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what is the appropriate assessment of any level 1 trauma patient?

rapid assessment: determine if the patient was stable, unstable, dying or dead.

primary survey: assess and stabilize the patients Airway, Breathing, Circulation, Disability, and Exposure (remove patients clothing to assess for additional injuries).

if stable enough, secondary survey: head-to-toe examination, radiographs, diagnostic procedures, lab testing.

tertiary survey: within first 24 hours, reexamine patient to identify any clinically significant injuries that were missed


what is a primary survey?

1. airway and c-spine: examine for obstruction -may need intubation and stabilize c-spine
2. breathing/ventilation: examine chest wall for subQ emphysema or tracheal deviation
3. circulation: start two large-bore IV catheters and start IVF resuscitation if HD unstable, may need O- blood
4. disability: GCS (consider intubation for GCS


name some cause of life-threatening chest trauma?

airway obstruction
tension ptx
massive hemothroax
open ptx
flail chest
cardiac tamponade


how do you calculate GCS?

Eyes: does not open (1), opens to pain (2), opens to voice (3), opens spotaneously (4)
Verbal: makes no sound (1), incomprehensible sounds (2), inappropriate words (3), confused/disoriented (4), normal (5)
Motor: no movement (1), extension to pain/decerebrate (2), flexion to pain/decorticate (3), withdrawal (4), localizes (5), normal (6)


what is the secondary survey?

should only be performed once patient is stabilizing, otherwise resuscitation efforts should be continued.
head-to-toe history and physical. further testing as indicated (lab, radiology, diagnostic procedures)


name some immediate concerns for a burn patient.

potential for difficult airway (c-collar, inhalation injury, third-spacing of fluid leading to progressive airway edema), significant hypovolemia (hemorrhage, edema, third-spacing), hyperglycemia (endocrine response to burn injury), hyperkalemia (tissue destruction), carbon monoxide poisoning.


name some immediate concerns for crush injury.

DVT, vascular trauma (pain, pulselessness, pallor, paresthesia, paresis), fat embolus, occult hemorrhage, compartment syndrome, rhabdomyolysis


how do you calculate TBSA affected by a burn?

9% for each arm, chest, abdomen, head
18% each leg, back
1% groin

for children
9% arms, chest, abdomen
18% back, head
13.5% legs
1% groin


a burn patient has an initial BP of 98/62. does he require fluid resuscitation and how would you guide your therapy?

as he has suffered an over 30% TBSA burn, adequate fluid resuscitation will be necessary to prevent hypovolemic shock. however, resuscitation should be managed judiciously to avoid over resuscitation which can worsen edema in the airway, lungs, and limbs. it can even lead to abdominal compartment syndrome.
i would titrate resuscitation to urine output with goal output at 0.5-1 ml/kg/hr, hr 60 mmHg, and base excess


how does burn injury cause hypovolemia?

increased vascular permeability (esp in injured areas) with extravasation of proteins. the subsequent decrease in intravascular oncotic pressure leads to large volumes of fluid shifting out of the vascular compartment and into the interstitial space.
additionally, following a burn, circulating myocardial depressants, decreased coronary BF, increased SVR and diminished response to catecholamines can contribute to hypovolemic shock.


how do you calculate tbw?

2/3 intracellular 25L
1/3 extracellular 15L
1/5 plamsa 3L
4/5 interstitial 12L
very small amount (2.5%) transcellular


how could a pulm art catheter be used to guide resuscitation?

it can assess if the filling pressures are acceptable as well as an adequate mixed venous oxygen tension (normal 35-45 mmHg.


what is base excess and how does it indicate volume status?

+2 - alkalosis


what are the normal PA catheter values for:


CVP (right atrial pressure) - 1-6 mmHg
PAP - systolic 15-30 mmHg, diastolic 6-12 mmHg
PCWP (left atrial pressure, LVEDP) - 6-12 mmHg
CO (HR x SV) - 3.5-7.5 L/min
PvO2 (tension) - 35-45 mmHg
MvO2 (how well O2 is extracted) - 65-75%

CI = CO/BSA = 2.4-4.0 L/min/m2
BSA = sq root[Ht-cm x Wt-kg)]/60

SVI = CI/HR = 40-70 mL/beat/m2

SVR = 80(MAP-CVP)/CI = 1600-2400 dynes.sec.m2/cm5

PVR = 80(PAP-PCWP)/CI = 200-400 dynes.sec.m2/cm5


what is the Parkland formula?

formula used as guideline fluid resuscitation following burn injury.

