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Symptom
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Clinical Reference
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Arteriovenous Malformation (Ruptured)
Cardiovascular Presentations
Abdominal aortic aneurysm
Acute coronary syndrome (NSTEMI)
Acute coronary syndrome (STEMI)
Acute decompensated heart failure
Acute limb ischemia
Acute mesenteric ischemia
Aortic dissection
Aortic stenosis
Atrial fibrillation and flutter
Bradyarrhythmia and heart block
Cardiac arrest
Deep vein thrombosis
Myocarditis
Pericarditis
Pulmonary embolism
Stable angina
Superficial thrombophlebitis
Superior vena cava syndrome
Supraventricular tachycardia
Syncope (cardiogenic)
Unstable angina
Ventricular tachycardia
Respiratory Presentations
Acute bronchitis
Acute respiratory failure
Aspiration pneumonia
Asthma exacerbation
Bronchiolitis
Community-acquired pneumonia
COVID-19 pneumonia
COPD exacerbation
Croup
Croup (laryngotracheobronchitis)
Epiglottitis
Hemothorax
Hospital-acquired pneumonia
Pleural effusion
Pneumothorax (traumatic)
Pulmonary contusion
Spontaneous pneumothorax
Neurological Presentations
Bell's palsy
Benign paroxysmal positional vertigo
Brain abscess
Cauda equina syndrome
Cervical radiculopathy
Concussion (mild traumatic brain injury)
Encephalitis
Guillain-Barré syndrome
Hemorrhagic stroke (intracerebral)
Ischemic stroke
Lumbar radiculopathy
Malignant spinal cord compression
Migraine
Peripheral neuropathy (acute)
Retropharyngeal abscess
Schizophrenia (acute exacerbation)
Seizure (breakthrough:known epilepsy)
Seizure (first-time)
Spinal cord injury
Status epilepticus
Subarachnoid hemorrhage
Tension headache
Transient ischemic attack
Traumatic brain injury (moderate-severe)
Vestibular neuritis
Viral meningitis
Gastrointestinal Presentations
Acute appendicitis
Acute cholecystitis
Acute diverticulitis
Acute pancreatitis
Anal fissure
Choledocholithiasis and cholangitis
Clostridioides difficile colitis
Gastritis
Gastroenteritis (viral and bacterial)
Gastroesophageal reflux disease
Incarcerated or strangulated hernia
Inflammatory bowel disease flare
Large bowel obstruction
Lower GI hemorrhage
Peptic ulcer disease
Perforated viscus
Small bowel obstruction
Upper GI hemorrhage
Genitourinary and Reproductive Presentations
Acute prostatitis
Acute urinary retention
Ectopic pregnancy
Epididymitis
Orchitis
Ovarian torsion
Paraphimosis
Pelvic inflammatory disease
Priapism
Pyelonephritis
Renal laceration
Ruptured ovarian cyst
Testicular torsion
Tubo-ovarian abscess
Urinary tract infection (uncomplicated)
Urolithiasis (renal colic)
Vaginal bleeding (non-pregnant)
Infectious Disease Presentations
Acute sinusitis
Acute tonsillitis
Acute upper respiratory infection
Animal bite
Bacterial meningitis
Cellulitis
Conjunctivitis (bacterial)
Dental abscess
Endocarditis
Febrile neutropenia
Fournier gangrene
Hand-foot-mouth disease
Hepatitis (acute)
Herpes zoster
HIV-related illness
Human bite
Impetigo
Infected diabetic foot ulcer
Infectious mononucleosis
Influenza
Necrotizing fasciitis
Osteomyelitis
Otitis externa
Parasitic infection
Periorbital cellulitis
Peritonsillar abscess
Scabies
Sepsis
Septic arthritis
Spontaneous bacterial peritonitis
Tick-borne illness (Lyme disease)
Tinea infection
Tuberculosis
Viral exanthem
Wound infection
Trauma Presentations
Achilles tendon rupture
ACL and mceniscus tear
Ankle fracture
Ankle sprain
Burn
Calcaneus fracture
Cervical spine fracture
Clavicle fracture
Dental avulsion
Distal radius fracture
Drowning
Elbow fracture and dislocation
Electrical injury
Facial bone fracture
Facial laceration
Femur fracture
Fingertip amputation
Forearm fracture (radius and ulna)
Frostbite
Hand:finger laceration
Heat exhaustion
Heat stroke
Hip fracture
Humeral shaft fracture
Knee dislocation
Knee sprain
Lightning injury
Mandible fracture
Metacarpal fracture
Metatarsal fracture
Muscle strain
Nasal fracture
Non-accidental trauma
Orbital fracture
Patella fracture
Phalanx fracture (finger)
Proximal humerus fracture
Pulmonary contusion
Rib fracture
Rotator cuff tear (acute traumatic)
Scalp laceration
Scaphoid fracture
Shoulder dislocation
Skull fracture
Splenic laceration
Sternal fracture
Supracondylar pediatric fracture
Tendon laceration (hand:wrist)
Thoracic and lumbar spine fracture
Tibia:fibula fracture
Tibial plateau fracture
Toe fracture
Traumatic epistaxis
Traumatic hyphema
Toxicologic Presentations
Acetaminophen toxicity
Alcohol intoxication
Alcohol withdrawal
Anticholinergic toxicity
Anticoagulant overdose
Benzodiazepine overdose
Benzodiazepine:sedative overdose
Beta-blocker and calcium channel blocker toxicity
Carbon monoxide poisoning
Caustic ingestion
Digoxin toxicity
Drug eruption
Foreign body ingestion
Opioid intoxication
Opioid overdose
Opioid withdrawal
Organophosphate
Salicylate toxicity
Serotonin syndrome
Stimulant intoxication (cocaine, methamphetamine)
Tricyclic antidepressant overdose
Psychiatric Presentations
Acute anxiety
Acute psychosis
Agitation:behavioral emergency
Bipolar disorder
Conversion disorder
Major depressive episode
Neuroleptic malignant syndrome
Suicidal ideation and attempt
Musculoskeletal and Rheumatologic Presentations
Acute low back pain (mechanical)
Bursitis
Cervical radiculopathy
Costochondritis
Gout (acute)
Lumbar radiculopathy
Pseudogout
Tendinitis
Dermatology Presentations
Acute eczema (Eczema acute flare)
Allergic contact dermatitis
Erythema multiforme
Henoch-Schönlein purpura
Pressure injury
Psoriasis (acute flare)
Stevens-Johnson syndrome
Toxic epidermal necrolysis
Urticaria (acute)
Environmental and Exposure Presentations
Envenomation (snake, spider, insect)
High-altitude illness
Hypothermia
Hematologic and Oncologic Presentations
Acute chest syndrome
Coagulopathy
Hyperviscosity syndrome
Sickle cell crisis (vaso-occlusive)
Symptomatic anemia
Thrombocytopenia (severe)
Tumor lysis syndrome
Pediatric-Specific Presentations
Bronchiolitis
Croup
Emergency delivery
Febrile seizure
Kawasaki disease
Neonatal jaundice
Neonatal sepsis
Nursemaid's elbow
Pediatric fever 0 to 28 days
Pediatric fever 29 to 60 days
Pediatric fever 61 to 90 days
Pyloric stenosis
Slipped capital femoral epiphysis
Intussusception
