Neurosurgery Resident’s
Survival Guide
1st Edition (2013)
Neurosurgery Resident’s Survival Guide
The Division of Neurosurgery
The Ottawa Hospital
Copyright: August 2013 (1st Edition)
Authors:
Saad Alqahatani
Diana Ghinda
Hubert Lee
Table of Contents
INTRODUCTION ................................................................................................. 3
OBJECTIVES............................................................... Error! Bookmark not defined.
EDUCATIONAL ACTIVITIES AND RESPONSIBILITIES ........................................... 3
ROUNDS FOR RESIDENTS ROTATING TO NEUROSURGERY....................................... 4
CALLS ..................................................................................................................... 4
RESPONSIBILITIES............................................................Error! Bookmark not defined.
TECHNICAL SKILLS .......................................................................................... 10
EVD PLACEMENT ................................................................................................... 25
BASIC PATHOPHYSIOLOGIC PRINCIPLES...........................Error! Bookmark not defined.
Mass effect and cerebral herniations: ............................... Error! Bookmark not defined.
1.6.2 Hydrocephalus/shunt malfunction and EVD management .... Error! Bookmark not
defined.
7. COMMON PATHWAYS ............................................ Error! Bookmark not defined.
References ................................................................. Error! Bookmark not defined.
Intro
Service Description
Neurological Exam
Neurosciences / Management (ICP, Shunts, Tumour, Hemorrhage, Spine)
Technical Issues / Drains
Orders / Common medications
INTRODUCTION
Welcome to your neurosurgery rotation! This is a busy service with a typical census of
40-50 patients. The work can be overwhelming at times, but there are always other
residents and staff available to help you and the nurse practitioners are very helpful for
the floor issues.
EDUCATIONAL ACTIVITIES AND RESPONSIBILITIES
The senior residents direct the day-to-day running of the service on a team basis, which
begins in the Neurosciences Acute Care Unit (NACU) every morning. Rounds proceed
from NACU to the ICU, PACU, and lastly the emergency department for overnight
admissions after which the teams divide to complete D7/F7 rounds. The call schedule in
addition to the weekly schedules (distributed latest the weekend before) are
established by the chief resident indicating your daily assignment to OR or clinic if you
are not on call.
ROUNDS
Residents from other Divisions are always free to attend their specific seminars or other
formal educational programs connected with their specialty. Conversely, you are also
welcome and encouraged to participate in our weekly rounds which include:
 Tuesday: 4-6pm (Difficult Case Rounds / M & M’s – D7 Conference Rm)
 Wednesday: 7:30-8:30am (Neuroradiology Rounds – C2 Conference Rm)
 Thursday: 4-6pm (Academic Half Day – Didactic Teaching – D7 Conference Rm)
 Friday: 7-8am (Spine Rounds – C2 Conference Rm), 8-10am (Neurosciences
Rounds)
CALLS
During call you are expected to manage consults at the Ottawa Civic Hospital ONLY
from the emergency department, other services, and C2 clinic (clinic admissions).
During the day, the nurse practictioners will be available to help field a majority of the
floor issues within their range of practice. Any outside calls should be deferred to the
staff on call (including the Ottawa General Hospital).
THE NEUROLOGICAL EXAM
Consciousness
* May be confounded with sedation
 Alertness, Orientation (person, place, time)
 Mediated from the central pons and hypothalamus with neural tracts projecting
signals to relay nuclei in the thalamus up to the cortex, feed back from the
cortex to the thalamic nuclei promote arousal
 Glasgow Coma Score (GCS)
o Best verbal response
1. No response (Patients that are intubated give a T (counted as 1))
2. Incomprehensible sounds
3. Inappropriate words
4. Disoriented and converses
5. Fully oriented and converses
o Best eye response
1. Does not open eyes
2. Opens eyes to painful stimuli
3. Opens eyes to verbal command
4. Opens eyes spontaneously
o Best motor response
1. No motor response
2. Extension (decerebrate posturing)
3. Flexion (decorticate posturing)
4. Withdraws purposefully from painful stimuli
5. Localizes painful stimuli
6. Follows verbal commands
o Range: 3 – 15 (NO GSC 0!), specify the components (e.g. E4V5M6 = GCS
15)
o (GSC  13 – mild brain injury; GSC 9-12 – moderate injury; GSC  8 –
severe brain injury)
Cranial Nerves
 Midbrain
o CN II/III – pupillary light reflex, visual fields
 Midbrain-Pons
o CN III/IV/VI – extra-occular eye movements
 Pons
o CN V/VII – corneal blink reflex, facial sensation, facial movements
o CN VIII - occulo-cephalic reflex
 Medulla
o CN IX/X – gag/cough reflex
o CN XI – sternocleidomastoid and cervical trapezius m.’s
o CN XII – tongue movements
Motor
 Tone – normal, spastic, flaccid
 Bulk
 Strength
o 0 – no movement
o 1 – flickr of movement
o 2 – movement with gravity eliminated
o 3 – antigravity movement
o 4 – movement against resistance (gradient: 4-, 4, 4+)
o 5 – Full strength
 Reflexes
o Deep tendon
 0 – absent
 +1 – diminished
 +2 – normal
 +3 – hyperactive
 + 4 – hyperactive with clonus
o Plantar – upgoing, downgoing
Sensory
 Light touch
 Pain/Temperature
 Propioception
 Extinction
Cerebellar testing
 Coordination
o Finger-to-nose
o Heel-to-shin
o Rapid alternative movements (dysdiadokinesis)
 Gait
Trauma (ABC’s)
Airway - oropharyngeal reflexes associated with decreasing level of consciousness can
lead to compromised airway and require an airway adjunct or intubation
Breathing:
 Rate
 Pattern
1. Hypoventilation - shallow rapid respirations with decreased level of
consciousness or neuromuscular disease
2. Cheyne-Stokes breathing - waxing and waning (crescendo – decrescendo)
respirations attributed to decreased responsiveness of CO2 receptors in the
respiratory centers leading to CO2 retention stimulating compensatory rapid
respirations to reduce it
3. Apnea - episodes of absent respirations secondary to compression of
respiratory centers in the lower brainstem
4. Central hyperventilation - seen in brainstem lesions but most often
secondary to a systemic illness (metabolic acidosis - lactic acidosis,
ketoacidosis, uremia, or organic acid poisoning)
 Oxygen saturation (arterial blood gas)
Circulation:
 Heart Rate
o Tachycardia or bradycardia (supraventricular tachycardias most common
rhythm disturbance)
o Other non-CNS causes: pain, anxiety, agitation, fever, hypoxemia, and
volume depletion
 Blood pressure
o Hypertension often seen with cerebral ischemia and raised intracranial
pressure - represents a protective response to maintain cerebral
perfusion in these conditions and should not be treated rapidly into the
normal range
o Hypotension often seen in intracranial and spinal cord injury due to loss
of sympathetic tone (peripheral vasodilation)
Spinal Exam:
 Motor/sensory exam with rectal tone assessment as per ASIA Score
INTRACRANIAL PRESSURE & MASS EFFECT
The cranium represents a closed compartment – the Monroe-Kellie principle. The
contents of the cranium consist of 80% brain tissue, 10% cerebrospinal fluid, and 10%
blood. Due to lack of expansible properties, small increases in the volume can lead to
large increase in intracranial pressure (ICP).
Initial increase in mass effect in any
compartment is compensated by displacement of CSF to the spinal canal and with
increasing pressure may lead to obliteration of sulci and ventricles. Further increase in
volume in one compartment will push the normal contents into the other
compartments within the cranium, a phenomenon known as herniation. The main
forms of herniations are:
1. Subfalcine herniation
 Herniation of cingulate gyrus (possibly the anterior cerebral arteries (ACA)) under
the falx
 Etiology: lateral supratentorial mass
 Symptoms/Signs: often asymptomatic, leg weakness (with ACA infarct)
2. Central Tentorial herniation
 Downward displacement of the diencephalon through the tentorium
 Etiology: midline supratentorial mass or diffuse edema
 Symptoms/Signs: decreased level of consciousness, bilateral pupillary dilation
(subsequently fixed), impaired upgaze (“sunsetting eyes”), Duret’s (brainstem)
hemorrhage
3. Lateral Tentorial (Uncal) herniation
 Displacement of the uncus of the temporal lobe through the tentorial notch
 Etiology: Lateral supratentorial mass
 Signs/Symptoms: decreased level of consciousness, ipsilateral fixed, dilated
pupil, contralateral hemiplegia with upgoing plantar response (Kernohan’s
notch)
4. Tonsillar herniation
 Descent of the cerebellar tonsils through the foramen magnum
 Etiology: Infratentorial mass, post-lumbar puncture/drain with increased
intracranial pressure
 Signs/Sympsoms: decreased level of consciousness, cardiorespiratory
irregularities/arrest (watch for Cushing’s Triad – bradycardia, hypertension,
irregular respiratory rhythm), paralysis
CPP = MAP - ICP
Intracranial Pressure (ICP):
 Normal values = 5 – 15 mm Hg (8 – 18 cm H2O; 1cm H2O = 0.7 mmHg)
 Treatment threshold to reduce ICP = greater than 20mmHg
 Methods of monitoring
o EVD
o Intraparenchymal, subdural, epidural probe
Mean Arterial Pressure (MAP):

