Deep Vein Thrombosis (DVT)

Definition

• ROSEN's Emergency Medicine, p. 1196
• Bailey and Love's Short Practice of Surgery, 28th Ed., p. 345

Pathophysiology - Virchow's Triad

1. Venous stasis - reduced or stagnant blood flow (immobility, reduced muscular calf pump, obstruction to flow)
2. Vascular wall injury - venous trauma damages vessel walls and promotes thrombus formation
3. Hypercoagulability - abnormal levels of clotting factors such as antithrombin III, protein C, and protein S

• Gray's Anatomy for Students, p. 785

Anatomy of Relevant Veins

Diagram of leg vein anatomy - ROSEN's Emergency Medicine, Fig. 74.2

Risk Factors

• Bailey and Love's Short Practice of Surgery, 28th Ed., p. 345

Clinical Features

• Unilateral leg pain and swelling (calf pain is most common)
• Warmth, redness, and engorged superficial veins of the affected limb
• Tenderness on palpation along the deep venous distribution
• Homans' sign - calf pain on dorsiflexion of the foot (positive, but neither sensitive nor specific)
• Rarely, a palpable venous cord

Most patients will show no physical signs at all, making clinical suspicion essential.

• Because the left iliac vein is vulnerable to compression by the left iliac artery (May-Thurner syndrome), DVT occurs slightly more frequently on the left.
• Bilateral leg DVT is found in fewer than 10% of ED patients.
• ROSEN's Emergency Medicine, p. 1196-1197
• Bailey and Love's Short Practice of Surgery, p. 345

Differential Diagnosis

• Venous insufficiency
• Cellulitis (concurrent DVT found in only ~3% of cellulitis cases)
• Gastrocnemius muscle injury or Achilles tendon injury
• Ruptured Baker cyst (can mimic DVT in the calf/popliteal region)
• Calf muscle hematoma
• Systemic edema (e.g., heart failure causing asymmetric swelling)

Diagnosis

1. Wells DVT Score (Pre-test Probability)

• Score ≥2: DVT likely (High PTP)
• Score <2: DVT unlikely (Low PTP)

2. D-Dimer

• Measures breakdown of cross-linked fibrin from any intravascular thrombus
• Normal D-dimer with low PTP excludes proximal DVT with ~92% sensitivity
• Standard cutoff: >500 ng/mL = abnormal
• Age-adjusted cutoff: Age × 10 ng/mL (e.g., 80-year-old: <800 ng/mL considered negative), maintaining ~95% sensitivity

3. Venous Duplex Ultrasound

• Gold standard for diagnosis
• Key findings for DVT: no flow, non-compressible vein, no augmentation with calf compression, no respiratory phasicity
• A 3-point ultrasound covers common femoral, femoral, and popliteal veins
• Whole-leg ultrasound adds tibial, peroneal, and gastrocnemius veins
• ROSEN's Emergency Medicine, p. 1196-1197
• Gray's Anatomy for Students, p. 785

Treatment

Anticoagulation (First-line)

1. Initial therapy: Treatment-dose subcutaneous LMWH (low-molecular-weight heparin)
   • Patients with significant renal impairment: IV unfractionated heparin
   • HIT (heparin-induced thrombocytopenia): fondaparinux (anti-Xa) or bivalirudin (direct thrombin inhibitor)
2. Long-term oral anticoagulation for at least 3 months (longer if risk factors persist or recurrent DVT):
   • NOACs (preferred): rivaroxaban, apixaban (factor Xa inhibitors) or dabigatran (thrombin inhibitor)
   • These are equally effective as warfarin but with fewer major bleeding complications

IVC Filter

• For patients who cannot be safely anticoagulated (high bleeding risk)
• Temporary/retrievable filters are used until anticoagulation is safe or embolisation risk subsides

Endovascular Intervention

• Thrombus removal, thrombolysis, and stenting are increasingly used for acute DVT, particularly iliofemoral thrombosis
• Aim: restore patency and reduce risk of post-thrombotic syndrome (chronic leg swelling, pain, skin changes)
• Bailey and Love's Short Practice of Surgery, 28th Ed., p. 345

Complications

Prevention

• Compression stockings (avoid in peripheral arterial disease, neuropathy)
• Pneumatic calf compression pumps
• Pharmacological prophylaxis (LMWH)
• Bailey and Love's Short Practice of Surgery, 28th Ed., p. 344-345

Cortical Vein Thrombosis (Cerebral Venous Thrombosis)

Definition

• Bradley and Daroff's Neurology in Clinical Practice, p. 1409
• Grainger & Allison's Diagnostic Radiology, p. 1454

Classification

The superior sagittal sinus is the most frequently involved structure.

