Orotracheal intubation technique of choice
Manual stabilization of head and neck
O2 by NRB or BVM (using cricoid pressure) prior to intubation attempts
Surgical airway is ALWAYS an option
" Airway obstruction is probably the most frequent cause of asphyxia and may result from posteriorly displaced or lacerated pharyngeal soft tissues; cervical or mediastinal hematoma; bleeding; secretions, or foreign bodies within the airway; and/or displaced bone or cartilage fragments."
Clinical Anesthesia, pg. 1491
Secure the airway very carefully........
Protect the airway early: May struggle with edema and hematoma formation
Manual In Line Stabilization
one aligns the head in neutral position
the other stabilizes the shoulders by holding them against the stretcher
Provider can then secure the airway
Gold Standard for securing the airway in a trauma - may be more difficult but still the standard
The cervical spine is NEVER initially clear at first
MRI is the gold standard for ruling out C-Spine injury
Careful with cricoid pressure - even if it optimizes the view and we are doing an RSI due to "full stomach" precautions....we have to be wary of the "undue motion of the unstable spine if excessive force is used!"
High risk of:
epistaxis in a potentially already bloody airway
ETT --- into cranial vault
ETT --- into orbit
Patient may have a cranial base skull fracture and the signs may not be obvious immediately
Remember... Battle sign, Raccoon eyes, bleeding/CSF from nose?
Preferred Method of securing the airway?
Awake FOB with cooperative, sedated patient who has been topicalized and can maintain airway reflexes with little to no neck movement...and dont forget
what about that fluid...
"Serious airway compromise may develop within a few hours in up to 50% of patients with major penetrating facial injuries or multiple trauma, caused by progressive inflammation or edema resulting from....liberal administration of fluids."
Clinical Anesthesia Pg. 1496
Be very aware that in maxillofacial injuries, the edema and bleeding may severely inhibit the ability to secure the airway safely...may not have much time
Motor Vehicle: 5 types of collisions
Traumatic Aortic Rupture
Based on 3 interactive factors:
Type of instrument used to create the injury
Velocity: most significant determinate of wound potential
What type of tissue? Bone, blood vessels, organs...
femur trauma / pelvic fx
Can have 2 L of occult blood-femur or pelvis
Lateral positioning = may see worsening hypotension
Remember implications of lateral position?
Cardiac: decreased vascular resistance leads to decreased BP
Decreased volume of dependent lung
Increased perfusion of dependent lung
Decreased ventilation of dependent lung
types of Trauma
Blunt or penetrating?
Categorized as "Above or Below the waist"
The upper body - collides with dashboard, steering wheel, windshield - what injuries do you expect? (more to come)
The lower body - usually knee and femur injuries due to collision with lower dashboard
Acetabular fractures - common due to the legs tensing up preparing for the impact!
Of course: Always suspect cervical injury..
Blunt thoracic trauma:
Commonly results from not wearing a seat belt.
Injured structures include: chest wall, lungs, airway, heart, pericardium and great vessels of the thorax.
May compromise anesthesia due to poor gas exchange and cardiac output
Bleeding from heart and great vessels
Adequate fluid resuscitation before chest tube placement
Drainage of all bleeding cause massive hypotension
What is there to say...
"exsanguination is extremely rapid"
Traumatic Aortic Rupture
If complete - usually fatal
Intimal tear - dissecting aneurysm
Very infrequent to see ... most die at the scene
"Develops when lung is punctured within the thoracic cavity, creating a one way valve that traps air between the layers of the pleura. With each breath, more and more air becomes trapped in this space, increasing intrapleural pressures." Nagelhout pg. 916
Fixed low cardiac output
Life threatening emergency
Treatment - pericardiocentesis
Beck's Triad: 3 D's
Distended neck veins
Distant heart sounds
Decreased arterial pressure
Good induction method??
Subcutaneous emphysema of neck & chest
unilateral decrease breath sounds
diminished chest wall movement
hyperresonance with percussion, distended neck veins, tracheal shift
Large bore needle decompression - 14 gauge IV catheter 2nd intercostal space; above 3rd rib; midclavicular line
Avoid PPV and/or N2O
Chest Tube with water seal
40% of deaths are from head injuries
Tissue hypoxia creates a physiologic cascade
free radical generation
release of excitatory amino acids (Majority - Glutamate)
Lipid peroxidation - breakdown of cell membranes
entry of large quantities of Na, Ca, H2O into the cells
leakage of fluid and blood into the extracellular space
End result - cerebral edema + impaired cerebral circulation
Decreased O2 delivery from
during resuscitation still have the greatest impact on recovery
Perform baseline neuro assessment
CT Scan is gold standard for Dx TBI
AVPU system: Alert; responds to Verbal stimuli; responds to Pain; Unresponsive
Most importantly - avoid
Use vasopressers - Phenylephrine better because it does not constrict cerebral blood vessels
Studies show: even
episode of SBP <90 = increase mortality rate by 50%
Goal is to avoid secondary injury
Epidural & SubDural Hematoma
An epidural hematoma is located between the skull and the dura mater
Classically associated with displaced temporal bone skull fractures = laceration of middle meningeal artery
Arterial hemorrhage = rapidly expanding hematoma leading to herniation and death if not evacuated
Patients with acute epidural hematoma exhibit a "lucid interval" initially, then deteriorate.