Estimated by 2/3 diastolic blood pressure + 1/3 systolic blood pressure
Cerebral perfusion pressure (CPP):



Goal to maintain adequate cerebral blood flow and prevent cerebral ischemia
(typically > 70 mmHg)
Cerebral autoregulation maintains constant cerebral blood flow over a wide
range of MAPs
CPP can be increased by INCREASING MAP or DECREASING ICP
Signs of Increased ICP:
 Symptoms – Headache, nausea/vomiting, decreased level of consciousness,
confusion
 Signs – abnormal vitals (bradycardia, hypertension, apnea), declining GCS,
papilledema, upgaze palsy, fixed-dilated pupil, CN VI palsy
Management of Increased ICP:
General
1. HOB 30-45 degrees and the head midline – promotes venous return by relieving
any compression of the jugular veins
2. Oxygenation – pO2 > 60 mmHg to avoid hypoxic brain injury
3. Ventillation – normocarbia (35 – 40 mmHg) as CO2 promotes vasodilation,
hyperventilation effect temporary and only beneficial as temporizing measure
4. Maintaining blood pressure – for minimum CPP
Directed
1. Hyperosmolar therapy
 Target to serum osmolality of 300-320
 Mannitol 20% – an osmotic agent that increases serum tonicity drawing edema
away from the injured brain parenchyma while decreasing blood viscosity to
improve cerebral blood flow and oxygenation
o Dose: 0.5-1g/kg loading dose followed maintenance 0.25g/kg q6h
o Monitor kidney function
 3% Saline – treatment of edema and hyponatremia
o Dose: 150 cc q6h (max sodium of 155 mmol)
2. Hyperventilation – PaCO2 to 30 – 35 mmHg for acutely elevated ICP as temporizing
measure; risk of cerebral ischemia
3. Hypothermia – reduce cerebral metabolism and blood flow
4. Sedation/Paralysis
 Barbituates, Fentanyl, Vecuronium
5. Steroids
 Reduces vasogenic edema typically found in with tumours, absesses, and certain
hemorrhages
 Dose: dexamethasone 10mg IV bolus then 4mg PO QID
 Monitor blood sugars as can be come elevated
6. CSF drainage (if EVD in place)
7. Decompressive Craniectomy
Cerebral Edema:



