7: THE FOOT

7 THE FOOT



Clinical importance of the foot


In vertebrate anatomy, the ‘foot’ includes the carpus or tarsus and the regions distal to these joints. Contact between the foot and the potentially dangerous ground underfoot (frequently mud or concrete) produces a variety of disorders which cause many clinical problems. The lower limb is subjected to tremendous stress and strain through normal locomotion, and is frequently involved in trauma. Approximately 60% of the weight of a horse is carried on the forefeet and approximately 90% of all forelimb lameness occurs in the foot.


Correct foot balance is required and is sometimes forgotten. Various imbalances of conformation can occur. The foot has to be balanced and evenly placed around its centre of weight-bearing (midpoint of the circle of the laminar suspension). In dorso-palmar imbalance, the foot has a long toe and a low heel, so the load is transferred to the heels. Latero-medial imbalance is often the result of uneven trimming which results in sheared heels; one heel (usually the medial one) strikes the ground before the other.


In young horses, fractures of the growth plates are the most common. The younger the foal when the fracture occurs the better the prognosis. If the fracture is transverse, across the bone (as is usual in the pedal bone) rather than longitudinal, along the long axis, the bone heals more quickly. Approximately 80% of the fractures of the equine foot occur in the manus. Distal limb fractures are often acute, with severe ligament damage and soft tissue swelling. The fracture may be closed or open (exposed to potential infection). Bruised or sore shins (dorsal metacarpal disease) are the result of stress or fatigue to the bone as this part of the bone receives more stress compression than the other parts of the bone. Condylar, metaphyseal and diaphyseal fractures of the third metapodial (metacarpal and metatarsal) bones may occur. Chip fractures are also quite common. In the ‘proximal metapodial syndrome’ there are avulsion stress fractures of the proximal palmar and plantar cortices.


‘Splints’ are bony exostoses of the second or fourth metapodial bones. Fractures of the second and fourth metapodial bones usually occur in the distal third of the bone. They usually result from kicks, but may also occur spontaneously. Fractures of the middle phalanx occur frequently from the sudden compression and simultaneous torsion to which the foot is often subjected. This is particularly severe with sudden stops and starts.


Fractures of the distal phalanx (pedal bone) are not uncommon. They often occur when the horse kicks out and hits something solid. The digital pulse is increased in this fracture. If the distal interphalangeal joint (DIP) is also involved, there may be considerable effusions into the joint. Fracture of the proximal sesamoid bone may result from over-extension of the suspensory apparatus, degenerative changes in the bone, direct trauma or osteoporosis. Sesamoiditis (degenerative or bony change in the proximal sesamoid bones) is an important disease of the foot in the horse. ‘Ringbone’ is an enlargement of one or both of the bones which form the proximal or distal interphalangeal joint. The term ‘false ringbone’ is often used when only the shaft of the proximal or middle phalanx is affected.


There are several types of fracture (#) of the pedal bone (distal phalanx):









Inflammation of the distal phalanx (pedal osteitis) is quite common. ‘Sidebone’ is ossification in the ungular cartilages of the pedal bone and is relatively common, whereas bone-cysts in the pedal bone are much rarer. Fracture of the distal sesamoid (‘navicular bone’) may be in the form of a chip fracture or a simple sagittal fracture close to the ridge of the sesamoid bone. Comminuted fractures of this bone are fortunately rare, as they are impossible to repair.


Problems of the joints of the foot involve a considerable amount of the equine practitioners time, expertise, energy and patience. In the foal, the most common cause of acute lameness is septic arthritis/osteomyelitis. Most are septicaemic infections and in at least 50% of the cases, multiple joints are involved. There are basically three types of injury. One is related to the epiphyses, the second to the epiphyseal cartilages and the third to the cuboidal bones in the carpus and tarsus. Villonodular synovitis in the form of a chronic proliferative hypertrophic response is also not uncommon.


