Book 6, Case 7 emergent crani, vWD

Question 1

What is vWD?

Answer 1

most common inherited coagulation disorder,
caused by qualitative or quantitative defects of von Willebrand factor (vWF) in the plasma.
vWF plays an important role in both primary hemostasis and coagulation by mediating
platelet adhesion to the subendothelial surface of blood vessels (via the GPib receptor),
facilitating platelet-to-platelet aggregation (via the GPIIb/IIIa receptor), and functioning as a
carrier protein and stabilizer for factor VIII

Question 2

Look over vWD types in learning issues

Answer 2

Okay

Question 3

The family is not sure of the patient’s specific type of vWD or past treatment. How
would you evaluate her coagulation status?

Answer 3

I would perform a history, physical, and chart review to help identify the type
and severity of vWD; previous transfusion requirements; and episodes of abnormal bleeding,
such as easy bruising, hematomas, epistaxis, menorrhagia, and gingival, traumatic, or
perioperative bleeding. I would then order a CBC, platelet count, bleeding time, PT, and
PTT, recognizing that mild disease will likely produce near-normal studies, with severe
disease resulting in prolonged bleeding, thrombocytopenia, and a prolonged PTT, depending
on the type of disease. Given the severity of this patient’s condition and the urgency of the
case, I would not delay treatment to obtain studies designed to confirm and diagnose the type
ofvWD, such as vWF antigen, vWF activity (ristocetin cofactor or collagen binding
activity), factor VIII coagulant activity, and vWF multimer distribution by electrophoresis.
Rather, I would anticipate the possibility of significant bleeding and ensure the availability of
blood products, DDA VP, cryoprecipitate, FFP, and Humate P (a purified commercial
preparation of factor VIII-vWF concentrate containing large vWF multimers).

Question 4

You giving prophylactic DDAVP to vWD pts for crane?

Answer 4

Ahhhhh….
Considering the significant risk of bleeding associated with this major
surgery, and assuming I have been unable to identify the patient’s specific subtype of vWD, I
would provide prophylactic vWF replacement with either cryoprecipitate or Humate P (less
risk of transfusion-related infections with Humate P). While DDA VP (desmopressin), a
synthetic analogue of vasopressin that stimulates the release of vWF from endothelial cells, is
effective first-line therapy for many patients with Type I vWD (about 80% of patients with
vWD respond well), it provides little to no response in patients with Type 2A, Type 2M, and
Type 3 vWD, and will lead to thrombocytopenia in patients with Type 2B vWD. The lack of
a consistent response, a limited duration of action ( 6-12 hours), and the potential for
tachyphylaxis, render treatment with DDA VP inadequate for surgical prophylaxis during
major surgery where it is critical to control the patient’s bleeding tendency.
Clinical Note:
• To provide prophylaxis for major surgery, it is recommended to obtain initial vWF:RCo
and factor VIII levels of 2:100 IU/dL. Subsequent dosing should maintain VWF:RCo
and factor VIII levels above a trough of 50 IU/dL for at least 7-10 days following

Question 5

You lowering BP in pt with increased IcP?

Answer 5

Recognizing that this patient’s decreased level of consciousness, papilledema,
headache, and nausea are suggestive of severely elevated intracranial pressures and reduced
cerebral perfusion, and keeping in mind that cerebral perfusion pressure is equal to the mean
arterial pressure minus the intracranial pressure (CPP =MAP- ICP), I would be very
concerned that reducing her blood pressure may lead to worsening cerebral ischemia.
Therefore, while hypertension could potentially lead to hyperemia, increased cerebral blood
flow (CBF), and increased ICP (increased CBF -7 increased CBV -7 increased ICP), I would
not treat her hypertension at this time. My concern is that lowering the MAP of a patient
with elevated ICP and/or altered cerebral autoregulation (potentially abolished or rightward
shifted secondary to tumor affects or chronic hypertension, respectively), prior to undergoing
a procedure in the sitting position, could contribute to decreased cerebral perfusion pressure
and worsening cerebral ischemia. Rather, with this concern in mind, I would take immediate
steps to reduce her intracranial pressure prior to initiating any treatment to lower her blood
pressure.

