17: Tendon and Paratenon Lacerations

Tendon and Paratenon Lacerations

Linda A. Dahlgren, DVM, PhD, Diplomate ACVS


Due to their size and inability to ambulate on only three limbs, horses are uniquely dependent on the integrity of the structures supporting the distal aspect of the limb. Lacerations involving the tendons in this area represent a significant therapeutic challenge. Wounds are frequently associated with considerable soft‐tissue trauma and require surgical debridement and primary closure or management by second‐intention healing. Horses with a digital extensor tendon laceration can often be managed conservatively and have a good prognosis for return to athletic function, but when one or both digital flexor tendons have been transected, management is more complex. Tenorrhaphy to reduce gap formation and external coaptation to share loading may allow a more rapid return to function. This chapter describes the diagnosis and treatment of tendon lacerations in the horse and discusses the numerous associated factors that must be considered when managing wounds involving tendons.


Tendons are highly specialized soft‐tissue structures with unique anatomic features that make them critical to the athletic prowess of the horse. Because of the complex hierarchical organization of tendons and their essential role in locomotion, injuries to the tendons and ligaments of horses are a significant clinical problem. The supporting structures of the distal aspect of the limbs of horses are especially prone to injury because of their exposed location with respect to a variety of potentially damaging objects in the environment. The natural “flight” instinct of the horse in response to stimuli may lead not only to injury, but may exacerbate an injury as the horse attempts to flee a frightening situation. The result can be a devastating injury that sometimes leads to loss of function or necessitates euthanasia. Advances in veterinary medicine and surgery have led to more optimistic outcomes than historically described; despite these advances, however, tendon injuries still require a substantial commitment, on the part of the owner, to a protracted process of rehabilitation. This chapter reviews the basic anatomy and physiology of tendons, nuances of the basic principles of wound healing that pertain to tendons, and details relating to the management of tendon lacerations.

Tendon anatomy and function

Tendons are the fibrous extensions of muscles that connect muscle to bone, forming contractile units adapted to perform several specialized functions. By traversing the joints of the appendicular skeleton, tendons and their associated structures lend support to the limb by working with ligaments and joint capsules to maintain alignment of the bony column. More importantly, tendons function to translate muscle contraction into joint movement and enable highly efficient locomotion through the storage and release of elastic energy as the tendon lengthens under load and returns to its original length once unloaded. The impressive athletic ability of the horse is a remarkable example of this adaptation of form to function. The galloping horse must withstand extremes of force over endless repetition, resulting in maximal tendon stretch and return to rest. Maintenance of this finely tuned structural integrity of tendons was essential for survival when the horse was a prey animal and remains essential in the modern era where the horse is a domesticated athlete. Consequently, careful attention to the principles of wound management and tendon healing are paramount to a successful outcome after a tendon injury.

Tendons of the distal portion of the limb originate proximally, in the myotendinous junction, a transition zone between the muscle and tendon. The force generated by muscle contraction is transmitted, via the tendon, to its distal insertion(s) in the bone, resulting in joint movement. Distally, where the tendon inserts in the bone, lies a zone where tendon transitions to fibrocartilage, mineralized fibrocartilage, and finally bone. Between its origin and insertion, the tendon consists of tensile and compressive regions based on whether the tendon is oriented linearly or bends around a bony prominence. Injury may occur at any one of these tendinous segments, and injury to any segment presents a distinct set of challenges for the clinician. Knowledge of tendon anatomy and function and the ability to perform a thorough examination and arrive at a specific anatomical diagnosis provide the most accurate information so that the selected treatment results in the best possible outcome.

Tendon function is facilitated by a series of associated structures required to properly position and nourish the tendon and allow it to move in relation to surrounding tissues. As the tendon extends from muscle to bone, it spans a number of functionally distinct areas characterized by important adaptations. Tendon is surrounded by paratenon in regions of the limb proximal and distal to the joints where the tendon remains linear during locomotion (Figure 17.1). The paratenon is a layer of loose areolar tissue that allows the tendon to move independently beneath the skin and provides structural support for associated neurovascular structures.

Longitudinal schematic of a tendon within the paratenon, with lines depicting the blood vessel, paratendon, epitendon (peritendon), and endotendon.

