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LATERAL SINUS THROMBOPHLEBITIS (OTOGENIC SIGMOID/LATERAL SINUS THROMBOSIS)

A Comprehensive Discussion for 50 Marks — RGUHS University

CONTENTS AT A GLANCE

1. Introduction & Historical Note
2. Anatomy of Lateral/Sigmoid Sinus
3. Incidence & Etiology
4. Pathology & Pathogenesis
5. Clinical Features
6. Griesinger's Sign & Other Special Signs
7. Investigations
8. Radiological Imaging (with Images)
9. Diagnosis
10. Complications
11. Management — Medical & Surgical
12. Flowchart of Management
13. Recent Advances
14. Prognosis

1. INTRODUCTION & HISTORICAL NOTE

2. ANATOMY OF THE LATERAL (SIGMOID) SINUS

• Transverse sinus: runs horizontally in the tentorium cerebelli
• Sigmoid sinus: S-shaped continuation, runs in the posterior fossa → jugular bulb → internal jugular vein

Key Anatomical Relationships:

Superior Sagittal Sinus
        ↓
Transverse Sinus (horizontal part)
        ↓
Sigmoid Sinus (S-shaped, lies in sigmoid sulcus of mastoid bone)
        ↓  ← directly adjacent to mastoid air cells (KEY POINT)
Jugular Bulb
        ↓
Internal Jugular Vein (exits via jugular foramen)

• Via inferior petrosal sinus → Cavernous sinus (anterior)
• Via superior petrosal sinus → Cavernous sinus
• Via mastoid emissary vein → Scalp veins (→ Griesinger's sign)
• Downward → Internal jugular vein → Septic emboli to lungs

3. INCIDENCE & ETIOLOGY

Incidence:

• Pre-antibiotic era: ~40% of otogenic intracranial complications
• Post-antibiotic era: Rare but still seen; incidence ~3–4% of otogenic intracranial complications
• More common in children and young adults
• Male:Female ratio — roughly equal

Etiology:

Causative Organisms:

• Streptococcus species (most common — esp. S. pyogenes, S. pneumoniae)
• Staphylococcus aureus (including MRSA)
• Proteus mirabilis
• Pseudomonas aeruginosa
• Bacteroides (anaerobes — in cholesteatoma)
• Mixed flora common

4. PATHOLOGY & PATHOGENESIS

Pathogenesis (Dhingra / Cummings):

CSOM / Acute Mastoiditis
        ↓
Perisinus Abscess Formation
(erosion of bony sinus plate by cholesteatoma / granulation tissue / pressure necrosis)
        ↓
Inflammation of Adventitia of Sigmoid Sinus Wall
        ↓
Penetration of Venous Wall (endophlebitis)
        ↓
Infection reaches Intima → Triggers Virchow's Triad
(Endothelial damage + stasis + hypercoagulability)
        ↓
Mural Thrombus Formation (infected thrombus)
        ↓
Enlargement → Occlusion of Sinus Lumen
        ↓
Propagation of Thrombus (in both directions)
        ↓ ↑
[Toward jugular vein / IJV] [Toward transverse sinus / SSS]
        ↓
Septicemia (shower of infected emboli)
        ↓
Septic Emboli → Metastatic Abscesses (lung, brain, joints)

In AOM (osteothrombophlebitis route):

5. CLINICAL FEATURES

A. Symptoms

1. Picket fence fever — diurnal temperature spikes exceeding 103°F (39.4°C), rigor-free intervals, characteristic of septicemia
2. Headache — deep-seated, persistent, often occipital/temporal
3. Otomastoiditis symptoms — ear discharge, otalgia, mastoid tenderness

⚠️ Modern presentation caveat (Cummings, p. 2523): In the antibiotic era, the classic picket fence fever is less common. Affected patients, particularly children, may present initially with diplopia or other neurological symptoms rather than the classic fever pattern.

