Neurosurgery Flashcards
GCS score
Eyes: 4 spontaneous, 3 to verbal command, 2 to pain, 1 don’t open.
Verbal: 5 oriented, 4 confused, 3 wrong words, 2 incoherent mumbling, 1 nothing.
Motor: 6 command, 5 localizes to pain, 4 withdraws from pain, 3 decorticate, 2 decerebrate, 1 flaccid.
(take best response from UE, legs can have reflex withdrawal even if brain dead).
CN tests to r/o brainstem injury
Pupils: CN II and III (tests midbrain function).
Corneal reflex: test CN V and VII.
Gag reflex: tests CNIX and X
Signs of uncal (transtentorial) herniation.
Lesions to lateral supratentorial region cause uncus of temporal lobe to herniate through tentorial notch. Stretch CNIII resulting in compression of CST (cerebral peduncle/cortex) on ipsilateral size.
SS:
CN III palsy (ipsilateral non-reactive dilated pupil, ptosis).
CST: contralateral hemiparesis.
Decreased LOC (GCS <15).
Signs of acutely elevated ICP
Cushing’s triad: bradycardia, HTN with wide PP, irregular breathing.
Abnormal breathing patterns and associated brain areas.
Cheyne stokes: irregular respiration with periods of apnea. Apnea -> hypercarbia/acidosis -> worsening cerebral edema/increased ICP. May involve bilateral hemispheres, diencephalon, upper midbrain.
Central neurogenic hyperventilation: low midbrain/upper pons.
Ataxic: completely irregular rate and volume or no breathing. Lower medulla.
Immediate mxns of brain compensation for increasing ICP
Initially compensate by decreasing blood or CSF.
Ventricles become smaller and CSF is pushed down the spine. Dural venous sinuses become compressed .
Eventually can no longer compensate –> symptoms.
Acute mgmt of closed head injury with potential increased ICP.
Airway: intubate if GCS <8 with C spine precautions. Insert nasopharyngeal airway if potential for tongue obstruction of airway. Ensure smooth intubation to prevent increased ICP due to gag, cough, struggle.
Breathing: maintain PCO2 at 30-35 mmHg (increased CO2 results in vasodilation to try to increase O2 to area and subsequently increases ICP more). If acutely decreasing GCS, transiently hyperventilate to avoid herniation.
Circulation: HTN and reflex bradycardia. Do not aggressively lower BP as it may cause ischemia (CPP = MAP - ICP). Maintain CPP >70 mmHg by keeping MAP >90 mmHg and ICP <20 mmHg.
Order CT head non-contrast.
CTA: look for injury to blood vessels including carotids, vertebral arteries. With very elevated ICP, won’t see blood flow to brain.
Describe normal CPP autoregulation and how this changes with head trauma.
Autoregulation of CPP maintains CBF regardless of the MAP. With injury, lose autoregulation such that changes to CBF occur with changes to MAP.
Conservative mgmt for elevated ICP
Elevate head of bed to 30*, neck in neutral position: increases intracranial venous outflow. Use reverse Trendelenberg if thoracolumbar spinal injury.
Prevent hypoTN w/ pressors, fluid.
Ventilate to normocarbia: prevent vasodilation of blood vessels which would increase blood flow to brain. Hyperventilate for brief periods only to prevent hypoxia.
Oxygen to maintain PO2 >60 mmHg and prevent hypoxic injury.
Osmolar diuresis with mannitol: draw fluid from the brain into the blood then cause diuresis. Is rapid acting. Need to keep sBP > 90 tho.
Steroids have NO role in initial mgmt closed head injury. Decrease edema over subsequent days.
Aggressive mgmt closed head injury
Sedation or paralysis.
Draining CSF via ventriculostomy.
Barbiturate induced coma- reduce CBF and metabolism.
Decompressive craniectomy or lobectomy (last resort).
Primary vs secondary head injuries
1: due to trauma, present at the time of impact. Irreversible. E.g. basal skull #, cerebral contusion, diffuse axonal injury, hematoma.
2: complication of the 1* injury.
Give examples of secondary head injuries
1) loss of autoregulation –> edema, hydrocephalus.
2) increased ICP -> herniation, ischemia/hypoxia.
3) Delayed intracranial hematomas.
4) Meningitis.
5) Seizures.
6) Biochemical imbalance in neurons/glia –> acidosis, increased glutamate, Ca, free radicals, K+.
Ways to prevent secondary head injuries
Prevent hypotension (pressors, fluids), hypoxia (give O2), hypercarbia (hyperventilate). Early intubation/ventilation and fluid resuscitation important to prevent secondary brain injury.
Know SS, pathophys and CT results of: epidural, SAH, subdural (acute/chronic) hemorrhages).