Figure 17.1 Longitudinal schematic of a tendon within the paratenon, as occurs between sheathed regions.

The tendon itself is wrapped in a thin adherent layer of fibrous connective tissue called the epitenon that is contiguous with the progressively finer connective tissue organization within the tendon’s parenchyma. The network of connective tissue extensions from the epitenon, termed endotenon, carries the blood vessels, lymphatics, and nerves into the core of the tendon. The endotenon encases small collagen bundles (fibrils), binding them together into the larger bundles (fascicles) that ultimately form the characteristic hierarchical organization of tendon. Encasement of collagen bundles by the endotenon keeps the collagen bundles in longitudinal organization while allowing them to slide relative to one another as the tendon stretches and relaxes. Organization of collagen fibrils and fibers parallel to the lines of tension along the long axis of the limb is reinforced by covalent crosslinks between the individual collagen fibers. It is this uniquely ordered arrangement that imparts very high tensile strength to the tendons and allows them to withstand the repetitive high loads they experience as the horse gallops.

As tendons pass over a joint or bony prominence, the increased friction and change of direction result in distinct structural adaptations endowing the tendon with the ability to withstand the increased compressive forces generated in these areas and thereby ensure anatomic integrity during locomotion. The paratenon in these regions is replaced by a fibrous synovial sheath that encases the tendon, bathing it in synovial fluid similar to that found in high‐motion joints (Figure 17.2). The synovial sheath allows the tendon to glide smoothly as the joint flexes and extends and is composed of two layers: a fibrous support layer and an inner synovial membrane responsible for maintaining the health of the synovial environment (Figure 17.3). The inner synovial layer forms a contiguous layer lining the inside of the tendon sheath and the tendon. The mesotenon is a delicate sheet of connective tissue extending from the synovial membrane lining the sheath to the synovial membrane surrounding the tendon. It functions to carry the vascular supply to the tendon (Figure 17.4). Where movement or pressure is greatest, the mesotenon disappears entirely or is reduced to fine, thread‐like soft‐tissue structures called vincula that function to carry vascular supply to the tendon.1 Proximally, the synovial membrane of the sheath contains a sickle‐shaped fold of synovial membrane, which by its redundancy allows the tendon to move freely within its sheath (Figure 17.4).1 Another structural adaptation critical to the maintenance of anatomic integrity as tendons span joints are fibrous bands called annular ligaments, or retinacula, that cross from medial to lateral, gently encircling the tendon and binding it against the bone, thereby preventing it from slipping off to the side.

Illustration of the lateral view of the forelimb displaying individual sheaths that surround tendons, with line depicting the parts.

Figure 17.2 Lateral view of the forelimb showing individual sheaths that surround tendons where they cross points of friction such as joints or bony prominences.

Illustration displaying the longitudinal (left) and cross-sectional (right) views of the tendon within a synovial sheath, with lines depicting the parts.

Figure 17.3 Longitudinal (left) and cross‐sectional (right) views of a tendon within a synovial sheath.

Illustration of the tendon sheath, with lines depicting the tendon, sickle-shaped fold, blood vessel, synovial sheath, mesotendon, and fibrous sheath.

Figure 17.4 The proximal limits of the tendon sheath are characterized by a sickle‐shaped fold of redundant synovial membrane that enables free movement of the tendon within the sheath as the tendon stretches and relaxes.

Tendons receive their blood supply from four main sources. The proximal 25% of the tendon is nourished via the musculotendinous junction. The blood vessels that provide nutrition to the muscle via the endo‐, epi‐, and perimyseum continue to travel distally via the endo‐, epi‐, and paratenon to nourish the tendon. The distal 25% of the tendon receives its blood supply through its osseous insertions. Tendons receive an additional blood supply from surrounding soft tissue: the paratenon in unsheathed regions or the mesotenon or vincula in sheathed regions.2,3 In sheathed regions, the tendon also receives nutrition via synovial diffusion. After a tendon has been injured, its vascular network is expanded dramatically as part of the healing process so that it can provide the critical cellular and paracrine signaling needed to direct the healing process.4,5