Endocrine and Metabolic Presentations
Adrenal crisis
Diabetic ketoacidosis
Hypercalcemia
Hyperosmolar hyperglycemic state
Hypertensive emergency
Hypertensive urgency
Hypoglycemia
Myasthenia gravis crisis
Myxedema coma
Severe hyperkalemia
Severe hyponatremia
Thyroid storm
ENT and Maxillofacial Presentations
Acute laryngitis
Acute otitis media
Acute pharyngitis
Cerumen impaction
Epistaxis (anterior)
Nasal foreign body
Otitis externa
Tympanic membrane perforation
Ophthalmologic Presentations
Acute angle-closure glaucoma
Central retinal artery occlusion
Chemical eye injury
Corneal abrasion
Corneal ulcer
Globe rupture
Ocular foreign body
Orbital cellulitis
Retinal detachment
Obstetric Presentations
Hyperemesis gravidarum
Painful vaginal bleeding in pregnancy
Placenta previa
Placental abruption
Preeclampsia:eclampsia
Preterm labor
Threatened:inevitable:incomplete abortion
Systemic and Miscellaneous Presentations
Anaphylaxis
Angioedema
Cannabis-induced hyperemesis
Arteriovenous Malformation (Ruptured)
POCUS
Procedures
Calculators
Resuscitation
ECG Guide
Back
Clinical Assessment Checklist
Browse categories and answer follow-up questions to refine your symptom profile.
Approach to the Critical Patient
Immediate priorities
Airway and breathing threats
▶
GCS <= 8 requiring immediate airway protection
▶
Rapid sequence intubation preparation
Suction available at bedside
Herniation signs requiring emergent intervention
▶
Fixed dilated pupil unilateral or bilateral
Cushing triad: hypertension, bradycardia, irregular respirations
If GCS < 13, activate neurosurgery and neurocritical care immediately
▶
Non-contrast CT head within 25 minutes of arrival
CT angiography head concurrent if clinician available
Circulation and hemodynamic stabilization
▶
Blood pressure targets
▶
SBP target 130 to 140 mmHg per INTERACT-2 and INTERACT-3 data
Avoid SBP < 130 mmHg: associated with harm in hemorrhagic stroke
Avoid venous vasodilators: nitroprusside and nitroglycerin raise ICP
Large bore IV access bilateral antecubital
▶
Arterial line for continuous BP monitoring and titration
Central access if vasopressors anticipated
If active coagulopathy, immediate reversal
▶
Warfarin: vitamin K IV plus 4-factor PCC
Dabigatran: idarucizumab 5 g IV
Factor Xa inhibitors: andexanet alfa per weight and last dose
Thrombocytopenia: platelet transfusion if platelets < 100 x 10^9/L
Neurological stabilization and herniation prevention
▶
ICP management if herniation suspected
▶
Head of bed 30 degrees
Mannitol 0.5 to 1 g/kg IV bolus if herniation signs
Hypertonic saline 23.4% 30 mL IV for refractory herniation
Seizure management
▶
Levetiracetam 1000 to 3000 mg IV loading dose if clinical seizures
Prophylactic anticonvulsants not routinely recommended
Glycemic control
▶
Target glucose 6 to 10 mmol/l
Hyperglycemia worsens hemorrhagic stroke outcomes
Monitoring and targets
Continuous monitoring bundle
▶
Arterial line BP with continuous waveform
▶
SBP target 130 to 140 mmHg
Avoid hypertensive surges during procedures
Continuous cardiac monitoring
▶
Neurogenic cardiac injury pattern ECG
QTc prolongation with hypothalamic involvement
ICP monitoring indications
▶
GCS <= 8 with CT evidence of hydrocephalus or mass effect
External ventricular drain if obstructive hydrocephalus
Escalation triggers
▶
Declining GCS by 2 or more points
▶
Hematoma expansion CT
Emergent neurosurgery notification
Refractory hypertension SBP > 180 mmHg
▶
IV nicardipine or labetalol titration
ICU level care required
New herniation signs post admission
▶
Emergent repeat CT
Neurosurgery at bedside
Team activation and consults
Mandatory early consultations
▶
Neurosurgery
▶
All patients with ruptured AVM
Emergent for hematoma with mass effect or herniation
Interventional neuroradiology
▶
DSA for AVM characterization once stabilized
Embolization planning
Neurocritical care or ICU
▶
All patients requiring airway management
All patients with GCS <= 12
Hematology if coagulopathy or reversal agents required
▶
Complex anticoagulation reversal
Thrombocytopenia management
History
Symptom onset and characterization
Headache features
▶
Thunderclap headache or worst headache of life
▶
Maximal at onset characteristic of subarachnoid extension
Distinguishes from progressive tension headache
Associated nausea and vomiting
▶
Raised ICP marker
Meningeal irritation
Photophobia or phonophobia
▶
Subarachnoid hemorrhage extension
Meningismus correlation
Neurological symptom characterization
▶
Seizure activity at onset or after
▶
Approximately 20 to 25% of AVMs present with seizures
Todd paralysis mimicking focal deficit
Focal neurological deficits
▶
Hemiparesis or hemiplegia
Speech difficulty or aphasia
Visual field loss
Limb incoordination if posterior fossa
Altered consciousness
▶
GCS at scene and on arrival
Rate of deterioration
Prior symptoms and timeline
Preceding neurological symptoms
▶
Prior headaches different from usual
▶
15% of AVMs present initially with headaches
Sentinel headache preceding major rupture
Prior transient focal deficits
▶
Progressive focal deficits in less than 5% pre-rupture
May indicate steal physiology
Known AVM diagnosis or prior hemorrhage
▶
Annual re-rupture risk approximately 6% in first year post-hemorrhage
Returns to baseline 2 to 4% annually thereafter
Timing and triggers
▶
Exact time of onset or last known normal
▶
Critical for treatment window determination
Collateral history from witnesses essential
Activity at onset
▶
Typically spontaneous
May occur during exertion or Valsalva
Risk factors and past history
AVM rupture risk factors
▶
Prior hemorrhage: strongest predictor of re-rupture
▶
Annual re-rupture risk increases to 6% after first bleed
Deep venous drainage exclusive
AVM morphological features
▶
Small nidus size paradoxically higher rupture risk
Intranidal or feeding artery aneurysms
Single draining vein
Deep or periventricular location
Hypertension
▶
Modifiable risk factor for hemorrhage severity
Blood pressure control as secondary prevention
Relevant past medical history
▶
Prior seizures or unexplained headaches suggesting undiagnosed AVM
▶
Hereditary hemorrhagic telangiectasia family history
Prior neurosurgical procedures
Anticoagulant or antiplatelet use
▶