4 mL/kg/percentage of TBSA in the first 24 hours
deliver half in first 8 hours and other half over 16 hours


how are burns classified?

1st degree - injury limited to epidermis
2nd degree - epidermis and dermis
3rd degree - full thickness, complete destruction of epidermis and dermis
4th degree - muscle, fascia, bone


what is considered a major burn in an adult?

>10% TBSA if full-thickness
>25% TBSA if partial-thickness


list some indications for intubation of an adult after burn injury?

hypoxemia, hypercarbia, resp distress, stridor, loss of consciousness (inability to protect airway), altered mental status, major burn injury(>10% TBSA of third-degree), signs of inhalation injury


suppose you decide not to intubate a patient with 20% TBSA partial-thickness burns. what further evaluation, if any does he need?

fiberoptic bronchoscope to examine glottic and periglottic structures for edema or inhalation injury
ABG to check PaO2 (low PaO2 is suggestive of inhalation injury)
CXR, PFTs for baseline comparison (may appear normal in immediate post-burn period)


suppose the patient has 15% TBSA third-degree burns and 5% partial-thickness and you notice carbaceous material in his sputum. would you intubate now?

given the increased risk of respiratory compromise with major burn (>10% TBSA third-degree burns) and inhalation injury (as indicated by the carbaceous material in his sputum) I would prepare for immediate intubation.

he is at risk for difficult airway management for multiple reasons.
1. airway obstruction due to third-spacing of fluid and subsequent airway edema, coupled with having a c-collar in place
2. aspiration secondary to trauma and possible full stomach
3. questionable neurologic damage (cannot assess due to distracting injuries)

to intubate this patient i would:
1. administer aspiration prophylaxis - H2 blocker, metoclopramide
2. dry his airway with glycopyrrolate to more adequately topically anesthetize his airway (lidocaine jelly in the oropharynx, aerosolized lidocaine, possible transtracheal block)
3. adequate preoxygenation
4. sedation as tolerated
5. difficult airway equipment, in-line stabilization
6. FOI


do you suspect significant inhalation injury?

the history of burn in a closed space (in a building) combined with carabaceous material in the sputum are suggestive of inhalation injury. i would examine for additional signs of injury, such as singed facial hair, burned mucosa, cough, stridor, hoarseness, difficulty swallowing, and pharyngeal edema.


what are the main concerns with upper airway inhalation injury?

glottic and periglottic edema, copious/thick secretions. edema is worsened by the aggressive fluid resuscitation necessary for the stabilization of the severely burned patient.


what are the main concerns with lower airway inhalation injury?

this is less likely to occur because the upper airways typically are very efficient at cooling inhaled air. however, the patient can experience bronchial obstruction, bronchopneumonia, and air trapping due to mucosal necrosis, edema, tissue sloughing, copious secretions, decreased surfactant, and reduced mucociliary function. however, parenchymal lung injury usually presents 1-5 days after injury as ARDS.


after successful intubation, the patient becomes hypotensive. what is your differential diagnosis?

1. anesthetic drugs
2. hemorrhagic shock (occult bleeding secondary to thoracic, abdominal, extremity injury)
3. neurogenic shock (cervical SC injury after intubation)
4. cardiogenic shock secondary to burn-induced release of myocardial depressants catecholamines, vasopressin, ang-II, peptide Y), decreased response to catecholamines, or myocardial ischemia
5. CO toxicity (direct myocardial toxicity secondary to effects on mitochondrial system)
6. cyanide toxicity (CV depression or arrhythmias)
7. hypovolemic shock (third-spacing, inadequate resuscitation)
8. vagal secondary to laryngoscopy
9. tension PTX (trauma, CVL placement)
10. fat embolus (limb injury)
11. hypothermia (inadequately warmed fluids)
12. allergic reaction
13. transfusion reaction if blood administered
14. citrate toxicity


ABG shows 7.22/108/36 with SaO2 98% on 6L O2. What is your interpretation?

metabolic acidosis without resp compensation.
causes include:
1. DKA
2. hypothermia with rapid rewarming
3. CO poisoning
4. cyanide toxicity
5. increased metabolic rate (and O2 consumption) associated with burn injury


would you treat the acidosis with NaHCO3-?

