Hemodynamic Disorders — Edema, Thrombosis, Embolism & Infarction
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Rapid summary for last-minute revision before your exam.
Virchow’s Triad (3 factors promoting thrombosis):
- Endothelial injury
- Abnormal blood flow (stasis/turbulence)
- Hypercoagulability
DVT prophylaxis: Early ambulation, compression stockings, anticoagulation (heparin/LMWH).
Pulmonary embolism: Sudden dyspnea, pleuritic chest pain, tachypnea, hypoxia; S1Q3T3 pattern on ECG (deep S in I, Q in III, inverted T in III); CT pulmonary angiography (CTPA) = gold standard.
Infarction types: Red (hemorrhagic) = venous occlusion or dual supply (lung, liver); White (pale) = arterial occlusion in solid organs with end-arterial supply (heart, kidney, spleen).
⚡ Exam tip: “Cellophane keratopathy” = band-shaped keratopathy due to hypercalcemia in long-standing hypocalcemia; “nutmeg liver” = chronic venous congestion of liver (right heart failure).
🟡 Standard — Regular Study (2d–2mo)
Standard content for students with a few days to months.
Edema
Pathophysiology
Starling forces governing fluid movement across capillaries:
Forces favoring filtration (outward):
- Capillary hydrostatic pressure (Pc): ~35 mmHg (arterial end) to ~15 mmHg (venous end)
- Interstitial oncotic pressure: ~5 mmHg
Forces favoring reabsorption (inward):
- Plasma oncotic pressure (πc): ~25 mmHg (albumin, globulins)
- Interstitial hydrostatic pressure: ~–1 mmHg (slight suction)
Net filtration pressure = (Pc + πi) – (πc + Pi) ≈ 35 – 25 = ~10 mmHg (arterial end favors filtration; venous end favors reabsorption). Lymphatics return ~90% of filtered fluid.
Types of Edema
| Type | Mechanism | Example |
|---|---|---|
| Cardiac edema | ↓ cardiac output → RAAS → Na⁺/H₂O retention + ↑ venous pressure → ↑ capillary hydrostatic pressure | Right heart failure, CHF |
| Hepatic edema | Portal hypertension → ↑ capillary hydrostatic pressure in splanchnic circulation; hypoalbuminemia | Cirrhosis, portal hypertension |
| Renal edema | ↓ GFR → Na⁺/H₂O retention; hypoalbuminemia (nephrotic) → ↓ πc | Nephritic syndrome (GFR↓), Nephrotic syndrome (protein loss) |
| Nutritional edema | ↓ protein intake OR ↓ synthesis OR ↑ loss → ↓ πc | Kwashiorkor, marasmus |
| Inflammatory edema | ↑ capillary permeability (mediators: histamine, bradykinin, cytokines) | Infection, allergy |
| Lymphedema | Blocked lymphatics → ↑ interstitial protein → ↑ πi | Post-mastectomy (axillary node dissection), filariasis |
Nephrotic vs Nephritic Syndrome Edema
| Feature | Nephrotic Syndrome | Nephritic Syndrome |
|---|---|---|
| Primary defect | Glomerular barrier → massive proteinuria (>3.5 g/day) | Glomerular inflammation → hematuria, ↓ GFR |
| Protein loss | Albumin → hypoalbuminemia → ↓ πc | Variable |
| Edema | Generalized, severe (due to ↓ πc) | Periorbital, dependent (due to Na⁺/H₂O retention + ↓ GFR) |
| Blood pressure | Normal or low | Hypertension |
| Lipids | ↑ (increased hepatic synthesis) | Normal |
| Other | Hypercoagulable (ATIII loss) | Oliguria, hematuria (RBC casts) |
Thrombosis
Virchow’s Triad (3 Determinants of Thrombosis)
1. Endothelial Injury (most important):
- Direct damage to endothelium → platelet adhesion + activation + aggregation
- Examples: Atherosclerosis, vasculitis, myocardial infarction (endocardium), Reynolds manifolds (malignant hypertension)
2. Abnormal Blood Flow:
- Stasis: Slow flow → platelets don’t get swept away; coagulation factors accumulate
- Turbulence: Disrupts laminar flow → endothelial activation + platelet deposition
- Sites of stasis/turbulence: Deep veins (DVT), cardiac chambers (atrial fibrillation → left atrial appendage thrombus), diseased heart valves, bifurcations (where flow is turbulent)
3. Hypercoagulability (thrombophilia):
- Primary (genetic): Factor V Leiden (APC resistance, most common), Prothrombin gene mutation (G20210A), Antithrombin III deficiency, Protein C deficiency, Protein S deficiency
- Secondary (acquired): Malignancy (Trousseau syndrome), DVT/PE history, pregnancy, oral contraceptive pills (OCPs), smoking, hyperhomocysteinemia, HIT (heparin-induced thrombocytopenia), DIC
Factor V Leiden
- Most common inherited thrombophilia (5% of Caucasians)
- Point mutation (R506Q) in Factor V gene → Factor V cannot be inactivated by activated protein C (APC) → “APC resistance” → hypercoagulability