The tendon’s extracellular matrix (ECM) is composed of fibrous elements (collagen and elastin) and amorphous ground substance (proteoglycans and structural glycoproteins), and is maintained by a small number of highly differentiated fibroblasts, or tenocytes, that are embedded within the connective tissue matrix. Mature tenocytes are characterized by an elongated cell body with multiple cytoplasmic extensions that reach between the surrounding collagen bundles and participate in cell‐to‐cell and cell‐to‐ECM interactions. These active communications are important in maintaining the homeostasis of the matrix and in transmitting load information that enables adaptation to training. Type I collagen, which makes up 80–86% of the dry weight of tendon, is the primary structural protein of tendon, and is largely responsible for the high tensile strength of tendon.6 Elastin makes up as little as 1% of the dry weight of tendon but makes an important contribution to tendon’s elastic properties.7 Proteoglycans comprise less than 5% of the dry weight of tendon, but they play a central role in maintaining the viscoelastic properties of tendon. Proteoglycans perform the vital functions of regulating the water content of tendon, providing lubrication and spacing between fibrils, and imparting resilience and flexibility to the connective tissue matrix. They also play a role in the control of the diameter of collagen fibers and fibrillogenesis.8–10 The specific type and amount of proteoglycan in tendon varies in response to the mechanical forces exerted on the anatomic segment and is an example of biologic adaptation to environment.9–11 Regions under tension contain only small amounts of proteoglycan of small size (e.g., decorin, biglycan), whereas regions under compression contain larger amounts of proteoglycan of larger size (e.g., aggrecan and versican).9

The aforementioned unique macroscopic and microscopic adaptations of tendon are critical to normal locomotion. Should the tendon or its associated structures become damaged as a result of trauma or infection, debilitating lameness may ensue. An understanding of this relationship between structure and function can be exploited when treating horses with tendon injuries to make an accurate diagnosis and implement optimal treatment with the goals of returning the horse to athletic function.

Tendon healing

Because of the dense organization of collagen, sparse cellular population, and complex structural hierarchy, injuries to tendon present a therapeutic challenge. This is especially true in horses because of their large size and the resulting forces on their tendons, the risk of support limb laminitis, and the inability to prevent a horse from bearing weight on an injured limb during convalescence. Return to athletic function is hampered by the formation of scar tissue that lacks the viscoelastic properties and strength of normal tendon, resulting in a high incidence of re‐injury.

Tendon undergoes the same general physiologic healing processes after injury, as do other soft tissues. The acute inflammatory and debridement phases may be prolonged in injured tendon because of the high content of collagen, which is resistant to proteolysis and slow to turnover.12 Although the surrounding soft tissues may enter into the repair/proliferative phase of healing and form granulation tissue, the damaged collagen may still be undergoing debridement, extending the inflammatory phase beyond 10–14 days and well into the repair phase. The damaged collagen acts as a foreign body within the wound and delays healing. Healing of tendon is also slowed by the sparse blood supply to the tendon compared to that to some other tissues, such as muscle. The repair or proliferative phase of tendon healing begins at 3–4 days and lasts as long as necessary to produce adequate fibrovascular callous to stabilize the transected tendon ends; this is the first step critical to re‐establishing the strength of tendon.

In tendon, the proliferative phase can last 21–45 days or longer. Even after the gap between the ends of the severed tendon is filled by a mass of collagenous scar tissue, the tensile strength of the tendon unit is low. To support the weight of the horse, the immature repair tissue must undergo the remodeling or maturation phase of tendon healing, which can last 6–12 months and is characterized by an increase in the tensile strength of the tendon and a decrease in the tissue’s cellularity. As collagen is realigned along lines of tension, the content of type I collagen and the number of chemical crosslinks formed between the newly assembled collagen fibers rise. This brings about a gradual increase in tensile strength so that the injured tendon is able to withstand the forces required for standing and walking within a stall, without the need for external coaptation.

The nature of the cells that participate in the healing process remains a source of debate because few comprehensive studies have tracked the origin and migration of cells during healing of tendons. Tendon is not as inert a structure as was once thought. Healing is known to occur through extrinsic and intrinsic mechanisms.13,14 Extrinsic healing occurs as fibroblasts migrate from the surrounding paratenon and/or tendon sheath into the injured area. The paratenon and tendon sheath represent a significant source of cells that contribute to the regenerative response, and for many years extrinsic healing was thought to be the sole mechanism whereby tendons underwent repair.

