"dural arteriovenous fistula" AND "cerebral venous thrombosis"

dural AV fistula causes recurrent cerebral venous thrombosis mechanism plasmapheresis treatment 2024

mkdir -p /home/daytona/workspace/davf-cvt-ppt && ls /home/daytona/workspace/davf…

~/davf-cvt-ppt/create_ppt.js

const pptxgen = require("pptxgenjs");
let pres = new pptxgen();
pres.layout = 'LAYOUT_16x9';
pres.title = 'Dural AV Fistula & CVT';

// ─── COLOR PALETTE ───────────────────────────────────────────────
const BG_DARK   = "0A1628";   // deep navy  – title/section slides
const BG_MID    = "0D2137";   // mid navy   – content slides
const ACCENT1   = "E63946";   // arterial red
const ACCENT2   = "00B4D8";   // venous blue
const ACCENT3   = "FFB703";   // warning amber
const TEXT_MAIN = "E8F0FE";   // near-white
const TEXT_SUB  = "9DB8D2";   // muted blue-grey
const WHITE     = "FFFFFF";
const DIVIDER   = "1A3A5C";   // subtle separator

// ─── HELPERS ─────────────────────────────────────────────────────
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// ══════════════════════════════════════════════════════════════════
// SLIDE 1 — TITLE
// ══════════════════════════════════════════════════════════════════
titleSlide(
  "Dural Arteriovenous Fistula",
  "Recurrent CVT  |  Clinical Features  |  Management  |  Plasmapheresis"
);

// ══════════════════════════════════════════════════════════════════
// SLIDE 2 — WHAT IS DAVF?
// ══════════════════════════════════════════════════════════════════
contentSlide("What is a Dural AV Fistula?", [
  { text: "Abnormal arteriovenous shunts within the leaflets of the dura mater", bold: true, color: ACCENT2 },
  { text: "Acquired lesions — NOT developmental (unlike brain AVMs)" },
  { text: "Fed by: dural arteries (ECA branches, meningeal branches of vertebral artery)" },
  { text: "Drain to: dural venous sinuses ± cortical veins" },
  { text: "Account for 6% supratentorial and 35% posterior fossa vascular malformations" },
  { text: "Peak incidence: 50–60 years | No gender predilection", color: ACCENT3 },
  { text: "Locations: transverse-sigmoid sinus (most common), cavernous sinus, SSS, tentorial" }
]);

// ══════════════════════════════════════════════════════════════════
// SLIDE 3 — CLASSIFICATION
// ══════════════════════════════════════════════════════════════════
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  // Borden box
  const bordeRows = [
    ["Type", "Drainage", "Risk"],
    ["I", "Anterograde into dural sinus", "Benign"],
    ["II", "Sinus + retrograde into cortical veins", "Moderate"],
    ["III", "Direct retrograde cortical vein drainage", "HIGH – hemorrhage"],
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  // Cognard box
  const cognardRows = [
    ["Type", "Drainage", "Risk"],
    ["I", "Anterograde into sinus", "Benign"],
    ["IIa", "Sinus + retrograde sinus", "Low"],
    ["IIb", "Sinus + retrograde cortical vein", "Moderate"],
    ["III", "Direct cortical vein, no ectasia", "High"],
    ["IV", "Cortical vein with ectasia (>5 mm)", "Very High"],
    ["V", "Spinal perimedullary veins", "High"],
  ];
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  s.addText("⚠  Cortical Venous Drainage (CVD) = KEY risk factor for hemorrhage and progressive neurological deficits", {
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// ══════════════════════════════════════════════════════════════════
// SLIDE 4 — SECTION HEADER: dAVF → CVT Link
// ══════════════════════════════════════════════════════════════════
sectionHeader("Why Does dAVF Cause Recurrent CVT?", "The Bidirectional Pathogenic Loop");

