UBP Book 1, Case 1 (Trauma/Critical Care-Head Injury)

Question 1

What is the GCS?

Answer 1

A scoring system based on eye opening, best motor response, and best
verbal response that has a strong correlation with severity of head injury and patient
outcome.

Question 2

Little things that can be helpful when describing how you will intubate the patient:

Answer 2

place the patient in 30° reverse-trendelenburg to
improve respiratory mechanics, facilitate intubation, and reduce the risk of passive

regurgitation (make sure that this positioning is hemodynamically tolerated)

Question 3

How can you tell if someone is cleared from c-spine?

Answer 3

The
criteria for C-spine clearance include: 1) the absence of cervical pain or tenderness, 2)
the absence ofparesthesias or neurologic deficits, 3) normal mental status, 4) no

distracting pain, 5) >4 years of age. If the above criteria are not met, then a cross-
table lateral film showing C1 through Ti, an open mouth odontoid view, and an

anterior/posterior view are required. Even with an appropriate radiographic
examination, 7% of fractures are missed

Question 4

What’s so bad about a basilar skull fracture-why wouldn’t you want to nasally intubate when people have one? What signs do they have?

Answer 4

Given the presence of periorbital ecchymosis and hemotympanum, it
would be inappropriate to perform a blind nasal intubation as these findings suggest a
possible basilar skull fracture. With this type of fracture, there is a risk of advancing
the ETT into the brain when attempting a blind nasal intubation.

Question 5

When considering vital signs in these types of patients-remember:

Answer 5

Catecholamines are released with head injury!

Question 6

If they ask if the patient needs fluid resuscitation, what can you say?

Answer 6

Mention that they could be (unless you know they’re not), and that you would have to perform a thorough physical exam with special attention to
urine output (if a Foley catheter is in place), mucous membranes, cap refill, and blood
loss, recognizing that there could be hidden blood loss in the blah, blah, blah

Question 7

How do you feel about D5LR hanging in a brain injury patient?

Answer 7

I do have a problem with the D5LR since hyperglycemia may augment
ischemic brain injury. For this reason, glucose-containing solutions are usually avoided in patients with brain injury.

Question 8

So, in patients with elevated BP and head trauma-are you treating the hypertension?

Answer 8

without ICP monitoring it is very difficult to know whether his increase in blood
pressure is in response to an acute increase in intracranial pressure (i.e. reflex
response in order to maintain cerebral perfusion), or simply the result of pain,
hypoxia, hypercarbia, anemia, or hypovolemia. Therefore, I would first: (1) take
steps to reduce his intracranial pressure, (2) consult a neurosurgeon for potential ICP
monitoring, and (3) ensure adequate analgesia, intravascular volume replacement, and
ventilation. Ifl determined that treatment of his blood pressure was indicated, I
would carefully reduce his blood pressure by titrating a short acting agent (i.e.
esmolol), with the goal of bringing his blood pressure to a safer level without
compromising cerebral perfusion. I would not attempt to normalize his blood pressure
since higher than normal blood pressures may be necessary to provide adequate
cerebral perfusion in the presence of his elevated ICP (CPP =MAP - ICP).

Question 9

Cerebral perfusion pressure formula:

Answer 9

MAP-ICP (or CVP-whichever is higher)

Question 10

Autoregulation in the setting of head trauma: What numbers are the range? Can it be affected by trauma?

Answer 10

it is quite possible that this
regulatory mechanism is abolished in the presence of head trauma, making cerebral
blood flow pressure dependent. In the absence of chronic hypertension, intact
cerebral autoregulation maintains cerebral blood flow at a constant rate with mean
arterial pressure ranging from 60- 150 mmHg.

Question 11

What is normal CPP? What’s ideal in a patient with head injury?

Answer 11

Normal CPP is around 80-100 mmHg. In a patient with head injury
the optimum CPP is unknown. While earlier studies suggested improved outcomes
with a CPP of70-80 mmHg, there is more recent evidence showing that CPP > 70
mmHg may increase the incidence of ARDS. Additionally, some studies indicate that
cerebral ischemia may occur in the head injury patient with CPP below 50-60 mmHg.
Therefore, it would seem reasonable to try to maintain a CPP of 60-70 mmHg

Question 12

Do you always require ICP monitoring?

Answer 12

It’ll be case specific, but I would definitely discuss the possibility with the surgeon.

Question 13

Again-things you can do to decrease ICP without a drain:

Answer 13

There are several actions I can take to decrease ICP including: (1)
making sure there is no venous obstruction, particularly in this patient with a c-collar
in place; (2) elevating the patient’s head 15-30 degrees (ifhemodynamically
tolerated) to increase venous drainage; (3) administering mannitol, which reduces ICP
by osmotically shifting fluid from the brain compartment to the _intravascular
compartment, decreasing production of CSF (this affect is seen with hypertonic
fluids), and inducing reflex cerebral vasoconstriction secondary to decreased blood
viscosity (keep in mind that this drug may potentially worsen cerebral edema if the
BBB is not intact, and/or result in the expansion of an intracranial hematoma as
surrounding brain tissue shrinks with osmotic diuresis); ( 4) administering furosemide,
recognizing that in the presence ofhypovolemia, this diuretic could lead to
hypotension and worsening cerebral ischemia; and

Question 14

So, would you ever hyperventilate a patient with head trauma? What is the
problem with hyperventilation? How long do its effects last?

