01Approach to the Critical Patient/attcp61

Immediate priorities

›Airway and neurologic threats

›Declining level of consciousness

›GCS < 13 — immediate CT head without contrast

›Rapid decline — escalate to resuscitation bay

›Active seizure

›Benzodiazepine first line

›Levetiracetam loading for maintenance

›Signs of herniation

›Pupil asymmetry or fixed dilation

›Cushing response — hypertension with bradycardia

›Extensor posturing

›If herniation signs present, emergent neurosurgery consult

›Osmotic therapy as bridge

›Decompressive craniectomy may be lifesaving

›Hemodynamic and resuscitation targets

›IV access and continuous monitoring

›Cardiac monitor for arrhythmia screening

›Continuous pulse oximetry

›Hydration

›Dehydration is a recognized precipitant

›Normal saline resuscitation for volume depletion

›Fever control

›Treat if infectious etiology suspected

›Antipyretics for comfort and neuroprotection

›Key early decisions

›Anticoagulation initiation timing

›Intracranial hemorrhage does NOT contraindicate anticoagulation in CVST

02History/hx72

Cardinal symptoms

›Headache

›Present in approximately 90% of CVST cases

›Typically diffuse and progressive over days to weeks

›Worsened by coughing, bending, or head movement

›Onset pattern

›Subacute onset over more than 48 hours — most common pattern

›Thunderclap onset — rare, under 5% of cases; mimics subarachnoid hemorrhage

›Character

›Vertex or bifrontal location more specific for CVST

›Patients with migraine history often distinguish CVST headache from usual migraine

Neurological symptoms

›Focal deficits

›Hemiparesis or hemisensory loss in 20 to 50% of cases

›Bilateral leg weakness — superior sagittal sinus thrombosis with parasagittal infarction

›Aphasia — temporal lobe involvement via vein of Labbe

›Seizures in 20 to 40% of cases

›Usually focal onset

›Status epilepticus possible in severe cases

›Visual symptoms

›Transient visual obscurations

›Brief graying of vision on postural change — elevated ICP sign

›Diplopia from CN VI palsy — false localizing sign of raised ICP

›Progressive vision loss — papilledema with optic nerve compression

›Altered mental status

›Encephalopathy in up to 20% of presentations

›Diffuse sinus involvement or multiple cortical vein thromboses

›High mortality risk with encephalopathy

03Physical Exam/exam61

Vitals and general

›Vital sign interpretation

›Hypertension with bradycardia

›Cushing response — sign of brainstem compression and herniation

›Urgent neurosurgical emergency

›Fever

›Suggests infectious etiology — sinusitis, mastoiditis, meningitis

›Septic thrombophlebitis pattern

›Blood pressure

›Permissive hypertension in acute phase unless extreme elevation

›Avoid aggressive antihypertensive agents that may reduce cerebral perfusion

›General appearance

›Level of alertness and cooperation

›Encephalopathy as severity marker

›Irritability in patients with elevated ICP

Neurological exam

›Mental status

›Orientation and cognitive assessment

›New confusion or encephalopathy — high severity marker

›Memory impairment with medial temporal involvement

›Language

›Aphasia with dominant hemisphere temporal lobe involvement

›Dysarthria

›Cranial nerve exam

›CN VI palsy — lateral rectus weakness with diplopia

›False localizing sign of raised intracranial pressure

›Not specific to any venous sinus

›Visual fields

04Differential Diagnosis/ddx41

Life-threatening mimics

›Immediate threats requiring exclusion

›Subarachnoid hemorrhage

›ICD-10 I60.9

›Thunderclap headache overlap — CT then LP to differentiate

›Arterial ischemic stroke

›ICD-10 I63.9

›CVST infarcts cross arterial territorial boundaries

›Hemorrhagic transformation without arterial territory distribution should raise suspicion