Tendons are now known to be capable of intrinsic repair, which occurs when tendon fibroblasts embedded within the ECM up‐regulate their production of ECM components important to healing. Recent work suggests that progenitor cells embedded in the ECM may be activated in response to injury and thus contribute substantially to healing.15,16 Another important source of cells for intrinsic repair is the endotenon. Following experimental injury, the endotenon becomes more prominent as a result of hypercellularity and neovascularization.4,5 Big oval cells with large nuclei and nucleoli may represent progenitor cells that have migrated from the vasculature and/or have been quiescent within the endotenon and proliferate and differentiate in response to paracrine signals from the injured tissue. As knowledge of cell surface markers and cell tracking techniques increases, new studies may better define the cellular response that occurs within injured tendon. Although the extrinsic component of tendon healing is responsible for a robust cellular response, excessive scarring can result in the formation of adhesions between the tendon and the surrounding tissues past which the tendon must glide to function normally. This is especially important in the sheathed portions of the tendon where fibrous adhesions can significantly impair mobility, resulting in mechanical lameness and pain.

Diagnosis and treatment

Horses are prone to injuring themselves on a variety of objects found in their environment. Trauma can be self‐inflicted while the horse is at play or being ridden, or it can be the result of actions by another horse. As is the case with any injured horse, the attending clinician must perform a thorough physical examination to determine the systemic status of the horse and the precise anatomic structures affected. This examination enables an accurate diagnosis, helps determine the prognosis and options for treatment, and helps the owner decide on how to manage the situation. If environmental factors do not allow for a complete physical examination at the time the horse is initially presented, a preliminary assessment must be made, and the horse must receive appropriate interim treatment prior to being transported to a referral center. The goals of initial first‐aid are to immobilize the injured limb to prevent further damage to soft tissue or bone and to provide immediate life‐saving treatment to stop hemorrhage and treat for shock.

Physical examination

The horse should be examined for signs of hypovolemic shock, which include rapid, thready pulse, pale mucous membranes, delayed capillary refill time, and skin tenting. The superficial location of the median artery in the forelimb, the dorsal metatarsal artery in the hindlimb, and the digital arteries in the distal aspect of the limb make them prone to transection. Hemorrhage can typically be controlled, at least temporarily, by the application of a pressure bandage to the wound until the wound can be fully assessed. Immobilizing the injured limb by using a Kimzey Leg Saver Splint (Kimzey, Inc.) (Figure 17.5) or a piece of PVC pipe incorporated into a heavy bandage and extending down to the ground (Figure 17.6) prevents a partially lacerated tendon from disrupting completely and protects neurovascular structures from additional trauma. Splints are placed either dorsally or on the palmar surface of the forelimb and on the plantar surface of the hindlimb (the reader is referred to Chapter 7 for more information on splints). When the horse is able to balance on the stabilized limb, it is more likely to remain calm, enabling the exam to be completed.

Photo displaying Kimzeg Leg Saver Splint applied to the hindlimb of a horse.

Figure 17.5 Kimzey Leg Saver (Kimzey, Inc.) applied to the hindlimb to provide support and prevent further tissue damage.

Courtesy of Dr. Christophe Celeste.

Photo displaying forelimbs of a horse, with splint applied to the dorsal surface of the right forelimb with the dorsal bone column straight.
Photo displaying left hindlimb of a horse, with splint placed on the plantar surface with the limb in partial flexion.
Photo displaying left hindlimb of a horse, with splint placed on the plantar surface with dorsal bone column straight.
Photo displaying dorsal splint placement on the left hindlimb of a horse.

Figure 17.6 PVC splint applied to achieve immobilization and support for transport to a referral facility. Splints are usually applied to the dorsal surface of the forelimb with the dorsal bone column straight (a). For the hindlimb, splints are best placed on the plantar surface with the limb in partial flexion (b) or with the dorsal bone column straight (c); however, dorsal splint placement can be useful if plantar placement is not possible (d). Regardless of placement, the splint should extend to the ground and incorporate the foot for maximal stability. The flexed position (b) is indicated to relieve tension on the flexor tendons and prevent a partial flexor tendon tear from becoming complete.