// ══════════════════════════════════════════════════════════════════
// SLIDE 5 — PATHOGENESIS
// ══════════════════════════════════════════════════════════════════
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  s.addText("Mechanism: dAVF → Recurrent CVT (Bidirectional Loop)", {
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  // Arrow flow diagram
  const steps = [
    { label: "dAVF Creates\nHigh-Flow Shunt", col: ACCENT1 },
    { label: "Sinus Venous\nHypertension", col: "D62839" },
    { label: "Sinus Wall\nDamage / Stasis", col: ACCENT3 },
    { label: "Thrombosis\n(CVT)", col: ACCENT2 },
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  s.addText("▲ CVT → Venous stasis → Angiogenesis → New dAVF formation (feedback loop!)", {
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    { text: "1. Retrograde venous hypertension impairs cortical venous drainage → turbulent / stagnant flow", bold: false },
    { text: "2. Arterialized pressure in sinuses → endothelial shear stress → thrombosis trigger", bold: false },
    { text: "3. Post-CVT angiogenesis: VEGF / TGF-β released from thrombus → opens pre-existing AV shunts", bold: false },
    { text: "4. Incompletely recanalized sinus retains residual dAVF → perpetuates clot recurrence", bold: true, color: ACCENT3 },
    { text: "5. Thrombophilic states (Factor V Leiden, Protein C/S deficiency) amplify both dAVF and CVT risk", bold: false },
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// ══════════════════════════════════════════════════════════════════
// SLIDE 6 — CLINICAL FEATURES
// ══════════════════════════════════════════════════════════════════
sectionHeader("Clinical Features", "Presentation Depends on Location & Drainage Pattern");

twoColSlide(
  "Clinical Features of dAVF",
  "General / Intracranial",
  [
    "Pulsatile tinnitus (bruit) — most common",
    "Headache (often positional / progressive)",
    "Papilledema → pseudotumor syndrome",
    "Seizures (uncommon, cortical irritation)",
    "Cognitive decline / dementia (venous congestion)",
    "Subarachnoid or intracerebral hemorrhage",
    "Focal neurological deficits",
  ],
  "Location-Specific",
  [
    "Cavernous sinus: proptosis, chemosis, painful ophthalmoplegia, raised IOP",
    "Transverse/sigmoid sinus: pulsatile tinnitus ± otalgia",
    "Superior sagittal sinus: seizures, hydrocephalus, confusion",
    "Posterior fossa: lower cranial nerve deficits, cerebellar signs",
    "Tentorial: HIGH risk — SAH, mass effect",
    "Thalamic congestion → reversible dementia (rare)",
  ],
  ACCENT2, ACCENT3
);

// ══════════════════════════════════════════════════════════════════
// SLIDE 7 — CVT-SPECIFIC CLINICAL FEATURES
// ══════════════════════════════════════════════════════════════════
contentSlide("CVT in the Context of dAVF — Clinical Red Flags", [
  { text: "Headache — thunderclap or progressive; most common symptom (>90%)", bold: true, color: ACCENT3 },
  { text: "Focal deficits: contralateral weakness / sensory loss / aphasia" },
  { text: "Seizures (40%) — focal or generalized; more common than in arterial stroke" },
  { text: "Altered consciousness / confusion / encephalopathy" },
  { text: "Papilledema with visual obscurations" },
  { text: "CVT recurrence rate: 1–2%/year generally; HIGHER in dAVF-associated CVT", color: ACCENT1, bold: true },
  { text: "Recurrence risk factors: thrombophilia, male sex, no precipitant, underlying dAVF not treated" },
  { text: "New-onset dAVF reported in ~2.4% of CVT patients at 8-month follow-up (AHA 2024 guidelines)" },
]);

// ══════════════════════════════════════════════════════════════════
// SLIDE 8 — DIAGNOSIS
// ══════════════════════════════════════════════════════════════════
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  const diagRows = [
    ["Modality", "Findings / Role"],
    ["MRI + MRV", "Sinus occlusion (filling defect); cortical vein thrombus on SWI/GRE; venous infarct"],
    ["CT Venography", "Rapid screen; 'empty delta sign' in SSS; detects dAVF with CTA"],
    ["DSA (Angiography)", "GOLD STANDARD — defines feeding arteries, drainage pattern, Cognard/Borden grade"],
    ["MRA / CTA", "Non-invasive screening; early opacification of venous structures suggests AV shunt"],
    ["D-Dimer", "Elevated in acute CVT — useful but non-specific"],
    ["Thrombophilia workup", "Factor V Leiden, Prothrombin mutation, Protein C/S/Antithrombin, APLA screen"],
  ];
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// ══════════════════════════════════════════════════════════════════
// SLIDE 9 — SECTION HEADER: Management
// ══════════════════════════════════════════════════════════════════
sectionHeader("Management", "Acute CVT  |  Definitive dAVF Treatment");