›Bacterial meningitis or encephalitis

›ICD-10 G00.9 and G04.9

›Fever plus meningismus plus CSF pleocytosis

›CVST may coexist with CNS infection

›Hypertensive emergency with PRES

›Posterior reversible encephalopathy syndrome

›Bilateral posterior cortical T2 changes on MRI

›Severe hypertension trigger

Neurological mimics

›Conditions with overlapping features

›Idiopathic intracranial hypertension

›ICD-10 G93.2

›Headache plus papilledema plus CN VI palsy

›CVST must be excluded before diagnosing IIH

›Migraine with aura

›ICD-10 G43.109

›CVST headache usually distinguishable from patient's usual migraine

›Risk factor — OCP use elevates both migraine and CVST risk

›Brain abscess

05Laboratory Tests/lt44

Diagnostic biomarkers

›D-dimer

›Sensitivity approximately 94% at cutoff above 500 micrograms per litre

›High negative predictive value of 94 to 99%

›Negative D-dimer in low-probability patient makes CVST very unlikely

›False negatives occur with

›Isolated headache with no other symptoms

›Chronic symptoms lasting more than 6 days

›Limited sinus involvement or isolated cortical vein thrombosis

›Not a rule-out test in moderate to high clinical probability

›Thrombophilia panel

›Typically deferred to outpatient unless VITT suspected

›Factor V Leiden

›Prothrombin G20210A

›Protein C and S activity levels

›Antithrombin III

›Antiphospholipid antibodies — lupus anticoagulant, anticardiolipin, anti-beta-2 glycoprotein I

›JAK2 V617F mutation — myeloproliferative disorder screening

›Homocysteine level

›Timing consideration — acute thrombosis and anticoagulation affect some assay results

Hematologic and coagulation labs

›Complete blood count with differential

›Thrombocytopenia

›VITT — typically below 150 x 10^9/L with thrombosis

›DIC or HIT alternative explanations

›Polycythemia — erythrocytosis as thrombosis risk

›Leukocytosis — infection-driven thrombosis

›Coagulation panel

06Diagnostic Tests/dt84

Scoring Systems

›CVT Clinical Prediction Score

›Heldner et al. 2020 scoring system

›Seizure — 4 points

›Known thrombophilia — 4 points

›Oral contraceptive pill use — 2 points

›Symptom duration more than 6 days — 2 points

›Worst headache ever — 1 point

›Focal neurological deficit — 1 point

›Performance characteristics

›Combined with D-dimer above 500 micrograms per litre — AUC of 0.937

›Low score with negative D-dimer — CVST very unlikely

›Clinical application

›Not yet incorporated into major society guidelines as formal pathway

›Useful to stratify imaging urgency in ED setting

›ICP and prognosis markers

›Elevated ICP features

›Papilledema plus CN VI palsy plus headache — raised ICP syndrome

›Opening pressure on LP if performed

›Poor prognostic markers

›Advanced age

›Active malignancy

›Decreased level of consciousness on presentation

›Intracerebral hemorrhage on imaging

MRI

›MRI brain and MR venography — gold standard

›Indications

›Preferred modality per 2024 AHA Scientific Statement

›Best characterization of cortical vein thrombosis

›Parenchymal injury assessment — infarction, hemorrhage, edema

›Recommended sequences

›MR venography with contrast — filling defects in dural sinuses

›Gradient echo or susceptibility weighted imaging — blooming artifact in acute thrombus

