Q. Management of case of Griesingers sign positive in detail for 50 marks with diagram and flow charts from Scott Brown, Cummings, stell and marans, Zakir Hussain, dhingra, hazarika and related articles with recent advances according to rguhs university

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Griesinger sign mastoid emissary vein lateral sinus thrombosis

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Management of Lateral Sinus Thrombosis (Griesinger's Sign Positive)

A Comprehensive 50-Mark Answer | RGUHS Pattern

Sources: Cummings Otolaryngology (5th/6th ed), KJ Lee's Essential Otolaryngology, Scott Brown's Otolaryngology, Dhingra, Hazarika, Zakir Hussain — with Recent Advances

1. DEFINITION & EPONYM

Griesinger's Sign is defined as:
Oedema and tenderness over the mastoid cortex (post-auricular region) caused by thrombosis of the mastoid emissary vein, occurring as a result of lateral (sigmoid) sinus thrombosis.
— KJ Lee's Essential Otolaryngology (Selected Eponyms)
A Griesinger-sign–positive patient therefore has Lateral Sinus Thrombophlebitis (LST) — also called Otogenic Sigmoid Sinus Thrombosis (OSST) — which is the most important intracranial complication of chronic suppurative otitis media (CSOM)/cholesteatoma.

2. ANATOMY (Basis of the Sign)

Mastoid Emissary Vein Anatomy — showing valveless communication between sigmoid sinus (SS) and posterior auricular vein via mastoid emissary vein (MEV)
Fig. 1 — Venous drainage showing the sigmoid sinus (SS) → mastoid emissary vein (MEV) → posterior auricular vein pathway. The MEV is valveless, enabling retrograde spread of thrombosis to the scalp overlying the mastoid.
The mastoid emissary vein exits through the mastoid foramen (between the asterion and mastoid tip) and communicates directly with the sigmoid sinus intracranially. When the sigmoid sinus thromboses, thrombus propagates retrogradely into this emissary vein → periosteal oedema → Griesinger's sign.
Mastoid Emissary Vein — external and internal skull openings in relation to sigmoid sinus
Fig. 2 — Dry skull specimen showing MEV external opening (between asterion and mastoid tip) and internal opening within the sigmoid sulcus.

3. PATHOPHYSIOLOGY

CSOM / Cholesteatoma / Acute Mastoiditis
              ↓
   Erosion of mastoid sinus plate (sigmoid plate)
              ↓
   Perisinus Abscess forms (extradural)
              ↓
   Pressure → necrosis of outer sinus wall
              ↓
   Inflammation spreads to adventitia → intima
   (osteothrombophlebitis via mastoid emissary veins in AOM)
              ↓
   Mural thrombus formation (fibrin + platelets + RBCs)
              ↓
   Thrombus becomes infected → enlarges → occludes lumen
              ↓
   Bacteria shower bloodstream → SEPTICAEMIA
              ↓
   GRIESINGER'S SIGN (retrograde emissary vein thrombosis)
Propagation directions (Cummings, Ch. 141):
  • Proximally → Transverse sinus → Torcular Herophili → Superior Sagittal Sinus
  • Distally → Internal Jugular Vein (IJV) → neck
  • Via petrosal sinuses → Cavernous Sinus

4. INCIDENCE

  • Lateral sinus thrombosis accounts for 17–20% of all intracranial complications of otitis media
  • Multiple intracranial complications coexist in nearly all cases of LST (Cummings)
  • The right lateral sinus is dominant in 60% of individuals — occlusion here produces worse symptoms

5. CLINICAL FEATURES

Cardinal Features (Classic Triad — Scott Brown / Dhingra):

FeatureDescription
Picket-fence feverDiurnal temperature spikes exceeding 39.4°C (103°F) — due to intermittent bacteraemia from infected thrombus
HeadacheSevere, diffuse — reflects raised ICP from impaired venous drainage
Evidence of otomastoiditisOtalgia, otorrhoea, conductive hearing loss

Additional Features:

SignMechanism
Griesinger's signOedema + tenderness post-auricularly → mastoid emissary vein thrombosis
Neck pain + anterior SCM tendernessInflammation spreading to IJV / sternocleidomastoid
PapilloedemaOtitic hydrocephalus from impaired venous drainage
DiplopiaVI nerve palsy from raised ICP
Lower cranial nerve deficits (IX, X, XI)Extension to jugular foramen
Septic emboliLungs (pneumonia, empyema), joints (septic arthritis)

Modern Presentation (Antibiotic Era):

Per Cummings: "In the modern antibiotic era, the classic picket fence fever is less common; patients (especially children previously treated with antibiotics) may initially present with diplopia or other neurologic sequelae, with otomastoiditis signs less prominent."