Vasogenic edema
o breakdown of the blood-brain barrier leading to excess extracellular fluid
o etiology – tumour, abscess
o treatment - steroids
Cytotoxic edema
o cellular damage impairing the cell membrane transport system leading
to accumulation of water within the cells
o etiology – cerebral infarction
o treatment – refractory to steroids
Interstitial edema
o extravasation of fluid through the ventricular ependymal layer into the
parenchyma due to hydrocephalus
o treatment – ventricular CSF drainage
HYDROCEPHALUS
Classically defined as:
… an active distension of the ventricular system of the brain resulting from
inadequate passage of cerebrospinal fluid from its point of production within
the cerebral ventricles to its point of absorption into the systemic circulation
Classification:
1. Obstructive (Non-Communicating)
 Blockage of CSF flow proximal to arachnoid granulations
 Etiology – Intraventricular lesion (ie. colloid cyst), aqueductal stenosis,
compression of 4th ventricle, tentorial herniation
 Imaging – proximal ventrciulomegaly, sulcal effacement, transependymal
CSF flow
2. Non-Obstructive (Communicating)
 Impaired absorption of CSF at arachnoid granulations
 Etiology – following CNS infection, intracerebral hemorrhage (especially
SAH), choroid plexus tumour
 Imaging – ventriculomegaly affecting all ventricles
3. Normal Pressure (NPH)
 Ventriculomegaly with normal intracranial CSF pressure
 Presents with classic triad of:
o Gait ataxia/apraxia
o Incontinence
o Dementia
 Etiology – idiopathic
 Imaging – ventriculomegaly without sulcal effacement
4. Ex-Vacuo
 Ventriculomegaly secondary to cortical/parenchymal atrophy
Presentation
 Symptoms and signs of increased intracranial pressure
Investigations
 CT head plain
o Assess ventricle size
o Check catheter tip position within ventricle
 Lumbar puncture – measurement of opening pressure
 Shunt malfunction
o Shunt survey – skull/neck/chest x-rays to check for fracture in tubing
o Shuntogram (radionucleotide test)
o (suspected infection) CBC, ESR, CRP, blood cultures, CSF sample from
shunt reservoir
Management
 Temporary
o External ventricular drain
o Lumbar drain
 Permanent
o Surgical resection of obstructing lesion
o Shunt (see below for details)
o Third ventriculostomy
Shunts
 Types:
o Ventriculoperitoneal
o Ventriculoatrial
o Ventriculopleural
o Lumboperitoneal
(for
idiopathic
intracranial
hypertension,
communicating hydrocephalus)
 Clinical History and Physical Exam
o Symptoms of increased ICP (headache, nausea, vomiting, visual
disturbances)
o Symptoms of infection (fever, chills, neck stiffness, redness or
tenderness along the shunt tract, abodominal pain)
o Shunt details
 Reason for shunt insertion
 Type of shunt (low/medium/high pressure vs. programmable
valve, location of distal catheter)
 Last shunt revision
 Previous shunt malfunction / infections
o Rule out other sources of infection – respiratory, urinary, bowel
o Exam
 Depress shunt valve (ensure it empties and fills well)
 Palpate along shunt tract
 Check for meningismus
 Neurological Exam
NEUROONCOLOGY
Classification of Intracerebral Tumours:
 Primary (Benign vs. Malignant)
… a few examples
o Glioma (pilocytic, low grade, anaplastic, glioblastoma multiforme)
o Oligoastrocytoma
o Oligodendroglioma
o Ependymoma/Subependymoma
o Meningioma
o Hemangioma
o Vestibular schwanomma
o Pituitary adenoma
o Craniopharyngioma
o Lymphoma
o Choroid plexus tumour
o Pineal gland tumour
 Secondary
o Metastases
Clinical History and Physical Exam:
 Symptoms of increased ICP
 Focal sensorimotor deficits
 Seizures
 Full past medical history (especially previous history of cancer, smoker?)
 Constitutional symptoms
 Social history
 Functional status (Karnofsky Performance Scale) – prognostic value
Investigations:
 Basic labwork
 INR, PTT, type and screen (pre-op)
 Sellar lesions:


o Growth Hormone (IGF-1), LH, FSH, TSH, ACTH, Prolactin
o Neuro-opthalmology testing (visual acuity, visual fields)
Cerebellarpontine angle tumours:
o Audiometry
Imaging
o CT head plain
 tumour location/number, presence of edema, mass effect,
hydrocephalus
o MRI Brain (with and without contrast, Stryker Protocol (for
intraoperative neuronavigation), DTI (diffiusion tensor imaging /
tractography), MR spectroscopy, MR perfusion
o CXR, ECG
 pre-op and screening for lung nodules
o CT chest/abdomen/pelvis
 r/o other primary malignancy
Differential Diagnosis of Ring-Enhancing Lesions (MAGICAL DR):
Metastases
Abscesss
Glioblastoma Multiforme
Infarct
Contusion
AIDS (toxoplasmosis)
Lymphoma
Demyelination
Resolving Hematoma
Management:
 Surgical resection
o Tissue diagnosis
o Cytoreduction
o Indicated for single lesion, up to 3 metastases, or posterior fossa lesions
causing obstructive hydrocephalus secondary to 4th ventricle
compression
 Chemotherapy
o Adjunct to surgical resection, often requires tissue diagnosis unless
palliative therapy
 Radiation therapy (same as above)
 Steroids
o Dexamethasone (Decadron) often helpful for associated vasogenic
edema; can improve headache and neurological deficit