›FLAIR — cortical signal abnormality and subarachnoid blood

›DWI — cytotoxic edema and venous infarction pattern

›Findings

›Loss of normal flow void in sinus on T2

›T1 hyperintensity in subacute thrombus

›Hemorrhagic cortical infarcts not conforming to arterial territory

›MRI limitations

›Acute thrombus may appear isointense on T1

›Can mimic normal flow on some MRV sequences

›GRE or SWI sequences improve detection

›Availability constraints in acute ED setting

›CTV acceptable alternative for initial diagnosis

›MRI preferred for cortical vein thrombosis characterization

CT

›Non-contrast CT head — first-line in acute ED

›Direct signs of CVST

›Dense vessel or cord sign — hyperdense thrombus in cortical vein

›Dense triangle sign — hyperdense superior sagittal sinus

›Sensitivity approximately 25 to 57% for direct sinus signs

›Indirect signs

›Bilateral parasagittal hypodensities — venous infarction

›Hemorrhagic infarction not in arterial territory

›Gyral edema and sulcal effacement

›Normal in up to 30% of CVST cases

›Negative CT does not exclude CVST

›Proceed to CTV or MRI/MRV when clinical suspicion remains

›CT venography — confirmatory test in ED

›Indications

›Clinically suspected CVST with non-diagnostic CT

›Readily available in ED — acceptable alternative to MRV for major sinuses

›High sensitivity and specificity for dural sinus thrombosis

›Key findings

›Filling defect in dural sinus — empty delta sign on coronal reconstruction

›Absence of expected sinus opacification

›Collateral venous enhancement

›Limitations

›Radiation and contrast exposure

›Less sensitive than MRI/MRV for cortical vein thrombosis

›Contrast allergy and renal impairment considerations

Ultrasound

›Point-of-care ultrasound in CVST

›Role in CVST

›Not a primary diagnostic tool for intracranial venous thrombosis

›Transcranial Doppler may assess flow in superior sagittal sinus in some centres

›Adjunct applications

›Optic nerve sheath diameter greater than 5 mm suggests elevated ICP

›Sensitivity approximately 74 to 90% for elevated ICP when using 5 mm cutoff

›Bilateral measurements averaged

›POCUS for associated conditions

›DVT assessment

›Lower limb compression ultrasound if concurrent DVT suspected

›Relevant for anticoagulation duration decisions

›Jugular vein assessment

›Limited utility for intracranial sinus thrombosis

›May show abnormal flow in internal jugular thrombosis

07Disposition/dispo44

Admission indications

›All confirmed CVST require hospital admission

›Stroke unit or neuro-ICU preferred

›2024 AHA Scientific Statement — all patients admitted

›Neurology involvement mandatory

›Monitoring for neurological deterioration

›Seizure detection

›ICP monitoring in selected cases

ICU admission criteria

›High-acuity features requiring ICU

›Decreased level of consciousness

›GCS below 12

›Encephalopathy with safety concerns

›Large hemorrhagic infarction

›Mass effect or midline shift

›Perilesional edema with herniation risk

›Status epilepticus or refractory seizures

›Continuous EEG monitoring required

›Aggressive antiepileptic management

›Herniation signs

›Pupillary changes

›Need for ICP monitoring device

Consultation and transfer criteria

›Mandatory consultations before disposition

›Neurology — all confirmed cases

›Anticoagulation management

›Seizure prophylaxis guidance

›Neurosurgery — mass effect or herniation risk

08Treatment/t109

Anticoagulation — cornerstone of management

›Acute anticoagulation

›LMWH preferred over unfractionated heparin

›Enoxaparin 1 mg/kg subcutaneous every 12 hours

›Renal adjustment — use UFH if eGFR below 30 mL/min/1.73m2

›Anti-Xa monitoring in obesity or renal impairment

›2024 AHA Scientific Statement — Class I recommendation

›Intracranial hemorrhage is NOT a contraindication

›Unfractionated heparin alternative

›80 units/kg IV bolus then 18 units/kg/hour infusion

›Titrate to aPTT 60 to 100 seconds

›Preferred if renal failure or if rapid reversal needed

›Avoid in VITT — use non-heparin anticoagulant

›Transition to oral anticoagulation

›Timing of transition

›Lead-in parenteral anticoagulation for 5 to 15 days before oral agents

›Transition when neurologically stable

›Vitamin K antagonist — warfarin

›Target INR 2.0 to 3.0

›Overlap with parenteral anticoagulation until therapeutic INR on 2 consecutive days

›Bridging LMWH or UFH during warfarin loading

›Duration 3 to 12 months depending on underlying etiology

›Direct oral anticoagulants

›Reasonable alternative per 2024 AHA Scientific Statement

›Apixaban 10 mg twice daily for 7 days then 5 mg twice daily

›Rivaroxaban 15 mg twice daily for 3 weeks then 20 mg daily with evening meal

›Dabigatran 150 mg twice daily after 5 to 10 day parenteral lead-in

›DOAC-CVT trial 2025 — comparable safety and efficacy to VKA

›Anticoagulation duration

›3 months — transient reversible risk factor (OCP, pregnancy, infection)

›6 to 12 months — unprovoked CVST or mild thrombophilia

›Indefinite — recurrent VTE, severe thrombophilia, antiphospholipid syndrome, active malignancy

