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40 Cards in this Set

  • Front
  • Back

preop

preop

what is VWD?

the most common inherited coag disorder, there is a quantitative and qualitative defect of VWF in the plasma




vWF mediates platelet adhesion to the subendothelium, mediates platelet-platelet aggregation, and fucntions as a carrier and stabilizer of factor VIII

types of vWd

at least 50, but the 3 most common




type 1: most common, mild, quantitative defect




type 2: qualitative defects




type 3: most severe and rare form

the family is unsure of her type of vWD or previous treatment. how would you evaluate her coag status?

i would do a H&P and chart review to try to ID the type and severity, previous transfusion requirements, bleeding episodes and signs of easy bleeding or bruising




i would order a CBC, platelets, bleeding time, PT, PTT, knowing mild disease will give near normal values, severe disease will give prolonged bleeding time, PTT, and thrombocytopenia

would you delay surgery for testing to confirm the type of VWD?

no given the urgency of the procedure i would not delay, i would assume risk of bleeding and proceed with blood products, DDAVP, cryo, FFP, and humate P (factor VIII-vWF concentrate) available

is prophylactic DDAVP indicated in this case?

there is a significant risk of bleeding in this case, and assuming i couldnt identify which type of vWD she has, i would give vWF replacement with either cryo or humate P




while DDAVP causes the release of vWF from endothelial cells, and it is effective 1st-line therapy for type 1, it provides little help in type 2A and 3, and can lead to thrombocytopenia in 2B




therefore DDAVP is inadequate for surgical prophylaxis during this surgery

what is the recommended level of vWF and factor 8 for major surgery?

its recommended to obtain initial vWF and factor VIII levels of >100 IU/dl, and subsequent dosing should maintain levels >50 IU/dL for 7-10 days following surgery

would you lower her BP prior to surgery?

since she has signs of severely elevated ICP and reduced cerebral perfusion, and since CPP = MAP - ICP, i would be worried reducing her BP could lead to reduced CP, i would instead take steps to reduce ICP prior to initiating any BP treatment

arent you concerned that her high BP will result in inc ICP, placing the patient at inc risk of brain herniation?

since CBF becomes pressure dependent with MAPs above the range of autoregulation or when its abolished, i am concerned her HTN could lead to hyperemia and inc CBF with inc in CBV and ICP, nevertheless reducing her BP places her at risk of cerebral ischemia, therefore, i would attempt to lower ICP

how would you lower ICP?

1. hyperventilate to a CO2 30


2. ensure unobstructed drainage and elevate the head 30 degrees


3. give mannitol and diuretic


4. give a corticosteroid (thought to reduce ICP by stabilizing capillary membranes around the tumor


5. give a cerebral vasoconstricting anesthetic like propofol


6. ask the surgeon to do a ventriculostomy to drain CSF


7. avoid fcators which inc ICP and dec cerebral perfusion, such as hypercapnea, sympathetic stim, hypotension, and hypervolemia

could you just quickly place a lumbar subarachnoid catheter to drain some CSF and reduce her ICP?

no i would not, draining csf from the spinal compartment in the setting of noncommunicating hydrocephalus such as in a tumor could cause a dec in pressure below the foramen magnum without a concomitant drop above, and the pressure gradient that develops between the cranial and spinal compartments in a patient with severely elevated ICP could cause tonsillar herniation




in addition, pressure measurements from a lumbar catheter are not reliable since the compartments are not communicating

how does hyperventilation dec ICP? what is your target PaCO2?

the lower CO2 causes higher CSF pH around the walls of arterioles, which leads to vasoconstriction, dec CBF, dec CBV, and lower ICP




though this effect can be attenuated by the vasoconstricting or dilating effect of anesthetics, and/or transport of bicarb into the CSF which occurs in about 6-12 hrs and limits the effectiveness of hyperventilation long term




therefore i would reduce the CO2 to 25-30, since going lower provides little benefit while increasing the risk of cerebral ischemia and other complications assoc with resp alkalosis

complication of resp alkalosis?

prolonged opioid-induced resp depression

on exam you hear a midsystolic click and systolic ejection murmur, and note premature ventricular contractions at a rate of about 3 per minute. what preop cardiac workup would you require?

the midsystolic click and late systolic murmur with PVCs are consistent with mitral prolapse with MR




in the absence of symptoms like syncope, chest pain, or fatigue, these findings would not normally warrant further workup, bit in this case i would do an echo for several reasons:




1. to determine the severity of the prolapse and MR since she cant communicate her sx


2. to see if there are any atrial thrombi, since she is most likely taking propranolol for dysrhythmic control


