NeuroICU Board Review Question Book Flashcards
Treatment for cerebellar hemorrhage with clinical deterioration and evidence of brainstem compression (shift/herniation)?
Decompressive surgery
ICH Score
GCS: 2: 3-4, 1: 5-12, 0: 13-15
ICH volume 30 or more: 1
IVH: yes:1
Age: 80 or older: 1
Infratentorial: yes: 1
Otherwise = 0
5 or 6 = 100% 30 day mortality
Right middle cerebral artery stroke with ischemic cerebral edema and mass effect treament?
Decompressive hemicraniectomy
Location of ischemia causing ipsilateral dilated pupil, contralateral hemiparesis (sometimes bilateral), and abnormal extensor posturing
Middle cerebral artery (can have transtentorial herniation)
Kernohan Notch Phenomenon
Ipsilateral weakness to side of stroke,
“false localizer”
Charles Bonnet Syndrome
Partial or severe blindness resulting in complex visual hallucinations
“Visual release hallucinations”
Foster-Kennedy Syndrome
Frontal lobe masses
Ipsilateral optic atrophy with contralateral papilledema
Terson Syndrome
Intraocular hemorrhage associated with SAH
Usually associated with sudden aneurysm rupture
Anton Syndrome
Cortical blindness/visual agnosia from bilateral occipital damage
Patients unaware of visual deficit and confabulate visual scenes
Diagnosis of headache, blurred vision, seizures with severe hypertension with MRI with focal regions of confluent symmetric hemispheric vasogenic edema most commonly in occipital and parietal lobes?
Posterior reversible encephalopathic syndrome
Reversible posterior leukoencephalopathy syndrome
Presumed etiology of PRES
Failed autoregulation resulting in hyperperfusion and endothelial dysfunction/injury
Conditions associated with PRES
Eclampsia
Renal failure
Sepsis
Autoimmune disorders
Transplantation
Immunosupprassive therapies: cyclosporine and tacrolimus
Diagnosis
Posterior reversible encephalopathic syndrome - PRES
Reversible posterior leukoencephalopathy syndrome
Diagnosis: headache, seizures, temporal lobe hemorrahges or infarctions?
Thrombosis of the vein of Labbee
Side effect of IV alteplase and who is at increased risk of developing this complication?
Angioedema
Patients taking ACE-inhibitors
Treatment of IV alteplase angioedema?
Histamine antagonists: ranitidine and diphenhydramine
Corticosteroids
Lemierre syndrome
Thrombophlebitis of the internal jugular vein and bacteremia preceeded by recent oropharyngeal infection/abscess
Type of stroke in Sickle Cell patients by age
<10 - ischemic
20-30 - hemorrhagic - ruptured cerebral aneurysm
>30 - ischemic
Management of acute stroke in Sickle Cell patients
Thrombolytics and anticoagulation avoided but can be considered on a case-by-case basis
Exchange transfusion to lower % of sickle cell hb to 30% or less of total hemoglobin with total hb level 10 or less
Factor associated with thrombosis of dural sinus and/or cerebral veins? How many have seizures? What is the treatment?
Hereditary or acquired thrombophilias
Inflammatory conditions
Transient conditions: pregnancy, puerperium, dehydration, parameningeal infection
Some meds: tamoxifen, steroids, IV Ig, OCP
Head trauma
40% have focal or generalized seizures
Anticoagulation
Ischemic Stroke + Livedo reticularis diagnosis, pathology, etiology, Ab?
