Neuro II Flashcards

1
Q

Preoperative evaluation for neuro surgery?

A
  • Underlying medical conditions
    • Ex: Patent Foramen ovale- specific for sitting position/high risk VAE (sx near dural sinus)
  • Procedure length and position
  • Question optimized for surgery
    • Ex: subarachnoid hem, trauma pts → on mannitol, 3% NS, blood products
  • Negotiate hemodynamic/ventilation & position goals with surgeon
  • Determine need for:
    • Abx
    • Steroids- only for tumors (normalize edema ring → improve outcomes)
    • Diuretics
      • Bolus mannitol/3% NS prior to start
    • Anticonvulsants- Prophylactic admin
      • Common w/ trauma (brain exposed to blood)/brain tumors
        • Ex: phenytoin, phenobarb
  • Carefully assess fluid and electrolyte status – correct pre-op
    • Glucose levels: 90-180 mg/dL in diabetic patients
    • Avoid changes in Na+ > 3-4 mEq/L per hour (central pontine myelinolysis)
    • Plt count >100,000mm3
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2
Q

Considerations for neuro assssment?

A

where are they on compliance curve?

  • Level of consciousness
    • Awake/alert → can tolerate extra volume
  • ICP
    • Headache
    • Nausea
    • Papilledema
    • pupil size
    • respiratory pattern
      • any ICP issues → TIVA (propofol) approach
      • avoid hypoventilation/CO2 increase
  • Neurological deficits
    • Ex: look at brain – is it bulging?
  • MRI or CT results
  • Location of lesion
  • Surgeon’s impression of intracranial compliance and VAE risk
  • Supratentorial disease= ICP mgmt. problems
  • Infratentorial lesions = mass effects on vital brain stem structures w/ elevated ICP d/t obstructive hydrocephalus
  • ICP derangements can be identified radiologically – “slit ventricles” or shift in midline brain structures of more than 5mm – advanced pathology
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3
Q

Interventional neuroradiology uses, benifts, risks?

A
  • Emerging as the standard of care in some populations
    • International Subarachnoid Aneurysm Trial – meta analysis support widespread use of the this approach
      • most now repaired this way
      • *Grade 1 & 2 → better outcomes than open repairs
    • Uses: Angiography & embolization/devascularization of aneurysms, AVMs, brain tumors & spinal cord lesions
      • Technique: Insertion of occlusive material (detachable platinum coils, cyanoacrylates, “Onyx liquid embolic system,” & polyvinyl alcohol particles
      • Vasospasm treatment, Balloon angioplasty, thrombectomy (acute stroke), or endovascular stenting of occlusive cerebrovascular disease & extracranial carotid disease (often anti-plt therapy 5-7 days pre)
  • IR benefits:
    • Lower risk infection
    • Lower 3rd spacing
  • IR risks:
    • Sudden hemorrhage → space occupying lesion/hematoma
    • Stents/coils deployed to wrong place → occlusive
    • Vascular injury
  • Open procedures necessary:
    • Wide neck aneurysm
    • Abnormal anatomy
    • Disease/occluded vessels → cant pass catheters
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4
Q

Goals of neuro interventional radiology?

A
  1. GA not always required
    • conscious sedation often appropriate depending on procedural complexity
      • GA: TIVA vs VA (dep on intracranial compliance)
      • Sedation: fentanyl, midaz, propofol, precedex
        • Precedex issues:
          1. Interfere w/ cog testing
          2. HoTN
  2. Control sedation or anesthetic level for prompt neurologic evaluation
    1. Choosing → How important for neuro eval and can pt stay still?
  3. Keep the patient from moving during the procedure!
    • Mapping important
  4. Have the ability to manipulate cerebral hemodynamics on demand to meet procedural needs
    • Ex;
      • Alter CO2: Hyper/hypoventilate → change perfusion to certain area in brain
      • HyoTN → Use VA, propofol, esmolol, NTG/NTP (stronger)
    • Stent Deployment → Expect HoTN and bradycardia (pharmacologic

treatment)

  • INR procedures w/ IV sedation:
    • Ex: diagnostic angiography, carotid angioplasty and stenting, AVM embolization, etc.
      • GA required: intracranial angioplasty, embolization of aneurysms, uncooperative patients, etc.
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5
Q

Intervnetional neuroradiology procedure considerations? monitors needed?

A
  • 6-7 Fr gauge sheath in femoral artery
  • Anticoagulation utilized ~ 24 hrs: Heparin
    • Need preop baseline coag panel!
    • Dose: 3000-5000 units Heparin + infusion
      • ACT 1.5-2.5 X baseline
        • Catheters are foreign bodies → clot!
  • Extensions on ventilation & IV tubing- bed turned 90-180 deg
  • Monitors:
    • ETCO2- manipulate for radiologist
      • Patho: Lesions = local vasodilation surrounding
        • Hyperventilate → vasoconstrict vessels aroung healthy brain to lesion (receiving device)
    • Art BP- manipulate for radiologist
      • HoTN → asked when deploying occlusive material/coil/glue (greater control)
        • Don’t want HTN d/t pushing occlusive material beyond intended area
    • Bilateral LE pulse oximetry
      • If use femoral artery → assess vasospasm, thromboembolism, mechanical obstruction
  • May have to alter anesthetic plan:
    • EEG
    • evoked potentials
    • transcranial doppler
    • awake patient feedback
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6
Q

What are some sudden and severe complications in interventional neuroradiology?

A
  1. Hemorrhagic
    • Protamine
      • Dose: 1 mg per 100 units heparin admin
    • Controlled HoTN
      • Deepen anesthetic
      • Esmolol
      • NTG
      • NTP
  2. Occlusive – device (coil/balloon) deployed to unintended area → worry of ischemic damage distal to occlusion
    • Deliberate HTN – enhance collateral flow through CoW.
      • BP > 30-40% baseline or until neurologic symptoms resolve
        • Phenylephrine
        • Dopamine
    • Direct thrombolysis
  3. Anaphylaxis
    • Contrast media = anaphylaxis risk
      • Admin Epi
      • 3rd spacing → have fluids available
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7
Q

Overall goals for treatment in interventional neuroradiology?

A
  • Overall treatment → Neuroprotective measures
    • Hyperventilate – decrease ICP
      • ETCO2 26-30 mmHg
    • Rapid fluid admin – for hemorrhagic
    • Diuretic admin
      • Mannitol 0.5 g/kg
    • Anticonvulsants
      • Phenytoin
      • Phenobarb
    • induce Hypothermia (33-34 deg C)
    • EEG suppression- TPL coma (burst suppression)
      • reduce CMRO2 → preserve marginally perfused cells
        • Ensuring O2 going to maintenance of cell integrity
    • HOB 15 deg and neutral
  • Make sure you have access to all of these agents in the event of an emergency because rapid response will be required. Hypothermia to 33-34 degrees C B6th767
  • For deliberate hypertension consider phenyephrine or dopamine – get BP 30-40% > than baseline or until neurologic symptoms resolve. For controlled hypotension consider esmolol, NTG or NTP. Dose of protamine is 1mg for each 100U heparin given. Head up 15 degrees and neutral, PaCO2 around 28-30mmHg, give 0.5g/kg mannitol, rapid IV infusion, phenytoin and phenobarbital, TPL coma (burst suppression), temp 33-34C.
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8
Q

What are supratentorial tumors? symptoms?