// ══════════════════════════════════════════════════════════════════
// SLIDE 10 — ACUTE CVT MANAGEMENT
// ══════════════════════════════════════════════════════════════════
contentSlide("Acute CVT Management", [
  { text: "ANTICOAGULATION — cornerstone even with hemorrhagic infarction", bold: true, color: ACCENT2 },
  { text: "Acute: IV Heparin (UFH) or LMWH (subcutaneous)" },
  { text: "Transition to: Warfarin (INR 2–3) — DOACs under study (RE-SPECT CVT, SECRET trials)" },
  { text: "Duration: 3–6 months provoked; 6–12 months unprovoked; indefinite in thrombophilia", color: ACCENT3 },
  { text: "ICP management: acetazolamide, repeat LP in pseudotumor; head elevation" },
  { text: "Seizure prophylaxis: AEDs if cortical involvement / hemorrhagic infarct" },
  { text: "Endovascular thrombectomy / thrombolysis: for deteriorating patients despite anticoagulation" },
  { text: "Decompressive hemicraniectomy: life-saving in malignant cerebral edema" },
  { text: "Treat underlying dAVF: essential to prevent CVT recurrence (see next slide)", bold: true, color: ACCENT1 },
]);

// ══════════════════════════════════════════════════════════════════
// SLIDE 11 — DAVF DEFINITIVE TREATMENT
// ══════════════════════════════════════════════════════════════════
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  const txRows = [
    ["Modality", "Details", "Best For"],
    ["Endovascular Embolization", "Transarterial (NBCA / Onyx) ± transvenous; obliterates >90% with multimodal approach", "Large, inaccessible dAVFs"],
    ["Surgical Excision", "Direct ligation/resection of fistula + feeding vessels", "Small, accessible dAVFs; embolization failures"],
    ["Stereotactic Radiosurgery (SRS)", "20–30 Gy to nidus; obliteration takes 2–3 years; not suitable if cortical vein reflux", "Residual / recurrent; not first-line"],
    ["Combined (Embolization + Surgery/SRS)", "Sequential debulking → definitive treatment; preferred for complex high-grade fistulas", "Cognard III/IV, Borden II/III"],
    ["Anticoagulation alone", "Not curative; slows progression; risk: paradoxical venous thrombosis in draining sinus", "Bridge or palliation only"],
  ];
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// ══════════════════════════════════════════════════════════════════
// SLIDE 12 — SECTION HEADER: Plasmapheresis
// ══════════════════════════════════════════════════════════════════
sectionHeader("Plasmapheresis in dAVF & CVT", "Rationale, Evidence & Protocol");

// ══════════════════════════════════════════════════════════════════
// SLIDE 13 — PLASMAPHERESIS SLIDE
// ══════════════════════════════════════════════════════════════════
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  s.addText("Plasmapheresis (Plasma Exchange) — Role in CVT/dAVF", {
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  const rationale = [
    "Removes pro-thrombotic factors: fibrinogen, antiphospholipid antibodies (APLA), von Willebrand multimers",
    "Removes pro-inflammatory cytokines driving endothelial damage",
    "Corrects acquired deficiencies: Protein C/S, antithrombin (via FFP replacement)",
    "Reduces blood viscosity — improves flow in congested sinuses",
    "Targets APLA-associated recurrent CVT — removes pathogenic IgG/IgM",
  ].map((t, i, arr) => ({ text: t, options: { bullet: true, color: TEXT_MAIN, fontSize: 12, breakLine: i < arr.length - 1 } }));
  s.addText(rationale, { x: 0.3, y: 1.55, w: 4.3, h: 3.7, fontFace: "Calibri", valign: "top", margin: 3, paraSpaceBefore: 6 });

