8.3 Hypertension, Venous Thromboembolism (VTE) & Anticoagulation

7.3 Hypertension, Venous Thromboembolism (VTE) & Anticoagulation

Hypertension and venous thromboembolism (VTE) represent two major contributors to preventable hospital morbidity and mortality in Ireland. Registered General Nurses (RGNs) routinely encounter patients presenting with acute hypertensive crises, manage thromboprophylaxis protocols, detect life-threatening pulmonary emboli, and administer high-alert anticoagulant medications. This section provides an evidence-based clinical guide to the classification and management of hypertensive emergencies versus urgencies, the diagnostic assessment and prevention of deep vein thrombosis (DVT) and pulmonary embolism (PE), and the complex pharmacology, therapeutic monitoring, and emergency reversal of anticoagulant therapies.

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1. Hypertension Classification & Acute Hypertensive Crisis

Blood pressure (BP) classification in Irish acute and primary healthcare adheres to the standardized criteria established by the European Society of Cardiology (ESC) and the European Society of Hypertension (ESH).

ESC/ESH Blood Pressure Classification (Office Measurements)

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|                       HYPERTENSIVE CRISIS BIFURCATION (BP ≥ 180/≥ 110)          |
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|                               IS THERE ACUTE TARGET ORGAN DAMAGE?               |
|                                                │                                |
|                     ┌──────────────────────────┴──────────────────────────┐     |
|                     NO                                                    YES   |
|                     ▼                                                     ▼     |
|             HYPERTENSIVE URGENCY                               HYPERTENSIVE     |
|                                                                 EMERGENCY       |
| • No immediate threat to organ systems        • Acute end-organ failure present:|
| • Asymptomatic or headache, epistaxis           - Encephalopathy, Stroke, SAH   |
| • Oral antihypertensive therapy (Amlodipine,    - Acute Pulmonary Edema / HF    |
|   Labetalol, Ramipril)                          - Acute Aortic Dissection       |
| • Gradual reduction over 24-48 hours            - ACS / STEMI / NSTEMI          |
| • Outpatient / Ambulatory monitoring            - Acute Kidney Injury (AKI)     |
|                                                 - Severe Pre-eclampsia/Eclampsia|
|                                               • ICU / HDU admission             |
|                                               • Invasive Arterial Line          |
|                                               • Controlled IV BP reduction      |
|                                                 (Max 20-25% MAP drop in 1-2h)   |
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Hypertensive Urgency vs. Hypertensive Emergency

A Hypertensive Crisis is defined as severe elevation of blood pressure, typically $\text{SBP} \ge 180\text{ mmHg}$ and/or $\text{DBP} \ge 110–120\text{ mmHg}$. The absolute level of blood pressure is far less clinically significant than the presence or absence of acute, life-threatening target organ damage.

1. Hypertensive Urgency:
   • Definition: Severe elevation of blood pressure without evidence of acute target organ damage.
   • Presentation: Patients may experience mild-to-moderate occipital headache, epistaxis, lightheadedness, or acute anxiety, but fundoscopy shows no acute papilledema, chest X-ray shows no pulmonary congestion, renal markers are stable, and cardiac enzymes are negative.
   • Management Principles: Patients do not require immediate intravenous infusions or intensive care admission. BP should be reduced gradually over 24 to 48 hours using oral antihypertensives (e.g., oral amlodipine 5–10 mg, oral labetalol 100–200 mg, or oral ramipril). Rapid, precipitous drops with sublingual or intravenous agents are strictly contraindicated because sudden hypoperfusion can trigger ischemic stroke, optic nerve infarction, or myocardial ischemia.
2. Hypertensive Emergency:
   • Definition: Severe elevation of blood pressure accompanied by acute, progressive target organ damage threatening life or organ integrity.
   • Target Organ Manifestations:
     • Central Nervous System: Hypertensive encephalopathy (altered consciousness, confusion, seizures, papilledema, cortical blindness), acute ischemic stroke, acute intracerebral hemorrhage, or subarachnoid hemorrhage.
     • Cardiovascular: Acute cardiogenic pulmonary edema (acute left ventricular failure), acute coronary syndromes (STEMI/NSTEMI), acute aortic dissection (sudden tearing interscapular pain, pulse asymmetry, wide mediastinum).
     • Renal: Acute kidney injury (hematuria, proteinuria, rapidly escalating serum creatinine, oliguria).
     • Obstetric: Severe pre-eclampsia or eclampsia (hypertension with proteinuria, hyperreflexia, clonus, right upper quadrant pain, seizures).
     • Ophthalmologic: Malignant hypertension with bilateral retinal flame hemorrhages, cotton-wool spots, and papilledema (optic disc swelling).
   • Management Principles: Immediate admission to a High Dependency Unit (HDU) or Intensive Care Unit (ICU), insertion of an invasive arterial line for continuous beat-to-beat hemodynamic monitoring, and administration of titratable intravenous antihypertensive infusions.

