Case: Wil Wright — MSK Trauma, Fractures, and Haemostasis

MICN 201, Integrated Cases, Tutorial 1. This tutorial is based on the case of Wil Wright, a 25-year-old commercial pilot involved in a light plane crash, presenting with multiple musculoskeletal injuries. We use this case to integrate anatomy, physiology, pathology, and clinical reasoning.

CASE SUMMARY

Wil Wright, 25-year-old male, commercial pilot. He was piloting a light aircraft that experienced engine failure and crashed on landing. He was restrained by a harness and the aircraft structure partially protected him, but he has sustained significant trauma. On arrival at the ED he is alert (GCS 15), in pain, with abrasion injuries to his chest and arms. Primary survey reveals: Airway patent; Breathing — tachypneic (RR 22), SpO2 95% on air, reduced breath sounds on the right; Circulation — tachycardic (HR 110), BP 108/70, peripherally cool; Disability — GCS 15; Exposure — multiple abrasions, right knee deformity, right forearm deformity.

FRACTURES: PATHOPHYSIOLOGY AND CLASSIFICATION

A fracture is a complete or incomplete break in the continuity of bone. Mechanisms: (1) Direct force (impact fracture at point of injury); (2) Indirect force (torsional — spiral fracture; compressive — vertebral crush); (3) Avulsion — muscular pull detaches a bony fragment (e.g., base of 5th metatarsal avulsion by peroneus brevis). Classification: closed (skin intact) vs open (compound — skin broken, bone potentially exposed, infection risk high); transverse, oblique, spiral (torsion), comminuted (>2 fragments), segmental (2 fracture lines); impacted, buckle/torus (paediatric); pathological (through abnormal bone — metastasis, osteoporosis).

Fracture healing: (1) Haematoma formation (0-24h): bleeding into fracture site, acute inflammation, fibrin clot forms scaffold; (2) Soft callus (days 1-3 weeks): fibroblasts and chondrocytes form fibrocartilaginous callus, bridging the gap; (3) Hard callus (weeks 3-12): woven bone deposited by osteoblasts, replaces fibrocartilage via endochondral ossification; (4) Remodelling (months-years): woven bone replaced by lamellar bone; Wolff's law — bone architecture remodelled along lines of stress; fracture line disappears on X-ray.

Complications: immediate (haemorrhage, neurovascular injury, visceral injury), early (infection in open fractures — prophylactic antibiotics + debridement, fat embolism syndrome in long bone fractures: fat globules enter bloodstream, lodge in lungs → hypoxia, petechiae, neurological features, within 24-72 hours), late (malunion, nonunion, avascular necrosis — especially head of femur/scaphoid, osteomyelitis, post-traumatic arthritis, complex regional pain syndrome).

HAEMOSTASIS OVERVIEW

In trauma, haemostasis is the process that limits blood loss. Three phases:

Primary haemostasis: vascular spasm + platelet plug formation. Endothelial disruption exposes subendothelial collagen and von Willebrand factor (vWF). Platelets adhere to collagen via GPIb-vWF axis and GPVI-collagen directly. Platelet activation: ADP (dense granule release), thromboxane A2 (TXA2, synthesised via COX-1), and thrombin activate platelets via their respective receptors. Shape change (pseudopods), degranulation, and activation of integrin GPIIb/IIIa (fibrinogen receptor, key to platelet aggregation) → platelet plug.

Secondary haemostasis (coagulation cascade): Extrinsic pathway: tissue factor (TF, exposed subendothelial) + Factor VIIa → activates Factor X (and IX). Intrinsic pathway: Factor XII → XI → IX → X (activated by negatively charged surfaces, relevant in vitro but less in vivo). Common pathway: Xa + Va (prothrombinase complex) → thrombin (IIa); thrombin → cleaves fibrinogen to fibrin (fibrin mesh reinforces platelet plug) + activates FXIII (crosslinks fibrin). Thrombin also positive feedback: activates FV, FVIII, FXI, and platelets (via PAR-1 receptor).

Fibrinolysis: plasmin (from plasminogen, activated by tPA and uPA) dissolves the fibrin clot. D-dimer is a fibrin degradation product — elevated in PE, DVT, DIC, trauma.

In massive trauma: coagulopathy of trauma (acute traumatic coagulopathy, ATC) — consumption of clotting factors, dilution from resuscitation, acidosis, hypothermia, and hypocalcaemia all impair coagulation (the "lethal triad" of acidosis + hypothermia + coagulopathy). Management: damage control resuscitation — balanced transfusion (packed RBCs : FFP : platelets in 1:1:1 ratio), TXA (tranexamic acid) within 3 hours of injury (inhibits fibrinolysis), correct temperature/pH/calcium.