A

Pathophysiology

  • Supratentorial – located ABOVE tentorium
    • Tentorium: process of dura mater between cerebrum and cerebellum supporting the occipital lobes (cerebellum and occipital lobe)
    • Most common for craniotomy
    • Ex:
      • Meningiomas-
        • large size
        • difficult location
        • highly vascular → considerable BL
          • surgically challenging → lengthy procedure
        • Necrotic hemorrhagic core
        • Wide border of brain edema
          • increased bulk
          • increased impaired autoreg area
      • Gliomas (oligodendrogliomas, astrocytomas)
        • Easy access location
        • Less vascular – less bleeding risk
        • Hard to get clear margins → often reoccur (often “Debulking procedures”)
      • Metastatic lesions (breast, melanoma, lung, kidney)
      • Chronic subdural hematomas-
        • Space occupying lesions → displace other structures (specific symptoms or HA or Sz)
  • Symptoms:
    • ICP problems. Small changes in BP= big changes CBF/ICP
    • appear when compensatory mechanisms exhausted by growing lesion
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9
Q

Considerations for supratentorial tumors

A
  • Consider tumor location & size (blood loss & surgical position)
    • Locations:
      • Hypothalamus: SNS disturbance, altered LOC, temp, fluid reg, DI, cerebral salt wasting syndrome
      • Dural sinus: concern for VAE
        • Low risk except lesions encroaching on sagittal sinus
    • Size: Ability to displace structures
      • → ICP increase risk → CPP/herniation issues**
        • Generally: tumors = vascular
          • Necrotic hemorrhagic core
          • Wide border of brain edema (ischemic penumbra)
            • increased bulk
            • increased impaired autoreg area → maintain CPP
        • Tx: Steriods 24-48 hrs prior
          • stabilize edema ring
          • stabilize BBB
  • VAE risk:
    • Low, except lesions encroaching on sagittal sinus
  • Small changes in BP = big changes CBF/ICP
    • Impaired autoregulation area near tumor
  • Bilateral Subfrontal approach (retraction/irritation frontal lobes) - “frontal lobey
    • Consequence of frontal lobe retraction
      • delayed emergence
      • disinhibition
      • both (delayed emergence & disinhibition)
    • Considerations:
      • reduced IV anesthetic drugs (lower midaz/opioids)
        • to ensure whether its cognitive irritation or too much sedative
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10
Q

Anesthesia considerations for craniotomy for supratentorial, intracrnail tumors?

A
  • Control ICP (*top priority*)
    • Institute measures before open dura → then visually assess
  • Diuretics
    • Mannitol: 0.25-1.5 g/kg
    • 3% NS: 50-100 ml/hr
      • hourly Na+ checks → don’t change levels too fast
  • Corticosteroids
    • Dexamethasone: 10 mg q6hrs (48 hrs before and during case)
  • Hyperventilation
    • Goal: PaCO2 ~ 25- 30 mmHg
    • AVOID: PaCO2 < 25 mmHg → too much vasoconstriction (ischemic brain)
      • Aline → obtain CO2 gradient (assume 5 mmHg gradient in ABG and ETCO2)
  • Optimize hemodynamics
    • CPP adequate
  • Normovolemia
    • Avoid hyposmolar fluids
      • Ex:
        • Plasma = 295
        • LR = 273 mOsm/L (hyposmolar)
          • AVOID
        • *NS= 308 (hyperosmolar)
          • Hyperchloremic metabolic acidosis
        • *Plasmalyte/Normosol = 294 (isosmolar) <<< ideal choice
  • Normal blood glucose
    • Hyperglycemic → promotes anerobic metabolism → increase brain damage
  • Improve venous return (positioning)
    • HOB elevated 10-15 deg (adequate venous drainage)
    • Avoid PEEP
  • TPL, propofol
    • Parallel dec in CMRO2 & CBF
  • Mild hypothermia
    • Keep paralyzed → Prevent shivering
    • Rewarm slowly
  • Prevent coughing and bucking → could herniate through craniotomy
    • deep anesthesia
    • muscle relaxants
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11
Q

Preoperative preparation for supratentorial intracranial tumors

A
  • Pre-op LOC and CT scan evaluation
  • Medication regimen (hx of seizures, decadron 24-48 hrs?, mannitol or hypertonic saline)
    • Possible Lymphoma diagnosis → consider holding dexamethasone
      • Result in tumor lysis and complicate diagnosis.
  • Pre-medication w/caution if ICP ↑
    • Hypoventilation → ↑ PaCO2 → ↑ CBF → ↑ ICP
  • Routine monitors & arterial line (often pre-induction)
  • 2 large bore PIVs
  • Consider right atrial line to measure CVP if major blood loss or VAE concerns
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12
Q

Induction considerations for supratentorial intracranial tumor?

A
  • Place A line pre/post
    • Transducer at external auditory meatus (pressure perfusing CoW)
  • Optimize ICP
    • Caution w/ sedatives (hypoventilation)
  • Deep induction (avoid ICP change)
    • Lidocaine 1.5 mg/kg
    • Fentanyl 3-5 mcg/kg
      • Liberal → most pain @ case beginning (incision, bone flap, dura)
        • No pain receptors on brain → little surgical pain
    • Propofol 2 mg/kg
      • Small bolus right before intubation too (0.5 mg/kg)
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13
Q

Maintenance of supratentorial intracranial tumors

A
  • VA < 0.5 MAC
    • 1 MAC: Vasodilates → ↑ CBV (ok if brain looks ok)
  • Propofol drip 150 mcg/kg/min
  • Propofol 0.5-1 mg/kg
    • Pin placement → pain
      • Opioids
      • Esmolol
  • ABG – early
    • See CO2 gradient
  • Mannitol 1 g/kg
  • Dura open
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14
Q

Emergence supratentorial intracranial tumor

A
  • smooth
    • NO REVERSAL until pins out/head dressing on
    • Avoid → ↑ risk hemorrhage/edema
      • Shivering
      • Pain
      • Bucking
      • HTN
    • LTA
    • Precedex
      • Caution w/ HoTN
  • Overall:
    • Drugs easily titratable/adjust!
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15
Q

What is an infratentorial/posteiror fossa intracranial tumor? Symptoms?

A
  • BELOW tentorium
    • Small space
    • Structures of posterior fossa include: → when interrupted cause MAJOR problems
      • Medulla
      • Pons
      • Cerebellum
      • Major motor/sensory pathways
      • Primary resp/CV centers
      • Lower cranial nerve nuclei
        • Ex: Significant CV responses***
          • HTN
          • HoTN
          • Bradycardia
          • Tachycardia
  • Other symptoms:
    • Preop dysphagia
    • laryngeal dysfunction
    • respiratory abnormalities
    • chronic aspiration
  • More common in children (ex: medulloblastoma, pilocytic astrocytoma, ependymoma, brainstem glioma)
  • In Adults: acoustic neuromas, metastases, meningiomas, and hemangioblastomas
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16
Q

Posterior fossa tumor monitoring?

