Lateral sinus thrombophlebitis

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Lateral Sinus Thrombophlebitis (Sigmoid Sinus Thrombosis)

High-Yield Revision Notes for NEET PG / NEXT

Lateral sinus thrombophlebitis is a life-threatening intracranial complication of chronic ear infections. It involves inflammation and subsequent thrombus formation within the transverse and sigmoid dural venous sinuses, typically driven by direct extension of unsafe Atticoantral CSOM or acute coalescent mastoiditis.

Contrast-enhanced cranial axial CT scan demonstrating a classic filling defect inside the dural venous sinus, known as the Empty Delta Sign.

Pathognomonic Radiology: Post-contrast brain CT slice showcasing an enhanced dural wall surrounding a central, dark, non-enhancing clot matrix—the classic **Empty Delta Sign** (indicated by arrows).

Pathophysiology & Progression

The disease progresses predictably through anatomical stages due to the proximity of the mastoid antrum to the sigmoid sinus plate:

  1. Perisinus Abscess: Bony erosion of the sigmoid plate allows pus to accumulate between the mastoid bone and the outer dural wall of the sinus.
  2. Endophlebitis: Intra-arterial inflammatory tracking damages the endothelial lining, activating coagulation cascades and leading to a mural thrombus.
  3. Occlusive Thrombus: The clot grows to completely block venous flow, frequently tracking backward toward the torcula or downward into the internal jugular vein (IJV).

Classic Clinical Signs & Named Eponyms

Clinical Feature Diagnostic Presentation & Mechanism
Picket-Fence Fever Hectic, intermittent septic spikes (often exceeding 104°F/40°C) accompanied by rigors and chills. Driven by the periodic release of bacteria/septic emboli directly into the systemic bloodstream from the liquefying clot. Patient is deceptively alert between spikes.
Griesinger’s Sign Edema and exquisite tenderness localized behind the mastoid process. Caused by thrombosis and backup of the mastoid emissary vein.
Cord-Like Neck Mass Tender, palpable, cord-like structure felt along the anterior border of the sternocleidomastoid muscle. Indicates downstream tracking and thrombosis of the **Internal Jugular Vein (IJV)**.
Tobey-Ayer Test Used during manual cerebrospinal fluid (CSF) pressure monitoring (manometry). Compressing the healthy IJV causes a rapid rise in CSF pressure, whereas compressing the *thrombosed* side produces **no rise in CSF pressure** due to pre-existing complete blockage.
Crowe-Beck Sign Engorgement of the retinal and conjunctival veins triggered by manual digital compression of the healthy, non-affected internal jugular vein.

Diagnostic Workup

  1. Contrast-Enhanced CT / MR Venogram (MRV): MRV is the single most sensitive non-invasive modality. On contrast CT, the diagnostic finding is the **Empty Delta Sign**—seen on axial slices as a triangular outline of dural enhancement around an unenhanced intraluminal clot.
  2. Blood Cultures: Highly critical. Often positive for pathogens during pyrexial septic spikes. The microbiology mirrors unsafe CSOM, with **Pseudomonas** and **Proteus** species predominating.

Management Protocol

1. Surgical Intervention (Definitive Management)

  • Mastoidectomy with Sinus Decompression: A complete cortical or modified radical mastoidectomy is performed to remove the culprit cholesteatoma or granulation tissue matrix. The bony sinus plate is carefully thinned and removed to expose the outer dural wall of the sigmoid sinus.
  • Sinus Incision & Thrombectomy: If the clot is highly septic, the sinus wall is incised. The non-adherent thrombus is evacuated until free bleeding is achieved from both the upper (torcula) and lower (jugular bulb) ends.
  • Ligation of the Internal Jugular Vein: Historically routine, it is now reserved only for cases where septic embolization continues to plunge into the lungs despite full clearance and aggressive systemic therapy, or if the IJV clot is grossly putrid.

2. Medical Support

  • High-Dose Parenteral Antibiotics: Broad-spectrum intravenous regimens directed at blood and ear culture sensitivities, continued for an extended course of 4 to 6 weeks.
  • Anticoagulation (Low Molecular Weight Heparin): Initiated selectively to stop further retrograde or anterograde extension of the thrombus into adjacent venous structures (e.g., cavernous or superior sagittal sinuses), provided there is no active intracranial hemorrhage.