The joints of the manus and pes of the older horse are also subjected to a wide range of abnormalities. Sub-luxations occur and must be repaired, but they have a very poor prognosis. Luxations occur in the proximal (PIP) and the distal (DIP) interphalangeal joints. Angular deformity (joint laxity) of the fetlock is also a possibility. This, and a similar interphalangeal disorder, have a poor prognosis. Flexural deformity of the fetlock is either congenital or acquired. It may be due to relative shortening of the musculo-tendinous part of the superficial digital flexor muscle, the deep digital flexor muscle, or the sesamoidean ligaments. Traumatic and degenerative arthritis of the proximal interphalangeal joint (PIP or pastern joint) and distal interphalangeal joint (DIP or coffin joint) has been described, and infectious arthritis of the joint is also known.


The joints of the foot are accessible for the collection of joint fluid samples, or the administration of anaesthesia, or treatments. The fetlock joint is accessible via its palmar/plantar synovial recess. This is located just proximal to the joint, between the palmar aspect of the distal metapodial bone III and the suspensory ligament, at a level distal to the distal end of metapodial II. With the limb in a weight-bearing position, the needle is inserted at right angles to the axis of the limb, in a slightly downward direction, to a depth of 2–3 cm. The PIP (pastern) joint is entered through a site dorsal and just lateral to the common (forelimb) or long (hindlimb) digital extensor tendon and at the level of, or just distal to, the palmar or plantar process of the proximal phalanx. With the limb in a weight-bearing position, the needle is inserted in a distal and medial direction. The DIP (coffin) joint is located by finding a depression that is approximately 2 cm dorsal to the coronary band and on the midline. The needle may be inserted just medial or lateral to the common (forelimb) or long (hindlimb) digital extensor tendon or directly through the tendon. With the limb in a weight-bearing position, the needle is inserted in a distal and palmar or plantar direction, to a depth of 2.5 cm.


Tendonitis is inflammation of the tendon sheaths. Usually the superficial (SDF) and deep (DDF) digital flexor tendons are affected. These tendons suffer severe stress in the leg of the horse. They are also damaged when the muscles are fatigued. The SDF is more likely to be damaged because it suffers much more strain in over-extension than the DDF. The damage is most likely to occur at mid metacarpal level in the SDF or, for the DDF, at the level of the fetlock joint. Both tendons are avascular and repair therefore takes time.


Tendon lacerations are quite common as a result of wire cuts, over-reaching, or striking injuries. Damage to the DDF causes lifting of the toe. Damage to the SDF causes sinking of the fetlock. If both the tendons are sectioned then the fetlock sinks to the ground.


The ligaments of the foot may also suffer damage, usually as a result of trauma. Desmitis (inflammation of a ligament) can affect the distal sesamoidean ligaments of the fetlock. Breakdown of the suspensory apparatus can also occur, usually in racehorses when going at full speed: an acute over-extension of the fetlock can disrupt any or all of the components of the suspensory apparatus – suspensory ligament, sesamoid bones, and distal sesamoidean ligaments. The most common site of any such injury is at the proximal attachment of the suspensory ligament to the proximal plantar cortex of the metacarpal/metatarsal bones.


The ‘navicular syndrome’ is responsible for 30% of all of forelimb lamenesses. The syndrome is chronic palmar foot lameness affecting the distal sesamoid (‘navicular’) bone. It involves the fibrocartilage of its flexor surface, the palmar part of the distal interphalangeal joint, the deep digital flexor tendon, the podotrochlear (‘navicular’) bursa, the collateral sesamoidean (‘navicular’ suspensory) ligaments and the distal sesamoid impar ligament. There are two theories for its cause: the vascular theory and the biomechanical theory. It is thought to be associated with abnormal pressure/vibration forces between the deep digital flexor tendon and the flexor surface of the navicular bone. Also, penetrating wounds can reach the deep digital flexor tendon and may result in necrosis in the tendon. Penetration into the podotrochlear (‘navicular’) bursa may also involve the impar ligament and progress into the distal interphalangeal joint (DIP) and result in infectious arthritis. The digital sheath of the deep digital flexor muscle extends to the midshaft of the middle digit. Penetration into this digital sheath may result in infectious tenosynovitis.