Warfarin, DOACs, aspirin, NSAIDs
Timing of last dose
Coagulopathies or bleeding disorders
▶
Hepatic disease
Hematologic malignancy
Family and social history
▶
Hereditary hemorrhagic telangiectasia
▶
Autosomal dominant: mutations in ENG, ACVRL1, SMAD4
10 to 20% of HHT patients have brain AVMs
Family history of hemorrhagic stroke or vascular malformations
▶
First degree relative with AVM or aneurysm
Family history of aneurysmal subarachnoid hemorrhage
Substance use
▶
Sympathomimetics precipitate hemorrhage
Smoking associated with higher mortality in deep-seated ruptured AVMs
Alcohol use and toxicology screen indications
Physical Exam
Vitals and general appearance
Hemodynamic snapshot
▶
Blood pressure
▶
Hypertension extremely common in AVM hemorrhage
Cushing reflex: severe hypertension with bradycardia indicates raised ICP
Heart rate and rhythm
▶
Neurogenic cardiac arrhythmias
Bradycardia as herniation sign
Respiratory rate and pattern
▶
Irregular respirations as herniation sign
Cheyne-Stokes pattern with bilateral hemispheric involvement
Temperature
▶
Hyperthermia worsens outcomes after ICH
Target normothermia
Neurological examination
Level of consciousness
▶
GCS: Eyes, Verbal, Motor components scored separately
▶
Baseline GCS determines airway management threshold
Serial GCS to detect deterioration
Orientation and cognition
▶
Confusion or agitation as ICP or herniation sign
Postictal state mimicking focal deficit
Pupillary assessment
▶
Size and symmetry
▶
Unilateral fixed dilated pupil: uncal herniation sign
Bilateral fixed dilated pupils: severe brainstem dysfunction
Reactivity to light direct and consensual
▶
Sluggish reactivity as early herniation
Hippus and Marcus Gunn pupil if optic nerve involved
Focal neurological deficits
▶
Motor function bilateral
▶
Hemiparesis or hemiplegia localizes hemorrhage hemisphere
Pronator drift subtle cortical sign
Cranial nerve exam
▶
CN III palsy with uncal herniation
Gaze preference indicating frontal or brainstem involvement
Facial asymmetry for hemispheric localization
Speech and language
▶
Aphasia with dominant hemisphere involvement
Dysarthria with posterior fossa lesion
Cerebellar function if posterior fossa suspected
▶
Ataxia
Dysmetria
Meningeal and fundoscopic examination
Meningismus
▶
Neck stiffness with passive flexion
▶
Subarachnoid extension of hemorrhage
Kernig and Brudzinski signs
Photophobia and phonophobia
▶
Meningeal irritation signs
May be absent in obtunded patient
Fundoscopic findings
▶
Papilledema suggesting raised ICP
▶
May lag acute ICP elevation by hours
Most reliable in subacute presentations
Subhyaloid hemorrhage (Terson syndrome)
▶
Blood in vitreous or preretinal space
Indicates subarachnoid hemorrhage with severe ICP spike
Skin and systemic findings
▶
Telangiectasias on lips, tongue, fingertips
▶
HHT screening for underlying genetic syndrome
Epistaxis history correlation
Cranial bruit on auscultation
▶
Rare but classic for large high-flow AVMs
Most common in children
Differential Diagnosis
Hemorrhagic stroke mimics
Life-threatening hemorrhagic diagnoses
▶
Ruptured cerebral aneurysm with subarachnoid hemorrhage
▶
ICD-10 I60.9 subarachnoid hemorrhage
Perimesencephalic or basal cistern blood pattern on CT
Differentiating clue: aneurysm blood pattern differs from AVM lobar hematoma
Hypertensive intracerebral hemorrhage
▶
ICD-10 I61.9 intracerebral hemorrhage
Typical locations: basal ganglia, thalamus, pons, cerebellum
Older patient with chronic uncontrolled hypertension
Ruptured dural arteriovenous fistula
▶
ICD-10 I67.1 cerebral arteriovenous malformation
Pulsatile tinnitus or orbital bruit history
DSA required for definitive differentiation
Secondary hemorrhage causes
▶
Hemorrhagic transformation of ischemic stroke
▶
Preceding ischemic symptoms and territory-specific infarct
Cortical ribbon pattern of hemorrhage
Hemorrhagic brain tumor
▶
Glioblastoma or metastasis with surrounding edema
Subacute onset with progressive symptoms
Ring-enhancing lesion on contrast CT or MRI
Cerebral venous sinus thrombosis with hemorrhagic infarction
▶
ICD-10 I63.6 cerebral infarction due to cerebral venous thrombosis
Parasagittal location, bilateral or multiple hemorrhages
Headache progressing over days before hemorrhage
Vascular lesion mimics
Cerebral cavernous malformation hemorrhage
▶
Typically smaller bleeds with lower acute morbidity
▶
Popcorn appearance on MRI from repeated small hemorrhages
Hemosiderin rim on gradient echo sequences
May be familial: CCM1, CCM2, CCM3 mutations
▶
Multiple lesions suggest familial form
Spinal cavernomas may coexist
Mycotic aneurysm
▶
ICD-10 I72.9 aneurysm of unspecified site
▶
Distal branch vessel location distinguishes from berry aneurysm
Endocarditis with septic emboli as underlying cause
Cerebral amyloid angiopathy
▶
Lobar hemorrhage in elderly patient
Recurrent hemorrhages
Cortical microbleeds on gradient echo MRI
Coagulopathy-related intracerebral hemorrhage
▶
Anticoagulant use with supratherapeutic levels
▶
Warfarin with INR elevation
DOAC with renal failure and drug accumulation
Liver disease with synthetic dysfunction
▶
Low platelets and elevated PT
Multiple hemorrhagic foci possible
Laboratory Tests
Core emergency labs
Hematologic assessment
▶
Complete blood count with differential and platelets
▶
Thrombocytopenia threshold for transfusion < 100 x 10^9/L in ICH
Leukocytosis as stress response versus infection
Coagulation panel: PT/INR, aPTT, fibrinogen
▶
INR > 1.5 requires reversal in hemorrhagic stroke
Fibrinogen < 1.5 g/L indicates consumptive coagulopathy
Type and crossmatch for surgical readiness
▶
Two units packed red cells on hold
Massive transfusion protocol activation criteria
Metabolic panel
▶
Electrolytes, glucose, renal function
▶
Hyponatremia common post-ICH: SIADH or cerebral salt wasting
Glucose target 6 to 10 mmol/l; hyperglycemia worsens outcomes
Renal function for contrast agent and drug dosing
Hepatic function panel
▶
Coagulopathy secondary to hepatic synthetic dysfunction
Drug metabolism implications for anticonvulsants
Cardiac and perfusion markers
Troponin
▶
Neurogenic myocardial injury common after large ICH
▶
Elevated troponin in 25 to 30% of severe ICH