I would not secondary to potential complications.
1. generation of additional CO2 (reacts with H to form CO2) which would then diffuse into cells and increase intracellular CO2)
2. left-shift of the oxyhemoglobin dissociation curve (resulting in impaired tissue delivery of oxygen). it may already be left-shifted as a result of CO or cyanide poisoning
3. hyperosmolarity due to excessive Na
4. hypokalemia secondary to movement of K from extra to intracellular


what are the considerations with carbon monoxide poisoning? why is a normal SpO2 possible? why does tissue hypoxia occur?

pulse oximeters only read two wavelenghts of light - 660 nm and 960 nm. carboxyhemoglobin and oxyhemoglobin absorb light both at 660 nm, potentially leading to falsely elevated SpO2 readings.

tissue hypoxia occurs bc of the high affinity of CO for Hb (thereby reducing the amount of oxygen that can bind to Hb). additionally CO-Hb causes a left-shift in the oxyhemoglobin dissociation curve, resulting in impaired tissue delivery of oxygen (binding of CO to Hb increases O2 affinity for the remaining O2 sites, making unloading more difficult)


how would you treat CO toxicity?

100% oxygen to improve oxygenation and promote elimination of CO (decreases the 1/2 life of CO-Hb from 4-6 on room air to 40-90 min), observe the patients for cherry-red blood (indicating very high levels of CO-Hb) and order a CO-Hb level.

If CO-Hb was >25-30% i would consider hyperbaric oxygen to promote CO elimination (decreases the half life to 20-30 minutes at 3 atm)


what are some conditions that may cause SpO2 to poorly approximate SaO2?

methemoglobinemia, carboxyhemoglobinemia, severe anemia, certain dyes, nail polish, excessive ambient light, poor perfusion, motion


can SaO2 on ABG appear normal with CO toxicity?

yes, because SaO2 is derived from PaO2 (which is unaffected by CO). co-oximetry is the only way to assess CO status


what is the intracompartmental pressure associated with compartment syndrome?

>30-40 mmHg OR


what monitors would you require to anesthetize the patient if he required emergent fasciotomy?

1. standard ASA
2. 5 lead EKG for myocardial ischemia
3. arterial line for hemodynamics (acidotic patient prone to major fluid shifts) and ABGs
4. central line for CVP and PA catheter access if necessary
5. foley for renal function and fluid resuscitation
6. core temperature for hypothermia

monitors to consider:
7. BIS if concerned hemodynamics will limit amount of anesthetic i can deliver (titrate to index


what are standard ASA monitors?

A qualified anesthesia provider and VOTC
Ventilation: ETCO2, inspired anesthetic gases
Oxygenation: SpO2 and inspired O2 (with an alarm)
Circulation: HR, BP q5m, EKG


what if ekg stickers will not transmit a signal due to the patient's burn injury?

you can use needle electrodes


anything else you would require?

2 large bore PIV, rapid infuser, warming blankets/heat lamps/IVF warmer


what HD changes do you expect to see immediately after a burn and then 48 hours later?

immediate: decrease in CO due to:
- circulating myocardial depressants
- increased SVR and hypovolemia (increased capillary permeability leads to movement of fluid from intravascular to interstitial space)
- decreased CBF
- decreased response to catecholamines

48 hours later: hyperdynamic state
- if resuscitation is adequate, capillary permeability should have returned to normal, leading to interstitial fluid resorption
- increased metabolic demand
- increased circulating catecholamines
- decreased SVR (due to circulating inflammatory mediators)
- increased CO (up to 2x)


if this patient is extubated on transfer and you are unable to ventilate, what is your ddx?

1. laryngospasm
2. airway swelling
3. tissue obstruction a/w OSA


what will you do?

1. call for help, difficult airway cart, surgeon capable of performing emergent trach
2. protect the cervical spine (ensure in-line stabilization and c-collar is in place)
3. cricoid pressure
4. open mouth and clear oropharynx
5. larson's maneuver - jaw thrust and firm pressure at the ascending ramus of the mandible
6. PPV with 100% O2
7. deepen anesthetic and give IV lidocaine (1-1.5 mg/kg)
8. 30 degree rev trendelenburg to help relieve obstruction and fascilitate intubation

small dose (0.1-0.5 mg/kg) IV sux

9. attempt intubation, if unsuccessful, LMA


what is the mechanism of laryngospasm?

stimulation of the mucosa from the epiglottis to the VC (superior laryngeal nerve off pharyngeal branch of the vagus) or the mucosa below the VC (recurrent laryngeal nerve). the muscles that tighten to cause spasm are the lateral cricoarytenoids (RLN), thyroarytenoids (RLN), cricothyroid (ext br of SLN).

other causes: hypocalcemia, painful stimuli, vagal hypertonicity, foreign body


is succinylcholine contraindicated in this patient?

it is not truly contraindicated within the first 24 hours following a burn injury, however due to his crush injury (possible rhabdomyolysis leading to increased K) and increased risk of difficult intubation it would be a last resort.


when is succinylcholine contraindicated and why?