The Controlled Reduction Rule & Clinical Exceptions

• The General Hemodynamic Rule: Under autoregulatory mechanisms, cerebral blood flow remains constant across a wide range of Mean Arterial Pressures ($MAP = DBP + \frac{1}{3}[SBP - DBP]$). In chronic hypertension, the cerebral autoregulatory curve is shifted to the right. Lowering BP too rapidly plunges cerebral perfusion below the critical ischemic threshold. Therefore, the general goal is to: $\text{Reduce Mean Arterial Pressure (MAP) by a maximum of } 20\%\text{ to }25\%\text{ within the first 1 to 2 hours}$ followed by a gradual reduction toward 160/100 mmHg over the subsequent 2 to 6 hours, achieving full normalization over 24 to 48 hours.
• CRITICAL CLINICAL EXCEPTIONS TO THE 20–25% RULE:
  1. Acute Aortic Dissection: The sheer force of left ventricular ejection ($dP/dt$) propagates aortic wall tearing. The rule of controlled 25% reduction is suspended. The target is rapid, aggressive lowering of SBP to $<120\text{ mmHg}$ and heart rate to $<60\text{ bpm}$ within 20 minutes, achieved with an IV beta-blocker (e.g., IV labetalol or esmolol) followed by an IV vasodilator (e.g., sodium nitroprusside or GTN). Vasodilators must never be given before beta-blockers, as reflex tachycardia increases aortic wall shear stress.
  2. Acute Ischemic Stroke: Permissive hypertension is maintained to preserve collateral perfusion in the ischemic penumbra. Blood pressure is not lowered unless $\text{SBP} > 220\text{ mmHg}$ or $\text{DBP} > 120\text{ mmHg}$. However, if the patient is eligible for intravenous thrombolysis (alteplase), BP must be carefully lowered and maintained $<185/110\text{ mmHg}$ before and during infusion.

First-Line Intravenous Antihypertensive Medications

• IV Labetalol: Combined competitive alpha-1 and non-selective beta-1/beta-2 adrenergic antagonist (ratio 1:7 IV). Reduces systemic vascular resistance without inducing reflex tachycardia. Administered as a 20 mg IV bolus over 2 minutes, followed by 40–80 mg boluses every 10 minutes (max 300 mg), or continuous infusion (1–2 mg/min). Ideal for hypertensive encephalopathy, ischemic stroke, and eclampsia. Contraindicated in asthma, acute decompensated heart failure, and high-degree AV block.
• IV Hydralazine: Direct arteriolar smooth muscle vasodilator. Administered 5–10 mg slow IV every 20 minutes. Preferred in severe pre-eclampsia/eclampsia. May induce reflex tachycardia.
• IV Glyceryl Trinitrate (GTN): Potent venodilator (arteriolar dilation at high doses). First-line in hypertensive emergency accompanied by acute pulmonary edema or acute coronary syndrome. Titrated at 10–200 micrograms/minute.

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2. Venous Thromboembolism (VTE): Deep Vein Thrombosis & Pulmonary Embolism

Venous Thromboembolism (VTE) encompasses Deep Vein Thrombosis (DVT) and Pulmonary Embolism (PE). Hospital-acquired VTE is the leading cause of preventable in-hospital death, necessitating rigorous nursing risk assessment.