Impairs cardiac contractility and may limit BP management
ECG correlation for Takotsubo pattern
▶
ST changes and QTc prolongation
Echocardiogram if significant troponin elevation
Lactate
▶
Perfusion assessment >= 2 mmol/l indicates hypoperfusion
▶
Serial measurement every 2 to 4 hours if elevated
Guides resuscitation adequacy
Blood gas
▶
Arterial blood gas if intubated or respiratory compromise
▶
PaO2 target > 80 mmHg: hypoxia worsens hemorrhagic stroke outcomes
PaCO2 target 35 to 40 mmHg unless herniation requires brief hyperventilation
Transient hyperventilation PaCO2 30 to 35 mmHg for herniation bridging only
Toxicology and special labs
Toxicology screen
▶
Sympathomimetics: cocaine, amphetamines precipitate ICH
▶
Urine and serum toxicology
History often unreliable
Alcohol level
▶
Confounds neurological exam
Independent risk for falls and head injury
Pregnancy test in women of childbearing age
▶
Alters imaging approach and medication selection
▶
Urine or serum beta-hCG
Result required before gadolinium and CT radiation decisions
Diagnostic Tests
Scoring Systems
AVM risk stratification: Spetzler-Martin grading system
▶
Nidus size component
▶
Small < 3 cm: 1 point
Medium 3 to 6 cm: 2 points
Large > 6 cm: 3 points
Venous drainage component
▶
Superficial only: 0 points
Deep component: 1 point
Eloquence of adjacent brain
▶
Non-eloquent: 0 points
Eloquent (motor, language, visual, basal ganglia, brainstem, cerebellar): 1 point
Total score 1 to 5: higher score correlates with surgical morbidity and mortality
▶
Grade 1 to 2: low surgical risk, resection favored
Grade 3: intermediate, multidisciplinary decision
Grade 4 to 5: high surgical risk, radiosurgery or observation considered
ICH severity scoring
▶
ICH Score
▶
GCS component: 3 to 4 = 2 points; 5 to 12 = 1 point; 13 to 15 = 0 points
ICH volume >= 30 mL: 1 point
Intraventricular hemorrhage: 1 point
Infratentorial location: 1 point
Age >= 80 years: 1 point
Score 0 to 6; score >= 3 associated with 30-day mortality > 70%
Limitations of scoring systems
▶
Scores designed for hypertensive ICH; AVM-related hemorrhage has better prognosis for same score
Clinical trajectory and underlying AVM treatability must inform prognosis
MRI
MRI brain indications for ruptured AVM
▶
Subacute phase after hemodynamic stabilization
▶
Defines AVM nidus anatomy with superior soft tissue detail
Hemosiderin staining on T2 and gradient echo detects prior hemorrhage
Sequences of value
▶
T1 and T2: flow voids characteristic of high-flow AVM nidus
FLAIR: perilesional edema and white matter involvement
Gradient echo or susceptibility-weighted imaging: hemosiderin and microbleeds
Contrast T1: nidus enhancement and venous drainage delineation
MR angiography
▶
Time-of-flight MRA provides vascular anatomy without contrast
Less detailed than DSA but non-invasive option in stable patients
MRI limitations in acute setting
▶
Longer acquisition time limits use in unstable patients
CT remains first-line in acute hemorrhage
MRI for surgical and radiosurgical planning
▶
Functional MRI for eloquent cortex mapping
▶
Language and motor mapping before resection
Reduces surgical morbidity in eloquent AVMs
Diffusion tensor imaging tractography
▶
White matter tract relationship to nidus
Informs safe surgical corridors
CT
Non-contrast CT head: first-line imaging
▶
Acute hemorrhage detection
▶
Sensitivity approaching 100% within first 24 hours
Identifies location, volume, and midline shift
Intraventricular extension suggests hydrocephalus risk
Hematoma volume estimation
▶
ABC/2 method: length x width x height / 2 in milliliters
Volume >= 30 mL associated with worse outcomes
Hydrocephalus detection
▶
Temporal horn dilation
Transependymal CSF flow on FLAIR equivalent CT cuts
CT angiography
▶
Rapid AVM nidus identification
▶
Good sensitivity for nidus, feeding arteries, draining veins
Identifies intranidal aneurysms requiring urgent treatment
CTA limitations compared to DSA
▶
Cannot assess flow dynamics or venous drainage timing
Misses small AVMs obscured by hematoma
ACEP Level B recommendation: CTA as initial vascular imaging in ICH
CT perfusion adjunct
▶
Assesses perihematomal penumbra
May guide BP management targets in research settings
Repeat CT indications
▶
Clinical deterioration: declining GCS
▶
Hematoma expansion in first 24 hours in 30 to 40% of cases
New or worsening midline shift
Post-treatment assessment
▶
After surgical evacuation or embolization
Before EVD weaning
Ultrasound
Transcranial Doppler (TCD) applications
▶
Cerebral autoregulation assessment
▶
Impaired autoregulation common after AVM rupture
Guides permissive versus tight BP targets
Vasospasm detection post-SAH extension
▶
Mean flow velocity > 120 cm/s suggests vasospasm
Lindegaard ratio > 3 indicates vasospasm versus hyperemia
POCUS for systemic assessment
▶
Cardiac function assessment
▶
LV function for neurogenic cardiomyopathy
Pericardial effusion screen
IVC assessment for volume status guidance
▶
Collapsibility index for fluid responsiveness
Limited utility in intubated patients
Lung ultrasound for ventilated patients
▶
B-lines for pulmonary edema from neurogenic etiology
Consolidation detection if aspiration occurred during seizure
Intraoperative ultrasound
▶
Real-time AVM nidus localization during surgery
▶
Reduces cortical opening size
Confirms complete nidus removal before closure
Disposition
ICU admission indications
All ruptured AVM patients require minimum step-down or ICU level care
▶
GCS <= 13: mandatory neurocritical care ICU
▶
Continuous ICP monitoring if EVD placed
Hourly neurological checks minimum
Intubated or airway protected patients
▶
ICU mandatory for ventilator management
Sedation-analgesia protocol to avoid ICP spikes
Hemodynamic instability
▶
Vasopressor requirement
Refractory hypertension requiring continuous IV infusion
Neurosurgery operative indications for emergent transfer
▶
Large hematoma with mass effect and herniation
▶
Volume > 30 mL with midline shift > 5 mm
Posterior fossa hemorrhage > 3 cm with fourth ventricle compression
Obstructive hydrocephalus requiring EVD
▶
IVH with hydrocephalus on CT
Acute decline in GCS associated with hydrocephalus
Transfer to neurosurgical center if not available locally
▶