Epidural hemorrhage: skull # leading to bleed from middle meningeal artery. Blood pools between bone and dura. Pt may be lucid before decreased LOC. Hyperdense lens appearance (convex from skull), does not cross sutures. Tx with craniotomy.
SAH: can develop anywhere in brain. Look for hyperdense blood in sulci/gyri, ventricles.
Acute subdural: due to ruptured subarachnoid bridging vessels (usually arterial bleeding). Blood between dura and brain. No lucid interval (hemiparesis, pupillary changes). Look for hyperdense crescent on CT that is panhemispheric (over whole surface of brain). Treat with craniotomy if >1cm thick.
Chronic subdural hematoma: slow developing subdural. Occurs in elderly pts with brain atrophy, propensity to fall. Small initial acute SDH becomes chronic liquid blood with formation of surrounding membranes –> made of granulation tissue with small blood vessels prone to bleeding. Look for HYPODENSE crescent on CT.
Pts often asymptomatic or may have HA, confusions, signs increased ICP. ‘Mimicker’ of depression, dementia, focal deficits, increased ICP. Tx with burr holes or craniotomy if recurrent.
Describe the clinical signs of the various basal skull #’s
Anterior fossa (orbital roof): periorbital hematoma (racoon eyes bilaterally), CSF rhinorrhea (# into paransal sinus with dural tear).
Petrous temporal bone: hemotympany, CSF otorrhea, mastoid bruising (delayed), facial nerve weakness (immediate or delayed), sensorineural hearing loss.
Scalp laceration: probe for underlying #.
CSF leak: usually will stop on its own.
Important Q’s on Hx for head injury/potential brain lesion.
LOC and its length, amnesia (retro/antero-grade), associated seizure (high likelihood mass lesion), age >60 (more likely to have mass lesion/die from injuries), bleeding disorder/anticoagulation, HA, persistent vomiting.
Symptoms associated with mass lesions/delayed neurological deterioration: high speed MVA, rollover or pt ejected, death in same MVA, pedestrian struck, intoxicated pt, fall >3 ft or 5 stairs.
Poor prognostic factors to consider with head injuries.
Low GCS on admission.
Absence of brainstem reflexes (pupillary, corneal, gag, occulocephalic).
Age >60.
Systemic insults: hypoxia, hypercarbia, hypoTN, prolonged seizure.
Penetrating head injury.
SS of SAH
Sudden onset thunderclap HA. N/v, photophobia, meningismus (neck stiffness), decreased LOC, focal neurological deficits, sudden death.
Common causes of SAH
Trauma.
Ruptured cerebral aneurysm (75%): sac-like outpouching of vessel wall at arterial bifurcation, thin secondary blebs may form at wall and rupture. Have close relationship with penetrating arteries. Most commonly affect main branches of Circle of Willis (ACA>PCA>MCA>carotid bifurc).
Other vascular malformations: usually cause ICH.
Vasculitis.
Bleeding disorders.
Hemorrhagic infarctions.
Angiogram negative- venous hemorrhage, much more benign.
Investigative steps for suspected SAH.
CT head 1st line. Hyperdense cisterns and fissures on CT.
If CT head negative, do lumbar puncture for cell count. If there is blood in the CSF, compare amount in first to last tube. If traumatic tap, # blood cells should decrease by last tube. Can look for xanthochromia.
CTA.
Mgmt SAH
BP control: sBP <140 to reduce risk of further bleeding.
Fluids and lyte monitoring (watch for SIADH).
ICP control: may require intraventricular drain.
Aneurysm tx:
1) microsurgical aneurysm clipping: craniotomy. Anatomical cure (definitive, durable). RIsk of vessel occlusion, perforation).
2) Endovascular aneurysm coiling (IR procedure): higher incidence of incomplete aneurysm occlusion. Potential for aneurysm recurrence and rebleeding.
Complications of SAH
Aneurysm rebleeding.
Hydrocephalus.
Cerebral vasospasm: narrowing of arterial caliber due to irritation from blood outside the artery. Related to amt of blood on CT scan. Onset day 4-7 (new neurological deficit), may cause cerebral ischemia, altered LOC, fluctuating neuro deficits. Manage with CCB to reduce spasm, statins, hydration, ‘Triple H therapy’ –> HTN (sBP >180), Hypervolemia, Hemodilution which together act to force blood through vessels. Get gradual resolution over 2-3 weeks.
RF for brain tumors
Ionizing radiation, genetic syndromes
Presentation + initial tx of brain tumors
Increased ICP –> mass effect, edema, obstructive hydrocephalus. SS = HA (worse in morning, lying down, n/v), drowsiness, visual obscuration, papilledema, CN VI palsy (horizontal diplopia).
Tx w/ steroids to decrease edema, anticonvulsants.
If no focal deficits, consider frontal lobe tumors.
Mgmt: mgmt of symptoms, surgical resection, EBRT, chemo.
