Book 4, set 2-compartment syndrome and Fasciotomy, Burn Flashcards
For burn pts, and even some trauma pts: don’t forget what?
At least 2 large bore IVs, rapid infusion device and equipment useful in preventing hypothermia-warming blankets, IV fluid warmers
what cardiovascular changes you expect to occur
following a significant burn injury.
Immediadte:
What if fluid resuscitation has been normal?
In the immediate post-bum period (first 24-48 hours), cardiac output is
decreased due to circulating myocardial depressant factors, increased systemic
vascular resistance, a contracted plasma volume (due to increased capillary
permeability leading to the movement of protein-rich fluid from the intravascular to
the interstitial space), decreased coronary blood flow, and a diminished response to
catecholamines. If fluid resuscitation has been adequate, the patient’s capillary
integrity returns to normal after 24-48 hours. Moreover, interstitial fluid re-
absorption, increased metabolic demands, and increased circulating catecholamines
lead to a hyperdynamic state, where cardiac output is increased (2 X normal) and
systemic vascular resistance is reduced (the latter may be the result of circulating
inflammatory mediators).
Don’t forget to ensure adequate manual in line stabilization when pts have a collar!
Okay
Your burn pt gets extubated and you are unable to ventilate-now what?
call for help
call for emergency airway cart and surgeon with ability to perform an emergency airway, apply cricoid, suction oropharynx, provide jaw thrust and give postive pressure with 100% O2, deepen the anesthetic and administer lidocaine (COULD BE LARYNGOSPASM), place pt in 30 degree reverse t berg position to relieve any obstruction from swelling. IF still apneic, I would CONSIDER sux (if under 24 hours), and place ETT. If htat was unsuccessful, i would place an LMA and have surgeon begin prep for cricothyrotomy or trahc
Even though sux can be given vefore the 24 hour mark, you have to KIM that there are still other reasons to not give it like-
High K+, crush injury (could result in rhabdo), increased risk for difficult intub/vent-so only use it as a last resort in these types of pts.
If they give you a random number of blood that was lost, and ask if you’ll transfuse-what are factors that you will weigh?
Other comorbidities: for example pts who have HTN, IDDM, HLD, sickle cell-need to be at a Hct of 30%. Mention that your decision also is based on current surgical hemostasis, hemodynamic stability and signs of tissue ischemia
you knew it was coming: what is the formula for estimated allowable blood loss?
Estimated Allowable Blood Loss = EBV X (Hi - Hf) / Hi
All over Hi
Remember-you can always ask for what intra op?
You can always ask for a TEE
During rodding of the femoral shaft the Sp02 suddenly
drops to 88% and the blood pressure falls to 76/50 mmHg. What do you think is
the cause? Surgeon also used bone cement
(1) fulminant fat
embolism syndrome (fat embolism may have occurred following the long bone
fracture and/or with placement of the intra-medullary device in the femoral shaft)
and/or (2) bone-cement implantation syndrome (the use of methyl methacrylate can
lead to circulating methyl methacrylate monomer and the embolism of intra-
medullary debris). However, I would also consider other potentially life-threatening
causes, such as (3) tension pneumothorax (trauma, line placement), (4) cardiac
tamponade (trauma, increased capillary permeability, and aggressive fluid
resuscitation), (5) significant hemorrhage (occult abdominal, thoracic, or extremity
bleeding, coagulopathy, inadequate surgical hemostasis), (6) dysrhythmia, and (7)
myocardial ischemia.
With hypotension, don’t forget to:
look at surgical field?
Pathophysiology of bone cement implantation syndrome?
hypotension, hypoxia,
dysrhythmias, pulmonary hypertension, decreased cardiac output, and even cardiac
arrest associated with bone-cement implantation syndrome may develop.
First, the
hardening and expansion of the bone cement results in increased intra-medullary
pressures and the embolization of bone marrow debris. When these emboli are of
sufficient size or quantity, they can lead to increased pulmonary vascular resistance,
right ventricular strain, and ventricular dysfunction. Second, circulating methyl
methacrylate monomer may lead to reduced systemic vascular resistance.
How can the effects of bone cement implantation syndrome be ameliorated?
maintaining euvolemia, creating a vent hole in the femur prior to implantation to
relieve intramedullary pressures,
How do you tx bone cement implantation syndrome?
largely supportive, I would provide 100% oxygen and administer fluids and
vasopressors as indicated.
Burn pt gets transferred toICU, but the cuff ruptures and they arent’ able to ventilate-what are you going to do?
Tube exchanger with jet ventilation capabilities.
First, I would (1) evaluate the adequacy of the patient’s airway,
ventilation, level of sedation, and ventilator settings. Assuming the nurse’s
assessment was correct, I would (2) obtain the appropriate difficult airway equipment,
including various sizes of endotracheal tubes; (3) ensure the presence of a surgeon
capable of performing emergent tracheostomy; ( 4) have the neck prepped and draped;
(5) ensure adequate sedation, and (6) replace the endotracheal tube using a jet-
ventilation exchange catheter.
Explain how you would supply jet ventilation through the airway exchange catheter.
obtain the appropriate difficult airway
equipment, (2) ensure the presence of a surgeon capable of performing emergent
tracheostomy, and (3) have the neck prepped and draped prior to placement of the
airway exchange catheter. I would then (4) ensure adequate sedation and (5) insert
the airway exchange catheter, being careful not to advance the catheter beyond 26 cm
(in adults) or when there was increased resistance, recognizing that this could lead to
perforation of the tracheobronchial treeAssuming the space within the
ETT were sufficient for adequate expiration after inserting the catheter (jet ventilation
through the exchange catheter should not be employed when the internal diameter of
the ETT is< 4mm following catheter insertion), I would (6) use an in-line pressure
regulator and (7) initiate jet ventilation with 100% Fi02, a pressure of 20-25 psi, and
an inspiratory time of less than 1 second. I would then (8) adjust these settings as
clinically indicated to provide adequate oxygenationemphysema). Finally, I would (9) remove the
damaged endotracheal tube (taking care not to remove the exchange catheter with it),
(10) perform careful laryngoscopy (visualization of the oropharynx helps to identify
problems with smooth passage of the new ETT over the exchange catheter - i.e. the
tip of the ETT catches on the right vocal cord or the arytenoid), and (11) insert the
new endotracheal tube over the exchange catheter.