Question 6

Aren’t you concerned that her high blood pressure will result in increased intracranial
pressure (ICP), placing the patient at increased risk of brain herniation?

Answer 6

Yeah, but I’m also concerned that lowering the BP will cause her to be at risk for cerebral ischemia….so….Therefore, prior to lowering her blood pressure, I
would attempt to lower her ICP by one or more of the following methods: (1) hyperventilate
the patient to a PaC02 of about 30 mmHg; (2) ensure unobstructed venous drainage and
elevating the head to 30° to facilitate venous drainage; (3) administer mannitol (the increase
in osmolarity draws water from the extravascular brain tissue) and/or a diuretic (particularly
useful for hypervolemic patients or those who will not tolerate mannitol - CHF or nephrotic
syndrome); (4) administer a corticosteroid, which is thought to reduce ICP by stabilizing
capillary membranes around the brain tumor (vasogenic cerebral edema often develops
around tumors) and /or decreasing CSF production; (5) administer a cerebral vasoconstricting
anesthetic, such as propofol or thiopental (this would be done at induction); and (6) ask the
surgeon to consider performing a ventriculostomy to allow for the drainage of CSF (and
provide a means of direct ICP measurement). Moreover, I would avoid factors that could
further increase ICP or decrease cerebral perfusion, such as hypoventilation (hypercapnia),
sympathetic stimulation (light anesthesia, especially during laryngoscopy), hypotension (i.e.
induction, sitting position, excessive anesthesia), and hypervolemia. My treatment goals
throughout this period of time would be to maintain adequate cerebral perfusion pressure
while avoiding ICP-induced brain herniation.

Question 7

Could you just quickly place a lumbar subarachnoid catheter to drain some CSF and
reduce her ICP? And if no, what would you rather have placed instead?

Answer 7

I would not do that, as I would be concerned that the pressure gradient between the
cranial and spinal compartments in a patient who already has severely elevated intracranial
pressures could result in tonsillar herniation. Since the pressure measurements of a lumbar
subarachnoid catheter are less reliable, and recognizing that patients with a posterior fossa
tumor are at increased risk for noncommunication hydrocephalus (obstruction of the CSF
outflow through the 4th ventricle), I would prefer a ventricular catheter to a lumbar
subarachnoid catheter, if possible.

Question 8

How does hyperventilation decrease ICP? What would be your target PaC02? and what are some bad things about hyperventilation to bring down CO2?

Answer 8

The decrease in PaC02 that occurs with hyperventilation leads to a higher
CSF pH around the walls of arterioles, which in tum leads to arteriolar vasoconstriction,
reduced CBF, reduced CBV, and, finally, lower ICP

the abrupt discontinuation of profound
hyperventilation could potentially lead to a rebound increase in ICP.
Therefore, when employing hyperventilation as a treatment modality, I would attempt to
lower the patient’s PaC02 to around 30 mmHg (possibly 25 mmHg ifl believed that cerebral
herniation was imminent). Further reductions in PaC02 may provide little benefit while, at
the same time, placing the patient at increased risk of cerebral ischemia (this is a theoretical risk) and other complications associated with respiratory alkalosis

Question 9

What does MVP with MR look like on EKG and sound wise? And would you require a work up in this emergent crane?

Answer 9

The auscultatory findings of midsystolic click and late systolic murmur along
with PVC’s on ECG are consistent with mitral valve prolapse associated with mitral valve
regurgitation.