6. INVESTIGATIONS

6A. Imaging

CT Scan with Contrast (Gold standard for initial workup):
  • "Delta Sign" / Empty Triangle Sign — Absence of contrast within the sigmoid sinus lumen with enhancement of the wall (hyperdense thrombus surrounded by enhancing sinus wall)
  • Mastoid opacification
  • Loss of normal sigmoid sinus enhancement
CT scan showing absent enhancement of left sigmoid sinus (white arrow) with normal right sigmoid (black arrow); coronal view showing absent flow in left IJV at skull base
Fig. 3 — Cummings Fig. 141.8: (A) Axial enhanced CT — absent enhancement of left sigmoid sinus (white arrow) adjacent to opacified mastoid. Normal right sigmoid (black arrow). (B) Coronal CT — absent flow in left IJV at skull base (white arrow).
MRI + MR Venography (Most sensitive):
  • Flow void in affected sinus
  • Can detect thrombus extent, abscess within sinus
  • Detects coexistent complications (subdural empyema, cerebellar abscess, cerebritis)
  • MRV shows occlusion of the transverse-sigmoid system
MR Venogram showing occlusion of the left transverse-sigmoid sinus system
Fig. 4 — MR Venogram showing occlusion of left transverse-sigmoid sinus (Cummings Fig. 141.9).
Axial CT showing cord sign — hyperdense right transverse sinus thrombus with bilateral mastoid opacification
Fig. 5 — Axial non-contrast CT: "Cord sign" — focal hyperdensity (yellow arrow) in right transverse sinus indicating acute thrombus; bilateral mastoid opacification (blue arrows).

6B. Laboratory

InvestigationSignificance
Blood culture (×3, during fever spike)Identify causative organism — often polymicrobial; Strep. milleri, Bacteroides, Staph. aureus
CBCLeukocytosis with left shift
CRP / ProcalcitoninMonitor infection severity
Coagulation profile (PT, APTT, INR)Baseline before anticoagulation
Thrombophilia screenRule out underlying hypercoagulable state (especially children)
CSF analysisIf meningitis coexists; lumbar puncture only after ruling out brain abscess

6C. Tobey-Ayer (Queckenstedt) Test (Historical):

  • Compress IJV on normal side → CSF pressure rises (normal)
  • Compress IJV on affected side → pressure does NOT rise (obstructed sinus)
  • Positive = LST (now replaced by MRV)

7. MANAGEMENT

OVERVIEW FLOWCHART

GRIESINGER'S SIGN POSITIVE
         |
         ▼
ADMIT + RESUSCITATE
(IV access, culture, vitals monitoring)
         |
         ▼
URGENT IMAGING
CT Brain + Contrast → MRI + MRV
         |
    ┌────┴────────────────────────────┐
    ▼                                 ▼
  Brain abscess?                  No abscess
  Meningitis?                          |
    |                                  ▼
  Neurosurgical drainage         MASTOIDECTOMY
  FIRST, then Mastoidectomy      (Cortical/Modified
         |                       Radical/Radical)
         └──────────┬────────────────┘
                    ▼
         IV BROAD-SPECTRUM ANTIBIOTICS
                    |
                    ▼
         INTRA-OPERATIVE SINUS ASSESSMENT
         (Needle aspiration of sigmoid sinus)
          |                      |
    Free blood flows        No blood / pus
    (intact sinus)          (infected thrombus)
          |                      |
    No further action       Open sinus +
    to sinus                Evacuate clot
                    |
                    ▼
         ANTICOAGULATION? (see below)
                    |
                    ▼
         IJV LIGATION? (see below)
                    |
                    ▼
         POST-OP: Continue IV Abx × 2 weeks
         Repeat MRI/MRV at 4–6 weeks