3. to rule out a PFO since shell be at inc risk of air embolism in the sitting position (PFO is a relative contraindication to sitting crani)

what if her condition does not allow for an echo tho?

i would proceed with the case and discuss alternative positioning with the surgeon such as prone or lat decub

would you order any premeds?

since its emergent i assume a full stomach, so id order aspiration prophylaxis in the form of H2 blocker and bicitra




considering her signs of significantly elevated ICP and altered mental status, id avoid:


1. CNS depressants which could prevent me from assessing mental status further


2. opioids which could lead to hypoventilation, hypercapnea, and further inc in ICP




i would continue propranolol and consider giving a corticosteroid to reduce ICP and/or dec CSF production

what are the current recommendations for periop antibiotics in someone with mitral valve prolapse?

MVP is no longer an independent indication for endocarditis antibiotic prophylaxis

recommendations for prophylaxis

reserved for conditions that are associated with the greatest risk of adverse outcomes from IE, including:




1. prosthetic valve or valve repair


2. previous IE


3. unrepaired cyanotic congential heart disease


4. for 6 mo following repair of a congential disease using prosthetic material


5. repaired congential heart disease with residual defects at the site of or adjacent to a prosthetic patch or device


6. cardiac transplant pts who develop cardiac valvulopathy

intraop

intraop

what monitors would you place for this case?

standard ASA monitors with capnography being esp important given the ICP




1. given her ICP id ask the surgeon to do a ventriculostamy for ICP monitoring and CSF drainage


2. given her cardiac status and the importance of maintaining CPP and monitoring CO2, id place an a line for HD monitoring and blood draws


3. given the sitting position id place a precordial doppler for VAE detection and a central line for aspirating it potentially


4. given the length of the sx id place a foley, and the potential need for diuresis related to ICP


5. esophageal temp probe to avoid hypo/hyperthermia


6. id discuss neurophys monitoring with the surgeon and neurophysiologist


7. assuming EMG was not planned, id use a peripheral nerve stimulator to ensure adequate neuromuscular blockade during the case

could you use TEE to monitor for intracardiac air?

yes it would be a good choice to monitor cardiac function and look for air




however it with other things in the mouth such as ETT, esoph temp probe, could obstruct venous drainage and cause macroglossia

the surgeon is planning ventriculostomy following induction. given the severity of her intracranial HTN, would you delay induction, intubation, and mechanical hyperventilation for placement of the a and central lines?

given her cardiac condition, her severely inc ICP along with dec intracranial compliance from the tumor, and potentially rightward shifted autoregulation curve, i want the a line before induction to more closely monitor and avoid hyper/hypo tension and ensure adequate CP




placing the central line can wait though





so would you do anything about her ICP during a line placement?

id attempt to hyperventilate her with cricoid pressure and gentle mask assisted ventilation until i establish the airway

what if the a line was a little difficult?

if i thought delaying to get the line was causing an unacceptable delay, id proceed with a BP cuff in stat mode assuming i was getting accurate cuff readings

where would you place the central line?

i would avoid the IJ due to the need to avoid head down positioning and more importantly the potential for obstruction for venous drainage from the head causing a further inc in ICP, so i would use a subclavian, and given the potential for VAE in the sitting position i would place the tip 2cm below the SVC-atrial junction to allow optimal aspiration of air

how are you going to induce this patient?

inducing a patient with significant intracranial HTN, i would have the goals to:




1. avoid hypotension which could dec CPP


2. maintain muscle relaxation and depth of anesthesia to avoid sympathetic-induced HTN and inc CBF, CBV, cerebral edema, and inc ICP


3. maintain ventilation and avoid hypoxia and hypercarbia


4. avoid anything, such as decs SVR and inc contractility which causes more complete emptying of the LV and worsens MVP/MR


5. avoid aspiration in a nauseous pt with a full stomach




so assuming a reassuring airway:


1. apply cricoid pressure


2. give lidocaine, fentanyl, and esmolol to blunt the sympathetic response to laryngoscopy


3. titrate etomodate while avoiding hypotension and give rocuronium, esnure adequate relaxation with a stim, perform careful intubation with a glidescope to minimize sympathetic stim, and be prepared to treat any HD instability

wouldnt you use sux?

i would avoid sux in this case bc even the transient inc in ICP associated with it may not be tolerated given her severely inc ICP and dec intracranial compliance from the tumor

following induction the BP drops to 88/40. are you concerned?

yes im very concerned given her significant intracranial HTN and this drop in MAP, which means a drop in CP and risk of cerebral ischemia, and im also concerned this may represent a potentially serious event other than excessive anesthesia or hypovolemia, such as:




1. tension pneumo from central line


2. brain herniation with subsequent autonomic instability


3. ventricular arrhythmias, myocardial ischemia, or HF due to worsening MR


4. anaphylaxis from ABx

after tumor resection the surgeon is unable to close the cranium bc the brain tissue is swollen. what will you do?

