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.
Complications of jet ventilation: supra vs subglottic
pneumothorax,
pneumomediastinum, pneumoperitoneum, pneumopericardium, subcutaneous
emphysema, and inadequate gas exchange (i.e. hypoxia and/or hypercapnia). With
supraglottic jet ventilation, gastric distention, regurgitation, and gastric rupture
would also be a risk.
Who is jet ventilation NOT appropriate for?
Jet ventilation may not be appropriate for patients with decreased chest wall
compliance (i.e. obesity), because this may lead to gastric distention (increased
risk of regurgitation; further reductions in pulmonary compliance).
Jet ventilation is probably not appropriate for patients with an upper airway
obstruction (i.e. glottic lesion) that would inhibit adequate exhalation between jet
applications (this can lead to progressively increasing airway pressures and
barotrauma).
Jet ventilation may not be appropriate for patients with advance COPD due to the
prolonged expiratory phase associated with this type of pulmonary disease.
Moreover, the risk ofbarotrauma would be significantly increased in the presence
of pulmonary bullae.
Burn pt has fever 4 hours post op-DDX?
FYI: early post operative fever is rarely indicative of an infectious process, fever is most likely due to a hypothalamus mediated increase inskin and core temps associated with major burn injury. It could also be a component of of the hypermetabolic response to thermal injury that includes increased
glycogenolysis, gluconeogenesis, severe fat and protein wasting, increased oxygen
consumption, and a negative nitrogen balance . Unfortunately, this
hyper-metabolism may lead to tissue hypoxia, renal failure, delayed wound healing,
and infection.
burn pt with early post op fever-wyd?
I would attempt to attenuate the detrimental effects of this hyper-
metabolic response by providing: (1) environmental heating, to minimize the
metabolic expenditure required to maintain adequate core temperatures; (2)
aggressive pain control, to reduce catecholamine release; and (3) adequate nutrition
(25 Kcal/kg body weight + 40 calories per % BSA burn injury per 24 hours) via
enteral feeding or TPN. I would, however, keep in mind that this aggressive hyper-
alimentation requires close monitoring of serum and urinary glucose levels (to avoid
hyperglycemia), liver function (to identify cholestasis or fatty infiltration), and
electrolytes.
Burn pt who had blood transfusion and crush injury now has cola colored urine-DDX and what would you do?
Considering this patient’s recent blood transfusion and crush injury
from the falling roof beam, this cola-colored urine most likely represents either
hemoglobinuria from incompatible blood transfusion, or myoglobinuria secondary to
skeletal muscle destruction. The specific diagnosis could be made by serum
electrophoresisRecognizing that both of these conditions potentially result in acute renal failure, I
would administer fluids and mannitol in an attempt to induce diuresis.
Burn pt with hx of abdominal trauma and agressive fluid resuscitation has bcome hypotensive and oliguric, has increased airway pressures and decreased CO-what do you think may be going on? How do you make the diagnosis, and then what would you do?
A recent history of abdominal trauma (roof beam struck his torso) and aggressive fluid resuscitation (for burn injury), combined with a constellation of signs and symptoms that includes oliguria, hypotension, increased airway pressures, decreased cardiac output, and a distended abdomen, is consistent with abdominal compartment syndrome (ACS).tension pneumothorax, severe acidosis, ARDS,
pulmonary embolism, FES, or cardiac tamponade. To determine whether his clinical
condition is the result of ACS, I would measure the intravesical pressure with a Foley
catheter to identify intra-abdominal hypertension(> 20-25 mrnHg). A diagnosis of
ACS would necessitate immediate abdominal decompression.
What is Abdominal compartment syndrome?
ACS results when trauma, fluid resuscitation, and/or
shock-induced inflammatory mediators results in massive edema of intra-abdominal
organs, with subsequent cardiac (i.e. decreased CO, decreased venous return,
hyper/hypotension, and increased SVR, PAOP, and CVP), pulmonary (i.e. increased
dead space, hypercapnia, increased ventilatory pressures), renal (oliguria),
gastrointestinal, hepatic, and CNS dysfunction (increased ICP and decreased CPP).
How are you going to evaluate your burn pt who is intubated (Or i guess any pt in this situation who is intubated)
an initial rapid
assessment to determine whether the patient was stable, unstable, dying, or dead
(a.k.a. rapid overview). This would be quickly followed by a primary survey to
assess and stabilize the patient’s airway, ventilation, circulation, and neurologic
function (Airway, Breathing, Circulation, and Disability). This primary survey would
also include a quick examination of the UNDRESSED patient, to identify additional injury
(Exposure).
I would perform a secondary survey to systematically evaluate the
patient from head-to-toe for additional injuries, and obtain radiographs, diagnostic
procedures, and laboratory tests as indicated. Finally, after initial resuscitation and
operative interventions were completed, I would plan to perform a tertiary survey
within the first 24 hours to identify clinically significant injuries that were missed
during the initial evaluation
Fluid resuscitation guidelines for burn pts:
I would titrate my initial fluid resuscitation to maintain
urine output of 0.5 to 1 mL/Kg/hour, a pulse of 80-140 beats/minute, a mean arterial
pressure of> 60 mmHg, and a base excess< 2. I could also use the patient’s
hematocrit (increased hematocrit suggests inadequate fluid resuscitation)
Base excess normal values:
Base Excess:
4) What is the Parkland formula?