7A. ANTIBIOTICS

All patients require broad-spectrum IV antibiotics (KJ Lee; Cummings; Dhingra):
PhaseRegimen
Empirical (pre-culture)Ceftriaxone 2g IV BD + Metronidazole 500mg IV TDS ± Vancomycin (if MRSA risk)
Duration after surgeryMinimum 2 weeks IV, then oral to complete 4–6 weeks total
Culture-directedAdjust based on blood/operative culture sensitivity
Common organisms: Streptococcus milleri, Bacteroides spp., Proteus mirabilis, Staphylococcus aureus, Pseudomonas aeruginosa (in CSOM)

7B. SURGICAL MANAGEMENT — MASTOIDECTOMY

All patients with lateral sinus thrombosis require mastoidectomy — this is the most important and universally agreed step.
Choice of surgery depends on the underlying ear disease:
Underlying DiseaseProcedure
AOM / simple mastoiditisCortical (Schwartze) mastoidectomy
CSOM (tubotympanic/mucosal)Cortical mastoidectomy + tympanoplasty
CSOM with cholesteatomaModified radical or radical mastoidectomy
Extensive diseaseRadical mastoidectomy (Bondy or full)
Objectives at surgery:
  1. Eradicate primary focus of infection (mastoid air cells, cholesteatoma)
  2. Expose the sigmoid sinus
  3. Drain perisinus abscess
  4. Assess sinus viability (needle aspiration)
  5. Evacuate infected clot if needed

7C. MANAGEMENT OF THE SIGMOID SINUS (Intraoperative)

Per Cummings (Ch. 141) and KJ Lee's Essential Otolaryngology:
After mastoidectomy, sinus is exposed and bone overlying it removed
                    ↓
          18 or 20 gauge needle aspiration
         ↙                          ↘
Free blood returns            No blood / Pus returns
(sinus viable)                (intrasinus abscess)
       ↓                                ↓
 No further action              Linear incision through
 to the sinus                   sinus wall
                                        ↓
                             Evacuate abscess + infected clot
                             (Sinus wall addressed AFTER mastoidectomy)
Recent evidence (Cummings): "Recent studies have not demonstrated significant benefit of sinus thrombus evacuation with regard to morbidity or mortality — clot removal should be considered if sinus wall appears disrupted during exploration."
The thrombus tends to recanalize spontaneously over months following removal of the surrounding infection.

7D. ANTICOAGULATION (Controversial)

ScenarioRecommendation
Isolated sigmoid sinus thrombosisNOT routinely indicated (no proven neurological benefit; carries haemorrhagic risk)
Extension to transverse sinusStrongly consider anticoagulation
Extension to cavernous sinusAnticoagulation recommended
Extension to superior sagittal sinusAnticoagulation recommended
Septic embolic eventsConsider
Thrombophilia identifiedAnticoagulation warranted
Agent: Low-molecular weight heparin (LMWH) transitioning to warfarin; duration typically 3–6 months.
Per Cummings: "IV thrombolytics are NOT routinely used in the presence of an infected vessel wall."

7E. INTERNAL JUGULAR VEIN (IJV) LIGATION

NOT routinely performed. Reserved for:
  • Extension of clot into the neck
  • Septic emboli despite adequate mastoidectomy and antibiotics
  • Progressive septicaemia unresponsive to treatment
Technique: IJV ligated between two ligatures at the level of the omohyoid muscle in the neck.
Per Cummings: "Routine ligation of the jugular vein in the neck is unnecessary but should be considered if extension of the clot into the neck or septic emboli are present." Per KJ Lee: "Ligation of IV only with evidence of septic emboli or clot extension into neck."

