Horse state part B - surgery & orthopaedics

Equine surgery and orthopaedics

1. Principles and indications of local anaesthesia.

Local anaesthesia = numbing an area of the body using medications called local anaesthetics.

• Gives temporary loss of sensation and pain.

• Used for surgical procedures and diagnostic conclusion.

• Reduces the required amount of anaesthetic agent and allows complicated procedures to be performed on a standing horse.

• Injected around the nerve at a site where the nerve is not covered by bone.

• Risks following this type of procedure, including epidural anaesthesia:

  • Ataxia of the hind limbs

  • Hind-limb motor blockage

  • Recumbence

  • Respiratory depression

Indications ✅

• Surgical procedures: removal of teeth, laparoscopy and wound management.

• Lameness diagnostics: pain blocking using peripheral nerve blocks, intraarticular and intrabursal injections, and ring blocks.

Contraindications ❌

• Fracture confirmation

• Septic inflammation, including:

  • Periarticular cellulitis

  • Hoof abscesses

Regional anaesthesia

Regional anaesthesia can be used to localize the area of pain:

➡ Apply local anaesthesia and register any improvement in lameness after 15 minutes.

Start with a palmar digital nerve block and go upwards on the leg if there is no improvement.

Regional anaesthesia is divided into two main regions:

1. Head

2. Limbs

Forelimb nerve blocks 🐴

• Palmar digital nerve (PDN) block – “heel block”

• Semi-ring block at the pastern

• Abaxial sesamoid nerve block – basisesamoid nerve block

• Low 4-point block – low palmar nerve block

• High 4-point block – high palmar nerve block

• Lateral palmar nerve block

Hindlimb nerve blocks 🐴

• Plantar digital nerve block – as in the forelimb

• Abaxial sesamoid nerve block – as in the forelimb

• Low 6-point nerve block – low plantar nerve block

• High 6-point nerve block – high plantar nerve block

• Tibial nerve block

Head nerve blocks 🐴

• Maxillary nerve block

• Infraorbital nerve block

• Mandibular nerve block – inferior alveolar nerve block

• Mental nerve block

• Auricopalpebral nerve block

• Diamond block – supraorbital, lacrimal, zygomatic and infratrochlear nerve blocks

• Retrobulbar nerve block – muscles of the eye

Teeth

• subgingival, supraperiostal, interincisival or intralesional infiltration

Epidural anaesthesia

⚠ Epidural anaesthesia is injected into the epidural space, not the subarachnoid space. Injection into the subarachnoid space is called intrathecal or spinal anaesthesia.

• Used in a standing horse.

• Analgesics should be warmed to body temperature before injection into the spine.

Indications

Analgesia or anaesthesia of the perineal area, including:

• Perineum

• Rectovestibular laceration repair

• Surgeries involving the rectum

• Anus

• Tail

• Urethra, Bladder, Vulva, Vestibule, Vagina

• Relaxation of abdominal contractions in dystocia

Location

• Between the 1st and 2nd coccygeal vertebrae

• Or the lumbosacral space

⚠ It is forbidden to use proximal epidural anaesthesia in horses because it may cause severe hindlimb motor blockade, ataxia and recumbence.

Drugs

Adjust the dose to prevent ataxia and recumbence because the horse is in a standing position!

• Local anaesthetics: lidocaine, mepivacaine

• Alpha-2 agonists: xylazine, detomidine

• Opioids: morphine, methadone, hydromorphone

• Tramadol: analgesia

• Ketamine: analgesia and systemic effects

• One can use lidocaine (2%, 7-9ml), xylazine or detomidine (alpha-2-agonists) or opioids like morphine (butorphanol) or methadone.

Types of local anaesthesia 💉

• Superficial, Infiltration, Perineural, Local perfusion

• Intrasynovial:

  • Intraarticular

  • Intrabursal

• Intrathecal

Local anaesthetic drugs and duration ⏱

Drug	Onset of effect	Duration
Procaine	5–10 min	—
Lidocaine	5 min	30–60 min
Mepivacaine	10 min	60–120 min
Bupivacaine	30 min	120–140 min
Etidocaine	3–5 min	5–10 hours
Proparacaine	<1 min	5–25 min

Equine sedation and incomplete general anesthesia

Sedation = the depression of a patient's awareness to the environment and reduction of its responsiveness to external stimulation.

Sedatives and tranquilizers are commonly used in combinations as pre-anesthetics before general anesthesia to relax and sedate the animal. Some sedatives also provide analgesia.

💊 Drugs

Alpha2-adrenergic agonists

• Xylazine, detomidine, medetomidine, romifidine → sedation + analgesia

• Can be used alone or in combination with opioids.

• Induce bradycardia, decreased CO, hyperglycemia, decreased bp, hypothermia, hypotension, diuresis, polyuria, can kick

• Xylazine: (Rometar) lasts about 15–20 min. Dose: 1.1 mg/kg IV.

• Detomidine: (Domosedan) 0.01-0.04mg/kg IV or IM, lasts about 30–60 min.

• Atipamezole to reverse the effect

Phenothiazines

• Acepromazine → sedative, mild tranquilizing, often in combo with alpha2 agonist or opioid, is anti-arrhythmic, and cause vasodilation.

• often used in oral surgery (reduces chewing).

• Contraindicated in breeding stallion (penis prolapse) or hypovolemic patients.

Opioids

• Butorphanol, morphine, buprenorphine, meperidine

• Analgesic → always in combo with sedative.

Benzodiazepines

• Diazepam, midazolam → sedative, muscle-relaxing.

• Induce ataxia → not used in standing procedures.

• Foals

⭐ Common sedation in horse: Detomidine + butorphanol (domosedan og tourbugesic IV, 0,1ml av hver per 100kg)
→ Just know that you combine an alpha2 agonist + opioid.

🐴 Standing sedation

Necessary for a variety of surgical and non-surgical procedures in the standing horse.

Common drug combination for 500–600 kg horse:
💉 Detomidine (0.5 ml) + butorphanol (1 ml)

Benefits:

• Smoother recovery than GA.

• Sometimes cheaper than GA.

• Simpler to do standing sedation in some procedures, like laryngoplasty, dental procedures.

• In head surgeries (a lot of bleeding) → less bleeding in standing position than recumbence.

• Decreased risk for horse compared to general anesthesia, but more risk for staff.

Indications:
- Dental procedures, stomatology
- Diagnostic imaging

- Sinus surgeries
- Urogenital
- Orthopedic
- Wound assessment
- Castration

🐴 Sedation of adult horse

Short-term sedation is achieved by administering a bolus of an alpha2 agonist, with or without an opioid.

When used in combo with an opioid:

1⃣ Alpha2 agonist FIRST → 2⃣ Opioid

The horse must first be sedated with the alpha2 agonist prior to opioid to avoid opioid-induced excitement.

A combo of opioid + alpha2 agonist is only done when:

• Heavy sedation is required.

• Additional analgesia is required.

🐴 Sedation and anaesthesia in foals

Sedation and anesthesia may be required in foal to allow diagnostic and therapeutic procedures.

Differences in foals compared to adult horses:

• ❤ Circulatory system (transition from in-utero to newborn)

• 💊 Metabolism of drugs

• 🌡 Susceptibility to hypothermia and hypoglycemia

❌ Avoid:

• Drugs that lower heart rate → xylazine, detomidine

• Drugs that decrease preload → acepromazine
  → May produce diminished cardiac output and tissue perfusion.

• Premedication if using gases.

• Halothane.

Sedation of foals:

• Neonatal foals become recumbent when sedated, and the foal should be supported until it assumes recumbence.

• avoid drugs that lowers heart rate (xylazine and detomidine) and dec. preload (acepromazine).

• In foals younger than 4 weeks one should avoid A2A and use benzodiazepines, opioids and ketamine/propofol.

Alpha2 agonist

• Given to healthy foals, minimum dose.

• Older foals are sedated as adult, but with higher dose.

Benzodiazepines – diazepam and midazolam

• Slow administration.

• Ataxia may prolong.

• Don’t repeat dose or give high dose.

• Not analgesic.

💉 Benzodiazepines + ketamine

• Combined for painful procedures.

• Light anesthesia.

• Diazepam/midazolam + ketamine

• Diazepam commonly used for sedation in foals because it provides tranquilization and muscle relaxation with relatively little cardiovascular depression, and is commonly combined with ketamine for induction of GA

Equine general anesthesia

General anaesthesia = controlled and reversible CNS-depression.

It gives:

• Analgesia, Amnesia, Immobility, Unconsciousness, Muscle relaxation

📋 Patient preparation

• Obtain medical history.

• Pre-anesthetic clinical exam, with focus on cardiovascular and respiratory system.

• Conditions affecting recovery or induction should be considered and implementing plans for assisting → like musculoskeletal injuries or neurological diseases.

• 🌾 No hay 12 hours before anesthesia.

• Mouth should be flushed to remove debris.

• 💉 A jugular catheter should be placed if GA is intended or prolonged sedation (MENTION THIS ON STATE)

• 💧 Preoperatory stabilization of cardiovascular system with IV fluids is necessary for horses undergoing emergency surgery!!! (IMPORTANT ON STATE)

• ⚠ Horses must be sedated before induction of any anesthesia → cause excitement in horse without sedative premedication.

Why sedation before induction?

Sedation:

• Improves ease of handling

• Makes induction safer

• Decreases dose of induction

• Decreases dose of maintenance drugs

• Provides analgesia

• Improves quality of recovery by prolonging the time until the first attempt to stand

➡ Sedate with alpha2 agonist / Xylazine → wait 3–5 minutes after apparent effect of sedation before induction of anaesthesia.

Filip’s master mix: Xylazine for sedation, diazepam + ket for induction and xylazine + ket every 5-7 min for maintenance

💉 Total Intravenous Anesthesia – TIVA

TIVA = the use of intravenous agents for induction and maintenance of anesthesia, by the injection of a liquid anesthetic in a vein and by catheterization of vein (infusion anaesthesia).

✂ Procedures

• Castration, Cryptorchidectomy, Crib biting, Ovariectomy, Wound management, Orthopedic → lag screw, implant removal

💊 Induction regimes

⚠ Always first sedate with alpha2 agonist → then induction agent

Induction agents:

• Ketamine + diazepam

• Ketamine + guaifenesin → muscle relaxant, analgesic

• Thiopental

• Propofol

⏱ Prolongation of anesthesia with injectable drugs:

Short periods:
➡ Bolus of xylazine + ketamine

Prolonged period:
➡ Thiopental + alpha2 agonist

• Never use ketamine alone!!

• For maintenance, do half the amount of actual dose.

• Triple dip → 1L of 5% guaifenesin and adding 1-2g of ketamine and 500mg of xylazine then administered up to a rate of 1ml/kg/h, and is used for maintenance of surgeries up to 90 min.

⭐ Importance of TIVA

TIVA is frequently used in horses.

It’s cheaper than standing anesthesia and many procedures can be performed.

TIVA provides:

• Smooth, excitement-free induction phase

• Slow lowering of the body into sternal or lateral recumbence

• Minimal cardio-pulmonary depression

• Calm recovery period

• Minimal ataxia

😷 Inhalation anaesthesia

Most common method of maintaining anesthesia in the hospital setting.

• Requires strict monitoring and a professional anesthesiologist

• Expensive and time consuming

• Used for surgeries >1 h

🏥 Equipment

• Endotracheal intubation

• Anesthetic machine

• Recovery box → soft covering, dark and quiet room

➡ Induction starts with injectable → then maintenance with gas.

💨 Gases

• Isoflurane, Sevoflurane, Desflurane

High oxygen flow rate should be used during the first 10–15 min of anesthesia to carry the inhalation anesthetic into the circuit and thereby into the horse.

Flow rates:

• First 15 min → 20 ml/kg/min

• Remainder → 10 ml/kg/min

• Foals → 40–60 ml/kg/min

✅ Pros

• Minimal drug accumulation

• Good monitoring

❌ Cons

• Cardiovascular decrease

• No analgesia

• Too rapid recovery

⚠ Recovery from iso and sevo is fast and sometimes uncontrolled.

➡ Sedation decreases speed of recovery.

📊 Monitoring

❤ Heart rate: 28–44 bpm

• Bradycardia → atropine to increase HR

🌡 Body temperature: 37.5–38°C

🫁 Respiratory rate: >4 breaths/min

🩸 Blood pressure: 120/70 mmHg

• Hypotension → dopamine increases BP

🩸 Direct arterial blood gas

• O₂

• CO₂

💨 Capnography

• CO₂ in expired air

❤ ECG

• Heart’s electrical activity

🫁 Pulse oximetry

• Measures oxygen level of blood

• Attached on tongue

🚽 Urinary catheter

• If procedure is >1 hour

• Prevents over-distention of the bladder

⚠ Risks associated with equine anaesthesia

Horse can be dangerous to itself and the veterinarians during excitation stage.

1⃣ Complications at induction

• Intracarotid injection

• Administration of incorrect drug

• Haematoma formation

• Perivascular injections

2⃣ Intraoperative complications

🫁 Hypoxaemia

• Common in all recumbent adult, full-sized horses

🩸 Hypotension

• Higher risk in injectable anaesthetics

• Mean arterial pressure should be >70 mmHg

💨 Hypercapnia

• PaCO₂ >45

• Due to depressant effects of anaesthetic drugs on respiratory function

3⃣ Post-operative complications

1.💪 Myopathy

Dorsal recumbency: gluteal and longissimus dorsi muscles are most likely to be affected due to inadequate circulation.