S/S of deterioration = depressed mental status ipsilateral fixed & dilated pupil, contralateral hemiplegia
CT Scan reveals herniation
If Arterial epidural hematoma = true surgical emergency - rapid intervention
Closed Head Injuries
"Focused Assessment with Sonography for Trauma (FAST) is a limited ultrasound examination directed solely at identifying the presence of free intraperitoneal or pericardial fluid. In the context of traumatic injury, free fluid is usually due to haemorrhage and contributes to the assessment of the circulation"
"As a decision making tool for identifying the need for laparotomy in hypotensive patients (Systolic BP < 90), FAST has a sensitivity of 100%, specificity of 96% and negative predictive value of 100% (NPV). This is based on only 133 patients taken from 3 separate studies"
Symptoms usually occur within 12 -40 hours after long bone or pelvic fractures
Triad of: dyspnea, confusion and petechiae
Fat globules released by the fractured bone - enter the circulation through tears in the vessels
Once released they travel to the pulmonary system acting as microemboli
Biochemical theory (toxic & obstructive):
Toxic - free fatty acids directly affect pnemocytes = ARDS
exacerbated by trauma induced catecholamines= increasing FFA
Obstructive - An unidentified chemical rxn - release of mediators that interrupt lipid solubility = formation of lipids into emboli
Fat Embolus Syndrome
Petechiae on the chest, upper extremities, axilla, and conjunctiva
Fat globules in the retina, urine or sputum
Coagulation abnormalities: Prolonged Clotting time or thrombocytopenia
Increase serum lipase
Increased pulmonary artery pressures
EKG: ischemic-appearing ST-segment changes and right-sided heart strain
Treatment: prophylactic and supportive
Stabilize fracture, fluids, "aggressive ventilatory support"
Chest wall moves paradoxically with respiration
(re-entry of thoracic wall)
(expansion of thoracic wall)
Occurs in an area where 4 or more ribs are fractured in at least 2 locations
DULL sound over injured lung is heard as compared to hyper-resonance in simple pneumothorax
Goals of Anesthetic Management:
SBP - keep mean >80mm Hg
PaO2 - >95
ICP - < 20 - 25mm Hg (N=5-15 mm Hg)
CPP - 50 -70 mm Hg (CPP = MAP-ICP or CVP, whichever is higher)
Keep patient's head at a 30 degree elevation
Sedation & paralysis as needed
Avoid Ketamine, N20
Avoid Succinylcholine if cervical spine injury or burn injury
Rapid restoration on intravascular volume =
Minimize further brain swelling
Brain swelling may occur regardless due to the increased permeability of the BBB
Monitor serum osmolality normal range = 285 -295
(2x (Na + K)) + (BUN/2.8) + Glucose/18)
Why not use LR or D5W?
LR = slightly hypotonic which may promote swelling in uninjured areas of the brain when given in large quantities.
D5W = Isotonic then hypotonic (once inside the body)
Autoregulation of Cerebral perfusion pressure
*Wide swings in MAP will continue to provide a consistent CBF of 50 ml/100 g/min
*This will continue with a MAP 60-160mm Hg
*The autoregulatory curve is shifted to the right in cases of chronic HTN
*Above & below these limits, CBF is pressure dependent as cerebral blood vessels are either maximally dilated or vasoconstricted
*Brain tissue has high O2 consumption and no reserve = disaster if hypoxic
Acute Spinal Cord Injury
*Support of ventilation and oxygenation must be provided in patients who lack capacity for adequate gas exchange, whether from cervical cord injury with paralysis of the muscles of respiration, associated chest trauma, or other causes.
*Hypoxia exacerbates the pathophysiologic cascade of SCI and must be prevented by supplemental oxygen, mechanical ventilation, or both.
The aim of treating post-SCI hypotension is to restore mean arterial pressure to normotensive levels.
Hypertension should be avoided, because of the theoretic risk of enhancing intramedullary hemorrhage and edema.
*No motor, sensory, reflex, or sympathetic function above T6
* Sympathetic loss produces hypotension at or above T6
*Bradycardia from loss of cardio-accelerator function
*Hemodynamic monitoring-A line
*Hypothermia - interventions?
Results from a selective denervation of the sympathetic chain in the cervical or high thoracic (T1–T5) region with consequent loss of vascular tone and unopposed vagal activity leading to bradycardia
Possibly from skeletal muscle paralysis and venous pooling below the level of injury
Above T6; long term - can be as low as T10
Response to noxious stimuli stimulus causes intense vasoconstriction below level of lesion - such as surgical stimulation
Inhibitory control of sympathetic system destroyed
Hypertension and bradycardia, especially during intubation
Vasodilation above level of injury
Vasoconstriction below the level of injury
Poikilothermic below level of lesion
Avoid hypothermia and associated metabolic acidosis
No ability to sweat
Left shift of oxyhemoglobin dissociation curve
Altered calcium and potassium > arrhythmia's
May need to clamp aorta-sometimes this is done to isolate and see if the blood loss is from below or above the clamp
Avoid the lethal triad of trauma:
Acidosis, Coagulopathy, Hypothermia
Massive Hemorrhage Management
Autonomic dysreflexia develops in individuals with a neurologic level of spinal cord injury at or above the sixth thoracic vertebral level (T6).
Autonomic dysreflexia causes an imbalanced reflex sympathetic discharge, leading to potentially life-threatening hypertension.
It is considered a medical emergency and must be recognized immediately.
If left untreated, autonomic dysreflexia can cause seizures, retinal hemorrhage, pulmonary edema, renal insufficiency, myocardial infarction, cerebral hemorrhage, and death.
Complications associated with autonomic dysreflexia result directly from sustained, severe peripheral hypertension.