A
  • Good communication w/ surgeon!! → very small surgical space
  • Warning signs of damage to adjacent cranial nerve nuclei & respiratory centers:
    • Bradycardia & hypotension
    • Tachycardia & hypertension
    • Bradycardia & hypertension
    • Ventricular dysrhythmias
      • Communicate!! Represent damage to pons/lower medulla
        • don’t treat dysrhythmias but talk with surgeon!
  • Dissection on floor of 4th ventricle
    • Possibility of injury to cranial nerve nuclei & swelling
      • Even small swelling has large consequence since sx area small
        • CN dysfunction IX, X, XII
    • Consequences: → extubate? Go to ICU for monitoring
      • upper airway patency loss
      • cranial nerve function loss
      • respiratory drive loss
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17
Q

Positioning and monitoring for infratentorial tumor?

A
  • Positioning:
    • Sitting, lateral, prone, park bench, or three quarters prone position (keep in mind CV effects and complications
      • Quadriplegia
      • Macroglossia
      • Pneumocephalus
      • VAE (incidence 39% in sitting position)
      • PAE
  • ECG- alterations rate, rhythm
  • Arterial line (CPP and brain stem alterations)
  • BAEP/SSEP may be monitored
    • TIVA (propofol) → wont interrupt monitors
  • MEP or Electromyographic monitoring of facial nerve
    • Need at least ~2/4 twitches on TOF at least
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18
Q

Induction considerations for infratentorial tumor?

A
  • Tumor detection → compression of vital areas
    • Baseline AW patency issues
    • CV
    • Dysphagia
    • Chronic aspiration
      • *RSI
      • *Resolve pulmonary infection 1st
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19
Q

Maintenance/emergence consideratiosn for infratentorial/posterior fossa tumor?

A
  • Maintenance:
    • Positioning
      • Sitting/HOB elevated →
        • central line/CVP cath
        • Doppler
        • ETCO2 detection
    • Monitor Aline → surgical interventions affecting rhythm
  • Emergence: → ICU for >24 hrs
    • Issues:
      • Edema
      • Hemorrhage
      • Obstruction hydrocephalus
      • CV/Resp changes
      • LOC changes (any signs need to come back for decompression)
    • Extubation:
      • Awake/alert
      • Ready to reintubate if needed
  • Choose anesthetics with cardiovascular performance in mid.
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20
Q

Anatomy/physiology review of pituitary gland?

A
  • Pituitary gland
    • lies in sella turcica (bony cavity in sphenoid bone) at skull base of skull
      • very close to optic chiasm, carotids, cavernous sinus (CN III, IV, VI) → very close to structures (hemorrhage possible!)
  • Anatomy: 2 Lobes
    • Anterior (adenohypophysis) lobe
      • Regulation: hypothalamus via complex portal vascular system
        • GH
        • PL
        • PSH
        • LH
        • ACTH (adenocorticotropin)
        • B-liptropin
        • Thyrotropin (TSH)
    • Posterior (neurohypophysis) lobe
      • Regulation: Infundibular stalk - connects posterior lobe to hypothalamus
        • ADH
        • Oxytocin
  • Hypothalamus regulates anterior lobe via through regulatory peptides, (hypothalamic releasing and inhibiting factors) that reach the anterior pituitary via complex portal vascular system. Hypothalamic secretion is complex and occurs from neuronal and chemical influences, including feedback from target organ hormones. The posterior pituitary = 2 hormones ADH and oxytocin which are synthesized in specialized hypothalamic neurons and transported as granules in axons down the pituitary stalk to the posterior pituitary gland. Anterior hormones are GH, PL, FSH, LH, ACTH (adrenocorticotropin), B-liptropin, thyrotropin (TSH)
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21
Q

What are functioning vs non-functioning tumors?

A
  • 1. NONFUNCTIONING
    • diagnosed when large and causing symptoms by impinging on adjacent structures (ICP issues)
      • ex: chromophobe adenomas, craniopharyngiomas, meningiomas
        • s/s: ICP, HA, visual changes, cranial nerve palsies
  • 2. FUNCTIONING
    • diagnosed when small symptoms related to production of an excess of 1 or more anterior pituitary hormones
      • ex: prolactinomas followed by GH and ACTH – secreting adenomas
        • s/s:
          • Prolactinomas: amenorrhea, impotence
          • GH:
            • Before puberty → gigantism
            • After puberty → acromegaly
          • ACTH: cushings dx (excessive cortisol) from bilateral adrenal hyperplasia
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22
Q

Preop assessment of pituitary tumors

A
  1. Panhypopituitarism?
    1. Tumor compressing gland → not secreting enough hormone
      1. Tx: Correct hypocortisolism & hyponatremia; hypothyroid, etc.
      2. Can rupture and be emergency
  2. Acromegaly?
    1. Evaluate airway, cardiac function (arrhythmias and hypertrophic cardiomyopathy)
      1. AW enlargement: Enlarged tongue, narrow glottis, hypertrophied nasal turbs, mandible enlargement, glottic stenosis
        1. Tx: fiberoptic intubation → diff AW d/t growth
          1. ½ size smaller ETT d/t glottic stenosis
      2. CV enlargement:
        1. Hypertrophic cardiomyopathy
        2. Arrythmias
  3. Cushing’s Disease?
    1. Evaluate- CV workup
      1. DM
      2. OSA
      3. hyperaldosteronism (hypokalemia and metabolic alkalosis)
      4. HTN
      5. CHF
      6. obesity
  • Know size and location of tumor
    • Ex: functioning/nonfx
      • Pituitary microadenomas = no mass effect (fxing type → no ICP issue)
      • Pituitary tumors w/suprasellar involvement- nonfxing
        • Larger → evaluate for ↑ ICP
  • Clear dexamethasone with surgeon –
    • false positive for post-surgical hypopituitary function
  • Visual exam
    • assess optic nerve integrity
  • Transsphenoidal
    • nasal culture → ABX
  • SIADH with sellar tumors (low sodium with fluid overload) → preop correction
    • Tx: Demeclocycline (tetracycline)
      • inhibits ADH activity at renal tubules (see on med list)
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23
Q

Anesthetic considerations for pituitary tumor?

A
  • Monitors
    • standard +/- arterial line (working around carotids/venous sinuses)
  • Position
    • Supine
    • VAE precautions (doppler + right atrial line) if >15 degree surgical site-heart gradient
  • Pharyngeal pack
    • Placed by surgeon → document pack removed after sx
  • ETT
    • RAE
    • secured lower jaw
    • opposite site surgeon dominant hand
  • Transcranial Approach:
    • > ICP mgt VS transsphenoidal
    • Brain retraction → brain irritation risk (sz, DI, blood loss)
  • Transsphenoidal Approach: incision under upper lip, through nasal septum
    • Better M&M
    • High risk:
      • CSF leak
      • Meningitis
    • LA: 4 % cocaine & 2 % lido w/epi infiltrated èwatch dysrhythmias
      • Cocaine: inhibits NE reuptake → vasoconstriction/analgesia
  • CO2 management – depends on surgical goals
    • Ex: Hypocapnia → minimize brain volume → minimize arachnoid bulge degree into sella
    • Ex: Hypercapnia: larger tumor w/ suprasellar extension = normal/increased CO2 → deliver lesion into sella for excision
  • VEP monitoring – MOST sensitive to VA
    • Optic nerve and chiasm
  • C-Arm Fluoroscopy
    • head & hands inaccessible after drape
      • Peripheral Nerve Stim on LE
      • IVs and Aline working well after tucking
      • Check compression of C Arm on body (nerve damage)
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24
Q

What are some considerationg for emergence following pituitary surgery?