Stabilize airway and blood pressure before transfer
Transport with neurocritical care capable team
Definitive treatment disposition
Copy
Neurosurgical options after stabilization
▶
Microsurgical resection for Spetzler-Martin grade 1 to 2
▶
Best outcomes in accessible non-eloquent AVMs
Definitive single-stage treatment
Stereotactic radiosurgery for small deep AVMs
▶
Nidus diameter < 3 cm optimal response
3-year obliteration rate 80% for small AVMs
Continued hemorrhage risk during latency period of 2 to 3 years
Embolization as adjunct or bridge
▶
Reduces intraoperative bleeding
Rarely curative as monotherapy
Pre-operative embolization for high-flow lesions
Discharge planning after acute hospitalization
▶
Rehabilitation facility for neurological deficits
▶
Physical, occupational, speech therapy
Seizure precautions and driving restrictions
Neurosurgery outpatient follow-up within 2 to 4 weeks
▶
Repeat MRI with MRA or DSA
Treatment planning multidisciplinary conference
Treatment
Acute blood pressure management
First-line antihypertensive agents IV
▶
Nicardipine IV infusion
▶
Initial 5 mg/hour IV
Titrate 2.5 mg/hour every 5 to 15 minutes
Maximum 15 mg/hour
Target SBP 130 to 140 mmHg
Labetalol IV bolus
▶
10 to 20 mg IV bolus over 2 minutes
Repeat every 10 to 20 minutes as needed
Maximum cumulative dose 300 mg per acute episode
Avoid in acute decompensated heart failure and reactive airway disease
Hydralazine IV bolus
▶
10 to 20 mg IV every 20 to 30 minutes
Less predictable response than nicardipine
Alternative when labetalol contraindicated
Agents to avoid
▶
Nitroprusside sodium: raises ICP via venous vasodilation
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Contraindicated in raised ICP settings
Nitroglycerin: venous vasodilation raises cerebral venous pressure
▶
Avoid in ICH with raised ICP concern
Antiplatelets and anticoagulants: contraindicated acutely
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No aspirin, NSAIDs, heparin, or DOACs in acute phase
Coagulopathy reversal
Warfarin reversal
▶
4-factor prothrombin complex concentrate (4-PCC)
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INR 2 to 4: 25 units/kg IV (max 2500 units)
INR 4 to 6: 35 units/kg IV (max 3500 units)
INR > 6: 50 units/kg IV (max 5000 units)
Administer within minutes of decision
Vitamin K IV
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10 mg IV slow infusion over 30 minutes
Onset 6 to 12 hours for lasting INR correction
Administer concurrent with PCC for durability
Direct oral anticoagulant reversal
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Dabigatran: idarucizumab (Praxbind)
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5 g IV (two vials of 2.5 g) administered within minutes
Class I recommendation for life-threatening bleeding
Rivaroxaban, apixaban, edoxaban: andexanet alfa
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Low dose regimen 400 mg IV bolus then 480 mg infusion over 2 hours
High dose regimen for rivaroxaban > 10 mg or apixaban > 5 mg within 8 hours: 800 mg bolus then 960 mg infusion
4-PCC as alternative if andexanet alfa not available
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25 to 50 units/kg IV
ACEP Level B recommendation
Platelet transfusion
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Target platelet count >= 100 x 10^9/L in surgical candidates
▶
One apheresis platelet unit or six pooled units raises count 30 to 50 x 10^9/L
Antiplatelet drug effect: platelet transfusion if symptomatic and on aspirin or clopidogrel
ICP management
Hyperosmolar therapy
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Mannitol 20% solution
▶
0.5 to 1 g/kg IV bolus over 15 to 20 minutes
Onset 15 to 30 minutes, duration 3 to 6 hours
Monitor serum osmolality: maximum 320 mOsm/kg
Serum sodium and renal function monitoring
Hypertonic saline 3%
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150 to 250 mL IV bolus over 15 to 20 minutes
Target serum sodium 145 to 155 mmol/l
Avoid rapid sodium correction > 10 mmol/l per 24 hours
Hypertonic saline 23.4%
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30 mL IV for refractory herniation via central line only
Fastest osmolar effect for herniation rescue
Head positioning and general measures
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Head of bed 30 degrees neutral position
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Facilitates venous drainage and reduces ICP
Avoid neck flexion or rotation
Avoid hyperthermia: target normothermia <= 37.5 C
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Acetaminophen 1 g IV every 6 hours for fever
Cooling blanket for refractory hyperthermia
Avoid hypoxia and hypercapnia
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PaO2 > 80 mmHg
PaCO2 35 to 40 mmHg except brief herniation rescue
External ventricular drain
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Indicated for hydrocephalus with GCS decline
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Provides ICP monitoring and CSF diversion
Drain at 10 to 15 cmH2O above external auditory canal
Risk of ventriculitis 5 to 10% per insertion
Lumbar drain contraindicated with mass effect or hydrocephalus
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Risk of downward herniation
EVD preferred for IVH with hydrocephalus
Seizure management
Acute seizure treatment
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Lorazepam IV first line
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0.1 mg/kg IV up to 4 mg per dose
Repeat once after 5 minutes if seizure continues
Levetiracetam IV loading dose for breakthrough or prophylaxis after clinical seizures
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1000 to 3000 mg IV over 15 minutes
Maintenance 1000 mg IV every 12 hours
Preferred over phenytoin for tolerability and interaction profile
Phenytoin or fosphenytoin as second agent
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Fosphenytoin 20 mg PE/kg IV at maximum 150 mg PE/min
BP and cardiac monitoring required during infusion
Prophylactic anticonvulsant policy
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Routine prophylaxis not recommended per current guidelines
▶