Additional Symptoms:

• Neck pain and stiffness — from sternocleidomastoid (SCM) inflammation (perijugular involvement) — differentiated from meningism
• Malaise, anorexia, weight loss
• Vomiting
• Diplopia — from raised ICP → 6th nerve palsy
• Blurring of vision / visual obscurations — if otitic hydrocephalus develops

B. Signs

Fever Pattern:

Temperature (°F)
105 |        *           *
104 |      *   *       *   *
103 |    *       *   *       *
102 |  *           *           *
101 | *                           *
    |________________________________
    Time (hours/days)
    ← "Picket Fence" Pattern (Septic spikes) →

6. SPECIAL SIGNS IN DETAIL

Griesinger's Sign:

Tobey-Ayer Test:

7. INVESTIGATIONS

A. Blood Investigations:

• CBC: Leucocytosis (↑ WBC, neutrophilia), ↑ ESR, ↑ CRP
• Blood culture: May grow causative organism (especially during fever spikes/rigor)
• Coagulation profile: Baseline before anticoagulation
• LFT, KFT: Baseline organ function

B. Cerebrospinal Fluid (CSF) Analysis:

• Opening pressure: Elevated (due to otitic hydrocephalus)
• Cell count: Normal or mildly elevated (a few cells)
• Protein: Normal or mildly elevated
• Glucose: Normal
• Culture: Usually negative (unless associated meningitis)
• Tobey-Ayer test performed during LP

C. Imaging (Most Important)

1. CT Scan (Contrast-Enhanced Temporal Bone CT):

On Axial CECT:
┌─────────────────────┐
│  Contrast-enhancing │
│  walls of sinus     │  ← "Delta" shape (Δ)
│   with NON-         │
│  enhancing clot     │
│  in the CENTER      │
└─────────────────────┘
= Classic "Empty Delta Sign" (Delta sign / Dark centre sign)

• Absent enhancement of the sigmoid sinus (compared to normal opposite side)
• Opacified mastoid air cells
• May show perisinus abscess

2. MRI + MR Venography (Gold Standard):

• T1W: Isointense clot → bright on T1 (subacute thrombus due to methaemoglobin)
• T2W: Variable signal in thrombus
• MR Venography: Shows absence of flow / filling defect in sigmoid/transverse sinus (see below)
• Can detect associated complications: meningitis, cerebellar abscess, temporal lobe abscess

3. Otomicroscopy/Ear Examination:

• Ear discharge (purulent/mucopurulent)
• Perforated tympanic membrane / cholesteatoma

4. Chest X-Ray:

• Septic pulmonary emboli (rounded opacities, cavitation — "cannon ball" lesions)

8. DIAGNOSIS

Diagnostic Criteria (Cummings):

DIAGNOSIS: Lateral Sinus Thrombophlebitis
┌──────────────────────────────────────────────────────┐
│ CLINICAL:                                            │
│ • History of chronic/acute ear disease               │
│ • Picket-fence fever + rigors                        │
│ • Headache, postauricular edema (Griesinger's)       │
│ • +ve Tobey-Ayer test                                │
├──────────────────────────────────────────────────────┤
│ RADIOLOGICAL:                                        │
│ • CT: Empty Delta / Absent sigmoid enhancement       │
│ • MRI: Thrombus signal in sinus                      │
│ • MRV: Absent flow in affected sinus                 │
├──────────────────────────────────────────────────────┤
│ INTRAOPERATIVE:                                      │
│ • Needle aspiration of sinus → thrombus confirmed    │
│ • Perisinus abscess found                            │
└──────────────────────────────────────────────────────┘

9. COMPLICATIONS OF LST

1. Otitic Hydrocephalus — raised ICP without true hydrocephalus; due to reduced CSF absorption when major venous sinus occluded (particularly right transverse sinus which is normally dominant)
2. Meningitis — most common associated intracranial complication
3. Cerebellar Abscess — adjacent to sigmoid sinus
4. Temporal Lobe Abscess — otogenic
5. Septic Pulmonary Emboli — cannon ball lesions
6. Metastatic abscesses — joints, liver
7. Jugular Foramen Syndrome (Vernet's) — CN IX, X, XI palsies
8. Cavernous Sinus Thrombosis — via petrosal sinuses
9. Death — in untreated/delayed cases

10. MANAGEMENT

MANAGEMENT FLOWCHART:

SUSPECTED LST (Otomastoiditis + Septicemia)
                    |
         ┌──────────▼──────────┐
         │ INVESTIGATIONS      │
         │ CBC, Blood C/S, CT  │
         │ MRI/MRV, CSF, CXR  │
         └──────────┬──────────┘
                    |
         ┌──────────▼──────────────────┐
         │ MEDICAL MANAGEMENT          │
         │ IV Antibiotics (broad spec) │
         │ + Anticoagulation (debate)  │
         │ + ICP management (if ↑ICP) │
         └──────────┬──────────────────┘
                    |
         ┌──────────▼──────────────────────┐
         │ SURGICAL MANAGEMENT             │
         │ Mastoidectomy (cortical / RMW)  │
         │ + Exposure of sinus             │
         │ + Perisinus abscess drainage    │
         │ ± Sinusotomy + thrombectomy     │
         │ ± IJV ligation (controversial)  │
         └──────────┬──────────────────────┘
                    |
         ┌──────────▼──────────┐
         │ POST-OP CARE        │
         │ Continue IV Abx     │
         │ Monitor ICP         │
         │ Anticoagulate PRN   │
         │ Follow-up MRV       │
         └─────────────────────┘

A. Medical Management

1. Antibiotics (Mainstay of Treatment):

• Duration: 4–6 weeks of parenteral antibiotics (prolonged course)
• Adjust based on culture-sensitivity reports

2. Anticoagulation (Controversial):

• Contraindications: active intracranial haemorrhage, cerebellar abscess
• Recent evidence: Meta-analyses support anticoagulation improving outcomes in paediatric LST

3. Management of Raised ICP (Otitic Hydrocephalus):

• Head elevation (30°)
• Acetazolamide (carbonic anhydrase inhibitor — reduces CSF production)
• Serial lumbar punctures (therapeutic, to relieve pressure)
• CSF diversion (shunting) in refractory cases

B. Surgical Management

Step-by-Step Surgical Approach (Cummings; Scott-Brown):

• The choice depends on whether CSOM with cholesteatoma is present
• Exenterate all mastoid air cells
• Identify and expose the sigmoid sinus plate

• If perisinus abscess is present → drain it
• Remove all granulation tissue around sinus
• Thin and remove the infected sinus plate with curettes/diamond burs

• After exposing the sinus wall → aspirate with needle to confirm thrombus
• Blood returns freely → no thrombus (conservative management)
• No blood returns → occluded sinus

• Incise sinus wall (sinusotomy)
• Evacuate infected thrombus (thrombectomy) with suction or curettes
• Pack sinus with Gelfoam or fat graft

SINUSOTOMY TECHNIQUE:
┌─────────────────────────────────────────┐
│ Mastoidectomy completed                 │
│           ↓                             │
│ Sinus plate thinned/removed             │
│           ↓                             │
│ Needle aspiration confirms thrombus     │
│           ↓                             │
│ Longitudinal incision on sinus wall     │
│           ↓                             │
│ Clot removal with suction / packing     │
│           ↓                             │
│ Check for bleeding above & below        │
│           ↓                             │
│ Pack sinus or leave open to cavity      │
└─────────────────────────────────────────┘

• Persistent septicemia/pyemia despite adequate antibiotics and mastoidectomy
• Evidence of propagating thrombus into the neck
• Septic pulmonary emboli (to prevent further embolization)

• Transverse neck incision along anterior border of SCM
• Expose IJV between carotid sheath structures
• Ligate IJV at the level of the jugular bulb
• This is rarely performed today due to availability of anticoagulants

Modern view: IJV ligation has been largely abandoned in favour of anticoagulation and aggressive antibiotic therapy.

C. Management of Associated Complications:

11. COMPLETE MANAGEMENT ALGORITHM

OTOMASTOIDITIS PATIENT
        │
        ▼
Signs of intracranial complication?
(Fever, headache, Griesinger's sign, diplopia, papilledema)
        │
        ▼
URGENT WORKUP:
CT Temporal Bone (contrast) + MRI Brain + MRV
Blood culture, CBC, CSF (if safe)
        │
    ┌───┴────────────────┐
    │                    │
   YES: LST             NO: Monitor
    │                    │
    ▼                    ▼
ADMIT TO ICU         Continue treatment
IV Antibiotics        of otomastoiditis
(Ceftriaxone +
Metronidazole ±
Vancomycin)
    │
    ▼
SURGICAL EXPLORATION
Mastoidectomy
    │
    ▼
Perisinus abscess present?
    │
  ┌─┴──┐
 YES   NO
  │     │
Drain  Continue
abscess  medical Rx
  │
  ▼
Needle aspiration of sinus
Blood returns? ──YES──→ Conservative (no sinusotomy needed)
  │
  NO
  │
  ▼
SINUSOTOMY + THROMBECTOMY
  │
  ▼
Persistent sepsis / propagating thrombus into neck?
  │
  ├──YES──→ Consider IJV Ligation (rarely done today)
  │         OR Intensify anticoagulation
  │
  NO
  │
  ▼
POSTOPERATIVE:
IV Antibiotics × 4–6 weeks
Anticoagulation (Heparin → Warfarin × 3–6 months)
Serial MRV at 3 and 6 months
Monitor ICP / treat otitic hydrocephalus