Virchow's Triad: The Pathophysiological Foundation

Thrombus formation within the low-shear venous system requires one or more components of Virchow's Triad:

1. Venous Stasis: Impairment of normal venous blood velocity, leading to blood pooling in the valve pockets of deep veins, local tissue hypoxia, and accumulation of activated clotting factors. Causes include immobility, prolonged bed rest ($>3\text{ days}$), general anesthesia, post-stroke limb paresis, congestive heart failure, and obesity.
2. Endothelial (Vascular Wall) Injury: Disruption of the vascular endothelium exposes subendothelial tissue factor and collagen, activating the clotting cascade. Causes include major orthopedic trauma (pelvic or femoral fractures), major surgery (total hip/knee replacement), previous deep vein thrombosis, and indwelling central venous catheters (PICC lines, internal jugular lines).
3. Hypercoagulability (Thrombophilia): Alterations in the balance of procoagulant and anticoagulant proteins favoring microvascular thrombosis:
   • Acquired: Active malignancy (tumors release tissue factor and procoagulant mucins), pregnancy and immediate postpartum (elevated estrogen increases fibrinogen and prothrombin while reducing protein S), hormonal therapies (combined oral contraceptive pill, hormone replacement therapy), systemic sepsis, nephrotic syndrome, and dehydration.
   • Inherited: Factor V Leiden mutation (activated protein C resistance), Prothrombin G20210A gene mutation, Antithrombin III deficiency, Protein C or Protein S deficiency, and Antiphospholipid Syndrome.

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|                         VIRCHOW'S TRIAD & VTE PATHOPHYSIOLOGY                   |
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|        VENOUS STASIS            ENDOTHELIAL INJURY         HYPERCOAGULABILITY   |
|    (Immobility, Surgery,       (Trauma, Orthopedics,        (Cancer, Pregnancy, |
|     Bedrest, Heart Failure)     Indwelling Lines)            Estrogen, Sepsis)  |
|               │                         │                           │           |
|               └─────────────────────────┼───────────────────────────┘           |
|                                         ▼                                       |
|                     DEEP VEIN THROMBOSIS (DVT) FORMATION                        |
|                     (Valve pockets of popliteal/femoral/iliac)                  |
|                                         │                                       |
|                     ┌───────────────────┴───────────────────┐                   |
|                     ▼                                       ▼                   |
|              LOCAL RESOLUTION                       THROMBUS DETACHES           |
|              (Fibrosis, Valve Incompetence,         (Traverses IVC, Right Heart)|
|               Post-Thrombotic Syndrome)                             │           |
|                                                             ▼                   |
|                                                 PULMONARY ARTERY EMBOLISM       |
|                                                 • V/Q Mismatch & Hypoxemia      |
|                                                 • Acute RV Pressure Overload    |
|                                                 • Obstructive Shock & Collapse  |
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Clinical Presentation & Wells Diagnostic Scoring

Deep Vein Thrombosis (DVT)

• Presentation: Unilateral lower extremity dull aching pain, calf tightness, erythema, localized warmth, and pitting edema. Dilated superficial collateral veins may be visible.
• Measurement: Measure bilateral calf circumference at a marked point 10 cm below the tibial tuberosity. A discrepancy of $>3\text{ cm}$ between the affected and unaffected leg is clinically significant.
• Clinical Trap (Homans' Sign): Passive dorsiflexion of the foot to elicit calf pain (Homans' sign) is completely non-specific, unreliable, and potentially hazardous (can dislodge a fragile thrombus); it is strictly obsolete in modern practice.
• Wells Score for DVT: Stratifies probability as Low ($<2$) or High/Likely ($\ge 2$). High-probability criteria include active cancer (+1), paralysis/plaster cast (+1), recently bedridden $>3$ days or major surgery within 12 weeks (+1), localized tenderness along deep venous system (+1), entire leg swollen (+1), calf swelling $>3\text{ cm}$ (+1), pitting edema (+1), collateral superficial veins (+1), and alternative diagnosis equally or more likely ($-2$).
• Diagnostics: In low-probability patients, a negative D-dimer reliably excludes DVT ($>99%$ negative predictive value). In high-probability patients or positive D-dimer, perform a Compression Duplex Ultrasound (non-compressibility of the vein lumen confirms thrombosis).