No mortality benefit shown in randomized data
Initiate only after clinical seizure confirmed
Short-term use reasonable in high-risk locations
▶
Cortical AVM with lobar hematoma
Duration limited to 7 days then reassess
Neuroprotective and supportive measures
Glycemic management
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Target glucose 6 to 10 mmol/l
▶
Insulin infusion protocol for persistent hyperglycemia
Hypoglycemia equally harmful: glucose < 4 mmol/l requires immediate correction
Frequent glucose monitoring every 1 to 2 hours if insulin infusion
DVT prophylaxis
▶
Sequential compression devices immediately post-admission
▶
Mechanical prophylaxis continued until ambulation
Pharmacologic DVT prophylaxis timing individualized
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Generally 24 to 48 hours after surgical hemostasis or hemorrhage stability confirmed
Hematology and neurosurgery joint decision
Nutrition
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NPO acutely in all patients
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Potential for emergent surgery or intubation
Swallow safety evaluation before oral intake
Enteral nutrition via NGT for intubated patients
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Start within 24 to 48 hours of ICU admission if hemodynamically stable
Standard polymeric formula at 25 kcal/kg/day
Special Populations
Pregnancy
Pregnancy-specific considerations
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AVM hemorrhage epidemiology in pregnancy
▶
AVM rupture risk approximately 3.5% per year
Risk not clearly increased during pregnancy in most studies
Hemorrhage accounts for approximately 5% of maternal deaths
Physiologic changes affecting management
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Increased plasma volume and cardiac output
Gestational hypertension may alter BP thresholds
Inferior vena cava compression: left lateral decubitus positioning
Imaging in pregnancy
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Non-contrast CT head generally acceptable
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Fetal radiation dose well below 50 mGy threshold for deterministic effects
CT angiography with additional iodinated contrast acceptable when needed
MRI preferred when available and patient stable
▶
No ionizing radiation
Gadolinium: avoid in first trimester; limited use thereafter
DSA in pregnancy
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Shielding of uterus mandatory
Deferred when possible until post-delivery if stable
Blood pressure targets in pregnancy
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SBP targets adjusted for gestational age and baseline BP
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Avoid SBP < 110 mmHg: fetal uteroplacental perfusion risk
Target SBP 130 to 150 mmHg in severe gestational hypertension
Safe antihypertensives in pregnancy
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Labetalol IV: preferred first-line in obstetric hemorrhagic stroke
Hydralazine IV: established safety profile in pregnancy
Nicardipine IV: acceptable, limited obstetric data
Avoid ACE inhibitors and ARBs: teratogenic
Delivery and surgical planning
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Multidisciplinary team: neurosurgery, maternal-fetal medicine, neonatology, anesthesia
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Cesarean section for viable fetus if neurological deterioration or hemorrhage instability
AVM treatment deferred to postpartum period in stable patients when feasible
Seizure management in pregnancy
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Levetiracetam relatively safe in second and third trimester
Magnesium sulfate for eclampsia-associated seizures
Avoid valproate: highest teratogenic risk
Geriatric
Age-related considerations for ruptured AVM
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AVM presentation in elderly is less common than in younger adults
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Most AVMs are congenital; incidental discovery in elderly more common
Hemorrhage in elderly more likely to be hypertensive ICH or amyloid angiopathy
Comorbidity burden alters risk-benefit of intervention
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Cognitive baseline assessment crucial for outcome prediction
Functional status and patient goals in treatment decisions
Hemodynamic management
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Higher baseline BP in elderly: relative targets may differ
▶
Aggressive SBP lowering below 130 mmHg may compromise cerebral perfusion
Autoregulation curve shifted rightward in chronic hypertension
Renal function decline affects drug clearance
▶
Levetiracetam dose reduction if eGFR < 50 mL/min
Contrast nephropathy risk with CTA and DSA
Coagulation in elderly
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High anticoagulant use for atrial fibrillation in elderly
▶
Prompt reversal essential; delays increase hematoma expansion
Thromboembolism risk management after reversal requires hematology input
Antiplatelet-related bleeding: aspirin or clopidogrel common
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Platelet transfusion if on dual antiplatelet therapy with active bleeding
Surgical and radiosurgery considerations
▶
Higher surgical morbidity with age > 65
▶
Spetzler-Martin grade incorporates size and eloquence but not age
Radiosurgery preferred for deep small AVMs in elderly
Goals of care discussion early
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Advance directives and healthcare proxy identification
Functional recovery potential stratification
Pediatrics
AVM epidemiology in children
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AVMs account for up to 70% of hemorrhagic stroke in children < 19 years
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Approximately 25% of hemorrhagic strokes in adults < 50 years
Annual rupture risk approximately 2 to 4% in unruptured pediatric AVMs
Seizure presentation more common in pediatrics
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20 to 25% present with seizures as first manifestation
Headache as presenting symptom in 15%