Prevention:

• Careful positioning

• Adequate padding

• Short operating time

• Maintain BP

2.🦴 Long bone fractures

• Higher after colic surgeries

3.Neuropathy

• Most commonly seen on peripheral nerves, e.g. radial nerve

• Ischemic in origin

4. Sweeney shoulder

🏥 Complications during hospitalization period

• 🩸 Shock

• ☠ Endotoxaemia → fluid + electrolytes are important

• 🐴 Postoperative Ileus (POI)

• 🤕 Colic → some horses suffer from one or more episodes of colic after colic surgery

• 🩹 Wound complications

• Adhesions

• 🩸 Thrombophlebitis

• 🦶 Laminitis → after acute abdomen

• 💩 Postoperative diarrhoea

• 🦠 Septic peritonitis → contamination of ingesta in peritoneal cavity
  → Atb, NSAIDs and hydration!

Equine wounds

Wound = a sudden and violent disturbance of soft tissue connections with simultaneous skin and mucosal damage due to mechanical, physical or chemical factors. fra lecture: a wound is a disruption of the anatomical and cellular continuity and integrity of the tissue.

Categorization of wounds

• Cause: accidental or intentional (surgical incision)

• Open wounds: Incisions (sharp cut, sharp edges), Lacerations (most common, ireegular skin edge, painful), Puncture, Avulsion (wound with tissue loss), combined, complicated

• Closed wounds (not entire skin thickness): Abrasion, Contusion, Burn (chemical, friction, freeze and sunburn, 1st-3rd degree)

• Location: head, thorax, abdomen, joints (heals completely different at different locations)

🔍 Wound Assessment

🐴 General assessment of horse

• History (what happened)

• Physical examination of patient (initial wound assessment, patient cooperative or not, restrain, sedation?)

• 💉 Important to know tetanus vaccination status! need tetanus toxoid administration if not vaccinated within 6 months, 13-20ml, but careful with pregnant mares (acute hepatitis/Theiler´s Ds)

• Penetrating wounds above abdomen/thorax: hemorrhage should be eliminated (Hematocrit, cavity liquid content assessment)

• Contraindicated to use phenotiazines (acepromazine) on horses with hemorrhagic wounds → cause vasodilation → worsening of hypotension → hemorrhagic shock

🔎 Initial assessment of wound

• Influence of healing

• Severity involving structures:

  • Nerves, Blood vessels, Ligaments, Bones, Joints

• Degree of contamination (initial cleaning before palpation)

• In joints, use sterile saline or contrast medium (water only in verry dirty wounds, water is hypotonic and is not sterile)

• Use sterile gloves to not contaminate the wound with human skin

• Remove foreign body!

⚠ Factors inhibiting healing:

• Infection, Contamination, Necrosis, Movement, Loss of blood supply, Hypoxia, Loss of tissue, Tumors (sarcoid = fibroblastic tumor, wound in this area will behave differently), Cutaneous habronemiasis, Phytiosis (fungal involvement)

Wound healing depends strongly on location:

• Head wounds → generally heal well because of good blood supply.

  • Eyelid → gentle debridement + suture

  • Lip/tongue → suture; severe tongue injury may require partial amputation

  • Nostrils → careful layered closure

  • Ear → suture soft tissue, not cartilage

• Neck, trunk & proximal limbs → may include lacerations, punctures and burns; treat according to wound type with cleaning/debridement, analgesia ± antimicrobials/supportive treatment.

• Distal limb wounds → poorer healing because of lower temperature/blood supply, contamination, movement and tension. Particularly important complications:

  • Tendon laceration

    • Extensor → partial injuries may heal conservatively; complete injuries may require suturing/support.

    • Flexor → repair + strong immobilization/support.

  • Digital tendon sheath penetration → risk of septic tenosynovitis → lavage + drainage ± systemic/local antibiotics.

  • Joint penetration → risk of septic arthritis/synovitis → lavage + intra-articular/systemic antibiotics + immobilization as indicated.

🩹 Methods of Wound Management

1⃣ Primary closure/healing (First intention healing)

• Union of tissue by sutering wound margins

• Minimal granulation tissue, desired type of healing, often very good outcome

• Clean and non-infected

• Sutured during golden period = 6–8 h (know on state)

• Signs not to: inflammation, swelling, exudate formation

• Preparation: Hemorrhage control, hair removal, clean, wound debridement (remove necrotic tissue), lavage (saline, lactated ringer´s, hydrogen peroxide)

2⃣ Secondary intention healing

• Left unsutured

• Heals via contraction + epithelialization

• Contraction begins after the lag phase (mainly by myofibroblasts)

• Done with wounds that:

  • Have lost tissue and/or are infected

• new epithelium is visible after ca 2weeks after injury on extremities, it grows at rate 1-1.5mm/10 days

• control with: counter pressure (bandage/cast), immobilisation, antimicrobials, topicals

3⃣ Delayed primary closure

• Apposition after golden period

• Before granulation tissue → 4–5 d

• Sutured when ready for primary closure

4⃣ Delayed secondary closure

• Closure after granulation tissue formation

5⃣ Grafting

• Used in wounds that are too large to heal or cannot be sutured

• Pedicle graft

• Free graft (full-thickness, split, sheet graft, island graft (pinch, punch/biopsy punches)

🚑 Initial Wound Treatment

🎯 Goal: Decontaminate the wound as much as possible and prevent further contamination.

• 💧 Flush/lavage with saline

• ✂ Sharp debridement of gross contaminants

• 💊 Local antiseptics or ATBs packed into wound to prevent further contamination

• 🦴 Limb immobilization according to injury

• 🩸 Pressure bandage applied directly over bleeding area to control hemorrhages

🔄 Stages of Wound Healing

1⃣ Inflammatory phase

⏱ 2–3 days after wounding

• Increased permeability

• Fibrin depositis and WBC (first neutrophiles)

• later in distal extremities

⬇

2⃣ Debridement phase (lag phase = debridement + inflammation phase. KNOW ON STATE)

⏱ Within 6–8 hours of injury

• Macrophages (made from monocytes) move into wound

• Remove debris

• Induce fibroblasts and cytokines

• Stimulate fibroplasia + angiogenesis

⬇

3⃣ Repair phase (fibroblastic/proliferative phase)

• Formation of granulation tissue

• Fibroblasts and blood vessels start to appear in the lesion by day 3 (fibroblasts are crucial for ct formation)

• Epithelial cells move from the wound edges across the granulation tissue (this is what we want)

⬇

4⃣ Remodelling/maturation phase

⏱ Begins 2 weeks after wounding → 6–12 months later

• wound contraction, granulation tissue and collagen production diminishment, collagen cross-linking → scar formation

🧠 Remember:
Inflammation → Debridement → Repair → Remodelling

🧼 Wound Preparation

1⃣ First treatment – Active immunization

💉 TAT = immunoserum tetanus

• Dosage: 4000–6000 IU (13–20 ml)

2⃣ Anaesthesia / sedation

3⃣ Preparation of wound environment

• Shave the area

• Clean wound with antiseptic soap

4⃣ Surgical debridement

🩸 Living tissue bleeds → dead tissue does not bleed

Can be done:

• Mechanically

• Dakin's solution → less discomfort

Mechanically:

• Cut new edges for wound

• Excise grossly non-viable or damaged skin with scalpel

⚠ If wound contains devitalized tissue or debris → wound should be left open:

• Secondary intention healing OR

• Delayed primary closure

5⃣ Lavage (flushing) of wound

💧 Sterile saline or electrolyte solution

Application under pressure:

• Betadine

• Chlorhexidine
  → antimicrobial activity

6⃣ Wound revision

• Palpation and control of wound for foreign objects

• Sterile gloves and probes

• X-ray examination?

• Bandaging

• Corticosteroid ointment?

• Honey?

🩹 Wound Dressings

Wounds on dorsal and palmar surface of fetlock, tendons and ligaments
➡ Fixation bandage (cast)

Functions of wound protection/bandaging

• 🛡 Protective

• 💧 Absorption

• 🩸 Compression

• 🦴 Stabilizing

🧻 Wound Covering

Types

• Biological → skin grafts

• Synthetic → semi-permeable, impermeable or permeable

1⃣ Underlying materials

• Bandage cotton wool / padding

2⃣ Bandage

• Elastic flexible cohesive bandage

• Plaster padding

• Cast

3⃣ Cast – fixation bandage

• Cast bandage embedded in polyurethane resin

• Hard and solid after 20–30 minutes

• ⭐ Radiolucent! Important for X-ray controls

🧩 Skin Transplant

Used for wounds that are healing unsatisfactory or not at all.

Preparation

• Clip

• Shave

• Disinfection

• ATB ointments + bandage for 3 days

💉 Sedation / anaesthesia

• Butorphanol

• Detomidine

• TIVA

Types

• Pinch grafting

• Punch grafting

• Meshing grafts

• Full-thickness sheet grafting

📍 Donor sites

• Ventrolateral part of abdomen

• Lateral shoulder area

• Cranial area of chest

• Side parts of neck

💧 Wound Drainage

Deep wounds → dead space → accumulation of secretion → bacterial growth → disturbed healing process

Types of drains

Passive:

• Penrose

• Tubular

Active:

• Closed suction systems

• Open suction systems

5. Second Intention Healing Wounds in Horses

Second intention healing = wounds left un-sutured to heal by second intention.

Indications:

Wounds that

• Have lost tissue

• Are infected

• Are susceptible to infection

🔄 Two mechanisms of healing

1. Contraction

2. Epithelization

➡ Both dependent on formation of granulation tissue.

🧼 Treatment

• 💧 Decontaminate/flush wound by lavage saline solution

• ✂ Debridement:

  • Mechanically → cut new edges or scrape off dead tissue

  • Dakin's solution → less discomfort

• 🧩 Skin grafting if needed

• 🍯 Apply topical ointment → Manuka honey (also aid in debride)

• 💊 Topical ATB → silver sulfadiazine

• 💧 Wet dressing with antiseptic → moisture + low pH

• 🩹 Bandage or cast

• 💊 NSAIDs

🔄 Stages of Second Intention Healing

1⃣ Wound Expansion

• Right after a wound is made, the wound enlarges from retraction of the surrounding skin.

• Wounds on the distal limb of horses may expand for 11–13 days before contraction begins.

⬇

2⃣ Granulation Tissue Formation

⏱ Appears 3–6 days after injury.

Granulation tissue provides:

• 🧱 Surface for migration of epithelial cells

• 🦠 Barrier for infection

• 🔄 Myofibroblasts for contraction

• 🧬 Fibroblasts for collagen formation

⚠ There is more granulation tissue in leg wounds VS other places on the body, because of the blood supply and lack of muscles on legs.

Factors promoting formation:

• Larger body size

• 📍 Location → distal portion of limbs, mobile areas

• 🌡 Environment → moisture, warmth, low pH, low O₂ tension

• 🍯 Topical medication → honey, scarlet oil

⬇

3⃣ Epithelization

Epithelialization = the first signs of reparation.

• Formed from the edges of the wound

• Migrating epithelium moves beneath the clot that covers the wound

• Can be seen at about 2 weeks after wounding

• More prominent in distal part because of big skin tension

Factors increasing rate

• 🔥 Heat

• 🫁 Increased tissue oxygenation

• Hyperbaric oxygen therapy

• 💧 Moisture

• 💊 Topical medication

➡ Therefore use:

• 🩹 Bandaging or casting

• 💧 Wet dressing

• 💊 Silver sulfadiazine

Factors decreasing rate:

• 🦠 Infection

• Necrotic tissue

• Exuberant granulation tissue

• Glucocorticoids

• Changing bandage too often

⬇

4⃣ Contraction Phase

Contraction = wound closure by active shrinking/reduction of the wound, by pulling the surrounding tissue centripetally.

• Contraction begins after the lag phase

• ⚠ Wounds distal to the carpus and hock/tarsus are not capable of significant contraction

Factors inhibiting contraction:

• Hypovolemic anemia

• Hypoalbumin

🧠 Remember the order:

1⃣ Expansion → 2⃣ Granulation → 3⃣ Epithelization → 4⃣ Contraction

EXPAND → FILL → COVER → SHRINK

Equine hernias

Hernia = a protrusion of an organ, or part of it, through a defect in the wall of the anatomical cavity in which it normally resides.

Most are reducible, but in some cases the contents of the hernia cannot be returned to their normal location due to:

• Incarceration

• Strangulation

• Adhesions

📚 Classification

🔹 Origin

• Congenital or Acquired

🔹 Direct vs. indirect

• Direct hernia → occurs through a tear

• Indirect hernia → occurs through a natural passage (inguinal canal, umbilicus)

🔹 External vs. internal

1. External hernia → occurs through the body wall producing a visible and palpable swelling covered by skin.

Examples:

• Umbilical, Inguinal/scrotal

• Traumatic abdominal wall hernias, Ventral

• Incisional hernias

2. Internal hernia → within the abdominal cavity.

• hernia where abdominal viscera protrude through a ring, rent, or aperture located entirely within the abdominal cavity, example:

• Epiploic foramen, Mesenteric, Diaphragmatic, Omentum, Mesocolon, Gastrosplenic ligament, Hepatogastric ligament, Hepatoduodenal ligament, Ductus deferens

⚠ Incarcerated vs. Strangulated

🟡 Incarcerated hernia

• Passage of ingesta through the protruding loop of intestine is arrested.

• Blood flow in its wall is maintained.

🔴 Strangulated hernia

• Both irreducible + incarcerated, AND blood circulation is also arrested ➡ Results in gangrene unless speedy relief is given.

🧠 Remember:
Incarcerated = contents blocked
Strangulated = contents + blood blocked

Umbilical Hernia

More common in fillies (young female horses) and may be hereditary.

Causes:

• Congenital: Present at birth, Failure of abdominal wall to close

• Acquired: Develop at 3–4 weeks of age, Excessive straining to defecate/urinate, Umbilical infection

Hernial sac comprises:

• Inner peritoneal layer

• Outer layer of skin

• Linked by connective tissue

May contain:

• Small intestine, Cecum, Omentum

⚠ Incarceration and strangulation of herniated intestine is rare!