A
  • Smooth emergence - especially if CSF space has been opened
    • Issues → Meningitis r/t CSF leak!!
      • Valsalva maneuvers (coughing/vomiting) may contribute to reopening of a CSF leak and worsen the risk for subsequent meningitis
  • Suction well
    • AW cleared of debris, including formed clots
    • Packs removed
  • Visual acuity should be assessed pre-extubation
  • Nose packed – remind patient to breath through mouth
  • fully awake extubation
    • LTA
    • Propofol bolus

notes:

  • Smooth emergence, especially if the CSF space has been opened (and resealed with fibrin glue or by packing the sphenoid sinus with fat or muscle). Valsalva maneuvers, as with coughing or vomiting, may contribute to reopening of a CSF leak and worsen the risk for subsequent meningitis. Inspect the pharynx with a laryngoscope. The airway should be cleared of debris, including formed clots. allows one to more confidently extubate promptly at the first signs of reactivity to the endotracheal tube.
  • The chosen anesthetic technique should permit gross visual acuity exam before pt. extubated. If visual acuity is worse then may need emergent decompressive surgery.
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25
Q

What are some complications of pituitary surgery?

A
  • CSF Leak/Rhinorrhea – meningitis (transsphenoidal*)
  • Damage to Surrounding Structures-
    • CN 3-6
    • cavernous sinus
    • internal carotid
    • hypothalamus
    • optic nerve
    • Optic chiasm
  • Pituitary/Adrenal Axis Malfunction – dexamethasone followed by prednisone for 5 days post-op or until testing clears pt.

Pituitary Surgery: Complications- Diabetes Insipidus

  1. Development: 12-48 hrs postop
    1. rarely arises intraoperatively
  2. Diagnosis:
    1. Polyuria: 2-15 L/day
    2. rising serum osmolality: > 300mOs/kg
    3. specific gravity: < 1.005
  3. Treatment:
    1. 1/2NSD5W = Hourly maintenance fluids plus 2/3 previous hour’s urine output.
      1. (or hourly urine output minus 50 mL plus maintenance)
    2. Hourly requirement > 350-400 mL → add desmopressin (synthetic ADH)
      1. DDAVP: 0.5-1.0 uG IV/SQ
  • One of the important surgical considerations is the avoidance, when possible, of opening the arachnoid membrane. Postoperative CSF leaks can be persistent and are associated with a considerable risk of meningitis. In situations in which one is concerned that a persistent CSF leak may occur, some surgeons will place a lumbar CSF drain to maintain CSF decompression in the early postoperative period.
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26
Q

Interentions with intracranial aneurysms/SAH?

Risks? Grading?

A
  • Discovered pre-rupture:
    • *elective endovascular coiling (favored approach)
    • surgical clipping used
  • Subarachnoid hemorrhage
    • CoW aneurysm rupture:
      • 1/3 functional survivors
      • 1/3 die before hospital
      • 1/3 vegetative state
    • Operative clipping versus the endovascular approach in IR
  • Risks: 50’s (peak risk), female, HTN
  • Aneurysmal SAH surgical risk and outcome predicted via grading systems
    • World Fed. of Neurosurgeons – 1-5 based on GCS and Motor Deficit
      • 1-2: less severe (more favorable in outcome)
      • 4-5: severe
    • Hunt and Hess (clinical symptoms)
    • Fisher Grade (radiologic bleeding)
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27
Q

Symptoms of intracranial aneurysm/sah? Diagnostic?

A
  • Symptoms:
    • N/V
    • severe HA
    • stiff neck
    • photophobia
    • LOC
      • Blood + subarachnoid space = abrupt increase ICP
      • Pressure increasing → SNS response → increase catecholamines
        • HTN
        • dysrhythmias
  • Dx: CT scan, angiography = size and location
    • Small < 10 mm
      • > 6 mm require treatment
    • Large 10-24 mm
    • Giant > 24 mm
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28
Q

ECG changes associated with SAH?

A

Canyon T waves

  • Hemorrhage → body recognizes threat → catecholamine surge
    • NE/Epi → Heart exposed → dysrhythmias
      • Canyon T Waves – dips in T waves
  • Other common changes
    1. ST depression or elevation
    2. T wave flattening
    3. U waves
    4. Prolonged QT
    5. Dysrhythmia
  • w/in 10 days resolves
  • Increase CV enzymes
29
Q

What are some complications of intracranial aneurysms/SAH?

A
  • Intracranial HTN
    • Emergency ventriculostomy
    • Diuretics- 3% NS/Mannitol
    • Intubation (higher grades 3-5)
      • LOC issues
    • Hyperventilation
      • Prevent herniation short term (> 6 hrs → Bicarb tx to brain to normalize pH)
  • Hydrocephalus
    • Obstructive- hematoma blocking flow through ventricular system or Hgb clogs arachnoid villi preventing flow out
      • V/P shunt placement
  • Rebleeding
    • Most common cause of death in hospitalized SAH patients
    • Risk: Spontaneous rebleed
      • 1st 24 hrs = 4% risk
      • > 24 hrs = 1.5%/day
        • 19% over 2 weeks
  • Cerebral Vasospasm
    • Max risk days 3 to 14 post-rupture
      • Highest risk: 7 -10 day (avoid sx these days → worst outcomes)
    • Mechanism unknown. – structural and pathologic changes have been demonstrated in the vessel wall. Removal of extravasated blood decreases the occurrence and severity of ischemic deficits. Oxyhemoglobin thought to be the blood component responsible for vasospasm
      • Theory: Exposure of cerebral vessels to blood promotes vasospasms
        • Remove blood to decrease risk
    • Symptoms: 30% symptomatic (occurs in 70% of pt)
      • HA, increase BP, confusion, lethargy, focal motor speech impairment
        *
30
Q

What is typical surgical managmenet of intracranial aneurysms?

A
  • Contemporary management = early (
  • Ideally to OR w/in 18-24 hours
  • If early intervention not feasible: surgery delayed 10-14 days (beyond max risk vasospasm period)
    • Ex: days 4-12 after SAH
  • Early intervention pros:
    • decrease risk of rebleed
    • decrease risk of vasospasm
    • better tolerance of vasospasm treatment if needed
    • less bedrest
  • Early intervention cons:
    • more hydrocephalus/edema
    • more ICP issues
    • clot poorly organized
31
Q

Diagnosis of cerebral vasospasm? Treatment?