• Bradley and Daroff's Neurology, p. 1409

Causes and Risk Factors

Infectious/Septic

• Facial, orbital, paranasal sinus, or middle ear infections
• Skull osteomyelitis, mastoiditis (lateral sinus thrombosis)
• Syphilis, varicella-zoster, HIV

Non-infectious/Aseptic

• Pregnancy and puerperium (peripartum period)
• Oral contraceptive pill use
• Smoking, dehydration
• Prothrombotic / hypercoagulable states:
  • Factor V Leiden mutation
  • Protein C or Protein S deficiency
  • Antithrombin III deficiency
  • Antiphospholipid antibody syndrome
• Hematologic disorders, disseminated cancer
• Vasculitis (especially Behcet's disease)
• SARS-CoV-2 infection (rare complication)
• Marasmus, dehydration, carcinoma

In approximately 15-20% of cases, no cause is found.

• Bradley and Daroff's Neurology, p. 1409-1410
• Goldman-Cecil Medicine, p. 2727

Epidemiology

• Mean age at presentation: ~39 years
• More common in young women, especially in the peripartum period
• Rare in children; about half of pediatric cases occur in neonates and young infants
• Rare overall (incidence ~0.08% among hospitalized patients)

Pathophysiology

1. Venous hypertension → cerebral edema (vasogenic, then cytotoxic)
2. Reduced CSF absorption → raised intracranial pressure
3. Venous infarction - often multifocal and bilateral, affecting gray matter AND subcortical white matter
4. Hemorrhagic transformation (approximately 1/3 of cases develop intracerebral hemorrhage)

Clinical Features

Suspect CVT in female patients under age 50 with stroke symptoms but no classic risk factors, unexplained new seizures, or refractory headaches. An elevated LP opening pressure in an appropriate clinical context should prompt venous imaging.

• Tintinalli's Emergency Medicine, p. 1293-1295
• ROSEN's Emergency Medicine, p. 1343

Imaging

MRI with MR Venography (MRV) - Gold Standard

• Loss of normal flow void in the affected sinus or vein
• Thrombosed vessel appears hyperintense on T1 and T2
• Very acute thrombus may be hypointense on T2 (can mimic flow void)
• MRV shows absent or severely reduced flow signal with irregularity and narrowing

Sagittal T1 MRI: Increased signal and enlargement of the superior sagittal sinus indicating thrombosis - Bradley and Daroff's Neurology, Fig. 65.35

MR venogram: Absent flow in right transverse and sigmoid sinus (arrowhead) with intact left-sided flow (arrows) - Goldman-Cecil Medicine, Fig. 376-6

CT / CT Venography

• Acutely thrombosed sinus appears hyperdense and expanded on non-contrast CT (NECT)
• Post-contrast CT: "Empty delta sign" - hypodense center within an enhancing periphery (classic for superior sagittal sinus thrombosis)
• Parenchymal changes: low-density edema, hemorrhagic infarction, small ventricles
• SWI (susceptibility-weighted imaging): "blooming" of thrombosed vein; serpiginous dilated collateral veins indicate venous congestion

Lumbar Puncture

• Elevated opening pressure is a key finding
• Can be safely performed in CVT (not contraindicated)
• May show raised protein, red cells if hemorrhagic infarction present
• Grainger & Allison's Diagnostic Radiology, p. 1454
• Tintinalli's Emergency Medicine, p. 1295

Treatment

1. Anticoagulation (Primary Treatment)

• Acute phase: IV heparin or subcutaneous LMWH (preferred over unfractionated heparin - associated with lower mortality in one trial)
• Anticoagulation is recommended even if hemorrhagic infarction is already present - the benefit outweighs the risk
• Long-term: Warfarin (INR target 2.0-3.0) or newer anticoagulants for at least 3 months; longer if underlying cause persists

2. Adjunct Measures

• Seizure management: Prophylactic antiepileptics
• Raised ICP management: Head elevation, diuretics, acetazolamide
• Antibiotics: If septic etiology (now rare)

3. Endovascular / Surgical Options (Severe / Refractory Cases)

• Local thrombolysis (tPA) via direct venous infusion - reserved for stupor/coma and severely raised ICP
• Thrombectomy within the occluded sinus
• Decompressive craniectomy - for malignant brain edema with imminent herniation

Note: A small clinical trial found no benefit of adding endovascular therapy to medical therapy compared to medical therapy alone. Local thrombolysis is reserved for extreme cases.

