The Wil Wright Case — MSK Trauma and Haemostasis

The Wil Wright Case — MSK Trauma and Haemostasis

Case Introduction

Wil Wright is a 28-year-old male builder who presents to the emergency department following a fall from scaffolding approximately 4 metres. He is brought by ambulance. On arrival: GCS 15, BP 90/60 mmHg, HR 126/min, RR 22/min, SpO2 97% on 15L O2 NRB. He has an obvious deformity of the right femur mid-shaft, an open wound with bone visible, and complains of severe right lower leg pain. His right lower leg is tensely swollen, pale, and he cannot dorsiflex his ankle.

This case integrates fracture classification, compartment syndrome recognition, coagulation physiology, and damage control resuscitation.

---

Fracture Classification (AO/Müller System)

Fractures are systematically classified to guide management and facilitate communication. The AO/Müller classification is the most widely used comprehensive system:

Bone designation: Each bone is assigned a number (e.g., 1 = humerus, 2 = radius/ulna, 3 = femur, 4 = tibia/fibula).

Segment: proximal (1), diaphyseal (2), distal (3). Hence "32" = femoral shaft.

Morphological types:

• Type A (simple fracture): Single fracture line; two fragments

- A1 = spiral; A2 = oblique (>30°); A3 = transverse (<30°)

• Type B (wedge fracture): Three fragments; cortical contact between main fragments after reduction

- B1 = intact wedge spiral; B2 = bending wedge; B3 = fragmented wedge

• Type C (complex fracture): No cortical contact between main fragments after reduction; comminuted

- C1 = spiral; C2 = segmental; C3 = irregular comminuted

Additional descriptors:

• Open/compound fracture (Gustilo-Anderson classification):

- Grade I: wound <1 cm, clean, minimal contamination

- Grade II: wound 1–10 cm, moderate contamination

- Grade IIIa: wound >10 cm, adequate soft tissue coverage of bone

- Grade IIIb: extensive periosteal stripping, poor coverage — requires flap

- Grade IIIc: any vascular injury requiring repair (limb-threatening)

• Wil's femur has bone visible → open fracture; grade depends on wound size

Management principles for open femoral fracture:

• ATLS primary survey first (ABCDE)
• Haemorrhage control (femoral shaft can lose 1–1.5 L into thigh)
• IV broad-spectrum antibiotics within 1 hour (cefazolin; gentamicin if Gustilo III)
• Wound irrigation and provisional stabilisation (backslab/traction splint in ED)
• Definitive fixation: intramedullary nail (IMN) for femoral shaft — locked IM nail within 24–72h if patient stable; external fixation in damage control orthopaedics for haemodynamically unstable patients

---

Compartment Syndrome

Compartment syndrome occurs when pressure within an osteofascial compartment rises above perfusion pressure, causing ischaemia of the enclosed muscles and nerves.

The "6 Ps" of compartment syndrome:

1. Pain — severe, out of proportion to injury; pain on passive stretch of muscles in the compartment is the earliest and most reliable sign
2. Pressure — tensely swollen, "wooden" compartment
3. Paraesthesia — numbness/tingling from nerve ischaemia (early, reversible)
4. Paralysis — weakness of muscles in compartment (late, implies significant ischaemia)
5. Pallor — reduced capillary perfusion of skin
6. Pulselessness — LATE sign; pulses may be preserved until compartment pressures are very high (not a reliable early sign — do NOT wait for absent pulse)

Wil's right lower leg: tense swelling + pallor + inability to dorsiflex (deep peroneal nerve and anterior compartment muscles ischaemia) = compartment syndrome until proven otherwise.

Measurement of compartment pressure:

• Normal: <10 mmHg
• Fasciotomy threshold: compartment pressure >30 mmHg OR within 30 mmHg of diastolic blood pressure (delta pressure <30 mmHg)
• Delta pressure = diastolic BP − compartment pressure

Fasciotomy: Emergency two-incision four-compartment lower leg fasciotomy releases:

• Anterior compartment (tibialis anterior, extensor hallucis longus, deep peroneal nerve)
• Lateral compartment (peroneus longus/brevis, superficial peroneal nerve)
• Superficial posterior (gastrocnemius, soleus)
• Deep posterior (tibialis posterior, FDL, FHL, tibial nerve, posterior tibial artery)
• Wound left open, closed by split-skin graft after oedema resolves (3–5 days)

Consequences of missed/delayed fasciotomy:

• Muscle necrosis → rhabdomyolysis → myoglobinuria → acute tubular necrosis (AKI)
• Volkmann's ischaemic contracture (chronic fibrosis of ischaemic muscle, especially forearm)
• Nerve death → permanent neurological deficit

---

Coagulation Cascade

Haemostasis involves three phases:

1. Primary haemostasis: Vascular spasm + platelet plug (GPIb binds vWF → platelet adhesion; ADP + TXA2 → platelet activation and aggregation via GPIIb/IIIa binding fibrinogen)
2. Secondary haemostasis: Coagulation cascade reinforces platelet plug with fibrin
3. Fibrinolysis: Plasmin degrades fibrin clot

Coagulation cascade — modern cell-based model:

*Extrinsic pathway (tissue factor pathway — initiates coagulation):*

• Tissue factor (TF, factor III) exposed at injury → binds factor VIIa → TF-VIIa complex activates factor X and factor IX
• TF-VIIa is rapidly inhibited by TFPI (tissue factor pathway inhibitor) → limited burst of thrombin generation