A
  1. Diagnosis: angiography/transcranial doppler
    • HA
    • HTN
    • Confusion
    • Lethargy
    • Focal motor/speech deficits
    • Coma
  2. Nimodipine (CCB): standard prophylactic therapy
    • Improved long-term outcomes
  3. “Triple H Therapy”- less popular
    • Hemodilution
    • HTN (increase SBP 20-30mmHg)- phenylephrine
    • Hypervolemia (traditionally hypervolemia thought to help, now moving towards euvolemia and HTN as mgmt)
    • Euvolemia
      1. → more likely to bleed tho
      2. HTN and euvolemia more recent preference for therapy
  4. Cerebral balloon angioplasty or intra-arterial vasodilators (verapamil, nicardipine. Milrinone, papaverine, etc.)
  5. Promising new approaches –
    • PDE (cilostazol): platelet inhibitor and vasodilator: small Jan 2013 non-blinded trial
      1. Findings: decrease vasospasm and delayed cerebral infarction
    • TXA- Crash 3 Trial just published October 14th 2019 highly favorable
      1. – will probably become standard of care in TBI
    • Fibrinolytics- increase incidence of ischemic symptoms and hydrocephalus
      1. Miller 9th → don’t cite any convincing studies
    • Endothelin A receptor antagonist- Improved mortality did not improve long term functional outcomes
    • Magnesium- large randomized trial did not show a benefit
    • Statins - meta-analysis not significant…. larger trial failed to demonstrate significant reduced incidence of cerebral ischemia and death
32
Q

Preop considerations intracranial aneurysms/SAH

A
  • Note severity, acuteness, stage of SAH
    • Grade 1-2 bleed → favorable outcome
    • >3 bleed → intubated, LOC
  • Surgery Timing
    • Difficulty swallowing? Pneumonia/DVT risk?
  • ICP status
  • Assess for hypothalamic dysfunction and sympathetic over-activity
    • CoW near hypothalamus → rupture → SNS overactivity, temp regulation issues, EKG changes, endocrine/electrolyte imbalances
  • Assess Fluid Status:
    • SIADH - too much ADH →
      • intravascular volume expansion
      • low Na
        • tx: Volume restriction
    • Cerebral salt wasting syndrome
      • contracted intravascular volume
        • hyponatremia after SAH is more likely to be consequence of cerebral salt-wasting syndrome d/t release of a natriuretic peptide by the brain (similar ot hear)
        • triad of hyponatremia, volume contraction, and high urine sodium concentration
      • Pt excrete Na (low Na) → water follows Na → dehydration
        • Tx: Fluid replacement
33
Q

What are the major anesthetic goals for management of intracranial aneurysm/SAH?

A
  1. Acute HTN = risk of rerupture = often FATAL
    • Risky times:
      1. Intubation
      2. Mayfield pins
      3. surgical stimulation
    • Keep DEEP and tx HTN
      1. Preinduction aline
  2. Brain relaxation facilitates surgical access
    • Measures reducing ICP:
      1. ETCO2 25-30, PaCO2 ~30
      2. mannitol prior to opening dura – 1 g/kg
      3. TIVA
      4. Avoid VA > 0.5 MAC
  3. High-normal MAP
    • → prevent critical reduction of CBF to ischemic penumbra around SAH
      1. Ex: allow lower during critical periods but after want high/normal
  4. Tight MAP control as surgeon clips aneurysm and/or controls bleeding from a ruptured aneurysm
    • Promote collateral flow
    • Lower BP ex: Propofol 1 mg/kg to deepen
      1. dec CMRO2 to burst suppression level
      2. reserving all O2 to cellular integrity
    • MAX safe clamp time (during “trapping”) = 14 minutes (@ nml temp and BP)
      1. > 30 min → 100% brain damage incidence

Be prepared: Major intraoperative complication = hemorrhage!!!!

34
Q

Why do we not routinely utilize controlled hypotension during aneurysm repairs?

A
  • Has been completely replaced with temporary clipping; Now reserved for emergency bleeding and during AVM embolization
    • Max reduction of MAP to 40-50mmHg
      • need to be prepared to decrease BP rapidly if needed during the case.
  • Surgeon may request an increase in BP during temporary arterial occlusion/clip (phenylephrine drug of choice)
    • Max collateral flow
35
Q

Consideratiosn during surgical clipping of the aneurysm?

A
  • Adenosine 0.3-0.4 mg/kg
    • temporarily halt circulation while a permanent clip is placed on the aneurysm
      • have fib pads
  • Burst suppression w/
    • Propofol 1-2 mg/kg (w/ phenylephrine → reduce CMRO and support CPP) or
    • VA
  • Temporary occlusion - < 14 minutes
  • Mannitol
    • Additional 1g/kg 15 minutes before temporary occlusion
    • might have CBF enhancing effect during periods of CBF reduction
  • SSEP and MEP – monitoring ischemic changes
    • Communicate propofol bolus
  • IF a rupture occurs…. Preparation must occur before the episode of bleeding- immediate control of MAP 40-50 mmHg range may be required
  1. Deep isoflurane VS adenosine VS sodium nitroprusside infusion prepared before induction
  2. Normovolemia prior to bleeding episode essential
    1. Don’t aggressively fluid load before aneurysm clip
  • After hemorrhage – once temporary clips have been applied normal BP is desirable. If the surgeon is unable to temporarily occlude the bleeding aneurysm and blood loss is not excessive can lower MAP to 50mmHg or lower to assist the surgeon to gain control of the bleed. Judgment call – if blood loss is excessive fluid resuscitation must be accomplished before using drugs to lower BP
36
Q

What is important to remember about autoregulation around ischemic penumbra?

A

(i.e. be careful with controlled hypotension!)

  • Ischemic penumbra – no autoregulation
    • Pressure passive
      • Ex: MAP 50 → low CBF
      • Want high/normal MAP to get CBF close to 50 (requires much higher MAP)

Normal and absent autoregulation curves. The “absent” curve indicates a pressure-passive condition in which cerebral blood flow (CBF) varies in proportion to cerebral perfusion pressure. This curve is drawn to indicate subnormal CBF values during normotension as have been shown to occur immediately after both head injury and subarachnoid hemorrhage. The potential for modest hypotension to cause ischemia is apparent.

37
Q

Monitor and induction consideratiosn for intracrnail aneurysm/SAH?

A
  • Monitors:
    • SSEPS – impact anesthetics
    • Aline- REQUIRED
    • CVP (higher grades) – 10-12 mmHg
  • Induction: how prevent rebleeding? Minimize ICP changes!
    • Agents suppressing intubation response (need deep!)
      • Lido 1.5-2 mg/kg
      • Esmolol – prevent rebleeding at only induction
        • Labetalol (long 1/2L and after this want high/N MAP)
      • Propofol* high dose
      • Etomidate (poor EF)
      • Opioid
38
Q

Maintenance and emergency concerns for intracranial aneurysms?

A
  • Maintenance:
    • Deep for pins, scalp incision, turning bone flap, clipping (dec CMRO + robust BP to promote collateral BF)
    • *SEVO –
      • Des- catecholamine surge (HTN)
    • Burst suppresion during clipping/aneurysm exposure 1-2mg/kg propfol + 100-150 mcg/kg/min + vasopressor to maintain CPP
    • Mild hypothermia – completely relaxed and rewarmed after
      • (32-34degrees C)
    • Prior to dura opening:
      • Hyperventilate
      • Mannitol
      • Antisz med
  • Emergence:
    • Grade 1-2: Extubate
    • Higher grade: remain intubated
39
Q

What are AVMs? S/S?