Courtesy of Dr. Larry Galuppo (a and b) and Dr. Olivier Lepage (c).

The injured horse may need to be sedated or otherwise restrained to complete the examination, always while keeping in mind the systemic state of the horse. Severe blood loss and associated hypovolemic shock dictate selection and dosage of a sedative or tranquilizer. It is important that the veterinarian, owner, and handlers be protected from harm and that the horse not suffer more injury to the damaged tendon. A severely lame horse, in pain, can be a challenge to handle, and care must be taken to thoroughly assess the situation.

Physical examination should begin with a basic assessment of the horse’s temperature, pulse, respiratory rate, color of mucous membranes, and capillary refill time. The horse’s history, including information as to the duration of the injury, the horse’s vaccination status, and the use of any medications, should be recorded. The “big‐picture” information, such as hemorrhage or evidence of prior hemorrhage, weight‐bearing status, and pain level of the horse, as well as the horse’s overall demeanor, can be useful in formulating an initial plan. It is critical that the entire horse be examined so as not to miss additional injuries that may affect prognosis.

Careful observation of how the horse is willing to use the limb provides key information. Is the horse able to weight bear when stationary and to lock the stay apparatus? Does the foot stay flat on the ground, or does the fetlock or hock drop when the horse bears weight on the affected limb? Is there an abnormal pattern of flexion and extension that suggests that the reciprocal apparatus is no longer intact? Is there a stable bony column to support the horse? Is there any evidence of fluid drainage suggesting that a synovial structure is open? An understanding of normal anatomy is important when examining the distal aspect of the limb specifically for laceration of a digital flexor tendon.

Observation as the horse bears weight or takes a careful step or two on the injured limb is one of the easiest ways to assess the integrity of the primary support structures, including the digital extensor and flexor tendons, suspensory ligament, and their associated structures (e.g., tendon sheath, digital annular ligament, neurovascular structures). Transection of the common digital extensor tendon of the forelimb, or both the lateral and long digital extensor tendons (or below where the two join) of the hindlimb, results in knuckling of the fetlock when the horse attempts to walk, because the horse has lost its ability to extend the toe as the limb is advanced (Figure 17.7). When the limb is manually placed in a normal weight‐bearing position, a horse with a severed digital extensor tendon is able to bear weight on the limb without hyperextending the joints. Knuckling of the limb causes most horses to exhibit a substantial degree of anxiety, making restraint and stabilization with a splint an important aspect of treatment.

Photo displaying the knuckling of the right hind fetlock associated with transaction of the long and lateral digital extensor tendons.

Figure 17.7 Knuckling of the right hind fetlock associated with transection of the long and lateral digital extensor tendons.

Transection of the tendons and ligaments on the palmar/plantar surface of the distal limb results in characteristic changes in joint position (Figure 17.8). Complete transection of the superficial digital flexor tendon (SDFT) at the metacarpal/metatarsal region or fetlock results in hyperextension of the metacarpo/metatarsophalangeal joint, characterized by “dropping” of the palmar/plantar aspect of the fetlock towards the ground (Figure 17.9). The toe remains on the ground. The pastern may subluxate dorsally after the SDFT is transected. A structure deep to the SDFT [e.g., the deep digital flexor tendon (DDFT) or suspensory ligament] may be injured in the absence of injury to a more superficial structure, such as the SDFT, but most lacerations involve the structures immediately underlying the skin before they involve deeper ones. The distinctive clinical sign indicative of complete transection of the DDFT is elevation of the toe off the ground (Figure 17.10), resulting from loss of the tension band produced by insertion of the DDFT on the palmar/plantar surface of the distal phalanx. Transection of both the SDFT and the DDFT leads to hyperextension of the metacarpo/metatarsophalangeal and distal interphalangeal joints, as well as elevation of the toe off the ground (Figure 17.11). When the suspensory ligament, in addition to both of the digital flexor tendons, is transected, support to the palmar/plantar aspect of the limb is completely lost, and the palmar/plantar surface of the fetlock rests on the ground with the toe pointing up (Figure 17.12). Because the DDFT and its associated sheath are the only support structures present on the palmar/plantar surface of the pastern, injuries in this area typically affect only the DDFT. The clinical signs associated with partial transection of a digital flexor tendon vary depending on the percentage of remaining intact tendon and the location of the injury.

