Hallux Valgus is defined as lateral deviation of the great toe from the medial plane of the body, first described by Carl Hueter in 1871. ^[1]

A "bunion" is used to describe any enlargement or deformity of the MTP joint. It could be hallux valgus, an osteophyte from MTPJ arthritis, gout, an enlarged bursa, or an overlying ganglion. ^[1]

Understanding the anatomy is essential because it explains why the deformity is progressive and why conservative treatment cannot reverse it.

Key anatomical points ^[1]:

• Sesamoid complex: Each flexor hallucis brevis (FHB) tendon contains a sesamoid bone. The sesamoid complex is attached distally to the base of the proximal phalanx via the fibrous plantar plate, but has no attachment to the 1st metatarsal head. Between the two sesamoids lies the intersesamoidal ligament and the bony crista (ridge).
• Tendons arranged in 4 groups: Dorsal (long/short extensors), Plantar (long/short flexors), Medial (abductor hallucis), Lateral (adductor hallucis).
• Ligamentous structures around the 1st MTPJ: Collateral ligament, hood ligament, and sesamoid ligament contribute to joint stability ^[1].
• No muscle attaches to the 1st metatarsal head – this makes the 1st MT head vulnerable to extrinsic forces (e.g., constricting footwear).

Once the metatarsal head is destabilized and drifts medially, the tendons drift laterally. Previous stabilizing forces become deforming forces because the pull is lateral to the axis of the 1st ray. ^[1]

The progression cascade ^[1]:

1. The sesamoid sling slides under the 1st MT head
2. The crista (bony ridge between sesamoids) is eroded
3. The 1st MT pronates
4. The axis of pull of the abductor hallucis becomes more plantar
5. → This is a 3D deformity that is progressive

This is why splints and toe spacers provide symptomatic relief but cannot prevent or slow progression.

Causes ^[1]:

• Juvenile type: Lateral deviation of the articular surface of the metatarsal head without subluxation of the MTPJ
• Acquired type: Associated with abnormal foot mechanics – contracted Achilles tendon, pes planus, generalized neuromuscular disease, CVA, hindfoot deformity, inflammatory arthritis (e.g., rheumatoid arthritis)

Inspection ^[1]:

• Hallux: Pronation deformity, bunion, 1st MT varus, surgical scars
• Lesser toes: 2nd overriding toe, lesser toe deformity
• Midfoot: Medial longitudinal arch
• Hindfoot: Hindfoot valgus

Shoes/Gait ^[1]:

• Check insole, toe spreader
• Gait: 3 rockers (heel strike → mid-stance → toe-off), reduced toe-off, foot progression angle

Sitting exam ^[1]:

• Plantar callosity (indicates abnormal pressure distribution)
• Tenderness at bunion, 1st MTPJ, 2nd MTPJ

Motion ^[1]:

• 1st MTPJ range of motion
• 1st IPJ motion
• 1st TMT joint hypermobility (important – if hypermobile, Lapidus procedure may be indicated)
• Silfverskiöld test – tests for gastrocnemius tightness vs soleus tightness (relevant because contracted Achilles tendon is a risk factor)

Special tests ^[1]:

• DP pulse – always check vascular status
• Medial toe sensation – check for neuropathy
• Beighton score – assess ligamentous laxity

The Achilles tendon (also known as heel cord, calcaneal tendon) is the thickest tendon in the human body. It attaches the plantaris, gastrocnemius, and soleus to the calcaneum, causing plantar flexion of the foot and flexion of the knee. It is the most commonly ruptured tendon. ^[1]

Blood Supply and Watershed Area

The Achilles tendon receives blood supply from three sources ^[1]:

1. Osseotendinous junction (calcaneal insertion)
2. Mesotenon (synovial sheath-like structure carrying nutrient vessels to the mid-tendon)
3. Musculotendinous junction (proximal)

The tendon's internal structure is organized hierarchically: collagen fibrils → collagen fibres → primary fibre bundles (subfascicles) → secondary fibre bundles (fascicles) → tertiary fibre bundles → tendon, surrounded by endotenon (between fascicles) and epitenon (outer surface) ^[1].

• The watershed area is approximately 4 cm from the calcaneal insertion ^[1] – this is the zone of poorest vascularity and where most ruptures occur
• Graphs from Carr & Norris (JBJS Br 1989) show that both the number of intratendinous vessels and the relative area occupied by vessels reach their minimum at ~4 cm from the calcaneum ^[1]

Why does the watershed matter? The region ~2–6 cm proximal to the calcaneal insertion has the least blood supply. Poor vascularity means:

1. The tendon is more susceptible to degenerative changes
2. Once ruptured, healing potential in this zone is lower
3. This is why most ruptures are mid-substance, not at the insertion or musculotendinous junction

"Weekend warrior" – age 30–40, men > women (roughly 3:1), certain antibiotics (quinolones). ^[1]

Injury often during sports that require jumping, pivoting, running. Usually as you push off your foot, rather than during landing (forceful contraction). ^[1]

Biomechanical analysis ^[1]:

• Slightly flexed trunk
• Extended hip
• Ankle transition to end range of dorsiflexion (~40°)
• Foot typically flat and pronated

The critical moment: the foot is on the ground, ankle is in maximal dorsiflexion, and the calf muscles fire maximally to push off → the eccentric-to-concentric transition is when the tendon fails.

Video analysis of professional football players shows a typical sequence: ball possession → initial foot contact with ground → sudden increase in ankle dorsiflexion (injury frame) → loss of balance ^[1].