Pulmonary Embolism (PE)

• Presentation: Sudden-onset unexplained dyspnea, pleuritic chest pain (sharp, knife-like, worsened on inspiration), tachypnea ($RR > 20\text{ breaths/min}$), resting tachycardia ($HR > 100\text{ bpm}$), dry cough, hemoptysis, and apprehension. In massive PE: acute right ventricular failure, syncope, systemic hypotension (SBP $<90\text{ mmHg}$), elevated JVP, and pulseless electrical activity (PEA) arrest.
• Wells Score for PE: Clinical signs of DVT (+3), PE most likely diagnosis (+3), tachycardia HR $>100$ (+1.5), immobilization $>3$ days or surgery in past 4 weeks (+1.5), previous DVT/PE (+1.5), hemoptysis (+1), malignancy (+1). Score $>4$ indicates PE likely.
• Diagnostic Gold Standard: Computed Tomography Pulmonary Angiography (CTPA) is the definitive diagnostic modality. In severe renal impairment or severe iodinated contrast allergy, a Ventilation-Perfusion (V/Q) Lung Scan is performed. Bedside echocardiogram in massive PE reveals right ventricular dilatation and McConnell's sign (RV free wall hypokinesia with preserved apex motion).

Hospital VTE Prophylaxis: Irish HSE Standards

Under HSE National Quality and Patient Safety Directorate standards, every adult patient admitted to an acute hospital must undergo a documented VTE Risk Assessment within 24 hours of admission.

1. Mechanical Prophylaxis:
   • Graduated Compression / Anti-Embolism Stockings (AES / TEDs): Exert a continuous graduated pressure gradient (18 mmHg at the ankle, decreasing to 8 mmHg at the thigh), accelerating femoral venous return.
   • Absolute Contraindications to TED Stockings: Known peripheral arterial disease (PAD), absent pedal pulses, or Ankle-Brachial Pressure Index (ABPI) $<0.8$; peripheral arterial bypass grafting; severe peripheral neuropathy; massive lower extremity edema or pulmonary edema; local skin gangrene, dermatitis, or open wounds.
   • Intermittent Pneumatic Compression (IPC): Inflatable sequential calf/thigh sleeves that provide intermittent cyclical compression, augmenting venous flow and stimulating endogenous fibrinolysis. Preferred in surgical patients with bleeding risks.
2. Pharmacological Prophylaxis:
   • Low-Molecular-Weight Heparin (LMWH):
     • Enoxaparin (Clexane): Standard dose is 40 mg subcutaneously once daily (administered into the abdominal subcutaneous tissue, avoiding the 5 cm perimeter around the umbilicus). In severe renal failure (Creatinine Clearance $<30\text{ mL/min}$), reduce dose to 20 mg daily.
     • Tinzaparin (Innohep): 3,500 to 4,500 units subcutaneously once daily.
   • Mobilization: Encourage early, frequent ambulation and adequate oral hydration.

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3. Anticoagulant Pharmacology, Monitoring & Reversal Protocols

Anticoagulants are classified as High-Alert Medications due to the catastrophic risk of fatal hemorrhage from dosing errors or inadequate monitoring.