1. since the quickest way to relax the brain is to drain CSF, i would start draining CSF through the ventriculostomy in 10ml intervals




if this was not adequate, i would then:


2. hyperventilate to a CO2 of 30 to dec CBV


3. give mannitol or hypertonic saline to inc plasma osmolarity and draw H2O from brain tissue


4. give lasix to promote diuresis and reduce intravascular volume


5. give steroids to reduce tumor related edema


6. eliminate any obstruction to venous flow


7. ensure adequate anesthesia to prevent sympathetic induced increases in BP and CBV


8. treat excessive HTn which could lead to inc CBV


9. ensure adequate Na level, since hypoNa can cause cerebral edema

postop

postop

the surgeon asks if youll extubate in the OR deep to avoid sympathetic stim and inc ICP. would you agree?

no given her high risk of aspiration and risk for CO2 retention, id wait until she was fully awake and demonstrating the return of airway reflexes and adequate spont ventilation, also following posterior fossa tumor resection edema or hematoma could lead to worsening neurologic status in the first couple of postop days, requiring prolonged intubation

what if the surgeon needs an immediate postop neuro exam?

i would give a short acting opioid, lidocaine, and esmolol, wake the patient, perform the exam, and sedate her for transport to the ICU with the ETT in

the patient is slow to awake. what is your differential for the delayed emergence of this patient?

given her recent crani and elevated ICP, it includes:




1. hematoma formation


2. tension pneumocephalus


3. cerebral edema


4. cerebral ischemia/infarction


5. hypoxia


6. hypercarbia


7. seizures


8. obstructive hydrocephalus




and would also include things for any anesthetic like:


9. prolonged NM block


10. residual anesthetic


11. acid base or electrolyte disturbance


12. significant hypothermia

how would you manage this patient?

examine her, review ICP pressures, optimize HDs, ensure proper ETT placement and adequate ventilation, order lytes and ABG, use peripheral nerve stim to check for residual blockade, check the temp, review meds and doses given, inform the surgeon, provide supportive care, and consider CT or MRI




if i thought this was from inc ICP, id consider draining CSF, hyperventilating more if possible, giving mannitol, lasix, or steroids

assuming you did not use nitrous during the case, could her delayed awakening be due to tension pneumocephalus?

while N2O after dural closure can inc the volume of any trapped intracranial air, it can also happen in the absence on nitrous, most often with post fossa cranis in the sitting position with air moving over the brain and becoming trapped in the upper cranium, and is worsened if aggressive measures are taken to dec brain swelling during the case

on POD2, the nurse calls and reports the patient has impaired dorsiflexion of the right foot. what do you think is the cause?

this is a foot drop injury, which could be due to dorsiflexor muscle injury, peripheral nerve injury, stroke, neuropathies, drug toxicities, or diabetes




given the sitting position, id consider injury to the sciatic or common peroneal nerve, such as from:


1. stretching of the nerve with excessive flexion of the hips or insufficient bending of the knees


2. compression injury from inadequate padding




considering her recent crani and inc ICP, id also consider parasaggital cortical or subcortical cerebral infarction

what are the risk factors associated with peripheral nerve injury?

male


hospital stay >14 days


intraop hypotension


hx of vascular dz or HTN


Dm


smoking


very thin or obese body habitus

prognosis?

fortunately more than half of all patients who develop this regain full sensory and motor function within 1 yr

if this was peripheral nerve injury, could it have been prevented?

while the cause is likely multifactorial and some injuries my not be preventable, the risks can be reduced by:




1. doing a careful preop assessment of the patients tolerance to the position


2. ensuring appropriate positioning, avoiding hip flexion >90, insufficient knee bending, and excessive neck flexion


3. pad all common pressure points, including the buttocks and the peroneal nerve at the fibular head


4. postop perform an assessment to early ID any injuries

how would you manage this patient? what would you tell her family?

i would review the chart, take a history, and do a physical to determine the type and severity of the injury




depending on the findings, i would consider sending her for EMG and nerve conduction studies to confirm the diagnosis




i would have ideally discussed the risks of this with her family preop, and at this time i would inform them of my concerns and plans for further workup




i would reassure them that most cases resolve within 6-12 weeks without intervention, and let them know I would arrange for consult with a neurologist and the appropriate followup care