A
  • Congenitally malformed blood vessels form an abnormal communication between arterial and venous systems
  • No intervening capillary bed = shunting blood from surrounding brain = ischemia
  • Clinical manifestations:
    • parenchymal hemorrhage or SAH (10-30% mortality)
    • focal epilepsy
    • progressive focal sensory-motor deficits
      • 50% pts experience seizures – preventative anti-seizure medications common
  • Statistics:
    • Males > Females
    • onset 10-40 yo
      • hemorrhage risk: 1-3% per year.
      • Rebleed 6% 1st yr
      • 2% each subsequent year.
      • Mortality from 1st hemorrhage:10-30%.
40
Q

Management options for AVMSs?

A
  1. Surgical excision
  2. IR Embolization
    1. Staged repair: embolization → surgical excision to ensure CBF not changed dramatically
    2. Technique:
      1. MAC- allow neuro exam and complication dx
        1. Uncomfortable as embolize → get asleep for that part
  3. Stereotactic radiosurgery
  4. No intervention
41
Q

Anesthetic mgmt of AVMs?

A
  • Similar to surgery for SAH/ aneurysm
    • Arterial line required
    • CVP recommended
  • Control ICP/ mass effect
    • Measures to decrease ICP
  • +/- Induced hypotension to reduce lesion size and blood flow
    • Normotensive*
  • Avoid acute HTN!!!! → vessels don’t have ability to autoreg high pressures
  • Capability of accurately manipulating BP w/ bleeding.
42
Q

What is the phenomenon known as “perfusion pressure breakthrough” or cerebral dysautoregulations r/t AVM repair?

A
  • Patho: Sudden engorgement & swelling of brain
    • cauliflower-like protrusion from cranium
    • cerebral edema
    • hemorrhage
  • Lengthy procedures on large AVMs
  • Theories:
      1. Neurogenic or paracrine cause VS
      1. Acute obliteration of high-volume/low-resistance pathway with abrupt diversion of AVM’s flow to vasculature that has long been max. vasodilated & lost ability to vasoconstrict → no autoregulation →
        * RESULT: massive edema/hemorrhage (not strongly supported by experimental studies)
43
Q

How do we prevent perfusion pressure breakthrough? treatment?

A
  • Prevention BEST
    • keep sedated/intubated VS
    • aggressive BP control at emergence (have meds ready)
      • labetalol
      • hydralazine
      • nicardipine
  • Treatment
  1. High dose barbiturates
  2. High dose propofol
  3. Osmotic diuretics
  4. Hyperventilation- PaCO2 ~30 (ETCO 26-28)
  5. Low-normal MAP
  6. +/- Hypothermia
44
Q

What is the patho behind head injuries? review of gcs?

A
  • Patho: 2 Injuries
  • Primary injury – we have no control
    • biomechanical effect of force applied to skull and brain (milliseconds)
  • Secondary injury (goal = prevention)
    • Excitotoxicity- glutamate
    • Ischemic penumbra- optimize chance of neurons here survive
      • Patho: Ischemia, brain swelling, edema, intracranial hemorrhage, increased ICP, herniation (minutes to hours)
    • Aggravating factors: → secondary injury worse
      • Hypoxia
      • Hypercarbia
      • Hypotension**- max CPP
        • hypoxia + hypotension significantly worse > 90% patients severe outcome or death
      • Anemia
      • Hyperglycemia
      • Seizures
      • Infection
        • 40% will have another life-threatening injury

Glasgow Coma Scale – defines neurologic function impairment

  • Eyes open – Never (1)-spontaneous (4)
  • Best Verbal Response None (1) – oriented (5)
  • Best Motor Response None (1) - obeys commands (6)
  • Mortality closely related to initial score
  • Scores < 8 = considered severe
    • require intubation and controlled ventilation for ICP & airway control
45
Q

COnsiderations for airway mgmt with head trauma?

A
  • Airway management → ICP is not the only priority! (ABC’s)
  1. Full stomach
    1. Succs- increases ICP but don’t want aspirating
      1. Succs + propofol suppresses response anyway
  2. Cervical spine stability?
    1. R/o w/ CT scan
  3. Airway injury?
    1. blood + structural injury (larynx, cricoarytenoid cartilage, etc.) 
  4. Skull base fracture
    1. avoid nasal ETT
  5. Volume status?
    1. Large blood loss examples:
      1. Lacerated liver
      2. Long bone fracture
  6. Uncooperative/combative
  7. Hypoxemia
  8. ICP
    1. Keep sight of the ABCs of resuscitation: securing the airway, guaranteeing gas exchange, and stabilizing the circulation are higher initial priorities than control of ICP is. Do not risk losing the airway or causing severe hypotension for the sake of preventing coughing on the tube or brief hypertension with intubation.
46
Q

What is involved with inline stabilization during intubation?

A
  • 3 person job
    • # 1- hold manual c-spine stabilization against bed (no flexion)
      • No sniffing position
    • # 2- laryngoscopist
    • # 3- cricoid pressure to prevent aspiration
47
Q

Management for various head injuries?

A

Decompressive craniectomy/craniotomy performed for:

  • depressed skull fractures
    • OR < 24 hrs to prevent infection/meningitis
    • Bony fragments and penetrating objects should only be removed in OR (potential for tamponading a lacerated vessel or dural sinus)
  • midline shift- herniation impending
  • vassal cistern compression
  • refractory ICP increases
  • Evacuation of hematomas:
    • Subdural-
      • Intracranial HTN- common w/ acute (symptoms w/in 72 hours) subdural hematoma → require major therapy to control edema and ICP before during and after evacuation
    • Epidural- middle meningeal arteries → EMERGENCY
      • Symptoms: Bleed → temporary LOC → vasospasm/clotting occurs → wakes up → lucid interval → then rapid deteriorates!
        • minimal deficits to unconsciousness and signs of mass lesion (hemiparesis, unilateral decerebration, pupil changes), lucid period
      • Management: O.R. ASAP for decompression!
    • Intracerebral
      • Anesthetic approach similar for all three:
        • Maximize BP
        • Control ICP
48
Q

Considerations for anesthetic mgmt of head trauma fro BP? temperature? ventilation? fluids?

A
  • Blood Pressure
    • Hypotension and ischemia are devastating to injured brain
    • Exact target BP controversial
    • CPP 60-70 mmHg
      • 2007 guidelines Brain Trauma Foundation
    • “maintain CPP at or just above 60 mmHg 1st 2-3 days” M9th1893
  • Hypothermia
    • 3 Recent large clinical trials show no benefit
  • Hyperventilation (Brain Trauma Foundation recommendations)
    • Routine use discouraged (especially 1st 24 hrs)
      • ischemic brain = Harmful → decreases CBF
    • May use for acute ICP management, herniation prevention, minimizing retractor pressure, improve surgical access
    • If used → recommend brain tissue PO2 monitoring
  • Fluids – maintain intravascular volume
    • Prevent reduced serum osmolarity and colloid oncotic pressure
      • Prevent brain edema
    • Check labs –
      • cumulative pre-op mannitol
      • fluid therapy impact
    • Products:
      • 0.9% saline
      • 5% albumin
      • Blood products/plasmalyte/normosol > LR (hypoosmolar)
        • NS- hyperchloremic metabolic acidosis, electrolyte imbalances
49
Q

Anesthetic mgmt for head injury in regards to coagulopathy? hyperdyanmic circulatory response? cushing’s triad?