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|                    ANTICOAGULANT CLASSES, TARGETS & REVERSAL                    |
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| 1. VITAMIN K ANTAGONISTS : WARFARIN                                             |
|    • Target: Factors II, VII, IX, X, Protein C & S                              |
|    • Monitoring: Prothrombin Time / INR (Target 2.0 - 3.0; 2.5 - 3.5 in valves) |
|    • Reversal: IV Phytomenadione (Vit K1) + Prothrombin Complex Concentrate (PCC)|
| 2. DIRECT ORAL ANTICOAGULANTS (DOACs):                                          |
|    • Direct Thrombin Inhibitor: DABIGATRAN -> Reversal: IDARUCIZUMAB (Praxbind) |
|    • Factor Xa Inhibitors: APIXABAN, RIVAROXABAN, EDOXABAN                      |
|      -> Reversal: ANDEXANET ALFA (Ondexxya) or PCC 50 units/kg                  |
| 3. HEPARIN THERAPIES:                                                           |
|    • Unfractionated Heparin (UFH): IV infusion, monitored by aPTT               |
|      -> Reversal: PROTAMINE SULFATE (1 mg neutralizes ~100 units UFH)           |
|    • Low-Molecular-Weight Heparin (LMWH): Enoxaparin, Tinzaparin                |
|      Weight-adjusted SC, no routine monitoring -> Partially reversed by Protamine|
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1. Warfarin (Vitamin K Antagonist)

• Mechanism of Action: Competitively inhibits the enzyme Vitamin K Epoxide Reductase Complex 1 (VKORC1), blocking the recycling of reduced Vitamin K. This prevents the post-translational gamma-carboxylation of glutamic acid residues on the Vitamin K-dependent clotting factors: Factor II (prothrombin), Factor VII, Factor IX, and Factor X, as well as endogenous anticoagulant proteins Protein C and Protein S.
• Pharmacokinetics & Bridging: Warfarin has no effect on circulating clotting factors already synthesized. Full therapeutic antithrombotic effect requires 48 to 72 hours (contingent on the clearance of Factor II, which has a 60-hour half-life). Protein C has a very short half-life (8 hours); its rapid initial decline produces a transient paradoxical hypercoagulable state. Therefore, when initiating warfarin for acute DVT/PE, the patient must be "bridged" with therapeutic parenteral heparin (LMWH) for a minimum of 5 days and until the INR is within therapeutic range for at least 2 consecutive days.
• Laboratory Monitoring: The International Normalized Ratio (INR): $\text{INR} = \left( \frac{\text{Patient's Prothrombin Time}}{\text{Mean Normal Prothrombin Time}} \right)^{\text{ISI}}$
  • Target INR 2.0 to 3.0: Standard indication for treatment of DVT, pulmonary embolism, and non-valvular atrial fibrillation.
  • Target INR 2.5 to 3.5: High-intensity indication for mechanical prosthetic mitral heart valves and antiphospholipid syndrome with recurrent thrombosis.
• Interactions & Dietary Education:
  • Diet: Maintain a consistent intake of dietary Vitamin K. Instruct patients not to make sudden drastic changes in consuming green leafy vegetables (spinach, kale, broccoli, Brussels sprouts), which overcome warfarin inhibition and lower the INR.
  • Drugs: CYP2C9 inhibitors (Amiodarone, Metronidazole, Fluconazole, Ciprofloxacin) impair warfarin metabolism, dangerously escalating the INR and bleeding risk. CYP inducers (Rifampicin, Carbamazepine, St. John's Wort) enhance clearance, dropping the INR and precipitating thrombosis.
• Emergency Reversal Protocols (HSE Standards):
  • High INR (4.5 to 10.0) without bleeding: Withhold 1 to 2 doses of warfarin, reduce maintenance dose, monitor INR.
  • High INR ($>10.0$) without bleeding: Withhold warfarin; administer oral Phytomenadione (Vitamin K1) 1 to 5 mg.
  • Major Life-Threatening Bleeding (Intracranial, Massive GI Hemorrhage):
    1. Stop Warfarin immediately.
    2. Administer Intravenous Phytomenadione (Vitamin K1) 5 to 10 mg via slow IV injection (stimulates hepatic synthesis of new clotting factors within 4 to 6 hours).
    3. Administer Prothrombin Complex Concentrate (PCC: Beriplex or Octaplex) 25 to 50 units/kg IV immediately. PCC contains concentrated human Factors II, VII, IX, and X, normalizing the INR and restoring functional hemostasis within 10 to 15 minutes. Fresh Frozen Plasma (FFP, 15 mL/kg) is used only if PCC is completely unavailable, as it requires blood group crossmatching, thawing, large infusion volumes (risk of TACO), and provides delayed, incomplete factor correction.