Sneddon syndrome
Rare noninflammatory thrombotic vasculopathy
Primary idiopathic or associated with primary autoimmune disorder: SLE, antiphospholipid antibody (up to 78% with these antibodies)
Reversal agent for dabigatran
Idraucizumab
Treatment/reversal of IV alteplase hemorrhagic conversion
Cryoprecipitate
Rivaroxaban reversal agent
Andexanet alfaH
Heparin reversal agent
Protamine sulfate
Cerebral amyloid angiopathy etiology
beta-amyloid deposits in small arteries of the leptomeninges and cerebral cortex
MCC lobar intraparenchymal hemorrhage in elderly (esp alzheimers)
Severe thunderclap headache with or without other acute neurologic symptoms and diffuse segmental constriction of cerebral arteries diagnosis, can have hemorrhagic or ischemic strokes
Reversible cerebral vasoconstrictive syndrome
Convexity/sulcal SAH
Imaging: segmental constriction of cerebral arteries, normalizes within 3 months on imaging
Controversial: use of nimodipine, verapamil and/or magnesium
Recovery within days to weeks
Cerebral small-vessel arteriopathy (nonhypertensive) with subcortical infarcts with alopecia and spondylosis diagnosis
Cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy (CARASIL)
Early adulthood onset
HTRA1 gene
CVA in 40’s and 50’s with migraines with subcortical infarcts diagnosis
Cerebral autosomal dominant arteriopathy with subcotial infarcts and leukoencephalopathy (CADASIL)
KRIT1 gene
Familial cerebral cavernous malformations
Fabry disease multation
GLA
Retinal vasculopathy with cerebral leukodystrophy mutation
TREX1
DAWN trial
Endovascular thrombectomy reduced poor outcome and disability in select patients up to 24 hours after ischemic stroke in patients with mismatch between clinical deficit and infarct volume (worse deficit then CVA volume would suggest)
Lindegaard ratio
Middle cerebral artery velocity / internal carotid artery velocity
Mean flow velocities >120 cm/s = abnormal
Ratio <3 = normal
>6 = distinguishes severe from moderate vasospasm
Thrombocytopenia, microangiopathic hemolytic anemia, neurologic symptoms, rneal failure and fever
Thrombocytopenic thrombotic purpura
ADAMTS13 activity reduced
Tx: plasma exchange transfusion
Most common segment involved in a spontaneous vertebral artery dissection
Distal V3 segment - relatively mobile and unfixed, susceptible to tearing with sudden motion and stretching
World Federation of Neurologic Surgeons Scale of SAH
GCS 15, no motor deficit = 1
13-14, no = 2
13-14, yes = 3
7-12, either = 4
3-6, either = 5
Hunt and Hess Scale for SAH
Who get screened for unruptured aneurysms?
Families with 2 first-degree relatives with know IA
Patients with a family history of IA
Autosomal dominant polycystic kidney disease
Type IV Ehlers-Danlos syndrome
Microcephalic osteodysplastic primordial dwarfism
Consider in patients with 1st degree relative and conditions with increased risk of IA - ex: coarctation of aorta or bicuspid aortic valve
Modified Fisher Scale
Rare complication of rTPA
Angioedema from activation of complement and kinin cascade from increased concentrations of plasmin especially in patients on ACEI
How is rTPA potentially neurotoxic?
Cross blood-brain barrier and increase ischemic injury via potentiation of N-methyl-D-aspartate (NMDA) -induced cell death and increase in NMDA-mediated intracellular calcium levels
Treatment of acute ischemic stroke under 4.5 hr from onset (NIHSS <25, <1/3 MCA involvement, no prior CVA and DM, any anticoagulant use)
IV r-tPA
Treatment of acute ischemic stroke under 8 hours from onset, with terminal carotid, MCA (M1 or M2) or basilar artery occlusion with <1/3 hemisphere territory infarcted with ability to perform arterial puncture within 8 hours from stroke onset)?
Intra-arterial prourokinase, r-tPA or mechanical clot extraction
Indications for IABP
- Acute congestive heart failure exacerbation with hypotension
- As prophylaxis or adjunct treatment in high risk percutaneous coronary intervention
- Myocardial infarction with decreased left ventricular function leading to hypotension
- Myocardial infarction with mechanical complications causing cardiogenic shock, i.e., acute mitral regurgitation due to papillary muscle rupture or ventricular septal rupture
- Low cardiac output state after coronary artery bypass grafting surgery
- As a bridge to definitive treatment in patients with any of the following conditions; intractable angina or myocardial ischemia, refractory heart failure, or intractable ventricular arrhythmias
Contraindications for IABP
- Uncontrolled sepsis
- Uncontrolled bleeding diathesis
- Moderate to severe aortic regurgitation
- An aortic aneurysm or aortic dissection
- Severe peripheral artery disease unless pretreated with stenting
Indications for ventricular assist device
- High-risk percutaneous intervention, there is no precise definition for high-risk percutaneous coronary intervention (PCI), and many factors should be taken into consideration like impaired LV function, left main stenosis, ostial stenoses, heavily calcified lesions, and cardiogenic shock.