🔍 Clinical signs

• Typical oval swelling in umbilical region

• Intestine or omentum inside

• Size varies

• Tense, painful swelling → irreducible

🔎 Diagnosis

Palpation of hernia:

• Can it be reduced/put back into abdomen?

• Check hernial ring → size, shape, rigidity

💊 Treatment

Conservative:

• Bandages, Metal clamps, Rubber rings

• Cheap but dangerous

⏳ Smart to wait with surgery until foal is 6–12 months old, because it can disappear by itself.

Surgical:

• GA and Dorsal recumbency

• Elliptical skin incision around hernia

• From here either open hernial sac but not peritoneum and push sac inside, followed by suturing the muscle or remove hernial sac by penetrating peritoneum.

• If no damage to hernial sac/intestine → can be returned to abdominal cavity, but chance of re-herniation

• Resection of hernial sac is the better option

• Suture ring with continuous suture pattern overlapping mattress

Inguinal Hernia

1⃣ Intravaginal (untrue scrotal) hernia in foals

Frequent problem in foals.

➡ Internal inguinal ring is very wide for passage of testes in scrotum up to 6 weeks of age.

➡ Small intestines can pass this ring and canal → enters vaginal process.

🔍 Clinical signs

• Asymmetric scrotum

• Possible to palpate testicles and distal intestine

🔎 Diagnosis

• USG → intravaginal dislocation of intestine

• Possible to reposition

💊 Treatment

• Reposition intestine until inguinal ring gets smaller

• Check every day

• Reposition if it falls back

• Check by palpation for signs of strangulation

➡ Often resolves spontaneously by 3–6 months old.

➡ Application of a truss/bandaging may hasten resolution.

2⃣ Intravaginal (untrue) hernia in adult stallions

Rare, but more dangerous due to narrow inguinal canal → may cause strangulation.

💊 Treatment

Conservative:

• Manual compression of vaginal process

Surgical:

• Laparotomy, Closure of inguinal canal, Resection

• Unilateral castration

• Inguinal surgical approach → expose herniated intestine → reduce intestine back into abdomen → assess viability → resect if non-viable → close/narrow the inguinal ring → often unilateral castration.

Diagnosis (ASKED ON STATE)

• ⚠ Sedate first (stallion + pain/colic can be dangerous!)

• Rectal palpation: palpate the internal inguinal/vaginal ring (cranially and laterally to pelvis). Normally you identify structures of the spermatic cord at the ring; with an inguinal hernia, intestine can be palpated entering the inguinal ring/canal.

• Transrectal USG → identify intestine entering the inguinal ring and assess the entrapped bowel.

• External/scrotal examination + USG can show unilateral scrotal enlargement/intestine.

3⃣ Extra-vaginal (true scrotal) hernia

➡ Rupture of vaginal process

➡ Intestine is in the cavum scroti + traumatisation of serosal surface.

🔍 Clinical signs

• Enlargement of scrotum

• Continuous enlargement

🔎 Diagnosis

• Subcutaneous localisation of intestine in scrotum

• USG shows black Olympic rings filled with fluid above strangulation.

• Growing enlargement of scrotum

• Colic

🚨 Treatment

SURGERY IMMEDIATELY!!

• Bilateral castration

• Ligature of processus vaginalis

• Close external inguinal ring with suture

4.Inguinal rupture (direct inguinal hernia)

• is a herniation through a tear in the peritoneum and abdominal musculature close to vaginal ring which lies subcut in inguinal/scrotal region. Surgery.

Ventral Hernia

= Hernia coming through any part of the abdominal wall other than umbilicus or inguinal canal.

Causes

Mainly seen in mares after:

• Perforation of abdominal cavity from kicks

• Rupture of prepubic ligament

Traumatic:

• Kicks

• Collisions with blunt objects

• Halfway-jump over straddling gates

• Traumatic lateral abdominal hernias: along costal arch, ventral midline, and low flank

Incisional/postoperative:

• Improper closure of incision

• Tearing of sutures or sutured tissue

• Postoperative wound infection

🔎 Diagnosis

Signs of:

• Depression

• Abdominal discomfort

• Cessation of defecation → indicates intestinal obstruction

⚠ Important to differentiate from an abscess:

• Palpate swelling

• Rectal palpation

• Ultrasound

• Exploratory surgery

💊 Treatment

Surgery
➡ Reposition intestine → reconstruct and close abdominal wall.

🫁 Diaphragmatic Hernia

Can be:

• Congenital

• Acquired → fractured ribs, dystocia, trauma

🔍 Clinical signs

• 🚨 Violent intermittent colic

• 🫁 Respiratory distress

🔎 Diagnosis

• X-ray

• USG

• Absence of lung sounds

• Intestinal sounds in chest

• Sanguineous fluid in thoracocentesis

💊 Treatment

Surgical repair

• Primary technique OR Mesh technique

🧠 Quick Overview

🐴 Equine hernias

Umbilical → young foals → often resolves spontaneously

Inguinal – foal → intravaginal → intestine enters vaginal process → often resolves by 3–6 months

Inguinal – adult → intravaginal → strangulation risk → unilateral castration

Extra-vaginal → rupture of vaginal process → 🚨 immediate surgery + bilateral castration

Ventral → trauma/incision → reconstruct abdominal wall

Diaphragmatic → colic + respiratory distress → surgical repair

Stallion castration

Castration = surgical removal of the testis.

• Performed at any age

• Most commonly at 12–18 months old

📌 Indications

• Remove masculine behaviour and management problems

• Trauma, Testicular neoplasia, Inguinal herniation, Torsion of the spermatic cord, cryptorchidism

Preoperative actions; starvation for 8-10h if GA, tetanus prophylaxis, maybe ATB, NSAIDs, physical exam → descended testicles, herniation, etc.

🔪 Procedure – Three ways

1. Closed

➡ Amputate whole vaginal process (do not open vaginal tunic)

2. Open

➡ Incision through vaginal process (both layers)

3. Semiclosed

• open tunica vaginalis, then closing it after

🐴 Standing Castration

⭐ Preferred by Zert For stallions up to 1 year old.

✅ Advantages

• Popular method, Easy, Quick

• Less assistance, Less space

• Avoid risk of recumbency and recovery

💉 Sedation

• Alpha2 agonist + opioid: Xylazine / detomidine + Butomidor

💉 Local anaesthesia

• 2% procaine

• S.C. incision

• 20 ml 2% procaine intratesticular

• 10 ml in spermatic cord

⚠ No need for suture material → cannot be done aseptically.

➡ Only use an emasculator. Possible to ligate.

• Often using open method

Recumbent Castration

💉 General Anaesthesia

• Xylazine, Ketamine, Diazepam

💉 Local anaesthesia

• Procaine: S.C., Intratesticular, Spermatic cord

Castration methods

• Standing or recumbent, open, closed or semi-closed method. Scrotal or inguinal approach

1. Open castration

• Parietal vaginal tunic is opened, and the testicle is exposed, the spermatic cord is uncovered

Procedure:

• Scrotal skin incision → tunica dartos/fascia → open parietal vaginal tunic → exteriorize testicle → transect caudal ligament of epididymis → separate/perforate mesorchium → expose spermatic cord → emasculate the uncovered cord.

• The spermatic cord may also be both twisted and ligated for additional hemostasis.

• The scrotal incision can then be left open for drainage and secondary intention healing, which is common, or closed under appropriate sterile conditions.

⚠ Open does NOT mean that the skin must remain open.
It means the vaginal tunic was opened!!

2. Closed castration

• The parietal vaginal tunic is not opened. The testicle remains enclosed within the tunic. The spermatic cord is covered.

Procedure:

• Scrotal or inguinal incision → dissect fascia away from intact parietal vaginal tunic → exteriorize testicle still covered by tunic → isolate the covered spermatic cord → ligate and/or emasculate the entire cord together with the vaginal tunic → remove testicle.

In closed method you can choose from these methods what to do with the covered spermatic cord:

• Emasculation

• Ligature + emasculation

• Henderson method → twisting/torsion

• Equitwister → twisting/torsion machine

The important sentence:

3. Semi-closed castration

• Testicle is initially isolated while enclosed in the parietal vaginal tunic, but the tunic is then incised and manipulated. The remaining tunic is retained with the spermatic cord during emasculation

Procedure:

• Scrotal incision → exteriorize covered testicle → small incision into parietal vaginal tunic → insert thumb/fingers and manipulate/invert tunic → strip scrotal fascia from spermatic cord → extend tunic incision → emasculate spermatic cord with associated tunic.

• uncovered method: open tunica vaginalis, emasculate and suture the spermatic cord, then do the same with the tunica vaginalis → semi-closed (som vi gjorde i timen)

Scrotal vs inguinal approach

• Inguinal approach: an incision is made over the superficial ring, rather than directly over the scrotum.

With ligation of vessels + closing of abdominal cavity + wound closure

• Can be used in horses older than 1 year

• Safer method for bleeding

• Insurance cover

• Primary healing

• ❌ More expensive

• ❌ Retention of wound secretion

• Done in dorsal recumbency

3 Types of Closed Castration:

1. Uncovered

➡ One ligature on spermatic cord
+
➡ One ligature on vaginal process

(som han gjorde i timen)

2. Covered ⭐ Zert prefers this

➡ One ligature around spermatic cord + vaginal process

⚠ More dangerous as spermatic cord might slip into abdominal cavity and bleed

3. Castration from Regio inguinalis

➡ Resection of vaginal process

• Opening vaginal process

• Ligation of spermatic cord

• Suture of wall of vaginal process

• Suture of skin

OPEN METHOD

Without ligature

• Recumbent castration

• Without closure and ligation

• Done with emasculator or twisting

• ➡ Stops the bleeding

Spermatic cord can be:

• Uncovered

• Covered

🔧 Emasculators

• Sandy

• Henderson

🔄 Twisting method

Henderson method + Equitwister

➡ Castration by machine and torsion of testicle
➡ Torsion of whole proc. vaginalis
➡ Closure of abdominal cavity

Mechanical twisting of the entire spermatic cord proximal to the testis (15–25 rotations) using a specialized drill-attached clamp until the cord severs.

Major post-operative complication: Bilateral evisceration of abdominal contents due to lack of a suture ligature on the open vaginal ring.

🩹 Scrotal Healing

1⃣ Secondary intention healing – MOST COMMON

• Common to stretch the incision to help post-operative drainage

• Ensure excess fascia is trimmed

2⃣ Primary intention healing

• With absorbable sutures

• If performed under sterile conditions

• Requires adequate hemostasis

• ⬇ Decreases risk of post-operative complications

Postop care

• → 2-3 weeks of healing.

• If open method one should restrict activity and of closed method one should confine horse to stall for 2 weeks and monitor closely.

• Do 15 minutes of exercise twice daily, starting 24h after surgery, to prevent preputial and scrotal swelling (edema).

• Tetanus prophylaxis, systemic IM procaine penicillin for 3–5 days, and IV/oral NSAIDs (e.g., flunixin or phenylbutazone) for 1–3 days.

⚠ Complications

1.🩸 Haemorrhage

➡ Grasp and re-crush with emasculator for >30 mins

Usually due to:

• Improper tying before removal of emasculator

• Cord was too large

• Too hard exercise of horse before castration

2. Evisceration

➡ Prolapse of intestinal or omental contents → must do laparotomy

• predisposing factors: Pre-existing wide superficial/deep inguinal rings, increased intra-abdominal pressure, slippage of cord ligatures, or unclosed open castration in draft breeds/older horses.

3.💧 Oedema

➡ Due to insufficient exercise after surgery or to short incision → give NSAIDs and drainage

4.🦠 Septic funiculitis

➡ Infection of remaining cord stump due to:

• Contaminated emasculator

• Ligature (using un-asbsorbable suture)

• → Give doxycycline and NSAIDs

• Poor wound drainage

5.🦠 Clostridial infection

➡ Tetanus (give penicillin)

6.🦠 Septic peritonitis → doxycycline and NSAIDs

7.⚠ Penile damage ➡ Uncommon

8.💧 Hydrocoele ➡ Idiopathic, painless, fluid-filled enlargement of the parietal tunic following open castration→ scrotal swelling

9.🐴 Persistent masculine behaviour ➡ Caused by improper castration resulting in retention of epididymal tissue, or failure to recognize and remove a cryptorchid testicle

10. Colic

🧠 Quick Overview

STANDING 🐴
→ Up to 1 year
→ Alpha2 agonist + opioid + local procaine
→ Emasculator
→ ❌ No suture
→ Secondary healing

RECUMBENT – CLOSED 🛏
→ Older than 1 year
→ Ligation + closure
→ Primary healing
→ Uncovered / Covered / Regio inguinalis

RECUMBENT – OPEN 🔴
→ No ligature
→ Emasculator or twisting
→ Uncovered or covered

🐴 Stallion castration — methods

OPEN

• No ligatures/closure.

• Emasculator or twisting controls bleeding.

• Scrotal wound left open → secondary intention.

CLOSED – 3 methods:

1. Uncovered

   • Open vaginal tunic → expose spermatic cord.

   • Cord: twist → emasculator → ligature/suture.

   • Vaginal tunic: twist → emasculator → separate ligature/suture.

   • 🧠 Two structures → two ligatures.

2. Covered

   • Cord remains covered by vaginal tunic.

   • Deal with them together.

   • One ligature around cord + vaginal process.

   • 🧠 One package → one ligature.

3. Regio inguinalis

   • Approach through inguinal region.

   • Resect vaginal process.

   • Ligate spermatic cord.

   • Close vaginal process + wound.

