Case 91 - CNS Flashcards
What is subarachonid hemorrhage (SAH) and what are risk factors for it?
SAH = extravasation of blood into SA space
- causes - traumatic head injury, ruptured aneurysm
Risk Factors for aneurysm SAH
- previous hx of SAH
- cocaine
- HTN
- smoking
- marfan and ehlers-danlos (inc risk of aneuyrsm formation)
how is SAH diagnosed? (what are the s/sx and radiological tests)
S/sx:
- worse headache of my life
- increase ICP: n/v, loss of conciousness, seziures, CN palsies
- focal neurologic deficit, muchal rigidity
Imaging:
- noncontrast CT
- Lumbar puncture
- presence of RBC in spinal fluid
-
Cebral angiography = gold standard
- aside from diagnosis, allows ability to treat (coil)
- CT angiogram
Patient comes with the worst headache of her life. You suspect SAH, how will you manage this?
- ABC
-
mental status examination
- continuous monitoring of mental status –> loss of consciousness, inability to protect airway, and resp failure = emergent intubation
-
Etiology
- traumatic vs nontraumatic SAH
- traumatic SAH (TBI) requires eval of other injuries (tamponade, pneumothorax, c-spine injury, intraabdominal organ rupture
- nontraumatic - cerebral aneurysm
- traumatic vs nontraumatic SAH
- Hunt and Hess Grading scale for SAH (mortality %)
- surgical vs medical management
- early surgical management improves outcomes
- surgical clipping vs endovascular coiling
- medical mgmt - focus on avoiding complications (vasospasm, rebleed, hydrocephalous, inc ICP, hyponatremia (SIADH)
What is the Hunt and Hess grading scale?
Hunt and Hess grading scale
- classifies severity and estimated risk of mortality after SAH
Grades
grade 1 = mild headache
grade 2 = mod to sev headache, nuchal rigidity, CN palsy
Grade 3 = lethargy, confsuion, mild focal deficit
grade 4 = stupor, mod-severe hemiparesis,
grade 5 - coma, moribund, decerebrate rigidity (77% mortality)
Where is the most common location for cerebral aneursym?
anterior communicating artery (30%)
patient has SAH, which surgical better is better, surgical clipping or endovascular coiling?
- decision to coil or clip is determined by size, shape, location of each anuerysm, patient condition, and experience of physician
- endovascular coiling
- shown to improve disability and death at 1 year
- surgical clipping assoc with higher mortality and seziure rates
- endovascular coiling assoc with early rebleeding
What are the complications associated with SAH?
- rebleed
- cerebral artery vasospasm
- hyponatremia (SIADH or cerebral salt wasting)
- hydrocephalus and inc ICP
- Seizures
discuss rebleed in SAH patients and how to prevent it?
- Most common complication in first 24 hrs s/p SAH insult
- aneurysm clipping or coiling = best way to prevent it
-
Antifibrinolytics
- aminocaproic acid, tranexamic acid
- limit use to first 3 days (associated with cerebral vasospasm)
- use cautiously in pt with hx of MI, PE, hypercoagulablity
-
Lower BP
- decreases stress of arterial walls
- labetolol, nicardipine (do not cause cerebral vasodilation)
patient suffered a SAH 5 days ago, he is monitored in the neuro ICU. All of a suddent he experiences acute altered mental status, and has new focal neuro deficits. What is he expericing, and what are the risk factors
Cerebral Vasospasm
- occurs between day 3 to day 14 after SAH
- symptomatic pts seen 20-40% of time despite radiological evidence of spasm
RF
- poor clinical status
- thick blood on CT (> 1 mm thick)
- HTN
- volume depletion
- low CO
- smoking
- vasospasm on inital angio
What imaging studies can be used to dx cerebral vasospasm?
1) transcranial doppler
- TCD - used at bedside
- mean flow velocities of middle cerbral artery
- when flow velocity increases –> suggestive of vasospasm
2) cerebral angiography
* gold standard
pt has cerebral vasospasm, how can you prevent this and how do you treat this?
prevention
-
Nimodipine
- only med in clinical trials to improve outcome
- given prophylactically to prevent vasospasm
TX - triple H
-
HTN
- increase SBP 20-30 mmHg above baseline (but not > 200)
-
hemodilutoin
- crystalloids to dilute HcT to 30% –> decrease viscosity of blood –> improve tissue blood flow
- hypervolemia
TX - direct intraarterial injection of CCB
- *
Patient has SAH, you would like to prevet associated complications, which include hydrocepahlus, inc ICP, seizures, and hyponatremia. How would you prevent/tx these complicatoins
1) hydrocepahlus
* tx with external ventricular device –> divert CSF flow
2) inc ICP
- external ventric device –> remove CSF to decrease CSF pressure
- mannitol, hypertonic saline –> dec brain swelling
3) seizures
* prophylactic anticonvulsant therapy for 7 days
4) Hyponatremia (SIADH vs cerebral salt wasting)
- SIADH
- hyponatremic + hypervolemic or euvolemic
- fluid restriction
- Demeclocycline - blocks binding of ADH to receptors (V2 receptor)
- V2 receptor antagonist -> tolvaptan
- cerebral salt wasting
- hyponatremia + hypovolemic
- salt tablets, hypertonic saline
What is ICP, and what determines your ICP?