- Acute myocardial infarction. Some patients with (STEMI) and non-ST-elevation myocardial infarction (NSTEMI) would benefit from circulatory support to unload the LV and improve the coronaries’ perfusion; however, no evidence of the benefit of the mechanical circulatory support in decreasing the myocardial injury in the setting of acute occlusion.
- Cardiogenic shock and advanced heart failure stabilize critically ill patients and serve as a bridge to recovery, surgical, mechanical circulatory support, or transplant.[4]
Selected high-risk patients undergoing percutaneous aortic valvuloplasty or aortic valve replacement.[8] - Patients with severe LV dysfunction undergoing electrophysiologic procedures as these high-risk patients will be intolerant to prolonged ventricular arrhythmia during the procedure.[9]
- Right ventricular failure using percutaneously inserted RVD. RECOVER RIGHT trial demonstrated the safety and the immediate hemodynamic stabilization in patients with acute RV failure.[6]
Contraindications to percutaneous inserted ventricular assist device
- Significant peripheral vascular disease
- Aortic stenosis (less than 1.5 cm) or insufficiency
- Ventricular septal defect. The percutaneously inserted LVD increases the left to right shunt significantly
- Left ventricular thrombus [3]
Inclusion criteria for extracorporeal cardiopulmonary resuscitation
- Age <70 years
- Cardiopulmonary arrest to first CPR <5 minutes
- Witnessed arrest
- Ventricular fibrillation (VF) or paroxysmal ventricular tachycardia (pVT) or pulseless electrical activity (PEA) as initial cardiac rhythm
- Recurrent VF or intermittent ROSC
- Absence of comorbidities like end-stage heart failure/chronic obstructive pulmonary disease/liver failure/end-stage renal failure or terminal irreversible illness
- No known aortic valve incompetence
Indications for VA ECMO
- VA ECMO is used to provide both respiratory and cardiac support.[15]
- Cardiac conditions with low cardiac output (cardiac index < 2L/min/m) and hypotension (systolic blood pressure <90 mmHg) despite inotropic and intra-aortic balloon pump support.
- Cardiogenic shock secondary to either acute coronary syndrome, refractory cardiac arrhythmia, sepsis leading to cardiac depression, myocarditis, pulmonary embolism, drug toxicity, cardiac trauma, anaphylaxis, acute decompensated heart failure, septic shock; where cardiac activity is compromised and unable to pump out the adequate blood to meet the body’s demand.
- Periprocedural for high-risk cardiac interventions
- Postoperative heart failure: Inability to wean from cardiopulmonary bypass after cardiac surgery; ECMO is very useful post-operatively to provide rest for the heart and helps in recovery after the surgery.
- Post heart transplant: after heart or lung-heart transplantation in cases of primary graft failure
- Bridge to long-term VAD support or bridge to heart/lung transplant.
Indications for VV ECMO
- VV ECMO is used for respiratory support in those who do not respond to mechanical ventilation or any acute potentially reversible respiratory failure.[15]
- Acute respiratory distress syndrome secondary to either severe bacterial or viral pneumonia, including COVID-19 or aspiration pneumonitis. ECMO bypasses the compromised activity of the lungs and maintains oxygenation and ventilation with the removal of CO2.[2]
- Covid-19 Severe Respiratory Failure: ARDS due to SARS-CoV-2 infection when prolonged mechanical ventilatory support fails. In some cases, when ventilation fails, ECMO support (venovenous ECMO) has been initiated.[5]
- Extracorporeal assistance to support lung in cases of airway obstruction, pulmonary contusion (barotrauma), smoke inhalation, drowning, air leak syndrome, hypercapnia, or hypoxic respiratory failure
- Status asthmaticus
- Massive hemoptysis or pulmonary hemorrhage
- Bridge to lung transplant
Support for lung resections in unstable patients.