In the absence of symptoms, such as syncope, chest pain, and fatigue, these
findings would not normally warrant further cardiac workup. However, in this case, cardiac
echocardiography would be desirable for several reasons: (1) to determine the severity of the
mitral valve prolapse and regurgitation of this patient who is unable to discuss recent
symptomatology; (2) to determine if there are any atrial thrombi present in this patient who is
most likely taking propranolol for dysrhythmia control; and (3) to rule out a patent foramen
ovale in this patient who will be at increased risk of experiencing an air embolism when
undergoing craniotomy in the sitting position. In fact, the presence of a patent foramen ovale
is a relative contraindication to the performance of a craniotomy in the sitting position, due to
the potential for paradoxical embolism to the coronary or cerebral circulations. If, however,
the emergent nature of the patient’s condition did not allow for further preoperative cardiac
evaluation, I would proceed with the case and discuss alternative patient positioning with the
surgeon

Basically, I would say that I understand the urgency of this case, and would ask the surgeon to do a different position due to risk for VAE

Question 10

Who needs antibiotic prophylaxis for infective endocarditis?

Answer 10

(1) a prosthetic cardiac valve or prosthetic material used for valve
repair; (2) a previous occurrence oflE; (3) unrepaired cyanotic congenital heart disease; ( 4)
the 6 month postoperative period following a repaired congenital heart defect using
prosthetic material or a device; (5) repaired congenital heart disease with residual defects at
the site or adjacent to the site of a prosthetic patch or device (which inhibits
endothelialization); and (6) cardiac transplantation recipients who develop cardiac
valvulopathy.

Also, always say you would discuss with surgeon

Question 11

Don’t forget to add what monitor?

Answer 11

TEE!!!!

Think of it in all sitting position patients, or patients who you think could benefit from a PAC.

Question 12

Types of catheters (central)

Answer 12

Silicone catheters (Hickman, Broviac) are too flexible and are inappropriate for ICU use – polyurethane catheters are stiffer, designed for shorter use, and more appropriate. Do not use heparin-impregnated catheters: they may reduce infection by a small amount but they have not been shown to reduce thrombosis-the heparin washes off after several hours, and they can cause HIT Antimicrobial-impregnated catheters should be considered if the infection rate in your ICU is above the national average

Single lumen catheters are associated with a lower infection rate and should be used when clinically feasible

Question 13

Where would you place your CVC in pt with increased ICP?

And where are you placing that tip? and what kind of catheter?

Answer 13

While
the subclavian approach carries a higher risk of pneumothorax, I would avoid placement in
the internal jugular vein due to the need to avoid the head-down position during placement
and the potential for obstruction of cerebral venous drainage following placement, which
could lead to increased ICP.

with the tip of a multi-orificed catheter 2 cm below the
superior vena caval-atrial junction to allow for optimal aspiration of intra-cardiac air. I
would then confirm the correct positioning using either x-ray or intravascular
electrocardiography (TEE can also be used).

Question 14

If airway info isn’t given, always say…

Answer 14

Assuming this patient had a reassuring airway!!!

Question 15

Sux in these increased ICP patients?

Answer 15

I think it can be okay if pt has mild signs and sxs, but with papilledema and other severe signs, I would still avoid it-even with the pre-dosing of roc.

Question 16

And if you’re giving a paralytic in a neuro case, always say what?

Answer 16

Assuming it will NOT interfere with monitoring. Don’t forget about the monitoring.

Question 17

Following induction, the patient’s blood pressure drops to 88/40 mmHg. Are you
concerned?
Neuro pt with central line with hx of mitral regurgitation

Answer 17

Considering this patient’s significant intracranial hypertension, and
recognizing the risk of cerebral ischemia with a drop in mean arterial blood pressure (CPP =
MAP - ICP), I am very concerned about this substantial drop in blood pressure. Moreover, I
am concerned that this significant hypotension may represent a potentially serious
complication other than hypovolemia and excessive anesthesia, such as: (1) tension
pneumothorax, possibly secondary to central line placement; (2) brain herniation, with
subsequent autonomic instability; (3) ventricular dysrhythmia, myocardial ischemia, and/or
cardiac failure due to acutely worsening mitral regurgitation (presumably due to increased
left ventricular emptying and worsening valve prolapse secondary to decreased preload,
decreased afterload, and/or increased inotropy); and (4) anaphylactic reaction, possible
secondary to antibiotic administration.