🧠 Memory

OPEN = no ligature, leave open

CLOSED:

• Uncovered = TWO separately

• Covered = ONE together

• Inguinal = approach from groin

8. Diagnosis and Castration of Cryptorchids

Cryptorchidism = failure of both or one of the testes to descend into the scrotum.

• Can be unilateral → usually still fertile

• Can be bilateral → usually sterile

• Left testicle most commonly affected

• If testicle has not descended by 3–4 weeks of age → unlikely to descend

• Doesn’t count as cryptorchid until 2 years old

🧬 Etiology

Hereditable:

• Genetics

• Improper gubernaculum function

• Too large testis to pass through inguinal canal

Hormonal:

• Inadequate stimulation of androgen or testosterone

⚠ These stallions should not be used for breeding.

📍 Types of Cryptorchidism

1⃣ Complete abdominal cryptorchidism

➡ Both epididymis + testis are within the abdomen

2⃣ Incomplete abdominal cryptorchidism

➡ Epididymis has descended into the inguinal canal, but testis remains in abdomen

3⃣ Inguinal cryptorchidism

➡ Epididymis + testis have descended into the inguinal canal, but NOT into scrotum

Also called “high-flankers.”

🔍 Diagnosis

1. History

• Is the horse castrated earlier?

2. Rectal palpation of inguinal rings

No structures in inguinal region
➡ Cryptorchidism is completely abdominal

Vessels in inguinal region
➡ Cryptorchidism is inguinal or incompletely abdominal

3. External palpation

• Give sedatives to relax m. cremaster → easier to palpate

• Can always palpate it in case of inguinal cryptorchidism

4. USG

➡ Typical homogenic echogenic appearance

5. Hormonal assays

• Testosterone concentration (hCG stimulation test)!! → Administration of hCG causes a significant rise in serum testosterone levels if functional testicular tissue is present. Measure testo before and after!

• Blood: ⬆ Anti-Müllerian hormone → from Sertoli cells in cryptorchid testes, ⬇ Testosterone

• Urine: Estrogen

✂ Treatment

➡ Surgical removal of BOTH testes under general anaesthesia

⚠ Always locate and remove cryptorchid testicle FIRST.

If you cannot find the testicle:
➡ Send horse to professional clinic → you will only ruin the situation for other vet.

Surgical method depends on location of testicle.

Other options:

• Laparoscopic surgery

• Immunological castration

💉 Immunological castration

Immunization against luteinizing hormone-releasing hormone (LHRH)

➡ Decreases serum concentration of testosterone
⚠ Variable result

🔪 Methods of Surgery

⭐ Zert's approach:

Open abdominal cavity close to the prepuce and remove both testicles from one operation wound.

1⃣ Inguinal Approach

📍 Used for:

• Inguinal

• Incomplete abdominal

Procedure

• Dorsal recumbency → Incise under inguinal canal → Cut rectus abdominis → Locate vaginal process from gubernaculum → Incise vaginal process to locate testicle and epididymis → Find proper ligament of testis → Pull testis through vaginal ring → Suture superficial inguinal ring with absorbable suture ➡ Prevents evisceration

2⃣ Para-inguinal Approach

📍 Used if inguinal method didn't work.

• Incision several cm medial to inguinal ring

• Incision between raphe scroti and left leg

• Incision in the aponeurosis of the external abdominal oblique muscle, parallel and several centimeters medial to the superficial inguinal ring.

  

3⃣ Paramedian Approach

📍 Used in abdominal cryptorchidism

Procedure

Skin
⬇
Subcutis
⬇
External fascia flava abdominis
⬇
Aponeurosis of oblique abdominal muscle → cut
⬇
Rectus abdominis → separate fibers with finger
⬇
Transverse fascia + peritoneum → perforate
⬇
✋ Introduce hand into abdomen
⬇
🥚 Locate + remove testicle
⬇
Ligature
⬇
Reposition stump of spermatic cord
⬇
Suture fascia transversalis

⭐ Fascia transversalis = main structure holding abdominal wall

4⃣ Flank Approach

• 10–15 cm incision

• Through skin + subcutis

• Paralumbar fossa of affected side

• Horse can be standing or recumbent

Layers

Skin + subcutis
⬇
Cut external abdominal oblique
⬇
Split internal abdominal oblique
⬇
Split transversus abdominis
⬇
Cut peritoneum
⬇
🥚 Locate + remove testis

5⃣ Laparoscopic Approach

• Minimally invasive

• Requires expensive equipment

• Dorsal recumbency in the Trendelenburg position (head tilted down, pelvis elevated).

Procedure

1. Distend abdomen with gas

2. Insert camera through umbilical region

3. Locate testicle(s) around vaginal ring

4. Remove testicle(s)

Dorsal recumbency in the Trendelenburg position (head tilted down, pelvis elevated).

🩹 Post-operative Care

• Stall rest 7 days

• Lead walking only

• Exercise gradually resumed over 10–14 days

• External sutures removed 7 days post-op

• give NSAIDs for 5 days, ATB for 7-10 days (trimetoprim sulphonamide)

After laparoscopy

➡ Less invasive
➡ Resume activity after first 72 hours

⚠ Complications

Rare, but include:

• Anaesthetic complications

• 🩸 Excessive haemorrhage

• Evisceration

• Bowel damage

• 🦠 Infection

• Post-op swelling

• Incision breakdown

• Continued stallion behaviour

🧠 MOST IMPORTANT TO REMEMBER

📍 Where is the testicle?

Complete abdominal
➡ 🥚 Testis + epididymis = ABDOMEN

Incomplete abdominal
➡ 🥚 Testis = ABDOMEN
➡ Epididymis = INGUINAL CANAL

Inguinal
➡ 🥚 Testis + epididymis = INGUINAL CANAL

🔪 Match location → surgery

Inguinal/incomplete → 🔪 Inguinal approach

Can't access by inguinal → 🔪 Para-inguinal

Abdominal → 🔪 Paramedian / flank

Abdominal, minimally invasive → Laparoscopy

Committee questions:

Diagnosis — VERY HIGH YIELD

• External + rectal palpation of inguinal rings/canal.

• For rectal: sedation + Buscopan was specifically asked.

• USG → retained testicle described in these reports as round/hyperechoic with a central vessel.

• Blood: AMH.

• Urine: estrogen.

• ⭐ hCG stimulation test → they repeatedly care about this:
  test testosterone before → give hCG → test testosterone after.
  Increase indicates functioning testicular tissue.

• Used particularly when deciding castrated gelding vs retained testicular tissue.

Hormones

• Testosterone → produced by Leydig cells.

• If they ask control:
  Hypothalamus GnRH → pituitary LH → Leydig cells → testosterone.
  ⚠ Don't say GnRH comes from pituitary—the Oct 2023 report phrases this incorrectly.

Surgical approaches
Know the names:

• Inguinal → especially inguinal/incomplete abdominal cryptorchid.

• Parainguinal

• Paramedian

• Flank

• Laparoscopy

⭐ Complete abdominal cryptorchid: they particularly asked about paramedian approach and the muscle layers, so know the layers from your notes.

Laparoscopy — only mention if prepared for follow-ups
October 2025 examiner immediately followed it with:

• 3 incisions/ports

• camera

• instruments

• gas/insufflation

• CO₂

• Ligasure → hemostasis

• advantages → faster recovery, fewer complications/less hemorrhage.

Equine laparotomy

Laparotomy = incision into the abdominal cavity, usually in the case of life-threatening gastrointestinal abnormalities.

Exploratory laparotomies can also be performed to address:

• Reproductive issues

• Lesions in other organs in the abdominal cavity

Upon incising the peritoneum, assess:

→ The color and character of peritoneal effusion,

→ The pattern/distribution of distended bowel

→ Any gross discoloration of visceral or peritoneal surfaces.

• Gas/fluid filled bowel may need to be decompressed before continuing

→ Large intestine: use needle to decompress

→ Small intestine: strip content into cecum in simple obstructions or do enterotomy

• Keep intestines warm and moist with Hartmann’s solution during laparotomy (warmed sterile isotonic saline)

• Monitor, give ATB and IV fluids post op, also look for incisional swelling, herniation and evisceration post op.

📌 Indications

• 🐴 Colic → diagnose exact cause of colic when obstructing lesion requires surgery

• No exact diagnosis, but enough evidence that surgery is required to save the horse's life

• No response to treatment of colic (persistent severe pain)

• Recurrent colic over a period of days or weeks

• Obstruction

• Neoplasia

🔪 Different Ways to Open the Abdominal Cavity

1⃣ Inguinal

• Rectus abdominis muscle is cut

• Does not alone allow a thorough exploration and decompression of the non-herniated bowel

• Used in conjunction with ventral midline incision

📌 Used for:

• Stallions with inguinal or scrotal hernia

• Cryptorchid (inguinal and incomplete abdominal) castration

2⃣ Parainguinal

• Incision located cranially to the external inguinal canal

• Rectus abdominis muscle is cut

3⃣ Flank

🐴 Standing approach

📌 Most common for:

• Small colon

• Nondistended large colon

• Uterine torsion

🔪 Incision

Made in a vertical line midway between:

Last rib ↔ Tuber coxae

➡ Starting dorsal → continuing ventral

Layers

Skin
⬇
🔪 External abdominal oblique → sharply divided
⬇
Internal abdominal oblique → bluntly divided parallel to fibers
⬇
Transverse abdominal muscle → bluntly divided parallel to fibers
⬇
🔪 Peritoneum punctured
⬇
Abdominal cavity

🧠 Muscles involved

• External abdominal oblique

• Internal abdominal oblique

• Transverse abdominal muscle

🪡 Closure

Closure is done for 3 layers:

• First two layers of muscles → appositioned and sutured with absorbable material

• Skin → sutured or stapled

4⃣ Paramedian

📍 10 cm lateral to the midline

• Incision on either right or left midline

• Through tunica flava abdominis and rectus abdominis muscle

⚠ Careful to avoid:

• Deep epigastric vessels

• Superficial epigastric vessels

🪡 Closure

➡ Suture external fascia of rectus abdominis sheath

5⃣ Ventral Midline ⭐

⭐ Mostly done in linea alba in case of colic

➡ Allows complete revision of abdominal cavity

Indication: Surgical colic, urolith removal, ovariectomy, and caesarean section

📏 Incision

• Small intestine → 15 cm

• Large intestine → 60 cm

🔪 Approach

Initial incision made accurately in midline → Through linea alba → Extending cranially from umbilicus → Open peritoneum → Enter abdominal cavity

🔍 When opening the peritoneum, assess:

• Color and character of any effusion, Distribution/pattern of distended bowel, Discoloration of visceral surfaces, Discoloration of peritoneal surfaces

🪡 Closure

⚠ Do NOT include peritoneum → causes more irritation/inflammation → adhesions

1⃣ Linea alba

• Suture 1 cm from wound edge

• Simple continuous suture

⬇

2⃣ Subcutaneous tissue

⬇

3⃣ Skin

• Ford interlocking suture, Prolene

→ A wound stent or incise drape is applied, followed by removal after 12 hours and placement of an abdominal bandage

🧠 Quick Overview

Approach	📍 Location	⭐ Main use
Inguinal	Inguinal region	Inguinal/scrotal hernia, cryptorchid
Parainguinal	Cranial to external inguinal canal	Alternative inguinal access. crypto, ovariectomy, inguinal hernia.
Flank	Between last rib + tuber coxae	Standing; ovariectomy, uterine torsion, small colon surgeries, impaction, rectal tear.
Paramedian	10 cm lateral to midline	Through rectus abdominis. colic, crypto, cystotomy.
Ventral midline ⭐	Linea alba	Colic + complete abdominal exploration

🧠 Most important:

COLIC → VENTRAL MIDLINE → LINEA ALBA → COMPLETE EXPLORATION

⭐ Approaches + what you cut

Approach	Important layers
Ventral midline / median	Linea alba → peritoneum
Paramedian	Rectus abdominis → peritoneum
Inguinal	Rectus abdominis
Parainguinal	Rectus abdominis
Flank	External oblique → internal oblique → transversus abdominis → peritoneum

Which approach for what?

• Ventral midline → most common for colic/exploratory laparotomy; report also mentions removal of uroliths.

• Inguinal → cryptorchid surgery, particularly inguinal/incomplete abdominal cryptorchid.

• Flank → know the approach/layers; the March 2023 report suggests Zert may ask about an important fascia flavis? here.

🚨 When does a colic need laparotomy?

Think:

• Severe/persistent pain despite analgesia + diagnostic findings suggesting surgical lesion.

Can assess:

• Clinical signs/pain

• Rectal examination

• Nasogastric reflux

• USG

• Abdominocentesis

• Bloodwork

⭐ Lactate was specifically asked.

↑ Lactate = tissue hypoperfusion/hypoxia, especially important with strangulated/ischemic intestine.

🧠 Persistent severe pain + ↑ lactate → think ischemia/strangulation → surgery

Equine enterotomy

Enterotomy = the surgical incision into the intestinal lumen.

Commonly performed in:

• Jejunum, Cecum, Small colon

📌 Indications for Enterotomy

• Remove foreign bodies → commonly in right dorsal colon:

  • Enteroliths, Fecoliths, Bezoars

• Removal of fluid and ingesta

• Right and left dorsal displacement

• Parasitic infestations → Ascarid larvae in small intestine

• Ileum and cecum → obstruction and impaction

• ⭐ Pelvic flexure enterotomy → most commonly performed, for evacuation of sand or feed impactions of the large colon, enteroliths, and colonic volvulus.