Pediatric-specific management
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Weight-based BP management
▶
Age-specific normal BP references required
Nicardipine 0.5 to 4 mcg/kg/min IV titration in children
Labetalol 0.4 to 1 mg/kg IV bolus (max 40 mg) in children
Seizure management weight-based dosing
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Lorazepam 0.1 mg/kg IV (max 4 mg) for acute seizures
Levetiracetam 20 to 60 mg/kg IV loading dose (max 3000 mg)
Fosphenytoin 20 mg PE/kg IV if second agent required
Hyperosmolar therapy in pediatrics
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Mannitol 0.5 to 1 g/kg IV for herniation
Hypertonic saline 3% 2 to 5 mL/kg IV bolus for ICP crises
Surgical outcomes in pediatrics
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Better surgical outcomes than adults for same Spetzler-Martin grade
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Greater neuroplasticity supports functional recovery
Longer expected life with untreated AVM hemorrhage risk accumulation favors treatment
Radiosurgery in children
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Effective but radiation exposure concerns for young brain
Long-term cognitive effects being studied
Family and developmental support
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Child life specialist and psychosocial support
Neurodevelopmental follow-up for school-age and younger children
Seizure management coordination with pediatric neurology
Background
Epidemiology
Incidence and prevalence
▶
Brain AVM prevalence approximately 0.01 to 0.5% in general population
▶
Detection rate increasing with widespread advanced neuroimaging
Annual incidence of symptomatic AVM approximately 1.1 per 100,000 person-years
Hemorrhagic stroke contribution
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AVMs account for approximately 25% of hemorrhagic strokes in adults < 50 years
Up to 70% of hemorrhagic strokes in children < 19 years
Sex distribution
▶
Slight male predominance in ruptured AVMs noted in population studies
No clear sex difference in overall AVM prevalence
Rupture incidence and mortality
▶
Annual rupture risk approximately 2 to 4% in unruptured AVMs
▶
Risk increases to approximately 6% per year in the first year after hemorrhage
Returns to baseline 2 to 4% annual risk after first year
Rupture mortality and morbidity
▶
10 to 30% 30-day mortality after AVM rupture
Up to 40% of survivors die or remain functionally impaired within 1 year
Hereditary hemorrhagic telangiectasia association
▶
10 to 20% of HHT patients harbor brain AVMs
Multiple AVMs suggest HHT as underlying etiology
Geographic and demographic patterns
▶
No clear racial or geographic clustering reported
▶
Detection bias from healthcare access disparities
Age of presentation typically 20 to 40 years for initial hemorrhage
▶
Mean age of diagnosis lower than other hemorrhagic stroke etiologies
Pathophysiology
Vascular anatomy of AVM
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Congenital direct artery-to-vein shunting without capillary bed
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High-pressure arterial blood enters low-resistance venous outflow
Absent capillary bed causes abnormal flow dynamics and wall stress
Nidus structure
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Abnormal tangled vessel channels of variable size
Lack of elastic support and media layer in nidus vessels
Intranidal aneurysms from hemodynamic stress in 10 to 15% of AVMs
Feeding artery aneurysms
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Hemodynamically related to high AVM flow
Higher rupture risk than de novo berry aneurysms
Treatment priority over nidus in acute rupture setting
Hemorrhage mechanics
▶
Rupture of nidus vessels or intranidal aneurysm
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High-pressure arteriovenous shunting causes vascular wall failure
Parenchymal, subarachnoid, or intraventricular hemorrhage patterns
Secondary injury mechanisms
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Mass effect from hematoma expansion in first 24 hours
Perihematomal edema peaks at 24 to 48 hours
Hydrocephalus from IVH or subarachnoid blood
Cerebral autoregulation failure
Genetic and molecular basis
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Sporadic AVM: somatic KRAS and BRAF mutations in endothelial cells
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RAS-MAPK pathway dysregulation drives abnormal angiogenesis
Implication for future targeted medical therapy
HHT-associated AVMs: germline mutations
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ENG gene (HHT type 1): encodes endoglin, TGF-beta co-receptor
ACVRL1 gene (HHT type 2): encodes ALK1 receptor kinase
SMAD4 mutation: combined juvenile polyposis and HHT
Flow-related changes
▶
High-flow state promotes angiogenesis and AVM growth
Venous hypertension from obstructed drainage contributes to rupture risk
Therapeutic Considerations
Treatment decision framework
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ARUBA trial (A Randomized Trial of Unruptured Brain Arteriovenous Malformations)
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Randomized 226 unruptured AVM patients to intervention versus medical management
Intervention arm had higher risk of stroke or death at 5 years
Criticized for heterogeneous treatment modalities and short follow-up
Does not apply to ruptured AVMs requiring definitive treatment
Ruptured AVM treatment consensus
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Definitive treatment generally recommended after hemorrhage given 6% annual re-rupture risk
Multidisciplinary AVM team required: neurosurgery, neuroradiology, radiation oncology
Spetzler-Martin grade guides modality selection
Medical management considerations
▶
No proven medical therapy reduces AVM rupture risk
▶
VEGF pathway inhibitors under investigation in HHT
Bevacizumab for HHT-associated AVMs in research context
Secondary prevention targets
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Blood pressure control after hemorrhage
Seizure management and anti-epileptic drug optimization
Activity restriction until definitive treatment completed
