LO2

πŸ”΄ 1. Haemorrhage

  • Definition: Acute loss of blood from the vascular system.

  • Classification:

    • Class I: <15% blood loss (usually well-compensated)

    • Class II: 15–30% (tachycardia, anxiety)

    • Class III: 30–40% (hypotension, confusion)

    • Class IV: >40% (severe hypotension, unconsciousness)

  • Causes: Trauma, surgery, obstetric complications, GI bleed.

  • Clinical signs: Tachycardia, hypotension, cool/clammy skin, delayed cap refill, decreased urine output.


🩸 2. Haemostasis

  • Phases:

    1. Vasoconstriction – to reduce blood flow.

    2. Primary haemostasis – platelet plug formation.

    3. Secondary haemostasis – clotting cascade activates fibrin.

    4. Fibrinolysis – clot breakdown.

  • Disorders: Haemophilia, Von Willebrand disease, thrombocytopenia.

  • Pharmacology:

    • Pro-coagulants: Tranexamic acid, fibrinogen.

    • Anti-coagulants: Heparin, warfarin.


πŸ’‰ 3. Rapid Infusion Devices

  • Used in emergency scenarios requiring rapid fluid/blood product administration.

  • Indications: Hypovolaemia, trauma, obstetric haemorrhage, burns, massive transfusion.

  • Types: Belmont Rapid Infuser, Level 1, Fluido system.

  • Safety: Temperature control (prevent hypothermia), pressure regulation, monitoring for air embolism.


🚨 4. Massive Haemorrhage Protocols (MHP)

  • Trigger: >1 blood volume loss in 24 hrs or >50% in 3 hrs.

  • Goals: Restore circulating volume, oxygen delivery, prevent coagulopathy.

  • Components:

    • RBCs, plasma, platelets (1:1:1 ratio)

    • TXA within 3 hours

    • Calcium replacement (citrate toxicity)

    • Monitor ABGs, electrolytes, coagulation (TEG)

  • Complications: DIC, hypothermia, acidosis, hypocalcaemia.


πŸ§ͺ 5. TEG (Thromboelastography)

  • Purpose: Real-time assessment of clot formation and stability.

  • Key parameters:

    • R-time: Time until clot starts forming.

    • K-time: Time to reach clot strength.

    • Alpha angle: Speed of clot strengthening.

    • MA (Maximum Amplitude): Clot strength.

    • LY30: % clot breakdown in 30 mins (fibrinolysis).

  • Used to guide: Transfusion (FFP, platelets, cryo), antifibrinolytics (TXA).


⚑ 6. Shock and Pathophysiology

  • Definition: Inadequate tissue perfusion causing cellular hypoxia.

  • Common Pathways:

    • ↓O2 delivery β†’ anaerobic metabolism β†’ lactic acidosis β†’ organ dysfunction.

  • Stages:

    1. Initial: ↓ perfusion

    2. Compensatory: ↑ HR, vasoconstriction

    3. Progressive: worsening hypoperfusion

    4. Irreversible: multi-organ failure


πŸ’§ 7. Hypovolaemic Shock

  • Cause: Fluid/blood loss β†’ ↓ preload β†’ ↓ CO β†’ ↓ perfusion.

  • Signs: Tachycardia, hypotension, poor cap refill, cold extremities.

  • Management: ABCs, control bleeding, IV fluids, blood products, vasopressors if needed.


🐝 8. Anaphylactic Shock

  • Cause: IgE-mediated allergic response β†’ histamine release.

  • Effects: Bronchospasm, vasodilation, ↑ permeability β†’ oedema.

  • Signs: Stridor, urticaria, hypotension, wheezing.

  • Treatment:

    • IM Adrenaline (0.5 mg adult)

    • IV fluids

    • Antihistamines

    • Steroids

    • Oxygen, airway support


🦠 9. Septic Shock (From PDF)

  • Cause: Infection β†’ systemic inflammation β†’ vasodilation + capillary leak.

  • Criteria (Sepsis-3):

    • Infection + organ dysfunction (↑ SOFA)

    • Persistent hypotension requiring vasopressors + lactate >2

  • Management:

    • Early broad-spectrum antibiotics

    • Source control

    • Fluids (30 mL/kg)

    • Vasopressors (noradrenaline)

    • Monitor lactate, urine output


🀰 10. Postpartum Haemorrhage (PPH) (From PDF)

  • Definition: >500 mL vaginal or >1000 mL C-section blood loss.

  • Causes (4 Ts):

    • Tone (uterine atony)

    • Trauma

    • Tissue (retained placenta)

    • Thrombin (coagulopathy)

  • Management:

    • Uterotonics (oxytocin, misoprostol)

    • Fundal massage

    • Bakri balloon

    • Blood products

    • MHP activation


🧬 11. Disseminated Intravascular Coagulation (DIC) (From PDF)

  • Trigger: Sepsis, trauma, obstetric complications.

  • Pathophysiology: Widespread clotting β†’ consumption of clotting factors β†’ bleeding.

  • Lab: ↓ platelets, ↑ PT/APTT, ↓ fibrinogen, ↑ D-dimer.

  • Treatment:

    • Treat underlying cause

    • Replace blood products (platelets, cryo, FFP)

    • Monitor TEG


πŸ”₯ 12. Burns and Haemodynamics (From PDF)

  • Fluid shifts: Capillary permeability ↑ β†’ plasma loss β†’ oedema.

  • Risk: Hypovolaemia, compartment syndrome, renal failure.

  • Resuscitation: Parkland formula

    • 4 mL x %TBSA x weight (kg)

    • 50% in first 8 hrs, 50% in next 16 hrs

  • Monitoring: Urine output, electrolytes, lactate.


πŸ’§ 13. TURP Syndrome (From PDF)

  • Cause: Absorption of irrigation fluid (e.g. glycine) during prostate surgery.

  • Pathophysiology: Fluid overload + hyponatraemia β†’ cerebral oedema.

  • Symptoms: Confusion, bradycardia, hypertension, nausea, seizures.

  • Management:

    • Stop surgery

    • ABCs

    • Diuretics

    • Correct Na⁺ slowly


🫁 14. Thromboembolic Disease (From PDF)

  • Types:

    • DVT

    • PE

  • Risk factors: Surgery, immobility, pregnancy, malignancy.

  • Signs of PE: SOB, chest pain, tachycardia, hypoxia.

  • Prevention:

    • Mechanical: compression stockings, devices

    • Pharmacological: LMWH, heparin

  • Treatment:

    • Anticoagulation (e.g. enoxaparin β†’ warfarin/apixaban)

    • Thrombolysis in massive PE


🧩 15. Shock Cascades (From PPT)

  • Shared outcomes:

    • ↓ perfusion β†’ cellular hypoxia β†’ lactic acidosis β†’ organ dysfunction β†’ death

  • Systemic effects:

    • Cardio: ↓ CO, tachycardia

    • Renal: ↓ urine output

    • Resp: tachypnoea, ARDS

    • Neuro: altered LOC

    • GI: ↓ motility, ischaemia