• Right ventral colon enterotomy → access cecum in cases of cecocolic intussusceptions

• Colonic volvulus → pelvic flexure enterotomy

• Small colon strangulation → pelvic flexure enterotomy to release ingesta

💉 Surgical Preparation

💊 Pre-medication

• Broad-spectrum peri-operative ATB

• Anti-inflammatory medication → Flunixin

🍽 Dietary

• Fasted if possible

• ⚠ Majority of cases are emergent

🔪 Procedure

1⃣ General anaesthesia ➡ Horse is put under GA

2⃣ Midline laparotomy ➡ Abdomen opened using midline laparotomy

3⃣ Secure bowel ➡ Fix with Forceps OR Stay suture

4⃣ Incise intestinal wall

➡ Longitudinally
➡ Antimesenteric side

5⃣ Limit spillage of intraluminal fluid

• Aspirate intraluminal fluid OR

• Restrict flow using extraluminal digital pressure

6⃣ Remove the problem

➡ Remove luminal obstruction / fix whatever problem / do the job

7⃣ Lavage

💧 Lavage bowel with sterile saline

8⃣ Close

🪡 One- or two-layer suture technique:

• Synthetic absorbable

• Cushing or Lambert

• Minimal inversion of serosa

• First layer with Cushing’s or lambert and 2nd layers appositional + inverting

➡ Staple closure with thoracoabdominal (TA) stapler

COLON Enterotomy

📍 Common locations

• ⭐ Pelvic flexure

• Left dorsal → cecocolic intussusception

• Right dorsal colon → enteroliths

• Most common sites: pelvic flexure, cecal apex, descending colon (small colon), right dorsal colon

Procedure

• Incision on antimesenteric side when possible

• Large colon is exteriorized

• Placed on a colon tray:

  • On left side OR Caudally between horse's hind legs

  • and isolated with sterile drapes

💧 One hose → inserted into colon
💧 Another hose → continuously lavages serosal surface

How is luminal fluid and ingesta evacuated during a pelvic flexure enterotomy?

→ A full-thickness stab incision is extended longitudinally (ca. 10 cm), and water hoses are used to flush and siphon out content into a receptacle.

🪡 Closure

• Thorough lavage of the enterotomy site and surrounding bowel with several liters of sterile saline BEFORE first suture layer

Two layers:

1⃣ Simple continuous
⬇
2⃣ Inverting musculoserosal layer using Cushing or Lambert

➡ Colon rinsed thoroughly with sterile saline
➡ Replaced into abdomen

Post-surgical complications:

1. Peritonitis (due to leakage or contamination)

2. Postoperative ileus / diarrhea

3. Abdominal adhesions

4. Incisional/luminal hemorrhage

SMALL INTESTINE Enterotomy

⚠ Enterotomy in SI should be avoided because closure can produce:

• Adhesion formation and Narrowing (stricture) of lumen

➡ More common to do enterectomy in SI than enterotomy.

📌 Indications

A longitudinal enterotomy on the antimesenteric surface of SI may be indicated for:

• Removal of obstructions

• Impaction with food components

• Foreign material

• Ascarids → anoplocephala, cyathostomin, parascaris equorum

• Empty a segment of distended bowel to facilitate reduction of a strangulation in the epiploic foramen

• Suture in small intestine: A single-layer inverting pattern (Cushing or Lembert) using synthetic absorbable monofilament suture

💧 Prevent adherence of intestinal contents to serosa

Use:

• Constant lavage with warm sterile saline OR

• Precoat site of affection with sodium carboxymethylcellulose

🩺 Aftercare

• Physical Monitoring: every 4h (adult) or 2h (foals) the first 24h

• 💧 Fluid therapy: Give oral fluid 24-36h post op

• Feeding: small amount of food after 48 hours (gradually 24-72h)

• Avoid thrombophlebitis.

• Give domperidone (or lidocaine IV) for SI and metoclopramide for LI → to increase peristaltic movement

• Lidocaine IV ⭐ — commonly used after equine abdominal surgery, especially for postoperative ileus (POI). It has analgesic/anti-inflammatory effects and may promote GI motility.

• Neostigmine — directly increases cholinergic activity → increases intestinal contractions/motility.

• 💊 Analgesia → Peri- and post-operative NSAIDs 3-5 days

• 💊 Antimicrobial → Peri- and post-operative broad-spectrum ATB 3-5 days (penicillin, aminoglycosides)

• other med: laxatives/lubricants

• follow up and evaluation after 30 days

⭐ Most Common Sites of Enterotomy

📍 Cecal apex
📍 Pelvic flexure ⭐
📍 Right dorsal colon
📍 Descending colon

🧠 QUICK MEMORY

ENTEROTOMY = ENTER the intestine

GA
⬇
Midline laparotomy
⬇
Exteriorize + secure bowel
⬇
Longitudinal ANTImesenteric incision
⬇
Remove obstruction / ingesta
⬇
Lavage 💧
⬇
Cushing/Lambert closure 🪡
⬇
Rinse + replace

⭐ Large colon → enterotomy common, especially pelvic flexure
⚠ Small intestine → enterotomy avoided if possible → enterectomy more common

• ⭐ Most common sites:

  • Pelvic flexure — #1

  • Cecal apex — #2

  • Descending/small colon

  • Right dorsal colon has also been asked.

• Cecum: incision specifically at the apex.

• Indications/causes: obstruction/impaction, and examiners specifically asked about left and right dorsal displacement.

• Know which displacement is more common and which is worse — this was directly asked.

• Important complication/progression of displacement → large-colon volvulus.

• ⭐ Closure: 2–3 layers.

  • Simple continuous/interrupted

  • Then Cushing or Lembert

  • Also know inverted/vertical mattress — specifically requested once.

• ⭐ Drugs to restart intestinal motility:

  • Neostigmine

  • Physostigmine

• Small intestine: previous answers emphasize that enterotomy is mainly performed on large intestine; SI may instead require enterectomy.

Enterectomy

Enterectomy = surgical removal of a portion of the intestine.

📍 Commonly:

• Jejunum

• Ileum

📌 Indications

• Any intestine with:

  • Abnormal color

  • Decreased motility

  • Thickened appearance

⚠ Dead jejunum wall:

• Black serosa

• ❌ No pulsation of vessels

• Strangulation → most commonly

• After correction of obstruction which caused secondary vascular damage without return of:

  • Normal color, Motility, Pulsation

Resection of the Small Intestine

📏 Physiological limit of small intestine resection = maximum 8 metres

➡ SI is 18–21 m long

⭐ End-to-end anastomosis is the simplest and most physiologically compatible method.

🔪 Procedure

1⃣ Isolate bowel

• Fluid-filled ischaemic bowel should be isolated with intestinal clamps before manipulation begins.

⬇

2⃣ Select resection sites

• Suitable site proximal and distal to the strangulated bowel

⬇

3⃣ Ligate vessels

• Mesenteric vessels to compromised bowel are double ligated

⬇

4⃣ Transect intestine

• Distal end of gut is transected

• Mesentery incised between ligatures

⬇

5⃣ Cut vessels

• Each vessel is cut

⬇

6⃣ Anastomosis

• Remaining healthy intestine is joined together

• Long end of proximal gap of mesentery is closed when anastomosis is completed

🪡 Closure Alternatives

Use synthetic absorbable monofilament suture material.

A) ⭐ Zert!

Two-layer closure:
➡ Simple interrupted suture pattern in two layers

• Mucosa

• Serosa

B)

1st layer: Simple continuous
2nd layer: Cushing seromuscular suture

C)

Single layer:
➡ Interrupted Lembert sutures

Resection of the Large Intestine

⚠ Large intestinal resection is performed very rarely in horses.

Why?

1⃣ Most obstructions don't require resection

Many obstructions are caused by:

• Displacement with no/minimal interference of blood supply

• Simple obstruction of lumen → e.g. enteroliths

➡ Can usually be relieved by a simple enterotomy.

2⃣ Strangulation may involve too much bowel

If strangulation obstruction is present:

➡ Length of bowel involved may be so great that resection + anastomosis is not considered

➡ Euthanasia

🔗 Anastomosis

Anastomosis = surgical joining of tubular structures (arteries, veins, intestine) together so they can become continuous.

1⃣ End-to-End Anastomosis ⭐

➡ Connects two open ends of intestine together

Intestine:
━━━━✂　✂━━━━
　　　 ↓
━━━━━━🔗━━━━━━

🪡 Suture

• Simple continuous → serosa

• Cushing → seromuscular layer

⭐ Simplest and most physiologically compatible method.

2⃣ End-to-Side Anastomosis

➡ Connects end of intestine to a larger piece

━━━━━━┓
　　　　┃
　　　　┃

3⃣ Side-to-Side Anastomosis

➡ Connects the sides of intestine together

Used for:
➡ Jejunal anastomosis

━━━━━━━
　　↕
━━━━━━━

⚠ Post-operative Complications

• 💧 Leakage of content

• 🕸 Adhesions

• 🚫 Obstruction / stricture

• 🩸 Bleeding

• 🦠 Infection

💊 Post-op Care

• NSAIDs

• ATB

• Stool softener

🧠 QUICK MEMORY

Enterotomy vs. Enterectomy

ENTEROTOMY
➡ ✂ Cut INTO intestine
➡ Remove obstruction/content
➡ Intestine stays

ENTERECTOMY
➡ ✂ Remove a SECTION of intestine
➡ Usually because bowel is dead/damaged
➡ Join healthy ends = ANASTOMOSIS

⭐ Most important sequence:

Strangulation
⬇
🖤 Dead/damaged intestine
⬇
✂ Resection / enterectomy
⬇
🔗 Anastomosis
⬇
⭐ Usually end-to-end

Disorders of teeth exchange and exodontics

Equine dental developmental abnormalities can involve:

• 🔢 Tooth number

• 🦷 Morphology

• 📍 Position in the dental arcades

🦷 Tooth Anatomy

Horses have hypsodont teeth = continue to grow their whole life → 2–3 mm each year.

Tooth divided into:

• Crown → visible

• Reserve crown → hidden in alveolar bone

• Apex/root of tooth

Tooth consists of:

Outer → inner:

• Cementum, Enamel, Dentin, Pulp

Types

• Incisors, Canines, Premolars, Molars

🔢 Numbering System

Two systems:

1⃣ Based on type of teeth

• PM1, M2, etc.

2⃣ Triadan system

🧮 Dental Formula

Deciduous teeth

I 3/3, P 3/3 × 2 = 24

• 12 incisors

• 12 molars

🐴 Permanent teeth

I 3/3, C 1/1, P 3 or 4/3, M 3/3 × 2 = 36–44

➡ Depends on presence of:

• Canines

• P1 = wolf teeth

⏰ Eruption Schedule

• Foals are born with 4 premolars

• ⚠ Critical age = 2.5 years

• Replacement of 12 teeth
  ➡ Can impact food processing, decline performance and cause health problems

Deciduous Teeth

Foals get deciduous teeth at around 6 weeks old.

🦷 Incisors – RULE OF 8 ⭐

• Central → 8 days

• Intermediate → 8 weeks

• Corners → 8 months

🧠 8 days → 8 weeks → 8 months

Premolars

P2, P3, P4
➡ Erupt immediately after birth or within 2 weeks

🐴 Permanent Teeth

Horse has complete set of permanent teeth at 5 years.

🦷 Incisors

All erupted at 4.5 years:

• Central → 2.5 years

• Middle → 3.5 years

• Corner → 4.5 years

🧠 2.5 → 3.5 → 4.5

🐺 Wolf teeth – P1

• 1st premolar

• In maxillary arcades

• Only in some horses

🦷 Premolars

All erupted by 4 years:

• PM2 → 2.5 years

• PM3 → 3 years

• PM4 → 4 years

🦷 Molars

All erupted by 3 years:

• M1 → 1 year

• M2 → 2 years

• M3 → 3 years

➡ Have 2 infundibulum in maxillary arcade

🧠 M1 = 1, M2 = 2, M3 = 3

🦷 Canines

• 4 in stallions

• May not be developed

• Rudimentary

• Erupt around 3.5–5 years

📅 Age Determination of Horse

1⃣ Eruption of teeth

• Presence of deciduous teeth

2⃣ Occlusal surface of lower incisors

• Infundibulum wears away over time

• Gone in central by 8 years

3⃣ Shape of incisors

• Flattened → until 10 years

• Oval → 12–13 years

• Round → 15–20 years

• Triangular → >20 years

4⃣ Angle of incisors

• Young → more vertical/flat

• Older → greater/sharper angle

5⃣ Galvayne's groove

➡ Mark on upper corner incisors that appears and disappears in ageing horse

⚠ Congenital & Developmental Defects

1⃣ Oligodontia

Congenital absence of a tooth germ OR retention and inclusion of a tooth within jaw.

Consequences

Missing tooth →

• Mesial drift

• Tipping of neighboring teeth

• Lack of wear of antagonist

• Dental elongations

• Abnormal mastication

🔎 Diagnosis ➡ X-ray

2⃣ Polyodontia / Supernumerary Teeth

➡ Too many teeth

Can be:

• Retained deciduous teeth

• Supplementary teeth

Often:

• Mandibular premolar

• Maxillary molar

Remnants called “caps.”

Consequences

• Difficulty eating

• Unusual facial development

• Maxillary sinusitis

• Nasal discharge

• Facial swelling

🦷 Developmental Defects

1.Delayed tooth eruption

➡ Due to overcrowding
➡ Usually small breeds with limited jaw space

2.Retained deciduous dentition

➡ Caps retained because of entrapment between adjacent teeth

3.Maleruption / misalignment

➡ Cheek teeth → cause overgrowth of tooth erupting first

4.Dental dysplasia

• Abnormal bending

• Abnormal size

• Double teeth

5.Diastema

➡ Abnormal spaces between teeth
➡ Most common form of periodontitis
➡ Food impaction

6.Abscess

• Apical

• Root

• Periapical

7.Dental caries

➡ Bacterial destruction of dentin
➡ Extraction if caries result in fractures

🕳 Infundibular Caries

Very common in maxillary cheek teeth because they have 2 infundibulums:

• 1 rostral

• 1 caudal

Incisors have 1 infundibulum.