Classic complaint ^[1]:

"Doctor, I felt like someone kicked me from behind." Frequently will hear a pop sound. ^[1]

Physical exam – examined in prone position ^[1]:

What the Achilles clinical photos show: a circled gap above the heel on the ruptured side (examine prone) — feel before you order USG. ^[1]

It is recommended to rely primarily on clinical information and evaluation and to use imaging for ruling out other injuries and providing additional clinical information. ^[1]

MRI is not mentioned in the lecture as a primary investigation – USG is preferred because it allows dynamic assessment (can see whether ends approximate with plantar flexion).

Ulcer: Discontinuity or break in a bodily membrane that impedes normal function of the affected organ. ^[1]

Causes ^[1]:

• Diabetes (focus of this lecture)
• Peripheral vascular disease
• Cancer (neoplastic ulcer)

The learning objectives also mention arterial, venous, and neuropathic causes. You should be able to differentiate these:

Over 6 million ulcers annually – one every 2 seconds. 50% become infected. 20% of infected ulcers hospitalized. 15–20% of hospitalized patients undergo some form of amputation. One amputation every 19 seconds, major amputation every 53 seconds. ^[1]

Mortality for dialysis patients with foot ulcers: 2-year mortality 53%; 59% if foot ulcer at baseline; 74% if amputation. Mortality after amputation increased by 290%. ^[1]

Diabetic foot ulcer carries higher mortality than many cancers. ^[1]

5-Year Mortality Comparison [1]

Patients fear amputation more than death. ^[1] — Patients with diabetic foot complications had OR 2.36 (p = 0.002) of fearing amputation most, while those without foot complications feared death more (OR 0.51, p = 0.002) ^[1].

These statistics underscore why the lecture's attitude objective is about recognizing the serious complications and managing/monitoring expediently.

IWGDF 2023 Best Practice ^[1]:

• Routine referral: Patient with foot ulcer and signs of ischaemia, OR deteriorating/non-healing wound ( < 50% healing at 4 weeks) despite standard of care
• Urgent referral: Patient with critical limb ischaemia, infection or gangrene, OR considering a major amputation (above ankle)

Lower Limb Angiosomes [1]

Understanding vascular territories helps guide revascularization targets:

Onychocryptosis = ingrown toenail = unguis incarnatus = ungualabial hypertrophy. ^[1]

"Ingrown toenail" is misleading because it implies the nail plate grows laterally. All evidence indicates the germinal matrix determines the width and growth of the nail, and there is no evidence that the matrix becomes wider. ^[1]

The problem is actually hypertrophy of the lateral nail fold (soft tissue grows over/into the nail edge), not the nail growing into the soft tissue. This is why the alternative term "ungualabial hypertrophy" is more accurate.

Key nail anatomy ^[1]: The nail unit comprises the germinal matrix (beneath the proximal nail fold, responsible for nail growth), nail bed, nail plate, lunula, cuticle/eponychium, hyponychium, lateral nail folds, and distal nail fold. The germinal matrix determines nail width and growth direction.

• Improper nail cutting technique (cutting too short or rounding corners exposes the lateral nail fold to spicule pressure)
• Trauma (e.g., stubbing toe, tight shoes)
• Hyperhidrosis (excess sweating softens surrounding skin, making it vulnerable to penetration by nail edge)

Conservative treatment (for mild/early disease):

• Relieve pain
• Prevent progression
• Topical steroid and topical antibiotics
• Taping (pull lateral nail fold away from nail edge)
• Dental floss/cotton wick (place under nail corner to elevate it from the fold)
• Gutter treatment (place a plastic tube along the nail edge to protect the fold)
• Cotton nail cast

If failed conservative treatment → proceed to surgical management. ^[1]

Surgical options ^[1]:

• Partial nail avulsion (most common procedure) – the outer edge of the nail plate is elevated proximal to the cuticle, the nail border is incised longitudinally, and a longitudinal portion of the nail is removed to relieve symptoms of acute infection. Phenolization of the corresponding germinal matrix prevents recurrence.
• Wedge resection (Winograd procedure)
• Total nail avulsion (for severe/recurrent cases)

• Rheumatoid arthritis can cause hallux valgus, clawing, and crowding of toes ^[2]. RA is listed as an acquired cause of hallux valgus in the lecture.
• The 1st MTP joint is the classic site for gout – differentiate from hallux valgus bunion.

• Peripheral vascular disease causing leg ulcers and toe gangrene – complement the diabetic foot section ^[3].
• ABI measurement, angiography, and revascularization principles.

• Diabetic foot infections may progress to osteomyelitis – probe-to-bone test, MRI, and surgical debridement principles apply here.

• Pes planus in children is usually physiological (flexible) and resolves < 10 years ^[4]. Pathological (rigid) flat foot has different causes (tarsal coalition, JIA). The lecture notes the controversial association between pes planus and hallux valgus.

• Quinolone antibiotics cause Achilles tendon rupture – this is a well-known drug side effect tested across multiple blocks. Mechanism: quinolones are toxic to tenocytes and increase MMP activity.

1. Name the clinical tests for Achilles tendon rupture – Thompson test (calf squeeze), Matles test (loss of resting tension), palpation of gap
2. Interpret ABI – know the thresholds (0.9 = PAD, > 1.3 = calcification)
3. List the angles on weight-bearing XR for hallux valgus – HVA, IMA, DMAA
4. Name the management principles of diabetic foot ulcer – sharp debridement, off-loading, diabetic foot education
5. When to refer to vascular surgery – non-healing at 4 weeks, critical limb ischaemia, infection/gangrene, major amputation consideration