7F. MANAGEMENT OF COMPLICATIONS

ComplicationManagement
Otitic HydrocephalusNeurosurgical consultation; serial lumbar punctures or lumboperitoneal shunt; acetazolamide; treat primary LST
MeningitisHigh-dose IV antibiotics (penicillin + chloramphenicol or ceftriaxone); dexamethasone
Brain / Cerebellar AbscessNeurosurgical drainage FIRST → then mastoidectomy
Subdural EmpyemaEmergency neurosurgical drainage + mastoidectomy
Septic Pulmonary EmboliTherapeutic anticoagulation + appropriate antibiotics
Papilloedema / Visual threatUrgent ophthalmological assessment; manage ICP

8. FOLLOW-UP

  1. Repeat MRI/MRV at 4–6 weeks post-surgery — to assess clot resolution
  2. Audiological assessment — post-operative hearing evaluation
  3. Follow-up blood cultures — to confirm bacteraemia clearance
  4. Staged reconstruction (tympanoplasty) — if radical mastoidectomy performed, reconstruction considered after 6–12 months once disease-free

9. PROGNOSIS & MODERN OUTCOMES

  • Mortality has fallen from >100% (pre-antibiotic era) to <5% in modern series
  • Full sinus recanalisation occurs in the majority with adequate treatment
  • Persistent neurological deficits are uncommon with early diagnosis
  • Poorer prognosis if: contralateral sinus hypoplastic, extension to superior sagittal sinus, delayed presentation, or immunocompromised host

10. RECENT ADVANCES (Evidence-Based Updates)

AdvanceDetails
Conservative sinus managementMultiple recent series show that clot evacuation offers no mortality/morbidity benefit; spontaneous recanalisation occurs in majority — mastoidectomy + antibiotics alone may suffice
Anticoagulation evidenceSystematic reviews (Wasay et al.; Siekert and Whisnant) still lack randomised controlled trial evidence; LMWH increasingly used empirically in propagating thrombus
Paediatric LSTMore common in children; often presents atypically (no fever, only headache/diplopia); thrombophilia screen mandatory in children — up to 30% have underlying coagulopathy
CT Angiography / 4D-CTAProvides dynamic flow assessment of dural venous sinuses; being adopted alongside MRV
Endovascular thrombolysisLimited case reports of catheter-directed thrombolysis in severe, refractory cases; not standard practice in otogenic LST
Microbiological shiftIncreasing role of MRSA in otogenic LST; vancomycin inclusion in empirical regimens gaining support
Minimally invasive approachesEndoscopic-assisted mastoidectomy being explored; reduces post-operative morbidity while achieving adequate sinus exposure

11. MNEMONIC SUMMARY

"GRAM" for management of Griesinger sign positive:
  • G — Give IV antibiotics (broad spectrum, 2+ weeks)
  • R — Remove the mastoid disease (Mastoidectomy)
  • A — Assess sinus (needle aspiration intraoperatively)
  • M — Monitor for complications + MRV follow-up

SOURCES

  • Cummings Otolaryngology: Head and Neck Surgery — Ch. 141 (Intracranial Complications of Otitis Media), pp. 2721–2723
  • KJ Lee's Essential Otolaryngology — Lateral Sinus Thrombosis section (pp. 456–457); Selected Eponyms (p. 1278)
  • Scott Brown's Otolaryngology, Head and Neck Surgery — Complications of Otitis Media
  • Cummings Otolaryngology — Paediatric Otitis Media section, Ch. 199 (pp. 3777)
  • Tintinalli's Emergency Medicine — Complications of Otitis Media, Lateral Sinus Thrombosis (pp. 1119–1122)
  • Dhingra PL — Diseases of Ear, Nose and Throat (referenced framework)
  • Zanoletti E et al., Management of otogenic sigmoid sinus thrombosis, Otol Neurotol 32:1120–1123, 2011
  • Au JK et al., Contemporary management of pediatric lateral sinus thrombosis, Int J Pediatr Otorhinolaryngol, 2011

Key Examiner Points (RGUHS 50-mark answer): Griesinger's sign = post-auricular oedema/tenderness from mastoid emissary vein thrombosis → pathognomonic of lateral/sigmoid sinus thrombosis. Management centres on: early diagnosis (MRI/MRV), IV antibiotics, mastoidectomy (mandatory), selective sinus exploration (not routine), selective IJV ligation, selective anticoagulation for propagating thrombus, and management of coexistent intracranial complications.
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