- ** labs**: APC resistance assay (elongated PTT when exogenous APC is added); genetic testing for FV Leiden mutation
- Risk: 7-fold ↑DVT risk in heterozygotes; 80-fold ↑ in homozygotes
- Oral contraceptives dramatically increase risk in Factor V Leiden carriers
Deep Vein Thrombosis (DVT)
- Most common in deep veins of lower limbs (popliteal, femoral, iliac)
- Clinical: Unilateral leg swelling, pain, warmth, tenderness; Homans sign (calf pain on dorsiflexion — unreliable)
- Complications: Pulmonary embolism (most feared), Post-thrombotic syndrome (chronic venous insufficiency), venous stasis ulcers
- Diagnosis: D-dimer (high sensitivity, low specificity; useful to rule out), Compression ultrasonography (gold standard; non-compressible vein = thrombosis)
Embolism
Pulmonary Embolism (PE)
Source: DVT (most common); right heart thrombus; fat, air, amniotic fluid, tumor cells
Clinical: Sudden dyspnea, pleuritic chest pain (sharp, worse with breathing), tachypnea, tachycardia, hypoxia (low PaO₂), syncope, hemoptysis
ECG: Sinus tachycardia most common; S1Q3T3 (deep S wave in lead I, Q wave in lead III, inverted T wave in lead III) — classic but not sensitive; right axis deviation, RBBB
CT Pulmonary Angiography (CTPA): Gold standard; filling defect in pulmonary artery
Risk factors: Virchow’s triad, immobilization, surgery, malignancy, pregnancy, OCPs, previous DVT/PE
Treatment: Anticoagulation (heparin → warfarin or DOACs); thrombolysis (massive PE with hemodynamic instability); embolectomy (surgical or catheter-based)
Systemic Thromboembolism
- Arterial emboli: From left heart (mural thrombus post-MI, atrial fibrillation, valvular disease), aortic atherosclerosis, paradoxical embolism (through PFO)
- Sites: Brain (stroke), mesenteric arteries (ischemic bowel), renal arteries, peripheral arteries
- Venous emboli → lodge in pulmonary circulation (except paradoxical emboli through PFO/ASD)
Fat Embolism Syndrome
- Classic triad: Respiratory distress + neurologic symptoms + petechial rash (axillae, chest, conjunctivae)
- Timing: 24–72 hours after long bone fractures (femur, tibia, pelvis)
- Pathophysiology: Fat globules from bone marrow enter circulation → lodge in pulmonary capillaries → release free fatty acids → endothelial damage → ARDS, cerebral dysfunction
- Diagnosis: Clinical; CT chest shows diffuse alveolar infiltrates; fat globules in urine/sputum (non-specific)
- Treatment: Supportive; early fracture fixation reduces incidence
Air Embolism
-
100 mL air rapidly into circulation → fatal (coronary air embolism, cerebral air embolism)
- Sources: Central line placement/removal, surgery, diving (decompression sickness → nitrogen bubbles)
- Position: Left lateral decubitus with head down (Durant maneuver) — traps air in right atrium
Amniotic Fluid Embolism (AFE)
- Catastrophic; occurs during labor or immediate postpartum
- Triad: Sudden severe hypoxia + hypotension + coagulopathy (DIC)
- Pathophysiology: Amniotic fluid enters maternal circulation → fetal squamous cells + meconium → pulmonary vascular obstruction + massive cytokine release
- Prognosis: 80% mortality; leading cause of maternal death in developed countries
Infarction
Types
Pale (White) Infarcts:
- Arterial occlusion in solid organs with end-arterial blood supply
- Examples: Heart (MI), Kidney, Spleen
- Firm, white, well-demarcated; coagulative necrosis
Red (Hemorrhagic) Infarcts:
- Venous occlusion (e.g., mesenteric venous thrombosis, ovarian torsion)
- Organs with dual blood supply (lung — bronchial artery + pulmonary artery; liver — hepatic artery + portal vein)
- Loose tissue (allows blood to seep in): Lung, Liver
- Hemorrhagic, red-purple, ill-defined margins
Anemic (Pale) vs Hemorrhagic Infarction — Examples:
| Organ | Type | Reason |
|---|---|---|
| Heart | Pale (anemic) | End-arterial supply; firm (coagulative necrosis) |
| Kidney | Pale (anemic) | End-arterial supply; well-demarcated |
| Spleen | Pale (anemic) | End-arterial supply |
| Lung | Red (hemorrhagic) | Dual supply + loose tissue |
| Liver | Red (hemorrhagic) | Dual supply + loose tissue |
| Brain | Red (hemorrhagic) | Very high blood flow; liquefactive necrosis |
| Intestine | Red (hemorrhagic) | Venous occlusion (superior mesenteric vein); bowel is edematous, hemorrhagic, necrotic |
Factors Influencing Infarction
- Nature of blood supply (end-arterial vs dual vs collateral)
- Rate of occlusion (gradual = time for collaterals to develop = less infarction)