The hoof may be damaged by treading on something sharp or by being kicked and it is then easily infected by soil-borne pathogens. However, when the hoof is damaged, it can be supported and protected by casts and shoes.


Laminitis is a specific condition of the foot of the horse, usually affecting the forelimb. This is inflammation of the sensitive laminae of the corium (dermis) within the wall of the hoof. It is essentially a peripheral vascular disorder caused by systemic damage. Release of vasoactive substances (catecholamines) can cause ischaemic necrosis. There are many different predisposing factors, particularly grain overload and postoperative recovery after colic surgery. Laminitis can be graded as 1, 2, 3 and 4. Type 1 is developmental, type 2 foot pain and lameness, type 3 sub-clinical (recovery without mechanical failure) and type 4 chronic (this leads to displacement of the distal phalanx). The progression usually starts with excess grain overload, leading to a rise in lactic acid, then the caecal pH falls. Gram-negative bacteria rapidly multiply and extra endotoxin is released. Vasoactive agents are then released and circulate. This leads to vasoconstriction, ischaemia and necrosis. Another theory suggests that proteinases are activated in the distal lamellae and this degrades the type IV collagen which attaches the hoof to the distal phalanx. This results in loss of mechanical support.


Various other foot problems can be listed. ‘Mud rash’ (otherwise known as greasy-heel) is associated with bacterial infections caused by Dermatophilus and Staphylococci. Cracks in the hoof wall run vertically from the coronary band. ‘Seedy toe’ is separation of the hoof wall from the distal phalanx. ‘Thrush’ is a degenerative condition of the central and collateral sulci of the frog; it is associated with surface invasion by micro-organisms under anaerobic conditions. ‘Canker’ is a chronic, infectious, hypertrophic, moist, podo-dermatitis of the frog and sole. ‘Keratoma’ is an uncommon benign tumour of the horn between the laminar horn and dermis (corium) in the wall of the hoof. ‘White line disease’ is a rare, progressive crumbling of the hoof wall at the junction between the wall and sole. ‘Nail bind’ is a direct injury or bruising of the solar or laminar dermis caused by a shoe-nail. ‘Quittor’ is the necrosis of the ungular cartilages of the distal phalanx; it often results in purulent discharges and sinus formation above the coronary band.


The hoof wall is rigid except at the heels, where the laminae are attached to the ungular cartilages, which can ‘expand’ (move abaxially) on bearing weight. The structures within the ‘rigid’, box-like regions of the toe and quarters are also subjected to continuous movement on bearing weight, so there is a potential for problems of diminished blood supply to these regions. The hoof has a diminished response to injury and a slow rate of healing, yet it contains many important structures. Superficial wounds that penetrate only cornified tissue may, nevertheless, produce a sub-solar abscess. Pododermatitis is the inflammation of the solar dermis (corium) with or without secondary infection. Deep wounds that penetrate the germinal epithelium introduce infections, usually Clostridia. These are life-threatening emergencies with serious long-term consequences. Wounds that involve the synovial structures are particularly serious and require immediate and aggressive treatment.


Wounds greater than 1 cm in depth are dangerous as these penetrate the sole. Wounds of 1.2 cm will penetrate the hoof and wall. Wounds over 1.5 cm deep will penetrate the frog. These deep penetrating wounds can be classified into three groups: Type 1 wounds penetrate the corium and cause septic osteitis in the distal phalanx, with a distal cushion abscess. Type 2, penetrating deep puncture wounds, gain access into the caudal third of the frog and can enter many structures including the digital flexor tendons (the SDF and DDF). The hoof also contains other structures that can be penetrated, including the distal interphalangeal (DIP) joint, tendon sheaths, tendons (particularly the tendon of the DDF) and ligaments (the distal sesamoid impar ligament and the collateral ligaments of the DIP), the distal and middle phalanges and the distal sesamoid (‘navicular’) bone and its bursa. Type 3 wounds penetrate the coronary band, leading to septic chondritis of the cartilaginous structures such as the articular cartilages and ungular cartilages of the distal phalanx, and may subsequently extend into the distal interphalangeal (DIP) joint.