Three schematics illustrating the transection of SDFT (a), transection of SDFT and DDFT (b), and transection of the SDFT, DDFT, and suspensory ligament (c).

Figure 17.8 Schematic showing changes in joint position. (a) Transection of the superficial digital flexor tendon (SDFT) results in metacarpo/metatarsophalangeal hyperextension. (b) Transection of the SDFT and deep digital flexor tendon (DDFT) results in metacarpo/metatarsophalangeal hyperextension and toe elevation. (c) Transection of the SDFT, DDFT, and suspensory ligament results in complete loss of metacarpo/metatarsophalangeal support.

Source: Watkins 1999.17 Reproduced with permission of WB Saunders.

Photo displaying mild hyperextension (fetlock drop) of the right metacarpophalangeal joint resulting from complete transaction of the SDFT.

Figure 17.9 Example of mild hyperextension (fetlock drop) of the right metacarpophalangeal joint resulting from complete transection of the SDFT.

Photos displaying transection of the DDFT in the metatarsal region displaying toe elevation but no fetlock hyperextension (a–c). Photos displaying horse limbs with fishtail shoe applied, with inset (d–e).

Figure 17.10 (a)–(c) Transection of the DDFT in the metatarsal region showing toe elevation but no fetlock hyperextension (shown approximately 2 weeks following injury). Note that the toe is only slightly elevated when the horse is partially weight bearing (a, b) but when weight bearing is increased the toe elevation becomes more exaggerated (c). Because of the instability with increased weight bearing (c), it was difficult to catch the image without motion artifact. (d, e) The same horse 2 weeks later when the fishtail shoe was applied at the time of cast removal showing how the shoe works to support the limb and prevent toe elevation. The cast was removed early at 2 weeks because the horse developed cast sores. In its place the fishtail shoe and a bandage cast (d inset) was applied for support and changed every 4 days for 4 weeks. Image (d) was taken after 4 days when the first bandage cast was changed.

Courtesy of Drs. Mike Cissell and Elsa Ludwig.

Photo displaying hyperextension of the left metacarpophalangeal and distal interphalangeal joints and elevation of the toe off the ground associated with complete transection of both the SDFT and DDFT.

Figure 17.11 Hyperextension of the left metacarpophalangeal and distal interphalangeal joints and elevation of the toe off the ground associated with complete transection of both the SDFT and DDFT.

Courtesy of Dr. Gal Kelmer.

Photo displaying fetlock o a horse resting on a block of wood.

Figure 17.12 Complete loss of the palmar support structures occurs when the suspensory ligament and both digital flexor tendons are completely transected resulting in the fetlock resting on a block of wood and the toe pointing up. In this case, the toe elevation is less marked than normal because the extensor tendons were also transected.

Careful palpation of the injury can be useful in confirming the information obtained by observing the stance assumed by the horse when it bears weight on the injured limb and in determining the extent of a partial laceration. Hair surrounding the wound should be clipped and the wound cleaned. Sterile gloves should be worn to prevent further contaminating wound, and for one’s own protection against zoonotic infection. Many horses must be sedated and/or the region of the wound desensitized by regional or local anesthesia to ensure that the wound is examined thoroughly and safely. If the wound appears to be severe and clearly requires surgical repair, it can be assessed more thoroughly with the horse anesthetized. The potential risks associated with recovery from general anesthesia should be taken into account when deciding whether to anesthetize an injured horse for surgical treatment. External coaptation in the form a cast may be required to prevent more damage to injured structures while the horse recovers from general anesthesia. The systemic status of the horse must also be taken into consideration before general anesthesia is selected as the method of restraint; if the injury appears to be severe, however, the horse should be anesthetized so that the wound can be assessed thoroughly, irrigated, debrided, and repaired.