A
  • Coagulopathy
    • Brain tissue thromboplastin release → lead to DIC
      • Assess coags
      • Order products appropriately
  • Hyperdynamic Circulatory Response
    • Massive catecholamine surge (Epi) after head injury
      • → Tachycardia, HTN, increased CO, arrhythmia, CHF (prior CV impairment)
    • Tx:
      • Labetalol
      • esmolol
  • Cushing’s Triad – Need ICP reduction
    • Symptoms:
      • BP high → trying to enhance CPP
      • HR low → baroreceptors bring HR down
      • Irregular breathing
        • HERNIATION!!
    • Tx:
      • Diuretics
      • HOB 30 degrees
      • Barbiturates (more so propofol now)
      • PaCO2 30-35mmHg
      • ventricular drainage
      • consider mild hypothermia ~ 34-35 degrees C (controversial)
  • Multi-center large trial of hypothermia reduction within 8 hours of injury showed no benefit – question is….. If they are cooled sooner within 4 hrs is there potential for improved outcome? Study underway to evaluate.
50
Q

Use of TXA in head injury?

A
  • GOOD in head injury
    • TXA safe w/in 3 hrs of injury
    • Reduced brain injury death
      • ADMINISTER!!
51
Q

Montior, induction, maintenance, emergence for anesthesia for head trauma?

A
  • Monitors
    • Aline- pre/post?
    • Priority is to get cranim open as rapidly as possible
      • Never delay crani after IV accesss achieved
  • Induction
    • HoTN issue but also don’t want extra bleeding from HTN (similar to SAH)
      • Maintain normotension
      • Virtually any induction agent except ketamine can be used
  • Maintenance:
    • ICP issues → TIVA superior (CMRO dec and CBF maintained)
      • VA causes dilation at 1 MAC→ dec CBF
        • Keep < 0.5 MAC
  • Emergence:
    • Swelling peaks w/in 1st 3 days
      • Leave intubated past that period
52
Q

physiology of spinal cord?

A
  • Physiology similar to brain:
    • CO2 responsiveness
    • blood-“brain” barrier (blood “spinal” cord barrier)
    • autoregulation
    • high metabolic rate and blood flow
    • substantial ischemic vulnerability of gray matter
  • Measures to reduce spinal cord swelling analogous to ICP reduction are rarely used
    • Not issue being in intracranial vault
  • Considerations:
    • Robust BP important → Measures to prevent HoTN critical
53
Q

What are some extra tests/monitoring urilized during spinal procedures with major neuro risk?

A
  • Wake-up test
    • rehearse with patient, 45 minutes warning from surgeon, use short-acting agents
      • Technique: N2O → quick on/off
  • SSEP- Anesthetic restrictions
    • Less need for wakeup test
  • MEPs - Anesthetic/relaxant restrictions
  • Pedicle screw electromyogram - Relaxant restriction
  • Wake up test – wake patient up after instrumentation, before closure to see if can voluntarily move lower extremities, minimal sedation, pre-op preparation of patient, N2O narcotic (short-acting, moderate dose)
54
Q

Surgery in thoracolumbar region?

A
  • Position: Prone, lateral, or knee-chest
  • Unstable spine after trauma→
    • Awake intubation and position awake
  • Blood loss
    • especially if multiple levels involved, repeat operations, instrumentation, and spinal stenosis; risk of occult aortoiliac or major venous tear
  • VAE – rare
    • Risk → Frame that elevates spine above heart
  • Postoperative visual loss- d/t prone
    • Etiology unclear- associated with long prone procedures, low hematocrit, large estimated blood loss, and hypotension.
55
Q

Cervical region surgery? anterior/posterior aprroach? complications? anesthesia considerations?

A
  • Supine/anterior approach – diskectomies
    • Complications:
      • Retractor compression →
        • Airway
        • carotid arteries
      • Postoperative swelling →
        • airway compression
        • CN dysfunction
      • Traction required for anterior graft insertion?
  • Posterior approach (prone or sitting)- laminectomy & some diskectomy
    • Complications:
      • Eye damage
  • Anesthesia considerations:
  • Air embolism with sitting laminectomies
  • Maintain baseline MAP during sx
56
Q

Considerations during surgery after cervical spinal cord injury?

A
  • Hypotension (spinal shock) and respiratory insufficiency occurs with complete cervical cord injury
    • Spinal injury to cervical region
      • No signals to sympathetic reflex arch at cervical region
      • No sympathetic innervation impacting heart
        • Consequences:
          • Veins dilate
          • No CV accelerating fibers to mediate changes in CO to compensate dilation
          • HoTN- severe
          • Respiratory insufficiency
  • Keep MAP > 85 mmHg for 7 days post-traumatic injury
  • Awake intubation/Axial stabilization and position if unstable after trauma
57
Q

Considerations with vertebral metastasis?

spinal cord tumors?

A

Vertebral Metastasis

  • Large blood loss**
  • Position:
    • Prone or
    • anterolateral/retroperitoneal
  • Lesions > L1: Double-lumen tube

Spinal Cord Tumors

  • High normal MAP during retraction
  • Prone Positioning – Review considerations
58
Q

What is a communicating and non-communicating hydrocephalus?

What is a VP shunt?

A
  • Inserted to control hydrocephalus
    • Hydrocephalus: 2 types
        1. Communicating Hydrocephalus- free flow through ventricles, but not absorbed by arachnoid villi
          * r/t: infection or blood in CSF space, common after SAH
      • 2. Non- communicating Hydrocephalus- CSF obstructed in ventricular system, no free flow
        • r/t: blood/infection in ventricles or tumor
  • Ventriculoperitoneal shunt (most common)
    • Catheter via burr hole into lateral ventricle (non-dominant side)
    • A reservoir is placed SQ adjacent to burr hole
    • Drainage limb passes via SQ tunnel to a point near the epigastrium, where inserted into the peritoneal space through a small laparotomy
      • Muscle relaxation helpful
    • OG tube placement–
      • prevent distended stomach & inadvertent “gastrostomy” during laparotomy
59
Q

Anesthesia considerations during shunting procedures?

A
  • Invasive monitoring not generally required
  • Position:
    • Supine
    • 90 degree bed turned
  • Avoid further increases in ICP
    • Ex: PaCO2 25-30, avoid positioning obstructing venous outflow
  • Avoid dramatic ICP ↓ → keep flat
    • collapsing the ventricles can make it more difficult to place ventricular catheter
  • BP ↓ after ventricular cannulation
    • (+/- brief pressor support)- phenylephrine
  • Acute pain with tunneling/Minor postoperative discomfort
    • Burrowing SQ tunnel can produce a sudden painful stimulus.
  • Nursed flat - prevent rapid collapse of the ventricular system and formation of subdural hematoma

Empirically, there is a small incidence of subdural hematoma after shunting, and tearing of the bridging veins at the time of rapid brain shrinkage is a suspected cause

60
Q

Neuro physio review for peds?