2. Direct Oral Anticoagulants (DOACs)

DOACs are first-line agents for stroke prevention in non-valvular AF and for the treatment/secondary prevention of VTE, offering significant safety advantages over warfarin, including a $50%$ reduction in fatal intracranial hemorrhage.

• Direct Factor Xa Inhibitors: Apixaban (Eliquis), Rivaroxaban (Xarelto), and Edoxaban (Lixiana). Selectively bind to the active catalytic site of free and clot-bound Factor Xa, preventing prothrombinase complex assembly.
• Direct Thrombin Inhibitor: Dabigatran Etexilate (Pradaxa). Potent, competitive, reversible direct inhibitor of free and clot-bound thrombin (Factor IIa).
• Advantages: Fixed once- or twice-daily oral dosing; rapid onset of peak anticoagulation (2 to 4 hours); predictable pharmacokinetics; minimal food/drug interactions; no requirement for routine INR or coagulation monitoring.
• Renal Clearance Warnings: Dabigatran is 80% renally cleared and is strictly contraindicated in severe renal impairment ($\text{CrCl} < 30\text{ mL/min}$). Apixaban has the lowest renal clearance (27%) and is the safest DOAC in mild-to-moderate renal impairment.
• Specific DOAC Reversal Antidotes:
  • Idarucizumab (Praxbind): Specific humanized monoclonal antibody Fab fragment that binds dabigatran with an affinity 350 times greater than thrombin, immediately neutralizing its anticoagulant effect without procoagulant rebound. Dose: 5 grams IV (administered as two consecutive 2.5 g vials over 5–10 minutes).
  • Andexanet Alfa (Ondexxya): Recombinant modified human Factor Xa decoy protein that binds and sequesters oral Factor Xa inhibitors (apixaban, rivaroxaban), restoring endogenous Factor Xa activity.
  • If specific antidotes unavailable: Administer PCC (Beriplex) 50 units/kg IV off-label, combined with oral activated charcoal if ingestion occurred within the preceding 2 hours.

3. Heparins & Heparin-Induced Thrombocytopenia (HIT)

• Unfractionated Heparin (UFH): Binds to endogenous Antithrombin III (AT-III), producing a conformational change that accelerates AT-III inhibition of Thrombin (IIa) and Factor Xa by 1,000-fold. Administered as a weight-based IV infusion for acute pulmonary embolism. Monitored every 4 to 6 hours using the activated Partial Thromboplastin Time (aPTT), targeting an aPTT ratio of 1.5 to 2.5 times control. Has a short half-life (60–90 minutes). Specific antidote: Protamine Sulfate IV (1 mg neutralizes approximately 100 units of UFH; administered slowly over 10 minutes to prevent catastrophic hypotension and anaphylaxis; max single dose 50 mg).
• Low-Molecular-Weight Heparin (LMWH: Enoxaparin, Tinzaparin): Formed by enzymatic depolymerization of heparin chains. Selectively inhibits Factor Xa over thrombin (anti-Xa:anti-IIa ratio 4:1). Features high, predictable subcutaneous bioavailability ($>90%$), long half-life, and weight-based dosing without routine laboratory monitoring. Anti-Factor Xa activity monitoring is reserved for special populations: severe renal impairment, pregnancy, and morbid obesity ($>150\text{ kg}$). Protamine sulfate neutralizes only approximately 60% of LMWH activity.

Heparin-Induced Thrombocytopenia (HIT Type II)

HIT is an immune-mediated, life-threatening complication occurring in 0.5% to 5% of patients exposed to unfractionated heparin (and $<0.5%$ of patients receiving LMWH).