Several nerve blocks are used to localise the site of lameness in the manus or pes. Perineural analgesia of the distal digital region can be achieved by blocking the lateral and medial palmar/plantar nerves at the level of the middle phalanx. The needle is inserted subcutaneously over the palpable neurovascular bundle, just proximal to the ungular cartilage of the distal phalanx on each side. This is the Palmar/Plantar digital nerve block. These nerves can be blocked at a more proximal level by inserting the needle subcutaneously over the palpable neurovascular bundle, on the abaxial surface of the lateral and then the medial proximal sesamoid bone. This is the Abaxial sesamoid nerve block.


Perineural analgesia of the distal metacarpal and digital regions can be achieved by blocking the lateral and medial palmar, and palmar metacarpal nerves, proximal to the fetlock. The sites for subcutaneous injections are immediately distal to the distal extremities (‘buttons’) of the metacarpal bones II and IV, to block the palmar metacarpal nerves on both sides. At the same level, the sites for subcutaneous injections are located between the DDF and the suspensory ligament on each side, to block the palmar nerves. This is the Low 4-point nerve block for the forelimb. For the hindlimb, the same four injections are made, but there is an important anatomical difference. The dorsal metatarsal nerves exchange fibres with the plantar metatarsal nerves in the proximal phalangeal region and they innervate the hoof. It is therefore necessary to block these medial and lateral dorsal metatarsal nerves with subcutaneous circumferential ring-blocks at the dorsal aspect of the ‘buttons’ of the splint bones. This is the Low 6-point nerve block for the hindlimb.


Perineural analgesia of the metacarpal and digital regions can be achieved by blocking the lateral and medial palmar, and also the palmar metacarpal nerves, just distal to the carpus. The needle is inserted deeply, axial to metacarpal bone IV, until it reaches the palmar surface of metacarpal bone III. Here the lateral palmar metacarpal nerve is injected. The palmar nerve is blocked by inserting the needle subcutaneously at the same level into the space between the DDF and the suspensory ligament. This is repeated on the medial side in relation to metacarpal bone II. These constitute the High palmar nerve block. In the hindlimb, only one injection site is needed on each side to inject the nerves. The needle is inserted just distal to the tarsometatarsal joint and axial to metatarsal bone IV, until it reaches the plantar surface of metatarsal bone III. After injecting the lateral plantar metatarsal nerve at this site, the needle is partially withdrawn and a second injection is made between the DDF and the suspensory ligament, to block the lateral plantar nerve. This procedure is repeated on the medial side, in relation to metatarsal bone II and the tendon and ligament. This is the High plantar nerve block.



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Fig. 7.1 Surface features of the left manus: cranial view. Figs. 7.3, 7.5 and 7.7 show further views of this specimen. Palpable features have been shaved. Figs. 7.2, 7.4, 7.6 and 7.8 show the bones of the region. Fig. 7.9 shows the solar surfaces of the hoof.



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Fig. 7.2 The bones of the left manus: cranial view. The prominences shaved in Fig. 7.1 have been coloured red, except for the salient medial styloid process. For a comment on the lateral styloid process, see Fig. 7.4.





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Fig. 7.4 The bones of the left manus: lateral view. The prominences shaved in Fig. 7.3 have been coloured red. The distal epiphysis of the ulna fuses with that of the radius at about 1 year, to form the lateral articular condyle. The prominence just proximal to it is probably of diaphyseal origin, but it is commonly called the lateral styloid process of the radius.





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Fig. 7.6 The bones of the left manus: caudal view. The parts shaved in Fig. 7.5 have been coloured red, except for the salient medial styloid process. The inconstant and variable first carpal bone was not present on this skeleton, but its position is indicated in the drawing.

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Jul 8, 2016 | Posted by in SUGERY, ORTHOPEDICS & ANESTHESIA | Comments Off on 7: THE FOOT

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