Question 18

After resection of the tumor the surgeon is unable to close the cranium because the
brain tissue is too swollen. What will you do?

Answer 18

Recognizing that the quickest and most effective method of providing brain
relaxation would be to drain CSP via the ventriculostomy, I would begin by draining CSP in
10-20 mL aliquots as tolerated. If this were inadequate or not well tolerated, I would
consider one or more of the following interventions: ( 1) hyperventilation to a PaC02 of 30
mmHg to reduce cerebral blood volume (further reductions may cause more harm than
good); (2) the administration of mannitol or hypertonic saline to increase plasma osmolarity
and draw water from brain tissue (duration of affect is approximately 6 hours); (3) giving
furosemide to promote diuresis and reduced intravascular volume (particularly useful when
mannitol is inadequate or inappropriate~ i.e. CHF or nephrotic syndrome); (4)
administering dexamethasone to reduce tumor related edema; (5) eliminating any obstruction
to venous drainage from the intracranial compartment Gugular venous outflow); (6) ensuring
adequate anesthesia to prevent sympathetic-induced increases in blood pressure and CBV
(use propofol, thiopental, or etomidate rather than a volatile agent); (7) treating excessive
hypertension that could be leading to increased CBV; (8) reducing or discontinuing volatile
agents to avoid their cerebral vasodilatory affects; and (9) ensuring an adequate serum
sodium level, recognizing that hyponatremia could be contributing to cerebral edema.

Question 19

Pt had AMS prior to intubation and now got the tumor resected? You waking up? Why or why not? What if the surgeon needed an immediate neuro exam?

Answer 19

Immediate post-operative extubation under a deep plane of anesthesia is
desirable to allow for immediate neurological examination and to avoid excessive stimulation
due to coughing and/or straining. However, given this previously obtunded patient’s
increased risk of aspiration (questionable airway reflexes and preoperative nausea and
vomiting) and C02 retention (compromised mental status pre-operatively, intra-operative
opioid administration), I would delay her extubation until she was able to demonstrate intact
airway reflexes and adequate spontaneous ventilation. Moreover, following tumor resection
in the posterior fossa (especially near the brainstem), post-operative edema and/or hematoma
formation can lead to worsening neurologic status during the first couple of post-operative
days, necessitating prolonged intubation.
If an immediate neurological exam were necessary, I would administer a short acting opioid,
lidocaine, and esmolol (to avoid coughing, bucking, and hypertension); wake the patient;
perform a quick neurological assessment; and then provide adequate sedation for transport to
the ICU with the endotracheal tube still in place.

Question 20

The patient seems slow to awake.(s/p crane) What is your differential for the delayed emergence
of this patient?

What would you do?

Answer 20

Given her recent craniotomy and elevated ICP, my differential would include
hematoma formation, tension pneumocephalus, cerebral edema, cerebral ischemia/infarction,
hypoxia, hypercarbia, seizure, and/or obstructive hydrocephalus. However, my differential
would also include those causes associated with a routine anesthetic, such as prolonged
neuromuscular blockade, residual anesthetic, acid-base abnormality, electrolyte imbalance,
and/or significant hypothermia.
I would exam the patient; review ICP pressures provided by the
ventriculostomy; optimize hemodynamics; ensure adequate ETT placement and ventilation,
order electrolytes and an ABG; use a peripheral nerve stimulator to check for residual
neuromuscular blockade; review the chart for administered medications and their doses
(especially opioids, nondepolarizers, and neuromuscular reversal agents); check the patient’s
temperature; inform the surgeon; consider a CT or MRI, and provide supportive care. If I
believed her symptoms were the result of elevated ICP, I would consider draining CSF from
the ventriculostomy; initiating more aggressive hyperventilation; administering mannitol,
furosemide, or dexamethasone; and discuss surgical options with the surgeon.