In addition to visually assessing the injury and palpating the wound, the limb, while being palpated, should be flexed and extended, to better assess the injury. The ends of a completely severed tendon may retract a substantial distance proximally and distally to the wound, making the severed ends difficult to see or palpate. Ultrasonographic examination may be useful in assessing the extent of soft‐tissue injury; air trapped within the tissue planes of an open wound, however, creates artifacts that interfere with accurate sonographic examination. Nevertheless, use of ultrasound to assess vascular integrity in severe wounds remains an important adjunct to the rest of the examination. A horse with a completely disrupted or compromised blood supply has a grave prognosis for survival. Using radiography to rule out concurrent fracture is also warranted because the presence of bone involvement can impact the prognosis substantially.

General treatment considerations

Regardless of the structures involved, treatment of wounds involving a lacerated tendon is comprised of standard supportive care, including treatment of the horse for pain, dehydration, and/or hypovolemic shock, and of the wound for inflammation and contamination. Intravenous administration of fluids is indicated for horses suffering from hypovolemic shock resulting from hemorrhage or from dehydration resulting from decreased water consumption because of immobility and/or pain. In most cases, isotonic fluids, such as lactated Ringer’s solution, are adequate and should be administered at a rate appropriate to the horse’s needs. Administering plasma to treat for hypoproteinemia, or hypertonic saline solution or hetastarch to treat for hypovolemic shock, may be indicated in extreme circumstances. Additional nursing care specific to the horse’s systemic status and individual needs should be considered. This might be as simple as treating other less severe wounds, or more intensive, such as providing sole and frog support and cold therapy to prevent support limb laminitis. When bandaging or casting limits the mobility of the horse, care must be taken to provide bedding that enables easy movement within the stall.

For many horses, conventional non‐steroidal anti‐inflammatory drug (NSAID) therapy may suffice to keep them comfortable. In these cases, phenylbutazone (2.2–4.4 mg/kg) or flunixin meglumine (0.5–1.0 mg/kg) given twice daily provide excellent anti‐inflammatory and analgesic effects. Because most horses with a moderate or severe injury have an intravenous catheter in place for antibiotic therapy, the intravenous route is preferred for ease of administration and rapid, reliable effects.

Many horses with severe injuries may require analgesia beyond that provided by a NSAID, making it necessary to explore additional options to provide adequate analgesia. Administering an analgesic drug through a caudal epidural catheter is an excellent method of relieving pain in a hindlimb.18–22 Continuous peripheral nerve blocks are another option to consider in cases requiring adjunct analgesia.23,24 The goal of analgesic therapy is to make the horse comfortable enough to occasionally and modestly shift weight on to the injured limb just enough to prevent laminitis from developing in the contralateral limb. Other options for adjunctive analgesia include continuous intravenous infusion of lidocaine, ketamine, or butorphanol, fentanyl patches, morphine administered intramuscularly, and gabapentin;25–27 these drugs, however, are generally only required if the horse displays extreme signs of pain or during the first 24–48 hours after injury. Because supporting limb laminitis is a major potential complication after tendon laceration, vigilance with respect to supportive care and close monitoring for signs of laminitis are crucial elements of nursing care.

Antibiotic therapy is an important component of wound therapy and is especially critical for wounds involving tendons and their associated structures. Antibiotics are often administered systemically and regionally. Broad‐spectrum antibiotics, such as penicillin (22–44 000 IU/kg IV q 6 hours) or ceftiofur (2.2 mg/kg IV q 12 hours) and gentamicin (6.6 mg/kg IV q 24 hours) are indicated for most horses that have suffered a tendon laceration. Trimethoprim sulfa (30 mg/kg PO q 12 hours) may provide adequate coverage against most common contaminants, and its use may be sufficient if the wound does not involve a synovial structure. Whenever possible, a sample of (synovial) fluid or tissue from the wound for cytologic examination and/or culture and sensitivity testing should be collected to guide the selection of antibiotics. Based on lack of response to therapy, cytologic findings, or more appropriately, sensitivity testing, administering an antibiotic with a broad anaerobic spectrum, such as metronidazole, may be necessary. Duration of therapy is based subjectively on prior experience of the clinician, the severity, degree of contamination and duration of the wound, structures involved, and response to treatment. Antibiotics are administered intravenously as early as possible after tendon injury has been diagnosed; this is most likely to occur in consultation with a referral center with the aim to administer the initial dose prior to transport of the horse. Interim antibiotic therapy is an empiric drug selection, instituted while awaiting results of bacterial culture and antibiotic sensitivity testing. For all severely infected wounds, rational antibiotic therapy must be guided by culture and sensitivity results. Consequently, the referring veterinarian should collect a sample for culture and sensitivity testing prior to the initiation of interim antibiotic therapy and either submit it or send it along with the horse for testing at the referral hospital. The reader is referred to Chapter 16 for more information on the diagnosis and management of wounds involving synovial structures. Table 19.1 lists common bacterial isolates from various wounds in horses, and provides recommendations for interim systemic antibiotic therapy.