2
= metabolic acidosis
=normal
= alkalosis
What fluids do you give to burn pts?
LR
4 mL x %BSA burned x kg -deliver half in first 8 hours, the other 1/2 over the next 16 hours
Rule of 9’s:
And explain degrees of burn:
Head and neck, each upper extremity, the chest, and abdomen, as well as anterior and posterior aspect of each lower extremity represent 9%
First degree: injury limited to the epidermis
second: epidermis and dermis
third degree: full thickness iwht complete destruction of epidermis and dermal layers
4th degree: muscle, fascia and /or bone
Flow volume loop demonstrating a saw toothed or flattened inspiratory flow:
A flow volume loop demonstrating a saw-toothed or flattened inspiratory flow
and an extra-thoracic obstruction is suggestive of upper airway obstruction.
You determine that 15% of the patient’s injury is third-degree burns, with
second-degree burns making up the other 5%. Moreover, you note that his
sputum appears to be stained with carbonaceous material. Will you intubate
him now?
I would begin preparing for immediate endotracheal intubation
because of the risk of respiratory compromise associated with major burn (his bum
involves> 10% TBSA) and inhalational injury (carbonaceous material in the sputum
is consistent with inhalational injury).
Given this patient’s increased risk of difficult airway management (airway edema,
cervical collar in place), airway obstruction (i.e. third-spacing of fluid, inhalational
injury, aggressive fluid resuscitation), aspiration (i.e. trauma, diabetes mellitus,
possible recent food ingestion), and neurologic damage (unable to clear cervical spine
injury due to distracting pain), I would: (1) administer metoclopramide, an H2-
blocker, and glycopyrrolate; (2) provide 100% oxygen for several minutes; (3) ensure
adequate airway analgesia, manual in-line stabilization, and the presence of difficult
airway equipment; (4) perform an awake fiberoptic intubation, being careful not to
inflict any additional tissue trauma; and (5) provide sedation as tolerated.
signs of inhalational injuty:
Therefore, I would examine the patient for additional signs and symptoms of
airway injury, such as singed facial hair, burned mucosa, cough, stridor, hoarseness,
difficulty swallowing, and/or pharyngeal edema.
Burn pt with crush injury and c collar:following intubation, BP drops to 86/53-DDX
–Anesthetic drugs
hemorrhagic shock
–Neurogenic shock-cervical spinal cord injury following intubation
–Cardiogenic shock due to burn injury induced release of myocardial depressant factors
–Carbon monoxide poisoning-can cause myocardial toxicity
-Vagal responseto laryngoscopy
–Tension PTX
Keep MAP at lower end of cerebral autoregulation by maintaining a map above 50-thus allowing visualization of the aneurysm. Consider using adenosine for temporary arrest if the aneurysm can not be viusalized due to bleed,then immediately take measures to increase pressures.
What would you do for a ruptured aneurysm
Burn pt blood gas: pH= 7.22, P02 = 108 mmHg, PC02 =
36 mmHg, and Sa02 = 98% on 6 liters 0 2• What is your interpretation?
metabolic acidosis without respiratory compensation Potential causes of this condition in a
diabetic patient following trauma and major bum injury include shock, diabetic
ketoacidosis, hypothermia (especially with rapid rewarming, which may lead to the
release of accumulated metabolic products into the central circulation), carbon
monoxide poisoning, and cyanide toxicity.
Why does CO poisoning cause acidosis? What are you going to do if you suspect this toxicity?
Tissue hypoxia and acidosis develop with carbon monoxide poisoning for two
reasons: (1) carbon monoxide (CO) has a 200-250 fold greater affinity for
hemoglobin than does oxygen (reducing the number of available sites for binding of
oxygen …. somewhat like anemia); and (2) carboxyhemoglobin results in a left-ward
shift in the oxyhemoglobin dissociation curve, resulting in impaired tissue delivery of
oxygen
Suspect CO toxicity?
100% O2.If his CO-Hg level was> 25-30% and the delay of other
emergency care were acceptable, I would consider hyperbaric oxygen treatment to
further promote CO elimination
What is PaO2? and why is it unaffected by CO poisoning?
It’s a measure of oxygen tension in blood (amount of ffee O2 dissolved in plasma, so it is not affected by binding characteristics of hemoglobin)
What is SaO2? Pulse ox approximates what (SpO2)
Percentage of total arterial heme binding sites saturated with oxygen. This IS affected by oxygen binding to hemoglobin. This is measured by blood oximetry.
SpO2 approximates SaO2 under normal circumstances.
How to handle a pt that you are concerned about compartment syndrome?
confirm that
pulses in the extremity were weak or absent and look for other signs associated with
these conditions such as pallor, paresthesias (“pins and needles” is a common
description), paresis (usually a late finding). Swelling and tenseness in the affected
extremity would be more suggestive of compartment syndrome.
What i would want to get: doubt, I would consider arteriography or transducer measurement of intra-
compartmental pressures to obtain a more definitive diagnosis (immediate surgery is
required when the intra-compartmental pressure exceeds 30-40 mmHg or when there
is < 30 mmHg difference between the intra-compartmental pressure and the diastolic
blood pressure).