Question 21

Can you get a tension pneumocephalus even if you didn’t use N20? In which surgeries and positions is it more common?

Answer 21

a
tension pneumocephalus may develop even when N20 is avoided. This complication is most
commonly associated with posterior fossa craniotomies performed in the sitting position,
with air moving over the surface of the brain to become trapped in the upper cranium. This
is more likely to occur when aggressive brain relaxation measures are initiated
(hyperventilation, osmotic diuresis, etc.), creating an available space for air to occupy. The
patient becomes symptomatic (delayed emergence, headache) when this volume is
augmented by nitrous oxide, or with the reaccumulation of intracranial contents (CSF,
venous blood, arterial blood, extracellular fluid, etc.).

Question 22

On the second post-operative day, the nurse calls and reports the patient has impaired
dorsiflexion of the right foot. What do you think is the cause?

Answer 22

Her inability to dorsiflex her right foot is consistent with a foot drop injury,
which may be associated with a variety of conditions, such as dorsiflexor injuries, peripheral
nerve injuries (stretching of the sciatic or common peroneal nerves may occur in the sitting
or lithotomy position), stroke, neuropathies, drug toxicities, or diabetes. Given her recent
surgery in the sitting position, I would consider specific causes of sciatic or common
peroneal nerve injury related to this position, such as: (1) stretch injury with excessive
flexion of the hips and/or insufficient bending of the knees; or (2) compression injury
secondary to inadequate padding of the buttocks where the sciatic nerve emerges from the
pelvis.

Question 23

What are risk factors for intra-op nerve damage?

Answer 23

The risk factors for peripheral nerve injury include male gender, hospital stay
greater than 14 days, intra-operative hypotension, history of vascular disease and/or
hypertension, diabetes, smoking, and very thin or obese body habitus. Fortunately, more
than half of all patients who develop perioperative peripheral neuropathies regain full sensory
and motor function within 1 year.

Question 24

If this were a peripheral nerve injury, could it have been prevented?

Answer 24

Assuming it was due to improper positioning yes, but the mechanism of peripheral nerve injury is poorly understood I would have attempted to reduce the risk as much as possible by: (1)
performing a careful pre-operative assessment to evaluate the patient’s tolerance of the
planned operative position (probably not possible in this obtunded patient); (2) ensuring
appropriate patient positioning, particularly avoiding hip flexion beyond 90° (or beyond the
patient’s comfort level as determined by the pre-operative assessment), insufficient bending
at the knees, and excessive neck flexion (although this is not considered peripheral nerve
injury, excessive neck flexion when undergoing posterior fossa surgery in the sitting position
can lead to midcervical tetraplegia secondary to stretching of the spinal cord); and (3)
ensuring adequate padding to common pressure points, including the buttocks and peroneal
nerve at the fibular head. Post-operatively, I would perform a careful assessment of
extremity nerve function to facilitate early identification of any peripheral nerve injury.

Question 25

Nerve Injury: How would you manage this patient? What would you tell her family?

Answer 25

I would review the chart, perform a focused history, and evaluate the patient
to determine the type and severity of the injury. Depending on my findings, I would consider
a neurological consult with nerve conduction velocity studies and EMG to establish or
confirm the diagnosis. Ideally, given the preoperative mental status of the patient, I would
have discussed the risk of peripheral nerve injury with her family. At this time, I would
inform the patient and her family of my concerns and my plans for further evaluation. I
would then reassure them that most cases of peripheral neuropathy resolve within 6-12 weeks
without intervention and let them know that I would arrange for consultation with a
neurologist and the appropriate follow up care.