The large amount of tissue trauma and contamination in wounds involving a tendon result in a prolonged phase of debridement, which in turn, delays the formation of a healthy bed of granulation tissue. Antibiotic therapy should be administered for at least 3–5 days. Only for minimally contaminated wounds treated early (less than 3–6 hours after injury) would antibiotic therapy be maintained for as little as 3–5 days. Total duration of antibiotic therapy usually ranges from 7–28 days. A lengthy period of administration is most often associated with wounds involving a synovial structure and those with substantial contamination, a slow response to therapy, and/or persistent infection. For more information, refer to Table 19.5, which provides guidelines for duration of antibiotic therapy in specific types of wounds.

The increased use of regional antibiotic therapy in recent years has greatly improved the prognosis for horses with extensive tissue damage to a limb, with or without damage to a synovial structure. The antibiotic should be administered regionally and systemically for optimal results. Regional antibiotic delivery has the distinct advantage of achieving a much higher concentration of the antibiotic at the wound than can be achieved by systemic administration where high doses may be unacceptably expensive or cause detrimental side‐effects. Additionally, a wider range of antibiotic options that can be delivered regionally enables the selection of an antibiotic with a susceptibility pattern or spectrum of activity different to that being administered systemically. A complete review of regional antibiotic delivery is beyond the scope of this chapter, but many excellent resources on the subject are available28–30 and more information can be found in Chapter 19 of this book.

The choice of administering an antibiotic intravenously, intraosseously, intrasynovially, topically, or by sustained release from beads implanted at the wound is made on a case‐by‐case basis and depends on many factors, including the nature of the specific injury and the availability of a peripheral vein for delivery. Intravenous regional antibiotic delivery is a common choice because of general ease of administration and distribution to synovial structures and the surrounding soft tissues. Frequency of regional delivery depends on severity of contamination or infection, response to initial treatment, ease of delivery, and to some extent, prior experiences of the clinician. Although the literature contains various reports on the pharmacokinetics of regionally delivered antibiotics, the majority concern normal horses, and how these data may translate to horses with inflammation and possibly increased blood flow to the injured area is unknown. In many cases, therapy is administered by this route every other day, but frequency of administration can sometimes be reduced to every third day if the horse responds well to therapy.

In recent years, the use of regenerative therapies has gained popularity in veterinary medicine, especially in equine practice. Mesenchymal stem cells (MSC) are commonly delivered to the site of tendon and ligament injury caused by overuse, in the hope of stimulating a stronger healing response and reducing the incidence of re‐injury. Sources of cells include bone marrow and adipose tissue. Additional biologic therapies, such as platelet rich plasma (PRP), concentrated bone marrow aspirate, autologous conditioned serum (irap® plus, Dechra Veterinary Products), and ECM (ACell Vet™, ACell, Inc.), have also been described for treating tendinitis and desmitis. Application of regenerative therapies in general wound healing is covered in Chapter 22 of this book. The use of regenerative therapies has not yet been described for adjunctive treatment of tendon and ligament lacerations, but theoretically, their beneficial effects would apply. Use of PRP gel (with or without MSC) or ECM at the site of tendon injury may provide a structural scaffold and bioactive proteins capable of contributing to a regenerative response. Judicious use of products shown to be safe for use in open wounds, especially those that can be produced for point‐of‐care application, may be beneficial.

Extensor tendon laceration

Sep 15, 2017 | Posted by in GENERAL | Comments Off on 17: Tendon and Paratenon Lacerations

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