VITT-specific treatment

›Vaccine-induced immune thrombocytopenia and thrombosis

›Avoid all heparin products

›Unfractionated heparin contraindicated

›LMWH contraindicated

›IVIG administration

›1 g/kg IV over 4 to 6 hours on 2 consecutive days

›Neutralizes anti-PF4 antibodies

›Aim for platelet count recovery above 50 x 10^9/L before full anticoagulation

›Non-heparin anticoagulation

›Fondaparinux 7.5 mg subcutaneous daily for weight 50 to 100 kg

›Renal adjustment required

›Avoid if eGFR below 20 mL/min

›Argatroban IV infusion 2 micrograms/kg/minute

›Titrate to aPTT 1.5 to 3 times baseline

›Hepatic dose reduction if liver impairment

›Transition to DOAC when platelets adequate

Seizure management

›Active seizure control

›Benzodiazepine first line

›Lorazepam 0.05 to 0.1 mg/kg IV — maximum 4 mg per dose

›Repeat once if no response after 5 minutes

›Diazepam 10 mg IV alternative

›Second-line antiseizure medication

›Levetiracetam 60 mg/kg IV loading dose — maximum 4500 mg

›Maintenance 500 to 1500 mg twice daily

›Renal dose adjustment

›Valproate sodium 20 to 40 mg/kg IV loading dose

›Avoid in pregnancy

›Hepatotoxicity monitoring

›Prophylactic antiseizure therapy

›No routine prophylaxis without seizure occurrence — 2024 AHA recommendation

›May consider in patients with cortical lesions at high seizure risk

›Duration if started — typically 3 to 6 months minimum

›Levetiracetam preferred for prophylaxis

›Favorable safety profile

›No drug-drug interactions with anticoagulants

ICP management

›Conservative measures

›Head of bed elevation to 30 degrees

›Improves venous drainage

›Reduces ICP without compromising cerebral perfusion pressure

›Adequate sedation and analgesia in intubated patients

›Avoid coughing and straining

›Target PaCO2 35 to 40 mmHg — avoid hyperventilation unless acute herniation

›Osmotic therapy

›Mannitol 0.5 to 1 g/kg IV over 20 minutes

›Serum osmolality target below 320 mOsm/kg

›Repeat dosing every 4 to 6 hours as needed

›Hypertonic saline 3% NaCl

›150 to 250 mL IV over 15 to 30 minutes

›Serum sodium target 145 to 155 mmol/L

›Monitor for pulmonary edema and central pontine myelinolysis

›Pharmacological ICP reduction

›Acetazolamide for symptomatic elevated ICP without herniation

›250 to 500 mg twice daily orally or IV

›Reduce CSF production

›Glucocorticoids NOT recommended

›No benefit in CVST

›May worsen hypercoagulable state

›Surgical ICP management

›Decompressive craniectomy

›For malignant cerebral edema with herniation

›Lifesaving in selected patients

›2024 AHA Scientific Statement supports as rescue therapy

›Serial lumbar puncture or CSF diversion

›For refractory ICP without mass lesion

›Ventriculoperitoneal shunt for chronic hydrocephalus

Endovascular treatment

›Indications for endovascular intervention

›Neurological deterioration despite maximal anticoagulation

›GCS decline over 24 to 48 hours of therapeutic anticoagulation

›New hemorrhagic infarction or mass lesion

›Severe cases with venous outflow obstruction

›Endovascular options

›Mechanical thrombectomy

›Aspiration or stent-retriever technique

›Interventional neuroradiology expertise required

›Local catheter-directed fibrinolysis

›Alteplase infusion into sinus

›Higher hemorrhagic risk — reserved for selected cases

›Combined approach per institutional protocol

09Special Populations/sp69

Pregnancy

›CVST in pregnancy and postpartum

›Risk period

›Postpartum period carries highest risk — especially first 4 weeks

›Dehydration and hypercoagulable state synergistic risk

›Anticoagulation in pregnancy

›LMWH is the anticoagulant of choice throughout pregnancy

›Enoxaparin 1 mg/kg subcutaneous twice daily

›Does not cross the placenta

›Anti-Xa monitoring in first and third trimester

›Warfarin — avoid in first trimester and near delivery

›Teratogenic in weeks 6 to 12

›May be used in second trimester with informed consent in high-risk cases

›DOACs — contraindicated in pregnancy

›Cross placenta and associated with fetal harm

›Duration of anticoagulation postpartum

›Minimum 6 months total anticoagulation

›Reassess at 3 months postpartum for continuation decision

›OCP discontinuation

›All estrogen-containing contraceptives stopped at diagnosis