Antiepileptic medication
o Phneytoin for clinical seizures
o NO role for seizure PROPHYLAXIS
VASCULAR
General Management Guidelines for Intracerebral Hemorrhage
 Vitals
o Blood pressure parameters (sBP < 160 mmHg)
o Frequent neurovitals (q1-2h) if presence of hydrocephalus
 Investigations


o CT head
 Plain – to localize and assess extent of hemorrhage, presence of
hydrocephalus (repeat in 8-12 hours to rule out progression or if
neurological change)
 CT angiogram – rule out aneurysm, arteriovenous malformation
 CT venogram – rule out venous sinus thrombosis / venous cortical
vein thrombosis
o MRI Brain
 MRA – to rule out arteriovenous malformation (head and neck)
 SWI / GRE – identifies hemosiderin deposits to suggest
hemorrhage, to rule out cavernous malformation
o Catheter Cerebral Angiogram
 Consult interventional neuroradiology
 Aneurysms may be candidates for embolization (coiling)
 Arteriovenous malformations may be candidates for adjunctive
embolization (coiling/gluing)
o Lumbar Puncture
 CT head negative for SAH but suspicious clinical history
 Tube 1 – cell count / Tube 2 – Culture, Sensitivity, Gram Stain /
Tube 3 – biochemistry / Tube 4 – cell count
 Tube 4 to rule out traumatic tap (decreasing RBC count compared
to Tube 1)
 Xanthochromia – present by 12 hours and lasts 2 weeks
Coagulation Profile
o Check INR, PTT
o Elevated INR
 warfarin vs. hepatic dysfunction
 reversal agents: octaplex 40-80 cc IV (repeat INR 20 min post
infusion, duration of effect x 3 hours), vitamin K 5-10 mg PO/IV
(requires 6-8 hours for effect)
o Dabigatran
 Reversible, direct thrombin inhibitor
 Mildly elevated INR, prolonged thrombin time
 Call thrombosis/transfusion medicine for reversal regiment
(activated factor VII, octaplex, hemodialysis)
 Half-life 12-17 hours (prolonged with renal impairment)
Management
o ICP management
o External ventricular drain
 Indicated with presence of hydrocephalus (particularly with
decreased level of consciousness, seizures, focal visual/motor
deficits
o Seizure prophylaxis x 7 days
o Sequential compression stockings (SCDs)
Extra-axial Hemorrhage
 Epidural Hematoma
o Etiology – middle meningeal artery injury secondary to temporoparietal
skull fracture, middle meningeal vein, dural sinus, diploic veins
o Typically present with lucid interval following head trauma which
progresses to coma
o CT head findings:
 Lenticular shaped hematoma – restricted by suture lines
 Midline shift
 Skull fracture
o Management:
 Admit for observation initiating ICP management
 Follow up CT in 8 hours looking for progression
 Surgical evacuation (neurological deficit/decline)
 Subdural Hematoma
o Etiology - rupture of bridging cerebral veins, cortical artery
o May be asymptomatic or have focal neurological deficit
o CT head findings:
 Crescent-shaped hemorrhage
 Attenuation of blood on CT by age:
 Acute – hyperdense
 Subacute – isodense
 Chronic – hypodense
 Midline shift
o Mangement:
 Follow up CT in 8 hours looking for progression
 Admit for observation if symptomatic
 Seizure prophylaxis x 7 days – consider for acute hemorrhages
 Surgical evacuation
 Indications:
o Thickness > 10mm
o Midline shift > 5mm
o Decreased level of consciousness
o Focal neurological deficit
 Wide craniotomy (acute) – blood typically gelatinous
 Burrhole craniotomy (chronic)
Subarachnoid Hemorrhage
 Etiology
o Traumatic
o Spontaneous (aneurysm, arteriovenous malformation, vasculitis,
coagulopathy


Clinical History
o Thunderclap headache (sudden onset, severe)
o Nausea/vomiting
o Meningismus
o Photophobia
o Decreased level of consciousness
o Focal neurological deficit (ie. cranial nerve palsy)
o Risk factors:
 Smoker
 Alcohol abuse
 Coccaine abuse
 Hypertension
 Oral contraceptive use
 Pregnancy with pre-exiting arteriovenous malformation
 Connective tissue disease (Marfan’s, Ehler’s Danlos)
o Family History of aneurysms
Investigations
o CT head non-contrast
 98% sensitivity within 12 hours
 Location of hemorrhage:
 Aneurysmal - basal cisterns, suprasellar cistern, sylvian
fissure, interhemispheric fissure, tentorium