Contraindications (absolute and relative) to ECMO
Absolute
* Unwitnessed cardiac arrest
* Prolonged CPR without adequate tissue perfusion
* Not a transplant or VAD support candidate
* Unrepaired aortic dissection
* Severe aortic regurgitation
* Unrecoverable severe brain injury
* Disseminated malignancy
* Severe organ dysfunction, for example, emphysema/cirrhosis/renal failure
* Peripheral vascular disease in cases of peripheral VA ECMO
* Lethal chromosomal abnormalities
* Pulmonary hypertension (mean pulmonary artery pressure >50 mmHg) or cardiogenic failure: VV ECMO is contraindicated
Relative
*Obesity
*Advanced age
* Pre-existing chronic illness with long term poor prognosis
* Prolonged mechanical ventilation >14 days
Neurologic Complications to LVAD
Ischemic stroke - most common neurologic complication
Hemorrhagic stroke
TIA
Generalized hypoxic-ischemic event
Mycotic aneurysms
Cerebral abscess
Seizures
Encephalopathy
Neurologic Complications to ECMO
ICH - SAH, IPH, SDH - most common neurologic complication
Ischemic stroke
Seizures
Hypoxic-ischemic brain injury
Brain death
Harlequin syndrome: LV starts to recover while lungs are poorly oxygenated
Management of pulmonary hypertension
Diuretics for fluid retention and right ventricular failure
ACE inhibitors, b-blockers, angiotensin receptor-neprilysin inhibitors or ivabradine - NOT recommended for PAH unless other indications exist
Long term Oxygen if PaO2 <60
CCB - first line - amlodipine or nifedipine if bradycardic at baseline, dilt if tachy at baseline
Ambrisentan - endothilian receptro type A antagonist, bosentan and macitentan type A and type B
PDE type 5 inhibitors - sildenafil, tadalafil, vardenafil
Epoprostenol - prostacyclin analog
RTA diagnosis
Type 1 - impaired distal NH4 secretion, HCO3 <-15, low K, urine pH >5.5, + urine anion gap, common nephrocalcinosis
tx: correct electrolytes
Type 2 - reduced proximal HCO3 resorption, HCO3 -6 to -15, low-normal K+, urine pH <5.5 (increased urine HCO3), urine anion gap negative, rarely nephrocalcinosis
Tx: replace bicarb, citrate, potassium and sodium
Type 4 - decreased aldosterone secretion or resistance, HCO3 >15, high K+, urine pH <5.5, urine anion gap +, nephrocalcinosis: rare
tx: stop K+ retaining drugs, can give loop (lose K+) diuretics
FeNa calculation
AKI vs ATN
(Urine Na x Serum Cr) / (Serum Na x Urine Cr)
<1% = prerenal
>2% = ATN
Not accurate in mild AKI, AKI on CKD, recent diuretics
FeUrea calculation
AKI vs ATN
(Urine Urea x Serum Cr) / (Serum Urea x Urine Cr)
< 35% = prerenal
>35% = ATN
AIN vs ATN
AIN: allergic reaction causing interstitial inflammation, fever, rash, flank pain, arthralgia
ATN: no inflammation, kidney tubules
Bx for diagnosis
Renally eliminated anti-epileptic drugs
Levetiracetam
Gabapentin
Pregabalin
Topiramate
Eslicarbazepine
Lacosamide
Vigabatrin
IMPACT and CRASH trial looked at what?
Steroids in TBI
When to intubate MG patients?
VC < 20 mL/kg
NIF < -30
Maximal expiratory pressure <40 cm H20 or >30% or more decline in measurements on serial testing
Some use: VC <15 mL/kg or NIF < -20
What is discontinued during a myasthenic crisis? What is given?
Pyridostigmine
Tx: Corticosteroids, IvIg and Plasmapheresis
Contraindications to IvIg
Renal failure
Hypercoagulable states
Contraindications to plasmapheresis
Sepsis due to hemodynamic issues and bacterial colonization of plasmapheresis catheter
OD of pyridostigmine can trigger what?