What is an infundibulum?

➡ Funnel-like structure/layer consisting of cementum

⚠ M1 is the oldest permanent tooth in the cavity and is often predisposed to caries.

Hole fills with food
⬇
🦠 Tooth can rot/become infected
⬇
🦷 Tooth becomes weakened
⬇
💥 Fracture

💊 Treatment

• Grade 1 → clean + fill hole with composite

• Grade 2–4 → extract tooth

🔢 Grades of Infundibular Caries

0 = Normal

1 = Hypoplasia of cementum

2 = Cementum + dentinum hypoplasia

3 = Cementum + dentinum + enamel hypoplasia

4 = Fracture of tooth 💥

🧠 0 Normal → 1 C → 2 C+D → 3 C+D+E → 4 Fracture

🦷 Exodontics

Exodontics = teeth extraction

💉 Nerve Blocks

1. Maxillary nerve block

📍 Ventral to zygomatic arch, dorsal to facial vessel

➡ Blocks:

• Maxillary teeth, Maxillary sinuses

2. Infraorbital nerve block

➡ Blocks:

• Upper incisors, Canines, Wolf teeth, Upper Premolar 2

3. Mandibular nerve block

📍 Foramen mandibulae, medial side

➡ Blocks mandibular teeth

4. Mental nerve block

📍 Mental foramen

➡ Blocks:

• Lower incisors, Canines, Wolf teeth

📌 Indications for Extraction

🐺 Wolf teeth

Extract if:

• Rostrally displaced, Unerupted, Fractured, Mandibular wolf teeth

🦷 Incisors, canines & cheek teeth

Extract for:

• Apical infection, Fracture, Severe periodontal disease, Tooth mobility due to trauma

🔧 Extraction Procedures

1⃣ Intraoral Extraction

• Forceps extraction

• Fragmentation

• Segmentation

• Fragment elevation/luxation

🐴 Done in standing sedation

💉 Alpha2 agonist + opioid

2⃣ Surgical Extraction

😴 Done in general anaesthesia

Methods:

• Surgical buccotomy

• Transbuccal extraction → minimally invasive

• Trephination extraction → minimally invasive

⚠ Transbuccal Extraction

Avoid:

• Facial nerve

  • Dorsal buccal branch

  • Ventral buccal branch

• Parotid salivary duct

• Facial artery

• Facial vein

💉 Local Anaesthetics

Drug	⏱ Effect after	⌛ Duration
Procaine	5–10 min	—
Lidocaine	5 min	30–60 min
Mepivacaine	10 min	60–120 min
Bupivacaine	30 min	120–140 min
Articaine	3 min	75 min

🧠 QUICK MEMORY

⭐ Deciduous incisors = Rule of 8

8 days → 8 weeks → 8 months

⭐ Permanent incisors

2.5 → 3.5 → 4.5 years

⭐ Molars

M1 = 1 → M2 = 2 → M3 = 3 years

⭐ Exodontics

Standing + alpha2/opioid
➡ Intraoral extraction

GA
➡ Surgical extraction

⭐ Nerve blocks

Maxillary nerve → maxillary teeth + sinus
Infraorbital → upper front teeth
Mandibular → mandibular teeth
Mental → lower front teeth

Sharp teeth

Sharp teeth = the most common dental/stomatological pathology in horses.

➡ Include minor sharp points → large unopposed overgrowths.

Etiology

Overgrowth of enamel due to:

➡ Lack of wear + continuous eruption

Causes

• Missing teeth

• Malerupted teeth

• Fractured teeth

• Overall disparity in apposition of arcades:

  • Parrot mouth

  • Diastema

• Lack of normal lateral movements of mandible during mastication → due to diet

⭐ Diastema – most common cause

Diastema = abnormal space between two teeth

➡ Leads to malocclusion of opposite tooth

⚙ Pathogenesis

Insufficient/excessive attrition of teeth
⬇
Sharp points/spurs of enamel
⬇
Lack of attrition of occlusal surface
+
Continuous eruption
⬇
🦷 Overgrowth

⭐ Why do sharp points form?

The maxillary arcades are set wider apart than the mandibular arcades.

This leads to areas of lack of wear during mastication.

MAXILLA

➡ Sharp points/spurs form on BUCCAL side

MANDIBLE

➡ Sharp points/spurs form on LINGUAL side

🤕 Consequences

Sharp points can cause:

➡ Abrasion and ulceration of:

• Cheeks and Tongue

🩺 Clinical Signs

⚠ Many horses are asymptomatic.

Most common:

• Dysphagia

• Soft-tissue trauma

• Quidding

• Riding problems

🔎 Diagnosis

Clinical examination

• 💉 Sedation

• Head gag

• Rinse mouth prior to examination

• ✋ Palpation

• 👀 Visual inspection

• 🔦 Light for visualization

• Occlusion probe → inspect for damage

🔧 Treatment – Rasping

➡ Rasping of teeth using:

• Hand rasp or Motorized instruments

Where do you rasp?

MAXILLA → BUCCAL side
➡ Because maxillary cheek teeth form spurs on the buccal side

MANDIBLE → LINGUAL side
➡ Because mandibular cheek teeth form spurs on the lingual side

This occurs because maxillary cheek teeth are wider than mandibular cheek teeth.

⚠ Important During Rasping

❌ Do NOT rasp away too much

➡ Secondary dentine protects the pulp.

When reducing an overgrowth:
➡ Maintain the normal lateromedial angulation of the occlusal arcades.

📈 Prognosis

✅ Good prognosis for most cases.

⚠ Excessive removal of occlusal surface OR heating of tooth structure using uncooled instruments can cause:

➡ Post-procedure quidding

⏱ Can take months to years to resolve.

🧠 QUICK MEMORY

Why sharp teeth?

Continuous eruption + ↓ wear = sharp teeth

Where are the sharp points?

🐴 Upper/MAXILLA
➡ BUCCAL 🫦
➡ Cuts CHEEK

🐴 Lower/MANDIBLE
➡ LINGUAL 👅
➡ Cuts TONGUE

Treatment

🔧 RASP/FLOAT

⚠ Don't rasp too much → protect secondary dentine + pulp

Surgical diseases of nasal cavity and paranasal sinuses

👃 DISORDERS OF THE NARES

1⃣ Wry Nose “campylorrhinus lateralis”

• Congenital damage

• Shortening of premaxilla on one side
  ➡ Upper jaw + nose deviate to one side

• Typically accompanied by deviation of nasal septum
  ➡ Problems breathing

• Different degrees, but often euthanasia is best

2⃣ Hypertrophy of Alar Folds

➡ Vibrant sound during inspiration = high blowing

• Causes exercise intolerance in performing horses

🔎 Diagnosis + Treatment

Confirm noise originates from alar folds during exhalation/inhalation:

➡ Place sutures from skin at dorsal aspect of nose across openings of false nostrils

➡ Compare noise before vs. after suture placement

Positive result
➡ Correct diagnosis
➡ Indication for resection of alar folds

3⃣ Atheroma of False Nostrils

➡ Development of epidermal inclusion cysts (sebaceous cysts) in lining of false nostril.

• Painless

• Usually no respiratory obstruction

• Mainly cosmetic significance

4⃣ Facial Paralysis

➡ Dysfunction of nasolabialis muscle

Causes:

• Facial surgery, Dental extraction

⚠ Can cause an aerodynamic disaster for sport horses

5⃣ Trauma

Usually when nose is caught in a hook.

➡ Requires anatomical restoration

👃 DISORDERS OF THE NASAL CAVITY

🩸 Progressive Ethmoidal Hematoma – PEH

Repeated epistaxis at rest → unilateral or bilateral.

Can progress to:

• Respiratory stridor

• Facial deformity

• ⬇ Airflow through affected nostril

➡ Unknown etiology.

⚙ Pathogenesis

Expanding sub-mucosal hemorrhages develop on surface of ethmoidal turbinate labyrinth

⬇

Mucosal capsule splits

⬇

🩸 Bloody discharge

More common in horses >4 years.

🩺 Clinical Signs

• ⭐ Repeated hemorrhages from one nostril at rest

• Dyspnoea → nasal obstruction, reduced drainage

• Dirty nasal discharge → not fresh blood

• Facial swelling

🔎 Diagnosis

• History, Physical exam, Endoscopy, X-ray, CT

💊 Treatment

First:
➡ Chemical ablation with formalin 10% (inject/apply it on lesion to remove it)

➡ Repeat at 2–3 week intervals until resolved

If not successful:
➡ Surgical removal through frontal flap

Other Nasal Cavity Disorders

• Trauma

• Intra-nasal foreign bodies

• Neoplasia

• Polyps

• Mucoid degeneration of nasal conchae

• Nasal septum deviation

• Hyperplasia of nasal septal mucosae

• Subcutaneous emphysema

• Concha necrosis and metaplasia

🦴 PARANASAL SINUSES

⭐ Five Paired Paranasal Sinuses

1. Frontal

   • Frontal sinus

   • Conchofrontal sinus

2. Caudal maxillary

3. Rostral maxillary

4. Ethmoidal

5. Sphenopalatine

⚠ Paranasal sinuses are not completely separated.

➡ All sinuses communicate with or drain into the middle meatus.

🦠 Primary Sinusitis

Pathogenesis:

Stagnation of mucus
⬇
Inhibited muco-ciliary clearance by URT viral agents
⬇
Opportunistic bacteria follow
⬇
Purulent exudate
⬇
Chronic sinusitis
⬇
Hyperplasia of lining
⬇
Narrowing of ostia + inspissation of pus

🦷 Secondary (Dental) Sinusitis

➡ Caused by dental periapical suppuration

Roots of 4th–6th maxillary teeth lie within maxillary sinuses.

Fracture or necrosis
⬇
Dental infection
⬇
🦠 Secondary sinusitis

🩺 Clinical Signs

Early:
➡ Mucoid unilateral nasal discharge

Later:
➡ Purulent + malodorous discharge

Also:

• Facial swelling, Nasal obstruction

🔎 Diagnosis

• Clinical signs, Percussion, Oral inspection, X-ray

• ⭐ CT = BEST / GOLD STANDARD – Zert

💊 Treatment

Conservative:

• Systemic ATB

• Volatile or steam inhalation

• Light exercise

Surgical:

• Catheter placement

• Radical surgery

🦷 Secondary Empyema

➡ Caused by problems with first molar (M1)

⭐ Most frequent problem of rostral maxillary sinus

Treatment

• Trephination (making a hole through the bone to access the sinus)

• Push tooth out

• Flush bulla

• Make drainage into oral cavity without extraction of tooth

💧 Sinus Cysts

• Unknown etiology

• Common features with PEH

• Often in region of drainage ostium (large sinus cyst → blocks drainage ostium → mucus can't drain → sinus expands → facial swelling/nasal obstruction)

• Cysts contain yellow fluid

🩺 Clinical Signs

• Nasal obstruction, Facial swelling

• Rarely ocular proptosis → exophthalmos

• Mucoid discharge

🔎 Diagnosis

• Clinical signs, Physical exam, Endoscopy, X-ray

🔪 Treatment

➡ Fronto-nasal flap surgery

🍄 Mycotic Rhinitis & Sinusitis

• Unknown etiology

• May be opportunistic fungal infection secondary to other supportive conditions

🩺 Clinical Signs

• Low-grade unilateral purulent discharge

• Maybe epistaxis

🔎 Diagnosis

➡ Endoscopy

💊 Treatment

• Topical benzimidazole

• Foley balloon catheter

🧬 Neoplasia & Polyps

Neoplasia ➡ True tumors are uncommon

Polyps

➡ Pedunculated inflammatory proliferations enclosed in mucous membrane

➡ Can develop from complication of dental periapical disease

🩺 Clinical Signs

• Putrid nasal discharge mixed with blood

• Ocular proptosis

🔎 Diagnosis

• Physical exam, Endoscopy, X-ray, CT

🔪 Treatment ➡ Fronto-nasal flap surgery

🧠 QUICK MEMORY

👃 NARES

Wry nose → congenital deviation
Alar fold hypertrophy → high blowing
Atheroma → painless cyst
Facial paralysis → nasolabialis dysfunction
Trauma → anatomical restoration

🩸 PEH

Older horse + repeated unilateral epistaxis AT REST
➡ Think progressive ethmoidal hematoma

Treatment:
Formalin 10% → if unsuccessful → frontal flap

🦷 SECONDARY SINUSITIS

Dental disease → unilateral → purulent + malodorous discharge

⭐ CT = GOLD STANDARD

💧 SINUS CYST

Facial swelling + obstruction + yellow fluid
➡ Fronto-nasal flap

🍄 MYCOTIC

Unilateral purulent discharge ± epistaxis
➡ Endoscopy → topical benzimidazole

Surgical Diseases of the Pharynx, Larynx & Guttural Pouch

PHARYNX

Pharynx = soft tissue passage for food and air.

Connected with:

• Nares, Middle ears, Oral cavity, Larynx, Esophagus

Supported by striated muscle for:

• Swallowing and Phonation

1⃣ Dorsal Displacement of the Soft Palate – DDSP

🏇 Only a problem in racing horses while exercising.

Likely due to abnormal contraction of muscles of soft palate → causing them to be flaccid.

⚙ What happens?