• Pathophysiology: Heparin binds to platelet factor 4 (PF4) released from circulating platelets. In susceptible patients, IgG autoantibodies form against the PF4-heparin macromolecular complex. The Fc portion of these IgG antibodies binds to platelet surface FcγIIa receptors, triggering massive, uncontrolled platelet activation, explosive release of procoagulant microparticles, and extensive consumption of platelets.
• Hallmark Clinical Presentation:
  1. Platelet Count Drop: A drop in platelet count by $\ge 50%$ from baseline, classically developing 5 to 10 days post-heparin exposure (or within 24 hours if the patient was exposed to heparin within the preceding 100 days).
  2. The Thrombotic Paradox ("White Clot Syndrome"): Despite severe thrombocytopenia, patients rarely bleed. Instead, massive in vivo platelet aggregation triggers catastrophic venous and arterial thrombosis (pulmonary embolism, extensive DVT, ischemic stroke, acute myocardial infarction, bilateral adrenal hemorrhagic necrosis, and acute peripheral arterial limb gangrene).
• Mandatory Nursing & Medical Interventions:
  1. IMMEDIATELY STOP ALL HEPARIN: Discontinue all UFH infusions, subcutaneous LMWH, heparinized flushes for arterial lines, and remove heparin-coated venous catheters.
  2. NEVER ADMINISTER PLATELET TRANSFUSIONS: Transfusing platelets injects more substrate into the antibody-driven thrombotic fire, causing catastrophic thrombotic occlusion and death.
  3. DO NOT INITIATE WARFARIN IN ACUTE HIT: Warfarin rapidly depletes protein C, tilting the microvasculature into gangrenous necrosis (venous limb gangrene).
  4. COMMENCE ALTERNATIVE NON-HEPARIN ANTICOAGULANT: Immediately initiate an alternative parenteral anticoagulant: Argatroban (direct thrombin inhibitor, metabolized by liver), Fondaparinux, or Danaparoid.
  5. Order laboratory screening for anti-PF4/heparin antibodies via ELISA and confirmatory Serotonin Release Assay (SRA).

Anticoagulant Comparison Matrix

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4. Clinical Traps & OSCE Pitfalls

| Clinical Scenario / Candidate Action | Underlying Hazard / Consequence | Correct Irish Practice / OSCE Behaviour | | :--- | :--- | :--- | :--- | | Candidate applies TED compression stockings to a patient with absent pedal pulses. | TED stockings compress calcified, stenosed peripheral arteries, precipitating acute limb ischemia, necrosis, and amputation. | Palpate pedal pulses and check for known peripheral arterial disease or $\text{ABPI} < 0.8$. Never apply TED stockings to an ischemic limb. | | Rapidly dropping blood pressure from 220/130 to 120/80 mmHg in 30 minutes in a hypertensive patient. | Plunges cerebral perfusion pressure below the shifted autoregulatory threshold, causing massive watershed cerebral infarction. | Follow the controlled reduction rule: Lower Mean Arterial Pressure by maximum 20% to 25% over the first 1 to 2 hours using titrated IV labetalol. | | Administering platelet transfusions to a patient who develops acute thrombocytopenia (platelets 45 x 10^9/L) on heparin. | Transfusing platelets in Heparin-Induced Thrombocytopenia (HIT) triggers widespread explosive microvascular thrombosis. | Stop all heparin immediately. Withhold platelets. Start an alternative non-heparin anticoagulant (argatroban or fondaparinux). | | Candidate tests Homans' sign (forcible calf dorsiflexion) to evaluate suspected DVT in an OSCE station. | Homans' sign is inaccurate, painful, and may dislodge a fragile popliteal thrombus into the pulmonary circulation. | Do not perform Homans' sign. Inspect for unilateral swelling, calculate Wells score, measure calf circumference 10 cm below tibial tuberosity, and request Duplex ultrasound. | | Administering Fresh Frozen Plasma (FFP) as first-line reversal for warfarin-induced intracerebral hemorrhage. | FFP requires blood grouping, slow thawing, large infusion volumes (risk of fluid overload/TACO), and takes hours to normalize INR. | Administer Prothrombin Complex Concentrate (PCC: Beriplex/Octaplex) alongside IV Phytomenadione (Vitamin K1) immediately. PCC reverses INR within 15 minutes. |