• Bradley and Daroff's Neurology, p. 1409
• Adams and Victor's Principles of Neurology, 12th Ed., p. 1056
• Goldman-Cecil Medicine, p. 2729-2730

Prognosis

• Most patients who are treated early do well, with good neurological recovery
• Mortality remains significant in severe cases - large hemorrhagic venous infarctions found in 10-20% of cases
• Coma with multiple cerebral hemorrhages is usually fatal
• It may take weeks for headaches to remit even after starting heparin
• Outcomes in neonatal CVT depend on the extent of infarct and hemorrhage

Anatomy of the Vein of Galen and Deep Cerebral Veins

Overview: Superficial vs. Deep Venous Systems

• Neuroanatomy through Clinical Cases, 3rd Ed.
• Grainger & Allison's Diagnostic Radiology, p. 1357

The Deep Cerebral Venous System - Step-by-Step Hierarchy

Medullary veins
    ↓
Septal vein + Thalamostriate vein
    ↓ (join at foramen of Monro = "venous angle")
Internal Cerebral Veins (paired, bilateral)
    ↓
    + Basal Veins of Rosenthal (bilateral)
    ↓
Great Cerebral Vein of Galen (midline)
    ↓
    + Inferior Sagittal Sinus
    ↓
Straight Sinus (Sinus Rectus)
    ↓
Confluence of Sinuses (Torcular Herophili)
    ↓
Transverse Sinuses → Sigmoid Sinuses → Internal Jugular Veins

1. Thalamostriate Vein (Superior Thalamic Vein)

• Runs in the groove between the thalamus and the caudate nucleus, in the floor of the lateral ventricle
• Drains the thalamus, caudate nucleus, internal capsule, and adjacent deep white matter
• Travels posteriorly to reach the foramen of Monro (interventricular foramen)
• Joins the septal vein at the foramen of Monro to form the internal cerebral vein
• The point of junction (venous angle) is a key radiological landmark

Clinical note: In birth trauma, rupture of the thalamostriate vein can lead to intraventricular hemorrhage in newborns.

2. Septal Vein

• Courses directly posteriorly along the septum pellucidum
• Drains the frontal horn of the lateral ventricle and adjacent white matter
• Joins the thalamostriate vein at the foramen of Monro to form the internal cerebral vein

3. Internal Cerebral Veins (paired)

• Formed bilaterally at the foramina of Monro by union of the septal and thalamostriate veins
• Run posteriorly along the roof of the third ventricle, near the midline, enclosed within the velum interpositum (a fold of pia mater)
• Receive tributaries from the choroidal veins (draining the choroid plexus) along their course
• The two internal cerebral veins travel parallel to one another and unite posteriorly, below the splenium of the corpus callosum, to form the vein of Galen

Deep cerebral veins: The thalamostriate vein and choroidal vein drain into the internal cerebral vein, which converges with its fellow to form the great cerebral vein of Galen - Gray's Anatomy for Students

4. Basal Vein of Rosenthal (paired)

• Formed near the anterior perforated substance by the union of the:
  • Anterior cerebral vein (runs adjacent to the anterior cerebral artery / ACA)
  • Deep middle cerebral vein (runs adjacent to the MCA in the Sylvian fissure)
• Courses posteriorly and medially, winding around the lateral aspect of the midbrain (through the ambient cistern)
• Drains the insula, basal ganglia (lentiform nucleus), hypothalamus, medial temporal lobe, midbrain, and uncus
• Joins the internal cerebral veins posteriorly to contribute to the vein of Galen

5. Great Cerebral Vein of Galen

• A short (~1 cm), midline, unpaired vein formed by the confluence of:
  • The two internal cerebral veins
  • The two basal veins of Rosenthal
  • Other tributaries (e.g., posterior fossa veins)
• Located in the quadrigeminal cistern (superior to the quadrigeminal plate/tectum), posterior to the splenium of the corpus callosum
• Drains deeply located structures: basal ganglia, thalami, hypothalamus, midbrain, choroid plexus, corpus callosum, deep white matter
• Joins the inferior sagittal sinus (coming from the lower border of the falx cerebri) to form the straight sinus (sinus rectus)

Inferior view of brain showing basal veins and the deep venous system - Color Atlas of Human Anatomy

6. Downstream: Straight Sinus to Torcular

• Straight sinus (sinus rectus): Formed by vein of Galen + inferior sagittal sinus; runs obliquely in the midline within the junction of the falx cerebri and tentorium cerebelli, toward the confluence of sinuses
• Confluence of sinuses (torcular Herophili): Where the superior sagittal sinus, straight sinus, and occipital sinus converge
  • Most blood from the superior sagittal sinus preferentially enters the right transverse sinus
  • Most blood from the straight sinus (and vein of Galen) preferentially enters the left transverse sinus
• Transverse sinuses → Sigmoid sinuses → Internal jugular veins

Superficial Deep Cortical Veins (Anastomotic Veins)

It is uncommon for both Trolard and Labbé to be well developed simultaneously. Thrombosis of the vein of Labbé causes posterolateral temporal lobe infarction.

Posterior Fossa Venous Drainage

1. Vein of Galen (receives superior cerebellar veins, precentral cerebellar vein)
2. Superior petrosal sinus
3. Direct tributaries into the transverse and straight sinuses

Clinical Correlations

• Grainger & Allison's Diagnostic Radiology, p. 1454-1455
• Neuroanatomy through Clinical Cases 3rd Ed., p. 10.11
• Gray's Anatomy for Students, p. 1311-1312