Soft palate displaces dorsally
⬇
“Sits” on the epiglottis
⬇
🚫 Obstructs opening to trachea
⬇
Difficulty getting air during exercise

🩺 Clinical Signs

• Loud expiration noises

• Unable to maintain speed while running

🔎 Diagnosis

• Clinical signs, History, Endoscopy at rest

• ⭐ Endoscopy during exercise = GOLD STANDARD

🔪 Treatment

• Laryngeal advancement – tie forward

  • Move larynx rostrally + dorsally

• Laser palatoplasty

⚠ Epiglottic Entrapment – Don't Mix with DDSP

➡ Enlargement/entrapment of epiglottis in younger horses

Treatment

➡ Gentle resection of epiglottic folds by laser

Other Pharynx Diseases:

• Choanal atresia/stenosis

• Palatal defects

• Instability of soft palate

• Dynamic collapse of pharyngeal walls

• Intra-palatal cysts

• Pharyngeal cysts

• Neoplasia

• Extra-mural distortion by:

  • Strangles, Abscess, Neoplasia

LARYNX

Larynx = symmetrical, tube-shaped musculo-cartilaginous organ connecting:

Pharynx → Larynx → Trachea

2⃣ Laryngeal Hemiplegia= Recurrent Laryngeal Neuropathy

Progressive functional loss of laryngeal nerves

⬇

Larynx collapses on affected side during inspiration

⬇

Permanent dysfunction of muscles

⬇

🚫 Partial obstruction of airways

⭐ Typical

• Higher prevalence in males

• Long-neck, large breeds . long vagus recurrent nerve, trauma or wear on the nerve

• Usually LEFT side

🩺 Clinical Signs

• Inspiratory noise during exercise (high pitched whistling/roaring sound)

• Exercise intolerance

• Usually asymptomatic at rest

🔎 Diagnosis

Palpation
➡ Atrophy of intrinsic laryngeal musculature

Other:

• Arytenoid depression test

• “Grunt-to-the-stick” test

• Endoscopy

🔪 Treatment

⭐ Prosthetic laryngoplasty

➡ Suture between cricoid + arytenoid

➡ Mimics action of CAD muscle

Other:

• Nerve/muscle grafting

• Permanent tracheostomy

• Cordectomy → Zert does not like

3⃣ Fourth Branchial Arch Defect – 4-BAD= Laryngeal Dysplasia

Syndrome of irreparable congenital defects due to failure of development of some/all derivatives of the 4th branchial arch.

Can be:

• Unilateral or Bilateral

❌ Defective Structures

4 structures:

1⃣ Wings of thyroid cartilage
2⃣ Crico-thyroid articulation
3⃣ Cricothyroideus muscles
4⃣ Crico-pharyngeal sphincter muscles

🩺 Clinical Signs

• Abnormal respiratory sounds during exercise, Eructation, Nasal discharge, Coughing, Recurrent colic

• 4-BAD→ missing/abnormal laryngeal structures → abnormal respiratory sounds + swallowing problems.

🔎 Diagnosis

• Palpation, Dynamic endoscopy, Ultrasonography

Palpation:
➡ Unusually wide gap between:

• Caudal margin of thyroid and Rostral edge of cricoid

Normally, these structures overlap.

❌ Treatment ➡ No way to reconstruct the absent structures

GUTTURAL POUCHES = Auditory Tube Diverticulum (ATD)

2 air-filled, balloon-like structures

📍 Located between:

• Base of cranium → dorsally

• Pharynx + esophagus → ventrally

Each pouch:

• Is in contact with the other

• Separated by thin areolar tissue → septum

• Connected to the nasopharynx

4⃣ Guttural Pouch Tympany

⚙ Pathogenesis

Guttural pouch ostium acts as non-return valve

➡ Air can enter
➡ ❌ Air cannot leave
⬇
🎈 Guttural pouch expands

Etiology

• Foals a few days after birth

• Congenital malfunction of pharyngeal opening of pouch

🩺 Clinical Signs

• 🎈 Tympanic swelling of parotid region

• Mucopurulent discharge

  • Bacterial infection → strangles

• Dysphagia, Dyspnea

🔪 Treatment

Improve airflow from guttural pouch:

➡ Opening into larynx OR
➡ Perforation of septum between the pouches

5⃣ Diverticulitis of Guttural Pouch

➡ Inflammation of ATD mucous membranes

Etiology

• Strangles

• Chronic diverticulitis → chronic catarrhal inflammation

• Empyema

• Chondroids

6⃣ Chronic Empyema & Chondroids

⚙ Pathogenesis

Failure of drainage
⬇
Mucus/pus accumulates in pouch
⬇
Pus becomes stagnant
⬇
Formation of solid concretions = CHONDROIDS

⚠ Risk of Streptococcus equi

🩺 Clinical Signs

• Bilateral purulent nasal discharge, Swelling of parotid region

🔎 Diagnosis

• Clinical signs, Lateral X-ray

💊 Treatment

➡ Liquify chondroids by repeated lavage

➡ Drainage via Foley balloon catheter

7⃣ Guttural Pouch Mycosis 🍄

➡ Invasive fungal plaque on mucosal wall of ATD.

🚨 Clinical Signs

⭐ Spontaneous epistaxis AT REST (plaqe erodes internal carotid artery lining the guttural wall)

• Minor hemorrhages

• Dysphagia

• Pharyngeal paralysis

  • ➡ Ingesta in nasal discharge

• Cranial nerve defects:

  • Laryngeal hemiplegia

  • Facial palsy

  • Horner's syndrome

  • Abnormal head posture

🔎 Diagnosis

• Clinical signs

• Endoscopy ⚠ can be dangerous

💊 Treatment

Conservative:
➡ Antimycotic drugs

Surgical:
➡ Occlusion of carotid artery branches

• Ligature OR Transarterial coil embolization (must also do surgery, will be a lot of bleeding. the potensial risk of severe hemorrhage is the risk, not the fungi itself)

Other Larynx Diseases

• Epiglottal hypoplasia

• Laryngeal granuloma

• Neoplasia

• Sub-epiglottal cysts

• Epiglottal entrapment → younger horses → laser

• Arytenoid chondropathy

• Axial deviation of ary-epiglottal folds

🧠 QUICK DIFFERENTIATION

🏇 DDSP

Soft palate → over epiglottis
➡ EXPIRATORY noise
➡ Exercise
➡ Dynamic endoscopy
➡ Tie-forward

🗣 Laryngeal hemiplegia

Usually LEFT arytenoid doesn't function
➡ INSPIRATORY noise
➡ Exercise
➡ Endoscopy
➡ Prosthetic laryngoplasty

🎈 Guttural pouch tympany

Foal + air trapped
➡ Parotid swelling
➡ Create drainage/airflow

Empyema/chondroids

Pus → stagnant → solid chondroids
➡ Purulent discharge
➡ Lavage + Foley catheter

🍄 Guttural pouch mycosis

Fungal plaque
➡ 🚨 Spontaneous epistaxis at rest
➡ Cranial nerve problems
➡ Occlude carotid artery branches

Diseases of the eyelid and conjunctiva

👁 Importance of the Eyelids

• Protect the eye

• Produce and distribute tears

• Aid tear drainage

• Help control the amount of light entering the eye

👁 DISEASES OF THE EYELID

Congenital Disorders

1⃣ Entropion

Entropion = inward rolling of the eyelid margin.

⭐ Common in foals.

Etiology

Foals:

• Dehydration and Congenital disorders

Adults:

• Trauma

⚙ Pathogenesis

• Eyelid edge turns inward → Eyelashes rub against eye surface → Irritation of conjunctiva + cornea

Long term:

• Scarring, Abnormal coloring, Slow-healing sores

🩺 Clinical Signs

• 💧 Epiphora = excessive tearing

• 😣 Blepharospasm = blinking

• Conjunctivitis, Keratitis

💊 Treatment

Temporary repair:

• Vertical mattress suture, Subconjunctival injections

Surgery: rarely required.

⚠ Not recommended until adult age → avoid over-correction / iatrogenic ectropion.

➡ Blepharoplasty = removal of skin below eye

2⃣ Ankyloblepharon

➡ Failure of eyelids to open after birth

3⃣ Dermoid

➡ Focal congenital masses of displaced skin/tissue

May include hair.

🔪 May require surgical removal if causing irritation.

4⃣ Agenesis & Coloboma

Coloboma (dysgenesis)

➡ Full-thickness absence of portions of normal eyelid

Agenesis

➡ Complete absence of eyelid

If ocular disease is present:
➡ Reconstructive blepharoplasty

🐴 ACQUIRED EYELID DISORDERS

5⃣ Trauma / Laceration

⭐ Common because of the horse's prominent lateral eye position.

⚠ All eyelid injuries should be treated ASAP to avoid further damage to eye.

🩺 Clinical Signs & Diagnosis

• Usually obvious: Edema, Bleeding

💊 Conservative Treatment

• Topical compress

• Topical ATB

• Systemic NSAIDs

🔪 Surgical Treatment

• Temporary tarsorrhaphy

• Re-apposition of eyelid margin

🚨 NEVER RESECT / CUT OFF AN EYELID LACERATION!

Preserve as much eyelid tissue as possible.

6⃣ Ectropion

Ectropion = eversion of eyelid margin.

Usually due to complication of eyelid trauma.

⚙ Pathogenesis

Eyelid turns outward → Conjunctiva exposed → Irritants + secondary bacterial infections → Long-term/recurrent conjunctivitis + scarring

🔪 Treatment

➡ Surgical V and Y blepharoplasty:

7⃣ Blepharitis

Blepharitis = inflammation of the eyelids.

🦠 Infectious Causes

Bacteria:

• Moraxella equi

Parasites:

• Oncocerciasis, Habronemiasis

❌ Non-infectious Causes

• Dermatological condition. Photosensitization, Abscess, Neoplasia

🩺 Clinical Signs

• Blepharospasm. Hyperemia, Swelling, Exudation, Alopecia, Pruritus, Epiphora

🔎 Diagnosis

• History, Clinical signs

💊 Treatment

➡ Depends on etiology and condition

8⃣ Neoplasia

Most common

• Squamous cell carcinoma (SCC)

• Sarcoid

• Melanoma

Etiology / Risk Factors

Depends on:

• Age, Breed

• Lack of ocular pigmentation

• Genetics

• ☀ UV radiation

• Infectious agents

• Chronic irritants

🔎 Diagnosis

• Histopathological examination, Biopsy

💊 Treatment

• BCG (Bacillus Calmette-Guérin) → injection used to dissolve sarcoid

• ⭐ Gamma-radiation = best

⚠ Resection could destroy the eyelid margin.

9⃣ Distichiasis

➡ Double set of eyelashes

Extra hair/cilia grow from Meibomian glands.

Treatment

➡ Surgical electrolysis

🔟 Trichiasis

➡ Inward direction of eyelashes

Eyelashes contact cornea
⬇
Irritation

1⃣1⃣ Prominence of Nictitating Membrane= Third Eyelid

Etiology

• Altered globe position or size, Inflammation

• Neoplasia → SCC

• Tetanus

• Horner's syndrome

• Prolapse of orbital fat pad

• Conjunctival amyloidosis

🔎 Diagnosis

• Clinical signs, Biopsy, Cytology

💊 Treatment

Depends on underlying cause:

• Surgical, Antitoxins

CONJUNCTIVITIS

The conjunctiva covers:

• Inner eyelids

• Third eyelid

• Sclera

Conjunctivitis = inflammation of the conjunctiva.

⭐ Common in foals due to:

• Reduced tear production

• Low corneal sensitivity compared to adults

🦠 Etiology

• Primary Irritants: Environmental, Allergic, Chemical

• Foreign bodies

• Infectious: Moraxella equi

• Parasites: Thelazia, Habronema musca, Onchocerca cervicalis

Secondary ⭐ More Common

Secondary to:

• Keratitis

• Disorders of tear production/draining

• Eyelid disease

• Uveitis

• Endophthalmitis

• Trauma

• Ulceration

• Neoplasia → SCC

• Systemic disease

Respiratory viral infections

• Equine influenza, Equine herpesvirus, Rhinovirus

Other infections

• Strangles, Equine viral arteritis, Actinobacillus spp., Corynebacterium spp.

🩺 Clinical Signs of Conjunctivitis

• Swelling, Edema,💧 Epiphora

• Discharge:

  • 💧 Serous → viral

  • 🟡 Purulent → bacterial

• 🔴 Hyperemia

🔎 Diagnosis

• Physical examination

• Scraping + culture

• 💧 Schirmer tear test

• Occasionally biopsy

💊 Treatment

➡ Depends on etiological agent.

• 💧 Flushing of conjunctival sac

• Ophthalmic preparation of ATBs

• Granulomatous lesions:

  • Antihelmintic therapy

  • Anti-inflammatory therapy

• 🪱 Mechanical removal of parasites

🧠 QUICK MEMORY

Eyelid position

Entropion = IN ↩ → eyelashes damage cornea
Ectropion = OUT ↪ → conjunctiva exposed

Eyelashes

Distichiasis = extra/double eyelashes
Trichiasis = eyelashes directed inward

Trauma

🚨 NEVER cut off eyelid laceration → re-apposition

Conjunctivitis

🔴 Inflamed conjunctiva
💧 Serous = viral
🟡 Purulent = bacterial

Useful terminology

Epiphora = excessive tears 💧
Blepharospasm = excessive blinking/squeezing eye 😣
Blepharitis = inflammation of eyelid
Conjunctivitis = inflammation of conjunctiva

Corneal diseases

👁 Anatomy of the Cornea

Outside → inside:

💧 Tear film
⬇
Corneal epithelium
⬇
Corneal stroma
⬇
Descemet’s membrane
⬇
Endothelium

Acquired corneal diseases are common and can be:

• Traumatic / non-traumatic

• Inflammatory / non-inflammatory

• Ulcerative / non-ulcerative

1⃣ Corneal Ulcer / Traumatic Keratitis

Corneal ulcer = loss of corneal tissue.

The cornea is widely exposed to the environment → prone to disease and ulceration.