  // Clinical use box
  s.addShape(pres.ShapeType.rect, { x: 5.1, y: 1.1, w: 4.7, h: 4.2, fill: { color: "0B1D30" }, line: { color: ACCENT3, pt: 1.5 } });
  s.addText("CLINICAL USE & PROTOCOL", { x: 5.1, y: 1.1, w: 4.7, h: 0.4, fontSize: 13, bold: true, color: ACCENT3, fontFace: "Calibri", align: "center", margin: 0 });
  const protocol = [
    "Indications: APLA-associated recurrent CVT; catastrophic APS (CAPS) with CVT; refractory CVT with severe thrombophilia",
    "Frequency: 5–7 sessions over 10–14 days (1–1.5× plasma volume per session)",
    "Replacement fluid: FFP (replenishes coagulation factors) OR 5% albumin",
    "NOT a standard guideline recommendation for CVT (AHA 2024) — used adjunctively",
    "Best evidence: CAPS protocol — combine PLEX + heparin + steroids ± IVIG",
    "Monitor: coagulation profile, calcium (citrate toxicity), BP, allergic reactions",
  ].map((t, i, arr) => ({ text: t, options: { bullet: true, color: TEXT_MAIN, fontSize: 12, breakLine: i < arr.length - 1 } }));
  s.addText(protocol, { x: 5.2, y: 1.55, w: 4.5, h: 3.7, fontFace: "Calibri", valign: "top", margin: 3, paraSpaceBefore: 6 });
}

// ══════════════════════════════════════════════════════════════════
// SLIDE 14 — KEY TAKEAWAYS
// ══════════════════════════════════════════════════════════════════
{
  let s = pres.addSlide();
  s.addShape(pres.ShapeType.rect, { x: 0, y: 0, w: 10, h: 5.625, fill: { color: BG_DARK } });
  s.addShape(pres.ShapeType.rect, { x: 0, y: 0, w: 10, h: 1.0, fill: { color: "14243A" } });
  s.addShape(pres.ShapeType.rect, { x: 0, y: 0.95, w: 10, h: 0.07, fill: { color: ACCENT1 } });
  s.addText("Key Takeaways", { x: 0.4, y: 0.08, w: 9.2, h: 0.82, fontSize: 22, bold: true, color: WHITE, fontFace: "Calibri", valign: "middle", margin: 0 });

  const takes = [
    { icon: "🔴", text: "dAVF and CVT are BIDIRECTIONAL — each can cause and perpetuate the other", color: ACCENT1 },
    { icon: "🔵", text: "Mechanism: venous hypertension → stasis → endothelial injury → thrombosis; post-CVT angiogenesis → new fistula", color: ACCENT2 },
    { icon: "🟡", text: "Cognard III/IV / Borden II/III = high-grade, high hemorrhage risk — treat urgently", color: ACCENT3 },
    { icon: "🟢", text: "Acute CVT: ANTICOAGULATE even with hemorrhagic infarction; address underlying dAVF", color: "4CAF50" },
    { icon: "🔴", text: "dAVF treatment: Endovascular embolization (first-line) ± surgery ± radiosurgery", color: ACCENT1 },
    { icon: "🟡", text: "Plasmapheresis: adjunct for APLA-associated recurrent CVT / CAPS — NOT routine first-line", color: ACCENT3 },
    { icon: "🔵", text: "Long-term follow-up imaging mandatory — new dAVF can form months-years after CVT", color: ACCENT2 },
  ];

  takes.forEach((t, i) => {
    s.addShape(pres.ShapeType.roundRect, {
      x: 0.2, y: 1.1 + i * 0.62, w: 9.6, h: 0.55,
      fill: { color: "0D2137" }, line: { color: t.color, pt: 1 }
    });
    s.addText(`${t.icon}  ${t.text}`, {
      x: 0.3, y: 1.1 + i * 0.62, w: 9.4, h: 0.55,
      fontSize: 13, color: t.color, fontFace: "Calibri",
      bold: false, valign: "middle", margin: 4
    });
  });
}

// ══════════════════════════════════════════════════════════════════
// SAVE
// ══════════════════════════════════════════════════════════════════
pres.writeFile({ fileName: "/home/daytona/workspace/davf-cvt-ppt/DAVF_CVT_Presentation.pptx" })
  .then(() => console.log("PPT saved successfully."))
  .catch(e => console.error("Error:", e));

cd /home/daytona/workspace/davf-cvt-ppt && node create_ppt.js