24 hours after burn injury due to up-regulation of extra-junctional cholinergic receptors. this effect is seen most prominently 5-15 days after injury and persists for up to 2 years after healing of all burned skin.


if patient loses 850 mL of blood immediately after fasciotomy, would you transfuse?

yes, i would want to keep his Hct around 30% due to his CO level of 20%. his allowable blood loss is around 650 mL, so i would transfuse 1-2 units pRBCs. my decision may also be affected by surgical hemostasis, HD stability, and signs of ischemia


how do you calculate allowable blood loss?

ABL = [EBV(Hi-Hf)]/Hi

neonates 90 mL/kg
pediatric 75 mL/kg
women 65 mL/kg
men 75 mL/kg


the SpO2 falls to 88% and the BP to 76/50 during femoral shaft rodding. what is your ddx?

1. fat embolism
2. bone-cement implantation syndrome (embolization of intra-medullar debris and circulating methyl-methacylate)
3. tension PTX
4. cardiac tamponade
5. occult hemorrhage
6. dysrhythmia
7. myocardial ischemia


how would you evaluate the patient to achieve a diagnosis?

auscultate the lung fields, observe the surgical field for blood loss, evaluate the EKG.

i would consider placing a pulm artery catheter and abd/thoracic ultrasound to assess occult hemorrhage. TEE for pericardial effusion, tamponade, wall motion abnormalities, or intramedullary debris in the right heart


what are the features of bone-cement implantation syndrome and what is the pathophysiology?

features: hypotension, hypoxia, dysrhythmia, pulmonary hypertension, decreased cardiac output.

1. hardening and expansion of bone cement results in increased IM pressure and embolization of bone marrow debris. if the emboli reach sufficient size or quantity, there is increased pulm vasc resistance, RV strain, ventricular dysfunction.
2. methyl methacrylate may lead to decreased SVR.
3. cytokine release during femoral canal reaming can lead to microthrombus formation and pulm htn


how can bone-cement implantation syndrome risk be decreased?

- maintain euvolemia
- create a vent hole in the femur prior to implantation
- high-pressure pulsatile lavage of the canal to remove debris
- avoiding its use


how can bone-cement implantation syndrome be treated?

supportive - 100% FiO2, fluids, vasopressors

glucocorticoids - controversial, but would not in this IDDM

alcohol, heparin have not been demonstrated to improve outcome


how do you supply jet ventilation through an airway exchange catheter?

insert the catheter but do not advance past 26 cm (in adults) or when there is increased resistance. the space within the ETT must be adequate for expiration (must be >4mm after catheter has been inserted).

i would use an in-line pressure regulator and initiate jet ventilation with 100% FiO2, a pressure of 20-25 psi, insp time


what are some complications of jet ventilation?

pneumothorax, pneumomediastinum, pneumopericardium, pneumoperitoneum, subQ emphysema, inadequate gas exchange

if its supraglottic, gastric distention, rupture, or aspiration


what patients are not good candidates for jet ventilation?

-obesity (decreased CW compliance, leading to gastric distention)
-upper airway obstruction (may lead to air entrainment and barotrauma)
-COPD (increased expiratory time, risk of bullae rupture)


four hours post-op the patient has a temp of 38.9C, what do you suspect is the cause?

early post-op fever is rarely indicative of infection and especially in this patient's condition, i would suspect a hypothalamus-mediated increase in core and skin temp. this is expected and also concerning because sit is most likely part of the hypermetabolic response to thermal injury.


what is the treatment?

-environmental heating, to minimize the metabolic expenditure required to maintain core temp
-aggressive pain control
-adequate nutrition


what is the equation for nutrition for burn patients?

25 Kcal/kg body weight + 40 cal per %BSA per 24 hours


the patient begins producing dark cola-colored urine, what is your ddx?

1. transfusion reaction (hemoglobinuria)
2. rhabdomyolysis from crush injury (myoglobinuria)

both produce ARF, so i would increase fluids and give mannitol


what is abdominal compartment syndrome?

massive edema of intra-abdominal organs (caused by trauma, fluid resuscitation, shock-induced inflammatory mediators)

-decreased CO and venous return, increased SVR, PAOP, CVP
-hypoventilation (hypercapnea), increased airway pressures
-increased ICP, decreased CPP

intravesical pressure >20-25 mmHg