›Progestin-only alternatives acceptable

›Intrauterine device is preferred non-hormonal option

›Breastfeeding and anticoagulation

›LMWH and warfarin compatible with breastfeeding

›DOACs — insufficient safety data — avoid during breastfeeding

Geriatric

›CVST in older adults

›Epidemiology in older patients

›Malignancy is the most common underlying cause in patients above 65 years

›Dehydration, infection, and immobility as precipitants

›Male sex more commonly affected above age 55

›Presentation differences

›Atypical presentations more common

›Encephalopathy without headache

›Headache may be attributed to other causes causing diagnostic delay

›Anticoagulation in older adults

›LMWH requires renal function assessment

›Dose reduce or switch to UFH if eGFR below 30 mL/min

›DOAC use requires creatinine clearance assessment

›Dabigatran contraindicated if CrCl below 30 mL/min

›Apixaban preferred if renal impairment — less renal excretion

›Fall risk assessment before anticoagulation

›Higher intracranial hemorrhage risk in falls

›Benefit typically outweighs risk given CVST severity

›Prognosis

›Advanced age is an independent predictor of poor outcome

›Higher rates of death and dependency compared to younger patients

Pediatrics

›CVST in children and neonates

›Epidemiology

›Bimodal distribution — neonates and adolescents

›Neonatal CVST often associated with birth-related complications

›Adolescent risk factors overlap with adults including OCP and thrombophilia

›Precipitants in children

›Dehydration — particularly important in infants and toddlers

›Head and neck infection — otitis media, mastoiditis

›Iron deficiency anemia

›Sickle cell disease

›Anticoagulation in children

›LMWH preferred for acute treatment

›Enoxaparin 1 mg/kg subcutaneous every 12 hours for infants and children

›Neonates may require 1.5 mg/kg subcutaneous every 12 hours

›Target anti-Xa level 0.5 to 1.0 units/mL

›Unfractionated heparin for neonates with significant hemorrhage risk

›75 units/kg IV bolus then 28 units/kg/hour infusion

›Lower starting dose than adult — titrate to aPTT

›Duration — typically 3 to 6 months

›Seizure management in children

›Levetiracetam weight-based dosing

›20 to 60 mg/kg/day divided twice daily

›Maximum dose 3000 mg/day in older children

›Phenytoin or phenobarbital as alternatives per pediatric neurology

10Background/b68

Epidemiology

›Incidence and demographics

›CVST accounts for 0.5 to 3% of all strokes

›Estimated incidence 1.32 per 100,000 person-years

›Higher incidence in low and middle income countries

›Age and sex distribution

›Predominantly affects young adults under age 55

›Female to male ratio of 3 to 1 in reproductive age group

›OCP use accounts for much of the female predominance

›Mortality and outcomes

›Death or dependence in 10 to 15% despite treatment

›Approximately 80% achieve good functional recovery

›Chronic sequelae common — headache, fatigue, cognitive disturbance, epilepsy

›Poor prognostic factors

›Advanced age

›Active malignancy

›Decreased consciousness at presentation

›Intracerebral hemorrhage on imaging

›Deep venous sinus thrombosis — straight sinus and deep cerebral veins

Pathophysiology

›Mechanisms of venous thrombosis

›Virchow's triad applied to cerebral veins

›Hypercoagulability — thrombophilia, OCP, pregnancy

›Venous stasis — dehydration, mass effect on sinus

›Endothelial injury — infection, trauma, surgery

›Dural sinus anatomy

›Superior sagittal sinus — most commonly affected

›Transverse and sigmoid sinus — second most common

›Cavernous sinus — typically septic origin

›Deep cerebral veins — straight sinus and internal cerebral veins — severe presentations

›Consequences of venous occlusion

›Impaired venous drainage

›Elevated cerebral venous pressure

›Reduced cerebral perfusion pressure

›Cerebral edema

›Vasogenic edema from elevated capillary pressure

›Cytotoxic edema with venous infarction

›Hemorrhagic transformation

›Venous infarction predisposes to petechial and confluent hemorrhage

›Unlike arterial hemorrhage — anticoagulation does not worsen outcome

›Raised intracranial pressure

›Impaired CSF resorption — arachnoid granulations drain into superior sagittal sinus