 Traumatic - perimesencephalic
o CTA / MRA / catheter cerebral angiography
o Lumbar puncture (RBC, xanthochromia)
Grading Systems
o Hunt & Hess Grading:
 0 - Unruptured aneurysm
 1 - Asymptomatic or mild headache and slight nuchal rigidity
 2 - Moderate to severe headache, nuchal rigidity, cranial nerve
palsy
 3 - Lethargy or confusion, mild focal deficit
 4 - Stupor, moderate to severe hemiparesis, early decerebrate
rigidity
 5 - Deep coma, moribund appearance, decerebrate rigidity
o Fischer Grading (predicts vasospasm post-SAH):
 1 – Absence of subarachnoid blood
 2 – Diffuse or vertical layers of SAH less than 1 mm thick
 3 – Diffuse and/or vertical layers of SAH greater than 1 mm thick
 4 – Intracerebral or intraventricular clot with diffuse or no
subarachnoid blood
Management (Aneurysmal SAH):
o Blood pressure control
o Vasospasm prophylaxis
 Nimodipine 60 mg PO q4h x 21 days (can change to 30mg PO q2h
if hypotension ensues)
 Statin therapy (Simvastatin 80mg PO Daily x 21 days)
 IV MgSO4 3-5 g (maintain normal to high serum levels)
 IVF (NS)
 Transcranial Dopplers q2days
o Securing the aneurysm:
 Surgical Clipping
 Endovascular embolization (coiling)
Complications
o Vasospasm
 SAH day 4-14, typically resolves by day 21
 Clinical (H/A, neurological deficit) vs. Radiological (narrowing of
cerebral vessels on neuroimaging) vasospasm (30% vs. 70%)
 Symptoms by involved vessel:
 ACA – confusion, leg weakness
 MCA – aphasia, face/arm weakness
 PCA – hemianopsia
 Basilar artery – decreased level of consciousness
 Diagnosis with CT angiogram and perfusion +/- MRA (if coils
present), catheter cerebral angiogram

o
o
o
o
o
Management:
 Triple H Therapy (hypertension, hypervolemia,
hemodilution)
 IVF (NS 150-200 cc/hr)
 Raising MAP until clinical improvement (pressors PRN);
with secured aneurysm can raise systolic blood pressure
up to 200-220 mmHg before risk of rebleed
 Endovascular methods for diagnosis and treatment with
intraarterial milrinone / angioplasty
Hydrocephalus
Hyponatremia (SIADH, cerebral salt wasting)
Hypernatremia (Diabetes Insipidus)
Cardiac Arrythmia
Neurogenic pulmonary edema
Intracerebral Hemorrhage



Etiology:
o Hypertension (basal ganglia, pons, cerebellum)
o Amyloid angiopathy
o Cerebral infarct with hemorrhagic transformation
o Vascular malformation (aneurysm, AVM, AVF)
o Venous sinus thrombosis
o Vasculitis
o Tumoural hemorrhage
o Coagulopathy
o Substance abuse and drugs (cocaine, amphetamines, alcohol,
anticoagulants)
o Trauma
Investigations:
o Non-contrast CT head (repeat in 8-12 hours to observe for progression)
Management:
o ABC’s
o Blood pressure control
o Correct coagulopathy if present (octaplex, vitamin K, fresh frozen
plasma, platelets)
o ICP management
o Seizure prophylaxis (if cortical)
o Supportive care
 Tracheostomy
 Gastric feeding tube
o Surgical
 Craniotomy for clot evacuation




Indicated if unable to control increased ICP
Rapid deterioration in neurological status
Favourable location (non-dominant hemisphere,
cerebellum)
 Treatable lesion (vascular malformation or tumour)
External ventricular drain – hydrocephalus (often with IVH)
INFECTIONS
Cerebral Abscess
 Clinical History and Physical Exam:
o Fever, chills
o Decreased level of consciousness
o Focal neurological deficit (hemiparesis, seizure)
o History of recent infection (otitis media, dental abscess, bacterial
endocarditis, respiratory infection)
o Recent penetrating head trauma
o Recent neurosurgical intervention
 Etiology:
o Streptococcus (most common)
o Staphylococcus (penetrating trauma)
o Gram negative/anaerobic bacteria
o Immunocompromised (toxoplasmosis, nocardia, candida albicans,
listeria, mycobacterium, aspergillis)
 Complications:
o Rupture of abscess – ventriculitis, meningitis
o Cortical/sinus venous thrombosis
o Hydrocephalus
 Investigations:
o Contrast enhanced CT head
 Ring-enhancing lesion
 Surrounding edema
o MRI with and without contrast
 Capsule is strongly contrast enhancing
 Diffusion restricting
o WBC
o ESR, CRP
o Intraoperative culture and sensitivity swabs
 Management:
o Craniotomy for urgent aspiration/excision
o Antibiotics (6-8 weeks duration)

Order PICC line on admission for outpatient antibiotic
administration
TRUAMA
Head Trauma:
 Primary Injury:
o Hemorrhage – epidural, subdural, SAH, contusion (can result in edema
(vasogenic, cytotoxic)
o Diffuse axonal injury
 From
the
shear
stress
induced
by
rapid
acceleration/deceleration of the neural tissue
 Neuroimaging:
 Suspect when prolonged loss of consciousness
following head trauma in the absnce of any mass
occupying lesion on CT head
 Punctate hemorrhages
 Neuropathology: hemorrhagic foci in the corpus callosum and
dorsolateral rostral brainstem with microscopic evidence of
diffuse injury to the axons (axonal retraction balls, microglial
stars, and degeneration of white matter tracts
 Secondary injury
o Results from hypotension or hypoxia
 Management:
o ABC’s
 Intubation if GCS ≤ 8
 Maintain PaO2 95-105 mmHg, CPP > 60 mmHg
o ICP Monitoring
 If GCS < 9 and abnormal CT head
 If GCS < 9 and (2 of 3 of the following)
 Age > 40
 sBP < 90 mmHg
 Motor posturing
o ICP Management – see Intracranial Pressure and Mass Effect
o Seizure prophylaxis x 7 days (phenytoin)
o Surgery
 Evacuation of hematoma
o Supportive care (consider early if not expected to recover within 2
weeks)
 Tracheostomy
 Percutaneous gastric feeding tube
Spinal Cord Trauma:



Initial component - contusion and intraparenchymal or extradural hemorrhage
Later component – release of prostaglandins from the breakdown of cellular
membranes leading to vasoconstriction and secondary ischemia in the local
tissue
Management:
o Steroids (controversial)
 Methylprednisolone witin 8 hours of injury - 30 mg/kg IV bolus
followed by 5.4 mg/kg/hour infusion for 23 hours.
 Presumably reduces the release and activation of prostaglandin
metabolites preventing secondary injury
o Blood pressure
 Avoid hypotension – sBP > 90 mmHg
 Spinal shock – peripheral vasodilation and subsequent
hypotension due to loss of sympathetic innervation (common
with high thoracic and cervical injuries)
 Often followed in 48-72 hours by increased sympathetic tone /
vasoconstriction
 Autonomic dysfunction – maintain foley catheter and good
bowel protocol
 Treat with aggressive intravenous fluids and vasopressors as
needed
o Ventillation
Consider in high cervical injuries
 May require mechanical ventilation
 Monitor maximal inspiratory/expiratory pressures
SPINE
Cauda Equina Syndrome
 Clinical History and Physical Exam:
o A CLINICAL DIAGNOSIS!
o Leg weakness
o Leg numbness
o Radicular leg pain
o Saddle anesthesia
o Bladder and bowel incontinence
o Hyporeflexia (patellar, ankle jerks)
o Sexual dysfunction
o Decreased rectal tone (DRE)
 Etiology:
o Lumbar disc herniation
o Trauma
o Tumour


o Hemorrhage
Investigations:
o MRI lumbar spine
o Post-void residual (in and out catheterization)
Management:
o Urgent surgical lumbar decompression (<48 hours)
SEIZURES
As with any urgent call, don’t forget ABCs before proceeding further. Monitor oxygen
saturation and give supplemental oxygen by mask. Monitor vitals frequently. Establish
IV lines and obtain STAT glucose via glucometer and blood work (CBC, electrolytes,
extended electrolytes, BUN, CR). Consider neuroimaging but only once stable.



Lorazepam (Ativan) 0.1-0.15 mg/kg (max 2mg/min)
if seizure persists … giving phenytoin (Dilantin) 15-20 mg/kg IV bolus (may attempt
additional 10 mg/kg IV if no effect)
if seizure persists … intubate, foley catheter, EEG monitoring (if possible), treat with:
o Phenobarbital 5-20 mg/kg IV loading dose, 0.5-10 mg/kg/hr infusion
o Propofol 3-5 mg/kg IV loading dose, 1-15 mg/kg/hr infusion
o Versed 0.2 mg/kg IV loading dose, 0.05-2 mg/kg/hr infusion
ELECTROLYTE ABNORMALITIES
Hyponatremia
 Most commonly due to SIADH BUT NOT ALL HYPONATREMIA IS SIADH
 Step 1: RULE OUT other causes
o Fictitious causes – hyperglycemia (DKA), hyperproteinemia (multiple
myeloma), hypoalbuminemia (chronic renal failure),
hypertriglyceridemia
o Hypervolemia
o Drug-induced – Phenytoin/Carbamazepine/HCTZ
o Endocrinological – dysthyroidism, mineralocorticoid depletion
(hyponatremia + hyperkalemia)
o Cerebral salt wasting
 Investigations:
o Assess volume status
o Serum electrolytes, osmolarity, urine electrolytes/osmolarity
 SIADH – typically hypotonic hyponatremia with normal volume
status (urine osmolarity higher than serum osmolarity due to
inappropriate ADH release leading to concentrated urine)
o Review medications – (ie. for diuretics, anti-epileptics)
 Management:
o SIADH
 Fluid restriction (<1 L of free water/day)
 Salt tabs 1-2 g PO TID
 3% hypertonic saline IV infusion
 Watch for rapid correction no greater than 8-10 mEq/L in 24
hours due to risk of central pontine myelinolysis
 Follow serum electrolytes and osmolarity q 4-6 hours
Hypernatremia
 Etilogy:
o Central DI – common post-pituitary surgery
o Unable to drink/loss of free water
 Investigations:
o Hourly monitoring of urinary output
o Serum electrolytes, osmolarity, urine electroltyes, osmolarity, specific
gravity q6h
 Management:
o PO fluid intake
o DDAVP
o Consider endocrinology consult
TECHNICAL SKILLS
Drains (External Ventricular Drain (EVD) / Lumbar Drain (LD):
EVD:
 Indications:
o Hydrocephalus
o ICP monitoring (e.g. trauma)
o ICP management
 Common orders:
o Drain Height
 Zero to external acoustic meatus (EAM)
 Typically start at 10 cmH2O (within normal ICP range) but can
adjust LOWER to drain MORE CSF or HIGHER to drain LESS CSF
 May titrate height (within provided range) to achieve particular
hourly drainage value