Normal ICP is 7 - 15 mm Hg
ICP > 20 = intracranial HTN –> needs rapid eval
Cranial Vault
- comprised of brain, blood, and CSF
- closed, noncompliant system
-
increase in 1 area needs to result in a decrease in another area (compensatory mech):
- CSF shifted from cranial vault SAH to spinal SAH
- increase CSF absoprtion to systemic circulation
- increase venous blood sent to systemic circulation
- eventually compensatory mechanism become exhausted, cranial compliance decreases, small change in volume results in large change of pressure
what are etiologies of increased ICP?
Cranial vault: blood, CSF, brain tissue
Brain tissue
- tumor
- hematoma
- abscess
- cerebral edema
- 2/2 vasogenic (mass), cytotoxic (ischemia), hypoosmolarity intravascular space (shifts water into brian cells)
CSF - Obstructive
- cerebral aqueduct stenosis
- obstructive tumor blocking flow of CSF
CSF - non-obstructive
- hemorrhage (SAH, IVH)
- infection (meningitis)
Blood
- loss of autoregulation
- sinus thrombosis (inhibit flow of venous blood to systemic circulation)
patient comes to the ER with n/v, headaches, mild confusion, papilledema. You suspect increase ICP. How will you manage this patient?
Goals: increase CPP, decrease ICP
1) surgical consultation
2) ABC
3) Increase CPP
- CPP = MAP - ICP/CVP
- CPP of 60 - 100 mm Hg
- increase CPP prevents ischemia (ischemia results in further cerebral edema and inc ICP)
- Vasopressors, fluids
4) decrease ICP
- elevate head of bed to facilitate venous drainage
- check tube ties around neck (do not compres jugular)
- isotonic mainteance fluids (LR, NS)
- short term hyperventilation (PaCO2 30-35)
- Mannitol (0.5 - 1 g/kg) or hypertonic saline
5) decrease CMRo2
- consider sedation (propofol)
- avoid hyperthermia
- avoid shivering
6) control pain
7) prevent seizures
8) avoid hypoglycemia or hyperglycemia
What kind of ICP monitoring can you do?
- Ventricular Catheter
- gold standard
- allows for CSF drainage
- intraparenchymal catheter
- easier to place
- measures localized pressure only
Patient comes to the ICU with ischemic stroke. How will you manage this patient?
1) ABC
2) rule out life-threatening complications
- brain herniation, status epilepticus, and obstructive hydrocephalus (from edema or hemorrhagic conversion)
- s/sx brain herniation: n/v, cushing traid (htn, brady, resp irregularity), apnea or abnormal breathing, assymetric pupil
3) After, complete neuro exam performed
4) noncontrast CT
* to rule out hemorrage or other findings that contraindicate use of thrombolytic
5) assess candidacy for thrombolytic therapy
6) euglycemia - 140 to 180
7) prophylactic antiseizure for ONLY those that are suspected to have seizure activity
who are candidates for tPA therapy, who is it contraindicated in?
tPA candidates
- > 18 yo
- onset of symp within 3 hrs
contraindications
- cerebral hemorrhage
- history of stroke within 3 months
- previous intracranial bled, aneursym, AVM
- s/sx suggestive of SAH
-
elevated BP
- systolic > 185; diastolic > 110 (risk of bleeding)
- lab findings - coagulpathic (dec plt, inc INR, PTT)
What is Status Epilepticus (SE)?
- epileptic seizure of greater than five minutes or more than one seizure within a five minute period without the person returning to normal between them.
- convulsive SE vs nonconvulsive SE
- convulsive SE: Loss of consciousness, genearlized convulsions, tonic and clonic phases
- nonconvulsive SE: loss of consciousness without generalized convulsions
Why is treating seizures of upmost importance?
- seziures = abnormal excessive paroxysmal cortical discharges with motor, sensory, or cognitive dysfunction
-
allowing seizures to continue leads to:
- increase CMro2
- hyperthermia
- acidosis
- rhabodmyloysis
- trauma
- cardiac arrhythmas
- cerebral damage/ischemia
How do you treat seizures?
Goals: break seizure, prevent future seizure
1) break seizure
- BZD (GABA A receptor agonist)
- for intractable seizures –> propofol or barbiurates
2) control seizures / prevent future recurrence
- phenytoin or fosphenytoin (dilantin)
- carbamazepine
- levetriacetam (keppra)
-
valproic acid (depakote)
*
who should prophylactic therapy seizure meds be given to, and who is not recommended for?
prophylactic seizure med
- give to hemorrhagic stroke pts
- intracranial tumors
not recommended
- acute ischemic stroke (b/c risk is low)
Describe what each of the four fundamentals mean in terms of brain death criteria: irrversibility, absence of neuro function, apnea, additional confirm tests.
brain death criteria - 4 elementsh
1) Irreversibility
- demonstration of mechanism of injury to brain and anatomic findigs to prove such injury (CT, MRI)
- account for all reversible factors:
- hypothermia, intoxication, sedative drugs
- residual NMBD agents, electrolyte abnormalities, acid-base derangements
- neuro exam should not be improving over time
2) absence of neuro function
- all brainstem functions are absent:
- pupils not reactive, no corneal, pharyngeal (gag), tracheal reflexes
- pt does not grimace to pain
3) Apnea
* upon disconnection from vent, PaCO2 should rise > 60 mmHg with no respiration
4) confirm test
* most sensitive confirm test = cerebral angiography