Answer 14

I would consider hyperventilation to a C02 of25-30 mmHg if other
methods to reduce ICP were unsuccessful and I thought the elevated ICP was severe
enough to place the patient at risk for brain stem herniation. However, there is a risk of exacerbating cerebral ischemia by inducing cerebral
vasoconstriction in a patient with lower than normal cerebral blood flow following
head trauma. I would also keep in mind that the effects of hyperventilation are
temporary (24-48 hours) because HC03 levels in the CSF adjust to compensate for
the change in PaC02.

Question 15

The patient’s temperature is 33 degrees. Does this concern you?

Answer 15

Yes-poor wound healing, coagulopathy, cardiac dysrhythmias

Question 16

Would you use N20 on a patient with traumatic brain injury (TBI) and elevated ICP?

Answer 16

No-
if cerebral oxygenation is a problem-I want them breathing O2
If air is trapped in cranium-N20 can expand air pocket
Hyperemia=N20 can cause increased CBF

Question 17

During the case the patient’s blood pressure progressively falls to 95/60 mmHg
and peak inspiratory pressures increase to the mid 40’s. His oxygen saturation
falls to the high 80’s. What is your differential? What are you going to do? (This happens all the time-the scenarios they give)

Answer 17

My differential would include migration of the ETT into the right
mainstem, an unrecognized and expanding tension pneumothorax, cardiac
tamponade, and fat emboli secondary to the patient’s fractured femur. Moreover,
given his increased risk for aspiration and my difficulty in securing his airway, I
would consider the possibility that his hypoxia and decreased pulmonary compliance
are secondary to aspiration pneumonitis (an acute increase in pulmonary vascular
resistance secondary to hypoxic pulmonary vasoconstriction could also be
contributing to his decreased blood pressure) .
In treating this patient, I would hand ventilate, auscultate the chest, make sure the
patient was breathing 100% 0 2, verify correct positioning of the ETT, and order a
CXR. I may order an ABG, place a pulmonary catheter, and/or order an
echocardiogram if the clinical picture is confusing

Question 18

Normal Cardiac index
Normal PCWP
Normal PA pressure
Venous oxygen saturation

Answer 18

Normal Values:

• cardiac index= 2.6-4.2
• PCWP = 2-15 mmHg
• PA pressure= 15-30/4-12 mmHg
• venous oxygen saturation (internal jugular)= about 70-80%

Question 19

Fat embolism syndrome: Major and minor criteria:

How many minor and major criteria are needed to make the diagnosis?

Answer 19

Major criteria include: (1) a petechial rash, present
on the conjunctiva, oral mucosa, axillae, and/or the skin folds of the neck; (2)
hypoxemia, with a Pa02 < 60 mmHg on a Fi02 < 0.4; (3) central nervous system
depression, unexplained by the patient’s hypoxia; and ( 4) pulmonary edema.

Minor: Minor
criteria include: (1) tachycardia,> 110 beats/minute; (2) pyrexia; (3) retinal fat
emboli; (4) fat microglobulinemia; (5) fat globules in the sputum; (6) unexplained

Major: CPR
Minor: TP Fat Thrombo
anemia; (7) unexplained thrombocytopenia; (8) increased erythrocyte sedimentation
rate; (9) urinary fat globules; and (10) jaundice.

Question 20

Assuming this is fat emboli syndrome (FES), what would you do?

Answer 20

I would administer 100% oxygen, treat his hypotension, correct any
hypovolemia, replace blood and platelets as required, continue mechanical
ventilation, monitor the patient carefully for further deterioration, and inform the
surgeon of his condition

Question 21

DDX of ARDS like picture:

Answer 21

This clinical picture is consistent with: (1) aspiration pneumonitis; (2)
cardiogenic pulmonary edema (possibly secondary to fluid overload during trauma
resuscitation and/or surgery); (3) neurogenic pulmonary edema (may occur after any damage to the CNS
and ‘(4) acute respiratory distress
syndrome (possibly secondary to fat embolism syndrome, head trauma, or aspiration).
If blood had been transfused, I would also consider (5) transfusion related acute lung
injury (TRALI) and (6) transfusion associated circulatory overload (TACO).

Question 22

What is ARDS and what is the pathophysiology of ARDS-what’s damaged? What scarring is happening to the lungs?

Answer 22

ARDS represents the pulmonary manifestation of the systemic
inflammatory response syndrome (SIRS). There is injury to the capillary alveolar
membrane resulting in bilateral diffuse infiltrates,The syndrome may lead to fibrosing alveolitis
and permanent scarring of the lungs.

Question 23

What is required for the diagnosis of ARDS?

Answer 23

(1) a Pa02/Fi02 ratio of< 300; (2) acute onset,
defined as occurring within 7 days of the inciting event (i.e. sepsis, trauma, aspiration,
or another accepted cause of ARDS); (3) bilateral infiltrates identified by chest
radiography (CT or chest x-ray); and (4) respiratory failure that, in the physician’s
best estimation, is “not fully explained by cardiac failure or fluid overload”.

Question 24

Treatment of ARDS:

Answer 24

Treat causative events and reversible pathology Mechanical ventilation should provide
sufficient PEEP to recruit collapsed alveoli and improve gas exchange while avoiding
high airway pressures and large tidal volumes (tidal volumes 6 ml/kg or less & and
static airway pressures < 30 cm H20). Permissive hypercapnia may be necessary to avoid higher tidal volumes and airway pressures. The Fi02 should be less than 50%
if possible to prevent iatrogenic lung injury.

Question 25

Steroids in ARDs?

Answer 25

No. Not shown to be helpful. Lower TV and lower pressures are better