o Drainage
 Maximum 20 cc/hr (if greater than 20 cc within 1 hour, clamp for
remainder of hour then re-open)
 500 cc CSF production per day / 24 hours = 20 cc/hr
o Clamping
 While transducing ICP there is no CSF drainage
 Trial of clamping used to determine dependence on external CSF
drainage and subsequent need for shunting (remember to have a
CT head before and within 24 hours of clamping to compare
ventricle sizes)
Troubleshooting (No Drainage):
o System currently clamped – check all stop-cocks and white clips
o Malplacement/ Dislodged ventricular catheter (confirm with CT head)
o Low ICP (lowering the collection chamber to a smaller value along the
cm H20 scale or physically to the floor to confirm flow)
o Catheter blockage
 May be from brain tissue, blood clot, catheter tip up against
ventricle wall, or air
 Gently aspirate (max 1-2 cc) with sterile 10cc syringe from
collection site and/or subsequently flushing catheter with sterile
saline (max 1cc) to see if debris/choroid plexus can be dislodged
*if all fails, may require a new ventricular catheter
Lumbar Drain:
 Indications:
o CSF leak
o CSF drainage for intraoperative brain relaxation
 Common orders:
o Drain Height
 Zero to
 external acoustic meatus (EAM) – cranial dural defect
 lower back – lumbar spine dural defect
 Titrate height (+10 to -5 cmH2O) to achieve particular hourly
drainage value
o Drainage
 Aim for 5-15 cc/hr x 48-72 hours
 Maximum 20 cc/hr (if greater than 20 cc within 1 hour, clamp for
remainder of hour then re-open)
o Clamping
 Trial of clamping for 24 hours if no CSF leak during duration of
drain prior to removal
 Troubleshooting (No Drainage):
o System currently clamped – check all stop-cocks and white clips
o Malplacement/ Dislodged catheter
 Ensure adequate amount of catheter remains in the back (should
not see any markings outside the skin)
 Search for fractures in the tubing
o Catheter blockage
 Drop drain to floor to verify patency
 Gently aspirate (max 1-2 cc) with sterile 10cc syringe from
collection site
ORDERS
General Admission Orders:
(ADDAVID … & Consults)
 Admit to Neurosurgery, Dr. (Surgeon on Call), F7/D7 (floor) OR NACU
o NACU for unstable patients
 SAH
 Hydrocephalus
 Cardiac/Respiratory issues requiring continuous monitoring
 EVD in-situ
 Spinal injury – in halo traction
o F7/D7 for stable patients (max vital frequency q4h)
 Diagnosis
 Diet
o Keep NPO after midnight if potential OR
 Activity
o AAT
o C-Spine / L-Spine precautions, Log Roll
o Bedrest (CSF leak – especially if lumbar drain in-situ, spine fracture - until
ORIF or spinal orthosis fitted and confirmed radiological stability)
 Vitals
o Neuro vitals and regular vitals
o BP parameters
 Intracerebral hemorrhage – sBP < 160 mmHg
 Aneurysmal SAH
 Unsecured aneurysm – sBP < 160 mmHg
 Secured aneurysm with clinical vasospasm
o Increase MAP parameters by 10-15 mmHg until
asymptomatic
o sBP < 200-220 mmHg
 Arteriovenous malformation - MAP < 60-70 mmHg
 Investigations

o CBC, Lytes, BUN, Cr
o Serum Lytes and Osmolality q6h
 Treatment with IV 3% Saline therapy
 Pituitary tumours post-resection
o INR, PTT, Type and Screen +/- Crossmatch pRBCs (if for OR)
o ESR, CRP (suspected infection ie. shunt, abscess, subdural empyema,
wound infection)
o Anti-epileptic drug levels (with albumin for phenytoin)
o Imaging (CT, MRI, catheter angiogram – need to call interventional
neuroradiology to arrange in addition to requisition)
o CXR + ECG – preadmission/op if > 50 yo
Drugs
*see common medications for more details

o General
 Analgesia
 Anti-emetics
 Bowel protocol
 DVT prophylaxis (if no hemorrhage – SCDs if yes)
o Specific
 Antibiotics
 Anti-epileptic drugs
 Blood pressure
 Anti-hypertensives
 Pressors (requires central line for delivery and arterial line
for monitoring)
 IV Fluids
 NPO – awaiting OR
 Post-SAH
 Steroids – vasogenic edema
 Tumours
 Certain cases of intracerebral hemorrhage
 ALWAYS order with PPI
 Vasospasm prophylaxis
 Nimodipine 60mg PO q4h x 21 days
 Statin (ie. Simvastatin 80mg PO OD)
 MgSO4 IV 3-5g
Consults
o Anesthesia – pre-op if significant co-morbidities
o Hematology (Malignant) – with diagnosis of Lymphoma
o ID
o Medical and Radiation Oncology – post-tumour resection
o Neurology – non-surgical neurological issues (ie. venous thrombosis,
refractory seizures)
o Physiotherapy/Occupational Therapy
o Social Work – disposition planning
o Thrombosis – if patient on anticoagulation or development of DVTs
Post-op Orders / Considerations