›Risk of optic nerve compression and visual loss

Therapeutic Considerations

›Evidence base for anticoagulation

›Anticoagulation despite intracranial hemorrhage

›Multiple observational studies confirm safety

›2024 AHA Scientific Statement — anticoagulate regardless of hemorrhage

›Hemorrhage in CVST is venous and self-limiting with anticoagulation

›DOAC evidence

›DOAC-CVT trial 2025 — non-inferior to VKA for efficacy and safety

›RE-SPECT CVT trial 2019 — dabigatran comparable to warfarin

›Anticoagulation duration evidence

›Provoked CVST — 3 to 6 months generally sufficient

›Unprovoked or severe thrombophilia — 12 months or indefinite

›Endovascular therapy evidence

›Observational data and case series only

›No randomized controlled trial data supporting routine endovascular use

›Reserved for cases with clinical deterioration despite anticoagulation

›TODAM trial — ongoing at time of 2024 AHA statement

›Glucocorticoids — not recommended

›Multiple studies show no benefit in CVST

›May worsen hypercoagulable state

›Increase infection risk in septic thrombophlebitis

›Exception — use only if underlying inflammatory disease (vasculitis, sarcoid) requires steroids

›OCP management

›Discontinue all estrogen-containing contraceptives at diagnosis

›Reduces ongoing thrombotic stimulus

›Counsel on alternative contraception

›Progestin-only methods acceptable

›Future estrogen use — individualize based on thrombophilia and recurrence risk

11Patient Discharge Instructions/pdi29

copy discharge instructions

›Cerebral venous sinus thrombosis — home care after hospitalization

›Blood thinner medication

›Take anticoagulant exactly as prescribed — do not skip doses

›If on warfarin — attend INR monitoring appointments as scheduled

›If on DOAC — do not stop without speaking to your doctor

›Activity

›Light activity is fine — avoid contact sports or activities with fall risk while on blood thinners

›Return to work or school only when cleared by your neurologist

›Hydration

›Drink adequate fluids daily — dehydration worsens risk

›Increase fluid intake during illness, heat exposure, or exercise

›Medications to avoid

›No estrogen-containing contraceptive pills — speak to your doctor about alternatives

›Avoid NSAIDs unless approved by your doctor — increase bleeding risk with anticoagulants

›No new medications without checking with your doctor first

›Warning signs — return to emergency department immediately for

›Sudden severe headache — worst headache of your life

›New weakness of arm, leg, or face

›Sudden difficulty speaking or understanding speech

›New seizure or shaking

›Sudden vision changes or loss of vision

›Confusion or unusual behavior

›Unusual bleeding — blood in stool or urine, prolonged nosebleed, unusual bruising

›Follow-up appointments

›Neurology within 1 to 2 weeks after discharge

›Blood tests as scheduled by your doctor

›Repeat brain scan at 3 to 6 months — to check if clot has cleared

12References/r30

Guidelines and key sources

›Primary guidelines

›Saposnik G et al. Diagnosis and Management of Cerebral Venous Thrombosis: A Scientific Statement From the American Heart Association. Stroke. 2024.

›doi:10.1161/STR.0000000000000456

›Comprehensive evidence-based framework for diagnosis and management

›Ropper AH, Klein JP. Cerebral Venous Thrombosis. New England Journal of Medicine. 2021.

›PMID not available — NEJM review article

›Comprehensive review of pathophysiology and treatment

›Saposnik G et al. Diagnosis and Management of Cerebral Venous Thrombosis. AHA/ASA Statement. Stroke. 2011.

›PMID 21293023

›Earlier guideline — superseded by 2024 AHA statement

Key trials and studies

›Anticoagulation and DOAC trials

›van de Munckhof A et al. DOAC-CVT: DOACs Versus VKA for Cerebral Venous Thrombosis. Lancet Neurology. 2025.

›PMID 39986309

›DOACs non-inferior to VKA for efficacy and safety

›Heldner MR et al. Prediction of Cerebral Venous Thrombosis With a New Clinical Score and D-Dimer. Neurology. 2020.

›PMID 32576633

›CVT clinical prediction score derivation and validation

›Dentali F et al. D-Dimer Testing in Diagnosis of Cerebral Vein Thrombosis: Systematic Review. Journal of Thrombosis and Haemostasis. 2012.

›PMID 22257124

›D-dimer sensitivity approximately 94% at 500 micrograms per litre threshold

›Emergency medicine references

›Spadaro A et al. Cerebral Venous Thrombosis: Diagnosis and Management in Emergency Department. American Journal of Emergency Medicine. 2021.

›PMID 33765589

›ED-focused approach and management summary

›Field TS, Fragata I. Current Management of Cerebral Venous Thrombosis. Stroke. 2026.

›PMID 41924888

Evidence & Review