A
  • Neuronal development continues into 3rd yr of life
  • Spinal cord ends at L3 (adult level at age 8)
  • Open fontanelles
    • provide some protection with ↑ ICP
  • Palpation of the fontanelles = trend monitoring of “ICP”
    • Posterior fontanelle: closes 2-3 mo.
    • Anterior fontanelle: closes 12-16 mo.
  • CBF infants and children: 100ml/100g/min
    • 2 x of adults
  • CMRO2: 5-6 ml/100g/min
  • Glucose utilization 6.8 mg/100g/min
  • ICP 2-4 mmHg (lower than adults)
61
Q

List of common ped neuroanesthesia procedures

A
  • VP shunt (most common?)
  • Craniosynostosis
  • Meningomyelocele
  • Supratentorial craniotomy
  • Posterior fossa craniotomy (common)
    • Hydrocephalus- tight space → anything can obstruct flow
    • VAE risk
    • CV and respiratory center risk
62
Q

What is craniosynostosis?

A
  • Purpose: Premature fusion of cranial sutures
  • ~ 2-8 months
  • Considerations:
    • Position: Supine or prone
    • IV access – blood loss (usually related to number of sutures involved)!!!!
  • Arterial line- required
  • VAE risk- sitting up
    • precordial Doppler indicated
63
Q

Meningomyelocele patho? risk? associated factors?

A
  • Patho: Failure of neural tube to close during gestation
  • Risks:
    • neural injury
    • infection
  • Associated factors:
    • Arnold-chiari malformation
    • Hydrocephalus- pressure on brainstem fx
      • Assess CV & respiratory/aspiration
    • Latex allergy*
  • Consider prone induction
  • Fluids – account for CSF leak & 3rd space (exposed SA)
  • Maintain temperature
  • Blood loss (15-50cc) – more with large defect
  • Arnold Chiari malformation - Impaction of posterior fossa contents into foramen magnum
64
Q

Is it possible to use inhalaitonal induction in peds neuroanesthesia?

A
  • Inhalation induction –
    • want to get control of ventilation ASAP however to avoid increased ICP issues.
    • Avoid if obvious signs of decreased intracranial elastance (behavioral changes, LOC changes)–
      • propofol/TPL/fentanyl may be best (cant do inhalational induction)
  • Maintenance
    • SEVO – use 2-3mcg/kg fentanyl for smoother emergence

Standard pediatric considerations:

  • Airway
  • Body surface area
  • Temperature
  • Fluids maintain cerebral perfusion isoosmolar isooncotic

(no peds case on oral)

65
Q

Sterotactic procedures

A
  • Derived from Greek word stereos, meaning three dimensional, and the Latin word tactus, meaning to touch
  • MRI/CT allows precise three-dimensional localization of specific sites within the CNS increasing the neurosurgeon’s accuracy

Overall → AW issue (cant bag/mask vent if needed)

  • NEED to have someone w/ you who can remove frame if necessary
    • Anesthesia:
      • Sedation/Awake
      • Scalp block
    • Use of Stereotactic Procedures:
      • biopsy of small deep-seated lesions
      • placement of deep brain stimulation electrodes
        • ex: Parkinson’s disease /movement disorders/Tourette’s/Depression
      • ablation of lesions close to critical speech, motor, short term memory centers (movement disorders & temporal lobe epilepsy)

Needle placement picture

  • ensure pt off meds that promote bleeding
    • herbals
    • anticoags
  • the future - intraparenchymal stimulators for control of epilepsy and stereotactic stem cell implantation for a variety of degenerative and ischemic disorders??
66
Q

Preop eval for sterotactic procedures?

Process of placing frame?

A
  • Preoperative evaluation:
    • coagulation status (platelet-inhibiting agents & herbals)
    • patient education – plan w/procedure duration & movement restraints
      • Planned awake → immediate feedback (bleeding/procedure working)
  • Stereotactic frame placed
    • local anesthetic (scalp block)
      • picture
    • (+/- sedation)
      • Ex: Propofol 100-150 mcg/kg/min → scalp block while sleepy → frame placed
  • The patient then undergoes imaging study prior to OR
  • Bag-mask ventilation may be impossible (frame) - anesthetist must know how to remove
  • Frame will prevent application of the mask and ventilation, laryngoscopy, or neck extension. If a general anesthetic is to be administered, awake intubation may be required. If sedation is to be used should have certain knowledge regarding how to remove the device rapidly in an urgent situation (including knowledge of the whereabouts of the requisite “key” or spanner device).
67
Q

Anestheisa consideratiosn for sterotactic procedures?

A
  • Restriction of airway access (frame)
  • Restriction in sedation/anesthetic depth
    • electro-physiologic recordings are to be performed as a guide to device placement
  • Detection & management of complications (seizures & intracerebral hematomas)
  • Thalamic/subthalamic stimulator placement
    • requires identifying electrophysiologic “footprint” of specific nuclei – why cant have sedatives
  • Some surgeons may request no sedative be given
    • Dexmedetomidine:
      • superior sedative (does not interfere with electophysiologic mapping)
    • Remifentanil: OK
    • Propofol: OK
      • Ensure not given during mapping periods (communicate w/ surgeon)
    • If sedatives are administered (necessary Parkinson’s for frame placement & occasionally for imaging) –
      • ensure the ability to perform neurological examination shortly thereafter- short action!
    • ****Avoid benzodiazepines

Notes:

  • However, for placement of thalamic and subthalamic stimulators, part of the localization process entails identifying the typical electrophysiologic “footprint” of specific nuclei. Because the nature and duration of the effects of anesthetics on these signals are not known systematically, some surgeons may request that no sedative whatsoever be given. If sedatives are administered, they must be given in a manner that ensures the ability to perform precise intermittent neurologic examination of the patient. An issue that arises in some patients with movement disorders (e.g., Parkinson’s disease) is the problem of obtaining high-quality radiologic images in the presence of a persistent tremor. Sedation immediately preceding stereotactic placement may therefore be inevitable. Propofol has been used, but the window between propofol administration and subsequent recording should be as long as possible.
68
Q

Maintenance considerations for sterotactic procedurs?

A
  • Aggressive control of HTN –
    • Concern: multiple needle passes through brain predispose pt. to an intracerebral hematoma
  • Be prepared for urgent craniotomy should hematoma occur*
  • Lengthy procedures with minimal sedation = patient restlessness
  • VAE risk
    • secondary to spontaneous ventilation (head higher than heart)
  • The concern is that in the face of multiple needle passes through the brain, hypertension will precipitate the development of an intracerebral hematoma. In the event of a substantial hematoma, an urgent craniotomy may be required, and the anesthesiologist should be prepared from the outset for this eventuality. These procedures are lengthy, and restlessness may occur, especially in unsedated patients. The nonsystematic experience, obtained in situations in which the options were to sedate the patient or abandon the procedure, has been that satisfactory recordings can be made in the presence of dexmedetomidine