- Vulnerability of tissue to ischemia (neurons most vulnerable; fibroblasts least)
- Oxygen-carrying capacity of blood (anemia → worse outcome; polycythemia → better)
Systemic Effects of Infarction
- Fever (IL-1, TNF-α from inflammatory response)
- Leukocytosis (neutrophils)
- Elevated ESR (acute phase reactants)
- Increased serum enzymes: LDH, AST, ALT, CK, troponin (cardiac), amylase/lipase (pancreatic)
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DIC (Disseminated Intravascular Coagulation)
- Widespread microvascular thrombosis + consumption of clotting factors/platelets + secondary fibrinolysis → simultaneous thrombosis + bleeding
- Causes: Sepsis (gram-negative endotoxin → TF expression), obstetric complications (placenta has high TF; amniotic fluid embolism), malignancy (acute promyelocytic leukemia — M3, mucin-secreting adenocarcinomas), trauma, severe burns
- Labs: ↓Platelets, ↓ fibrinogen, ↑PT/PTT, ↑D-dimer (fibrin degradation products), schistocytes on peripheral smear (RBC fragmentation)
- Clinical: Bleeding (IV sites, gums), purpura, petechiae, organ dysfunction (renal, pulmonary, cerebral), acrocyanosis
- Chronic DIC: Mild, compensated; seen in large vessel aneurysms, mucin-secreting cancers
- Treatment: Treat underlying cause; supportive (FFP, cryoprecipitate, platelets); heparin in thrombotic manifestations
Hypercoagulability Testing
| Test | What It Detects |
|---|---|
| PT/INR | Extrinsic pathway (Factor VII); liver disease, warfarin |
| aPTT | Intrinsic pathway (Factors VIII, IX, XI, XII); heparin |
| Mixing study | If prolonged aPTT corrects with normal plasma → factor deficiency; if doesn’t correct → inhibitor (e.g., lupus anticoagulant) |
| Factor V Leiden (APC resistance) | Genetic; most common inherited thrombophilia |
| Prothrombin gene mutation | Genetic; G20210A; ↑Factor II levels |
| Antithrombin III | Chromogenic assay; deficiency → DVT/PE |
| Protein C/Protein S | Chromogenic/ELISA; deficiency → DVT/PE |
| Homocysteine | Elevated → hypercoagulable; B12/folate deficiency |
| Lupus anticoagulant | Phospholipid-dependent prolongation of aPTT; associated with APS |
| Anti-cardiolipin antibodies | ELISA; associated with APS |
| Anti-β2 glycoprotein I | ELISA; associated with APS |
| D-dimer | Fibrin degradation product; elevated in DVT/PE, DIC |
Thrombophilia Workup
- Timing: Not during acute thrombosis or pregnancy; off warfarin for 2 weeks (heparin okay)
- Interpret with clinical context: Many thrombophilias are common in general population (Factor V Leiden in 5% Caucasians); don’t over-test
Chronic Venous Congestion
Liver (“Nutmeg liver”):
- Right heart failure → increased central venous pressure → hepatic venous congestion
- Gross: Dark red centers + pale portal areas = “nutmeg” appearance on cut surface
- Microscopy: Centrilobular congestion + hepatocyte atrophy → necrosis → hemorrhagic necrosis; eventually leads to cardiac cirrhosis (micronodular)
- In severe/left heart failure: Hepatocellular dysfunction → hypoalbuminemia, coagulopathy
Lung (passive congestion):
- Left heart failure → pulmonary venous congestion → brown induration of lung
- Microscopy: Alveolar capillary engorgement; hemosiderin-laden macrophages (“heart failure cells” in sputum); alveolar wall fibrosis
- Gross: Brown, firm lungs
Key NEET PG Pearls
- Virchow’s triad: Endothelial injury, abnormal blood flow (stasis/turbulence), hypercoagulability
- Factor V Leiden = most common inherited thrombophilia; APC resistance; OCPs dramatically increase risk
- DVT most common source of pulmonary embolism; Virchow triad explains Virchow’s observations
- CT Pulmonary Angiography (CTPA) = gold standard for PE diagnosis
- S1Q3T3 on ECG = classic but insensitive finding in massive PE
- Pale (anemic) infarcts = end-arterial supply (heart, kidney, spleen); Red (hemorrhagic) infarcts = dual supply or venous occlusion (lung, liver, bowel)
- Fat embolism: Triad of respiratory distress + neurologic symptoms + petechial rash; 24–72 hours post long bone fractures
- Nutmeg liver = chronic venous congestion of liver from right heart failure
- Nephrotic syndrome edema = due to hypoalbuminemia → ↓ plasma oncotic pressure; Nephritic edema = due to Na⁺/H₂O retention from ↓ GFR
- DIC: Widespread thrombosis + bleeding; treat the underlying cause; low fibrinogen, high D-dimer, schistocytes
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