Investigations
o CBC, lytes, BUN, Cr in PACU
o CT head plain POD#0
o Post-transphenoidal surgery for sellar tumour
 Serum lytes, osmolality, urine lytes, osmolality q6h
 Accurate urine output monitoring
 Call MD if urine ouput > 300cc x 2hours / urine specific gravity <
1.005, Na > 145, Osm > 320
Drains
o Foley
 Removal POD 1
 Consider keeping foley if requires frequent/accurate urinary
output monitoring (e.g. diabetes insipidus)
o Hemovac
 Remove when output < 100 cc/24 hours OR if predominantly CSF
 Note content – serosanguinous vs. CSF
o
Staples/Sutures removal
o POD 7-10 days in general
o POD 14 – posterior fossa, re-operation, previous radiation
Brace
o C spine - aspen collar, cervical-thoracic orthosis, sterno-occipitalmandibular immobilizer (SOMI)
o L spine – TLSO (Boston brace), Jewett brace
Medications:
o Antibiotics (prophylaxis) – continue minimum 24 hours, up to 72 hours
(ie. VP shunts)
o DVT Prophylaxis – start POD #1 if no hemorrhage on post-op CT head
o Post-transphenoidal surgery for sellar tumour
 Encourage oral fluids
 Hydrocortisone 100mg IV q8h to be tapered to 50mg IV q8h and
eventually 20mg PO qAM, 10mg PO QHS
 DDAVP 0.1mg PO PRN
Common Medications:
Analgesia
Avoid sedating drugs that can obscure neurological exam





Tylenol 650mg PO q4h PRN
Codeine 30-60mg PO q4h PRN
Tramadol 25-50mg PO q4-6h PRN
Dilaudid
o Start with low doses
o 1-2 mg PO q4h PRN
o 0.5-1 mg SC q2h PRN
AVOID NSAIDs post spinal fusion
Bowel Protocol
Particularly important in spine patients post-op or with increased use of opioids
DVT Prophylaxis
 Heparin 5000 U SC q8h (consider if awaiting OR or high risk of bleeding as
reversible with protamine)
 Enoxaparin 40mg SC q24h
Antibiotics
 Meningitis post-neurosurgery
o Ceftazidime 2g IV q8h
o Vancomycin 1.5 g IV q12h
 Abscess
o Ceftriaxone 2g IV q12h
o Metronidazole 500mg IV q8h
o Vancomycin 1.5 g IV q12h
Antiepileptic drugs
 Phenytoin (Dilantin)
o Dose: 15-20mg/kg IV loading dose, then 300mg PO/IV QHS maintenance
dose
o Duration: prophylaxis of 7 days for trauma or SAH
o Monitoring: dilantin level and albumin in 5 days (correction for
hypoalbuminemia = measured phenytoin level / ((albumin x 0.2) + 0.1)
 Leviteracetam (Keppra)
o Dose: 500mg PO BID, can increase by 250mg/dose every 3-5 days
o No monitoring required
Antihypertensives
 Labetalol
o Beta blocker – alpha 1, beta 1, beta 2 receptor blockade
o Dose: 5-10 mg IV q15min PRN (max dose 300mg/day)
o Hold if HR < 60 BPM
 Hydralazine


o Direct vasodilator, may also increase ICP
o Dose: 5-20 mg IV q1h PRN
Enalprilat
o ACEI – watch for angioedema and impaired renal function
o Dose: 0.625 – 1.25 mg IV q3h
Others:
o Nicardipine (calcium channel blocker), nitrates/nitroprusside
Steroids
 Dexamethasone (Decadron)
 Dose: 10mg IV bolus then 4mg PO/IV QID maintenance
 Discontinuation requires taper:
o Fast Taper (reduce dose every day)
o Slow Taper (reduce dose every 2-3 days)
 4 mg PO QID x 2 days then
 4 mg PO TID x 2 days then
 4 mg PO BID x 2 days then
 2 mg PO BID x 2 days then D/C
 ALWAYS order with PPI (e.g. Ranitidine 150 mg PO BID / 50 mg IV TID
NEUROIMAGING
C-Spine X-rays:
 Adequte coverage – Base of skull to T1 (at least the C7-T1 must be visualized)
o Swimmer’s view – to help visualize C7-T1
o Odontoid views – visualize transverse ligament injury, looking for greater
than 7mm overhang of lateral masses
o Flexion-Extension view – rule out ligamentous injury
 Aligment
o anterior/poserior marginal line
o spinolaminar line
o posterior spinous line
o curvature (lordotic (cervical/lumbar), kyphotic(thoracic))
 Bones
o Vertebral body width and height (?fracture/dislocation)
 Disc
o Spacing
 Soft tissue
o Prevertebral
 Normal 7mm anterior to C3, 21 mm anterior to C7
o Atlanto-dental Index (ADI) - normal  3 mm
Subdural Hemorrhage
Epidural Hemorrhage
REFERENCES:
1. Guidelines for the management of severe traumatic brain injury. Brain Trauma
Foundation, American Association of Neurological Surgeons, Joint Section on
Neurotrauma and Critical Care. www.braintrauma.org
2. Trauma XRay. http://www.radiologymasterclass.co.uk/tutorials/musculoskeletal/xray_trauma_spinal/x-ray_c-spine_normal.html. Accessed on June 28th.
3. Daniel H. Lowenstein & Brian K. Alldredge (1998). "Status epilepticus". The New
England Journal of Medicine 338 (14): 970
4. Neurosurgery Surviaval Guide, Stanford University.
http://med.stanford.edu/dura/Curriculum/Curriculum.html
5. Neurocritical care orientation, Stanford University.
http://med.stanford.edu/dura/Curriculum/Curriculum.html
6. Canadian NeuroSurgery Rookie Camp, Course Manual, July 2012
7. M.S. Greenberg, Handbook of Neurosurgery, ed 6. New York: Thieme Medical
Publishers; 2006.