Evidence base for treatment modalities
▶
Microsurgical resection
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Immediate cure if complete resection achieved
Cure rate > 95% for grade 1 to 2 AVMs
Intraoperative DSA or indocyanine green fluorescence to confirm obliteration
Stereotactic radiosurgery (Gamma Knife, CyberKnife, LINAC)
▶
Obliteration rate 80% at 3 years for nidus < 3 cm
2 to 3 year latency period with continued hemorrhage risk
Optimal for small deep AVMs in eloquent cortex
Endovascular embolization
▶
Rarely curative as standalone treatment (< 5%)
Adjunct to microsurgery or radiosurgery
Reduces flow, allows targeted feeder treatment, and decreases operative bleeding
Patient Discharge Instructions
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Copy
Brain AVM rupture discharge education
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What happened: a blood vessel malformation in the brain bled
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The malformation was present from birth
Treatment is needed to prevent another bleed
Activity restrictions until treatment completed
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Avoid heavy lifting, straining, and strenuous exercise
No contact sports or high-impact activity
No driving until cleared by neurosurgery
Medications at discharge
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Take all prescribed medications as directed
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Anti-seizure medication: do not stop without physician guidance
Blood pressure medication: take daily as prescribed
Medications to avoid until cleared by neurosurgeon
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Aspirin, ibuprofen, naproxen, and all NSAIDs
Blood thinners unless specifically prescribed
Warning signs requiring return to emergency department
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Sudden severe headache especially if worst of life
▶
Seek care immediately even if different from previous headache
New or worsening weakness or numbness on one side
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Facial drooping or arm weakness
Leg weakness or difficulty walking
Difficulty speaking or understanding speech
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Sudden confusion or memory loss
Vision changes
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Blurred or double vision
Loss of vision in one or both eyes
Seizure: any convulsion or loss of consciousness
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Call 911 immediately
Do not drive after a seizure
Severe nausea or vomiting with headache
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May indicate increased pressure in the brain
Follow-up appointments
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Neurosurgery within 2 to 4 weeks for treatment planning
▶
Bring a complete medication list
A family member or caregiver should attend if possible
Repeat brain imaging as scheduled
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MRI or CT angiography to reassess AVM
Primary care physician within 1 week
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Blood pressure monitoring and medication adjustment
Lifestyle guidance
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Blood pressure monitoring at home
▶
Target blood pressure as prescribed by physician
Log readings and bring to follow-up
Alcohol: avoid or minimize
▶
Alcohol raises blood pressure and increases bleeding risk
Smoking cessation strongly recommended
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Smoking associated with worse outcomes after brain hemorrhage
Seizure precautions if applicable
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No driving, swimming alone, or working at heights until seizure-free period met per local regulations
References
Guidelines and key sources
Society guidelines and consensus statements
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American Heart Association and American Stroke Association guidelines for intracerebral hemorrhage
▶
Hemphill JC et al. Stroke 2015;46:2032-2060
Blood pressure management, coagulopathy reversal, ICP management
AHA ASA guideline on cerebral AVMs
▶
Derdeyn CP et al. Stroke 2017;48:e200-e224
Treatment modality recommendations by Spetzler-Martin grade
ACEP Clinical Policy on headache and neurological emergencies
▶
Level B: CT angiography for initial vascular imaging in ICH
Level C: antihypertensive targets in hemorrhagic stroke
Landmark trials and key studies
▶
ARUBA trial: unruptured brain AVM management randomized trial
▶
Mohr JP et al. Lancet 2014;383:614-621
Applies to unruptured AVMs only; does not guide ruptured AVM treatment
INTERACT-2 trial: blood pressure lowering in ICH
▶
Anderson CS et al. N Engl J Med 2013;368:2355-2365
Intensive SBP < 140 mmHg safe; SBP < 130 mmHg associated with harm signal
INTERACT-3 trial: care bundle for ICH
▶
Anderson CS et al. Lancet 2023;402:9-18
Care bundle including BP, glucose, temperature management improved outcomes
Evidence base for treatment modalities
▶
Spetzler RF, Martin NA. A proposed grading system for arteriovenous malformations. J Neurosurg 1986;65:476-483
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Original Spetzler-Martin grading scale publication
Foundation for surgical risk stratification
Starke RM et al. Stereotactic radiosurgery for brain AVMs: review. Neurosurgery 2014
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Obliteration rates and complication data by AVM characteristics
Coding references
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ICD-10 coding for AVM
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Q28.2 arteriovenous malformation of cerebral vessels (congenital)
I60.9 subarachnoid hemorrhage unspecified if SAH component
I61.9 intracerebral hemorrhage unspecified for parenchymal component
SNOMED CT concepts
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Arteriovenous malformation of brain concept
Ruptured intracranial arteriovenous malformation concept
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Management Protocols
Arteriovenous Malformation (Ruptured)