12. RECENT ADVANCES

A. Anticoagulation Evidence (2010s–2024):

• Systematic reviews (Rodriguez et al., 2023; Funamura et al., 2014) support anticoagulation in paediatric LST, showing improved recanalization rates and reduced propagation
• Low-molecular-weight heparin (LMWH) — increasingly preferred over unfractionated heparin for ease of use and predictable dosing
• Direct oral anticoagulants (DOACs) — emerging role in adult LST (rivaroxaban, apixaban), though paediatric data limited

B. Conservative Non-Surgical Approach:

• Recent publications (Symms et al.; Ooi et al.) describe successful management with antibiotics alone + anticoagulation without sinusotomy in selected cases, particularly in the antibiotic era
• Sinusotomy with thrombectomy is now reserved for refractory cases

C. Diagnostic Advances:

• MR Venography (MRV) is now the gold standard — replaced Tobey-Ayer test
• Diffusion-weighted MRI (DWI) — identifies associated brain abscess
• CT angiography — alternative to MRV in emergency settings
• Blood D-dimer — elevated in active thrombosis; useful for monitoring treatment response

D. Microbiological Advances:

• Streptococcus milleri group increasingly recognized in otogenic LST
• MRSA-related LST — increasing; requires vancomycin/linezolid
• PCR-based identification of organisms from blood/sinus aspirate

E. Endovascular Approaches:

• Catheter-directed thrombolysis (intra-sinus tPA) — described in refractory adult cases; not standard practice
• Mechanical thrombectomy — case reports in literature; remains experimental

F. Outcome Studies:

• Long-term recanalization — occurs in 80–100% of cases with anticoagulation on follow-up MRV
• Mortality — reduced from >50% (pre-antibiotic era) to <5% with modern management
• Residual deficits — hearing loss most common; neurological deficits rare with early treatment

13. STAGING (Chandler Classification — Modified for LST)

14. PROGNOSIS

• Mortality in modern era: <5% with early diagnosis and treatment
• Morbidity factors: delay in diagnosis, associated intracranial complications, virulent organisms (MRSA), young age with immunocompromise
• Hearing loss — permanent conductive or mixed hearing loss expected from CSOM/cholesteatoma
• Sinus recanalization — occurs in majority with anticoagulation; monitored by serial MRV
• Cranial nerve recovery — jugular foramen syndrome usually recovers with antibiotic treatment

SUMMARY TABLE

KEY REFERENCES

• Cummings Otolaryngology Head and Neck Surgery (6th Ed.) — Ch. 141: Complications of Temporal Bone Infections, pp. 2720–2725
• Adams and Victor's Principles of Neurology (12th Ed.) — Septic Transverse (Lateral) Sinus Thrombophlebitis, p. 2144
• Tintinalli's Emergency Medicine — Complications of Otitis Media: Lateral Sinus Thrombosis
• Dhingra PL — Diseases of Ear Nose and Throat: Intracranial Complications of CSOM
• Hazarika P — Textbook of ENT and Head & Neck Surgery: Complications of Chronic Otitis Media
• Scott-Brown's Otorhinolaryngology, Head and Neck Surgery — Intracranial Complications
• Stell & Maran's Head and Neck Surgery — Otogenic Intracranial Complications
• Funamura JL et al. (2014): Anticoagulation in paediatric sigmoid sinus thrombosis — Int J Pediatr Otorhinolaryngol
• Symms MJ et al. (1999): Management of lateral sinus thrombosis — Laryngoscope 109:1616–1620

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