Cholinergic crisis in MG (generalized weakness, miosis, excess pulmonary secretions, muscle fasciculations, abdominal cramping, diarrhea, diaphoresis, bradycardia)
Tx: support, stop pyridostigmine, tx myasthenic crisis (steroids, IvIg, Plasmapheresis)
HUS vs TTP
CSF normal, bacterial, viral, fungal
Bacterial: turbid, elevated opening pressure, most WBCs, low glucose
Viral: lymphocytes, low protein
Fungal: lowest WBC, high protein, normal or low glucose
Toxidromes
Pupils
*Dilated: antichol and symatho
*Pinpoint: cholingergic, opiods
HR-BP:
Up: antichol, sympath
Low: opoids, sed
Resp
Up: sympath
Low: opoid, sed
Temp:
Up: antichol, sympath
Low: opoid, sed
Bowel tones:
None: antichol, opoid, sed
Hyperactive: chol, sympath
Diaphoresis: chol, sympath
Serotonin syndrome versus neuroleptic malignant syndrome
Terson’s syndrome
Blindness from vitreous hemorrhage in setting of ICH with elevated ICP
Abulia and LE motor deficits can occur in vasospasm of which artery?
Anterior Cerebral Artery
Aphasia and motor deficit of upper and lower extremities can occur in vasospasm of which artery?
MCA - can also cause temporal lobe seizures or hemiparesis
Aneurysm that can cause Horners
Cavernous segment of carotid artery (compresses postganglionic symathetic pathway)
Posterior Circulation aneurysms can cause what?
Weber syndrome
Brainstem compression syndromes
CN III, and CN VI
Lower cranial nerve palsy
What symptoms can anterior communicating aneurysms cause?
Dementia
Abulia
Pituitary dysfunction
Denver criteria
3.0 to 3.5 Hz irregular generalized spike and wave or polyspike and wave diagnosis, precipitating drugs and what medication to avoid?
Absence seizures
Precipitating drugs: phenytoin, carbamazepine, oxcarbazepine and tiagabine
Avoid phenytoin in kids
Mixed 4 to 7 Hz theta with 12-16 Hz spindle activity diagnosis and hallmarks? Differentiation between two? When else can it be seen? What does it indicate?
Spindles
Spindle coma (high mesencephalic/midbrain lesions) versus stage II sleep - can arouse from sleep, not spindle coma
Can also see in post traumatic or post encephalitic encephalopathies
Harbinger of favorable prognosis for some meaningful recovery
Monotonous diffuse alpha activity diagnosis and assocation? Location of lesions or etiologies?
Alpha coma
Poor prognosis
Brainstem lesion or just caudal to pontomesencephalic junction
Toxic or metabolic abnormalities including barbiturate OD and hyperglycemic, hyperosmolar coma
PML vs MS MRI lesions
PML: confluent demyelination at juxtacortical white matter or near deep gray matter
MS: periventricular white matter
Marburg’s variant
Rapidly progressing demyelination
Multifocal lesions in cerebral hemispheres, brainstem and optic nerves
Pseudotumor variant possible
Path: extensive necrosis, massive macrophage infiltration, severe and extensive demyelination
CSF: mononuclear pleocytosis
Tumefactive MS vs Marburgs (Marburgs has homogenous contrast uptake)
6 weeks after viral illness or immunization, rapid multifocal or focal neurologic symptoms (motor then sensory deficits, brainstem signs and cerebellar signs), encephalopathy, MRI: large and confluent white matter edematous lesions: multiple, bilateral but asymmetric and enhance simultaneously or nearly simultaneously with gadolinium diagnosis?
Acute disseminated encephalomyelitis
Most common after measles
MRI with symmetric areas of abnormal high signal intensity in pons on T2-weighted images
Central Pontine Myelinosis
MRI with increased signal intensity on T2 without evidence of restricted diffusion or contrast enhancement diagnosis
Low-grade glioma
Treatment for glioblastoma multiforme
Resection
Concurrent chemotherapy (temozolomide)
Radiation
Additional adjuvant chemotherapy
Bevacizumab slows progression of recurrence
Treatment for metastatic epidural spinal cord compression (MESCC)
Corticosteroids
Surgery
Radiation therapy
Most common symptom of carcinomatous meningitis?
Diplopia
CSF of carcinomatous meningitis?
Increased opening pressure (>200 mmHg)
Increased leukocytes (>4)
Increased protein (>50)
Decreased glucose (<60)