*Intrinsic pathway (contact/amplification pathway):*

• Factor XII activated by contact with subendothelial collagen or foreign surfaces → activates XI → activates IX
• IXa + VIIIa (tenase complex on phospholipid) → activates X

*Common pathway:*

• Xa + Va (prothrombinase complex) → prothrombin (II) → thrombin (IIa)
• Thrombin: (1) cleaves fibrinogen → fibrin monomers → polymerise; (2) activates factor XIII → cross-links fibrin (stable clot); (3) activates V, VIII, XI (amplification); (4) activates protein C (anticoagulation feedback)

Laboratory tests of coagulation:

• PT (prothrombin time): Tests extrinsic + common pathway (factors VII, X, V, II, fibrinogen); reported as INR; prolonged in warfarin therapy, liver disease, factor VII deficiency, DIC (early)
• APTT (activated partial thromboplastin time): Tests intrinsic + common pathway (factors XII, XI, IX, VIII, X, V, II, fibrinogen); prolonged in heparin therapy, haemophilia A (factor VIII↓), haemophilia B (factor IX↓), lupus anticoagulant, DIC
• Fibrinogen: Functional assay (Clauss method); low in DIC, liver disease, defibrination; normal 2–4 g/L; target >1.5–2 g/L in massive haemorrhage (administer cryoprecipitate or fibrinogen concentrate)
• Thromboelastography (TEG/ROTEM): Viscoelastic whole-blood test; guides component therapy in massive haemorrhage (identifies specific deficiencies)

---

Anticoagulation

Heparin (unfractionated, UFH):

• Mechanism: binds and activates antithrombin III (AT-III); AT-III-heparin complex inhibits thrombin (IIa) and factor Xa (1:1 ratio for UFH); also inhibits IXa, XIa, XIIa
• Monitoring: APTT (target 1.5–2.5× normal) or anti-Xa levels
• Reversal: protamine sulphate (positively charged, binds and neutralises negatively charged heparin)
• Complication: HIT (heparin-induced thrombocytopenia) — IgG antibodies against PF4-heparin complex → platelet activation → paradoxical thrombosis; treat by stopping heparin and using alternative anticoagulant (argatroban, danaparoid)

Low molecular weight heparin (LMWH, e.g., enoxaparin):

• Predominantly inhibits factor Xa (anti-Xa:anti-IIa ratio ~4:1); predictable pharmacokinetics; OD-BD subcutaneous dosing; monitoring not required (except in renal impairment, extremes of weight, pregnancy — measure anti-Xa levels)
• Partial reversal with protamine

Warfarin:

• Mechanism: vitamin K antagonist; inhibits vitamin K epoxide reductase (VKOR) → prevents recycling of vitamin K from its epoxide form → reduced synthesis of vitamin K-dependent clotting factors: II, VII, IX, X (coagulation) and protein C and S (anticoagulation — note these are depleted first due to shorter half-lives, explaining early prothrombotic state)
• Onset: 3–5 days (must bridge with heparin); monitoring: INR (target 2–3 for VTE/AF; 2.5–3.5 for mechanical valves)
• Reversal: vitamin K (oral — takes 6–12h; IV — 4–6h); 4-factor PCC (prothrombin complex concentrate, Beriplex) for urgent reversal; FFP

Direct Oral Anticoagulants (DOACs):

• Factor Xa inhibitors: rivaroxaban, apixaban, edoxaban — directly inhibit free and clot-bound Xa; no monitoring; reversal: andexanet alfa (recombinant Xa decoy, approved)
• Thrombin (IIa) inhibitor: dabigatran — directly inhibits thrombin; reversal: idarucizumab (monoclonal antibody fragment, Praxbind)

---

Massive Transfusion Protocol (MTP)

Definition: Transfusion of ≥10 units packed red blood cells (pRBC) in 24 hours, OR ≥3 units pRBC in 1 hour.

1:1:1 ratio: Evidence from military trauma (PROPPR trial) supports balanced resuscitation with FFP:platelets:pRBC in 1:1:1 ratio — mimics whole blood; reduces coagulopathy of trauma; improves 24h survival.

Hypothermia-acidosis-coagulopathy triad (lethal triad / trauma triad of death):

• Hypothermia (<35°C): Impairs enzymatic function of coagulation factors (10% loss of factor activity per 1°C drop); impairs platelet function; causes coagulopathy that worsens bleeding
• Acidosis (pH <7.2): H⁺ ions inhibit coagulation enzyme activity (e.g., TF-VIIa, prothrombinase complex); reduces fibrinogen function; worsens bleeding
• Coagulopathy (acute traumatic coagulopathy, ATC): Triggered by shock + tissue injury; tissue damage activates protein C; APC (activated protein C) degrades Va and VIIIa; thrombomodulin on endothelium sequesters thrombin → less fibrinogen conversion → hyperfibrinolysis (tissue plasminogen activator release). All three elements form a vicious cycle.
• Prevention: warm IV fluids, warming blanket, early haemorrhage control, balanced resuscitation, tranexamic acid (TXA — anti-fibrinolytic; CRASH-2 trial: 1g IV within 3 hours of injury reduces mortality)

Permissive hypotension:

• In penetrating trauma with uncontrolled haemorrhage, target systolic BP 80–90 mmHg (MAP 50 mmHg) until surgical haemorrhage control
• Rationale: higher BP dislodges clot, accelerates bleeding; avoid aggressive crystalloid resuscitation (dilutional coagulopathy, hypothermia, tissue oedema)
• Caution: NOT in TBI (require MAP >80 mmHg to maintain CPP) — TBI requires individualized approach