📏 Classification according to depth

• Superficial

• Deep

• Perforating

🔍 Etiology

⭐ TRAUMA

Also:

• Disorders of adnexa:

  • Ectopic cilia

  • Entropion / ectropion

  • Eyelid laceration

• Foreign bodies

• Infectious → Equine herpesvirus 2

🩺 Clinical Signs

• 💧 Epiphora, Ocular discharge, Miosis, Blepharospasm, Photophobia,⬆ Vascularization / erythema

• Loss of transparency → opaque cornea

➡ Damage of corneal epithelium causes absorption of water from precorneal tear film.

🔎 Diagnosis – Fluorescein Stain ⭐

🟢 Superficial wounds → stain GREEN

🟢 Deeper wounds → halo appearance

💊 Treatment

Superficial / deep epithelial wounds:

• Topical ATB, NSAIDs, Topical 1% atropine, EDTA → protease inhibitor

Full-thickness lacerations:

• 🔪 Surgery: Conjunctival flap, Corneal graft, Remove loose flaps of cornea

🚨 CORTICOSTEROIDS CONTRAINDICATED WITH CORNEAL ULCERS

➡ Corticosteroids speed up activity of proteases
➡ Worsen the ulcer

2⃣ Keratomalacia / Melting Ulcer 🚨

Keratomalacia = liquefactive necrosis of the corneal stroma.

🚨 OCULAR EMERGENCY

🦠 Etiology

Proteases produced by:

• Bacteria:

  • Pseudomonas, Streptococcus

• Fungi

• Inflammatory cells

⚙ What happens?

Proteases
⬇
Break down corneal stroma
⬇
🫠 Cornea begins to “melt”

🩺 Clinical Signs

• Greyish, edematous, gelatinous corneal opacity

• Blue color

• Blepharospasm

• Serous → purulent ocular discharge

🔎 Diagnosis

➡ Fluorescein stain

💊 Treatment

• Topical ATB, Antifungal, NSAIDs

• ⭐ Topical anti-proteases:

  • EDTA, Acetylcysteine

• Treatment every 4–6 hours

3⃣ Immune-Mediated Keratitis – IMK

Common non-infectious eye disease in horses.

Often affects one eye, but can affect both.

⚠ Serious → can threaten horse's sight.

Four Types – Based on Depth

1⃣ Epithelial / superficial

• Inflammation of eyelids

• Congestion of conjunctival blood vessels

• Swelling of conjunctiva

2⃣ Midstromal

3⃣ Deep stromal

4⃣ Endothelial
🚨 Most dangerous and damaging type
➡ Affects innermost layer → endothelium

💊 Treatment

⚠ Important to distinguish from other causes of keratitis, especially infectious keratitis.

• Topical NSAIDs

• Topical cyclosporine A

• ❌ No corticosteroids!

4⃣ Dry Eye Syndrome= Keratoconjunctivitis Sicca – KCS

KCS = aqueous deficiency of the precorneal tear film, causing progressive inflammatory changes of the cornea + conjunctiva.

Two types: tear-deficient dry eye due to insufficient aqueous secretion, and evaporative dry eye often linked to meibomian gland dysfunction or eyelid abnormalities

🔍 Etiology

• Tear deficiency, Evaporative disorders, Eyelid problems, Meibomianitis, Exophthalmos

• Can result from head trauma, damage to the facial nerve controlling tear production, or secondary systemic/local inflammation

🩺 Clinical Signs

• Ocular pain, Dull cornea, Corneal edema, Keratitis, Mucopurulent ocular discharge

🔎 Diagnosis

• Schirmer tear test → <10 mm/min

• Rose Bengal stain → Remains red if tissue is devitalized

💊 Treatment

Replace precorneal tear film:

• Synthetic mucins, Artificial tears, Topical cyclosporine A

5⃣ Corneal Stromal Abscess

Corneal stromal abscess = pus-filled sore in the connective tissue of the cornea.

🦠 Etiology

Healing ulcer / corneal defect
⬇
Bacteria or fungi become trapped inside
⬇
Stromal abscess

⚠ Can cause secondary uveitis.

It typically develops when a superficial corneal microtrauma or ulcer heals over, sealing bacteria or fungi (frequently fungal) inside the avascular stroma where the immune system and topical drugs struggle to reach.

🩺 Clinical Signs

• White/yellow material in connective tissue, Corneal inflammation + swelling, Formation of blood vessels

• Ocular pain

💊 Treatment

• Topical + systemic ATB

• Antifungal

• Painkiller, NSAIDs

🔪 Surgery may be required to:

• Remove abscess, promote corneal healing

⚠ Prognosis = guarded

🦠 Infection in Corneal Ulcers

Most ulcers are presumed to have secondary bacterial and fungal infection.

⭐ Take swabs BEFORE any topical treatment
➡ Microbiology

If fungal infection confirmed:
➡ Antifungal treatment 6–8 weeks

6⃣ Protozoal – Besnoitia benetti

Coccidia → Besnoitia benetti

• FH: Cats

• IH: Horse (mostly donkeys, rare in horse)

• Vector: Flies

🔄 Life Cycle

🐱 Cat sheds oocysts
⬇
🐴 Horse ingests from grazing/water
⬇
Formation of tissue cysts in skin/nostrils
⬇
Edema + hyperkeratosis + alopecia
⬇
Can also infect eyes/sclera
⬇
⚪ Small dots/cysts on surface

🩺 Clinical Signs

• Fever, Nasal discharge, Ocular discharge

• Salivation, Stiff gait, Orchitis

• Subcutaneous edema

• Multifocal pinpoint parasitic cysts:

  • Nostrils, Ears, Face, Body

  • crusty hard skin lesions

• 👁 Scleral pearls → tiny cysts in eyes

🔎 Diagnosis

• Skin biopsy

• Endoscopy of nasal cavity

• ELISA confirmation

💊 Treatment

⚠ Problematic → no drug stops formation of cysts in organs/skin.

Early infection:
➡ Try trimethoprim (stop cyst forming, but not kill parasite)

Otherwise:
➡ Mostly symptomatic treatment

7⃣ Equine Herpesvirus 2

🩺 Clinical Signs

• Superficial punctate keratitis

• Blepharospasm

• Lacrimation

🔎 Diagnosis

• Clinical signs

• Response to antiviral drugs:

  • Idoxuridine, Acyclovir

8⃣ Parasitic – Onchocerca cervicalis

Large nematode inhabiting:

• Subcutaneous tissue, Tendons, Tendinous ligaments

➡ Microfilariae in skin.

⚙ Pathogenesis

Migration + death of Onchocerca cervicalis microfilariae

⬇

Corneal + conjunctival tissues

⬇

👁 Keratitis / keratoconjunctivitis

🩺 Clinical Signs

• Pain, Hyperemia

• Corneal opacity

🔎 Diagnosis

• Clinical signs

• Demonstration of microfilariae in biopsy

💊 Treatment

• Ivermectin

• Corticosteroids

🧠 QUICK DIFFERENTIATION

Corneal ulcer

Loss of corneal tissue
➡ Trauma most common
➡ Fluorescein +
➡ ATB + NSAID + atropine
🚫 NO corticosteroids

🫠 Melting ulcer

Corneal stroma literally breaking down
➡ Proteases
➡ Gelatinous/blue-grey cornea
🚨 Emergency
➡ EDTA + acetylcysteine

🛡 Immune-mediated keratitis

Non-infectious immune disease
➡ Different depths
➡ Cyclosporine A

💧 KCS

Not enough tears
➡ Schirmer <10 mm/min
➡ Artificial tears + cyclosporine

Stromal abscess

Bacteria/fungi trapped INSIDE healing cornea
➡ White/yellow material
➡ Can cause secondary uveitis
➡ Guarded prognosis

⭐ One important rule

CORNEAL ULCER + CORTICOSTEROIDS = ❌

Corticosteroids
➡ ⬆ Protease activity
➡ ⬆ Corneal breakdown
➡ Ulcer gets worse

Uveitits

The uvea = middle layer of the eye, beneath the sclera. It consists of: IRIS, CILIARY BODY, CHOROID

Uveitis = inflammation of the uvea.

🚨 Most common cause of blindness in horses.

Can be:

• Acute, Chronic, Recurrent

🔍 Etiology

1⃣ Trauma

2⃣ Corneal Disease

• Keratitis, Corneal ulcers

3⃣ Equine Recurrent Uveitis – ERU ⭐

➡ Autoimmune disease ⭐ Most frequent!

4⃣ Infectious Causes

🦠 Bacteria

• Leptospira interrogans serovars, Rhodococcus equi, Streptococcus, Brucella, Salmonella

🦠 Viruses

• Equine herpesvirus, Equine influenza virus

🪱 Parasites

• Onchocerca cervicalis, Thelazia, Toxoplasma, Strongylus

5⃣ Reflex Uveitis

➡ Mediated by axon effect in trigeminal nerve

For example:

Corneal injury
⬇
Trigeminal nerve stimulation
⬇
Inflammatory response inside eye
⬇
Uveitis

6⃣ Neoplasia

⭐ Melanoma = most common

Treatment

• Sector iridectomy

• Enucleation

7⃣ Systemic Infections

• Endotoxemia

• Septicemia

🩺 Clinical Signs

🔥 Acute Uveitis

• 😣 Pain

• 💧 Lacrimation

• Blepharospasm

• ☀ Photophobia

• ⭐ MIOSIS

• Impaired vision

• Corneal edema

• ⭐ Reduced intraocular pressure – IOP ↓

🧠 Classic Acute Uveitis

PAINFUL + SMALL PUPIL + LOW IOP

🌫 Chronic Uveitis

➡ Cataract / cloudy eye ⭐ Typical for chronic uveitis.

🔎 Diagnosis

• Clinical signs

• 💧 Schirmer tear test → Increased tear production

• 👁 IOP → ↓ Decreased pressure

• Collection of:

  • Aqueous humor

  • Vitreous humor

➡ To identify etiological agent

🚨 Treatment

START TREATMENT IMMEDIATELY AND AGGRESSIVELY!

Untreated inflammation → Damage inside eye → Retinal detachment → Vision loss

1⃣ Mydriatics

Mydriatic = dilates the pupil

• Atropine → long acting

• ⭐ Tropicamide → short acting, preferred

Why dilate the pupil?

Uveitis → Miosis → Iris/lens irritation → Risk of adhesions + lens damage → Cataract

➡ Therefore give mydriatic → dilate pupil

2⃣ Topical NSAIDs

Example: Diclofenac

Reduces:

• Pain, Redness, Swelling

3⃣ Steroids

• Prednisolone, Dexamethasone

⚠ Remember from corneal ulcers:

UVEITIS → steroids can be used

BUT

CORNEAL ULCER → ❌ topical corticosteroids

➡ Always check the cornea first.

4⃣ Antibiotics

• Doxycycline, Gentamicin

🔄 EQUINE RECURRENT UVEITIS – ERU= Autoimmune Disease

An autoimmune condition where:

Horse's immune system
⬇
Attacks its own ocular tissues
⬇
Repeated episodes of uveitis
⬇
Progressive damage to uveal tract
⬇
👁❌ Can completely destroy vision

ERU occurs after an initial episode of uveitis.

⚠ But not every horse with uveitis develops recurrent uveitis.

🔍 Possible Triggers of ERU

Specific conditions/agents associated with ERU include:

• 🦠 Bacteria

  • Especially Leptospira

• 🪱 Parasitic worms

• 🦠 Viruses

  • Equine influenza

• 🦷 Tooth root abscess

• 🐴 Hoof abscess

• 👁 Eye injuries

Inflammation can also be stimulated by dead/dying parasite larvae that have migrated into the eye.

🔪 Treatment of Recurrent Uveitis

1⃣ Vitrectomy

Vitrectomy = aspiration/removal of material from the vitreous body

➡ Removes: Cells, Antigens, Organisms from corpus vitreum

2⃣ Cyclosporine A Implant

➡ Cyclosporine A implant:

• Intravitreally / sub-sclerally ➡ Suppresses immune response

Your notes also mention:

• Cephalosporin implant

⚠ Prognosis

Guarded → poor

🚨 Complications

• Glaucoma

• Cataracts

• Cloudiness of cornea

• Retinal damage/detachment

• 👁 Blindness

🧠 UVEITIS – QUICK MEMORY

Acute:

😣 PAIN
⚫ MIOSIS
⬇ LOW IOP
💧 TEARS

Chronic:

🌫 CATARACT / CLOUDY EYE

Treatment:

DILATE + CONTROL INFLAMMATION + TREAT CAUSE

➡ Mydriatic
➡ NSAID
➡ Steroid
➡ ATB when indicated

🪱 EYE PARASITES

1⃣ Thelazia lacrimalis

➡ Nematode transmitted by non-biting dipteran flies that lick conjunctival secretions.

🔄 Life Cycle

🪰 Fly carrying larvae → Fly feeds on horse's conjunctival secretions → Larvae migrate fly → eye → Mature into adult worms → Female sheds L1 into lacrimal secretions / tears → Flies ingest L1 → L1 → L3 inside fly → Fly infects another horse

🩺 Clinical Signs

• 💧 Excessive lacrimation, Conjunctivitis

🔎 Diagnosis

• 👀 Rapidly moving worms visible in eye

• L1 detected in sediment of flushing fluid

💊 Treatment

• Local anesthesia of eye

• ⭐ Mechanical extraction of worms

• SC ivermectin

• Protect horses against dipteran flies

2⃣ Onchocerca cervicalis

➡ Nematode normally residing in ligamentous tissue.

Can cause parasitic keratitis due to migration through nasolacrimal duct.

⚙ Pathogenesis

Microfilariae migrate → Eye/corneal tissues → Inflammation + irritation → Ulceration → Granuloma formation

💊 Treatment

• Ivermectin, Topical corticosteroids

If granuloma irritates cornea:
➡ 🔪 Surgical removal

3⃣ Habronema musca

➡ Nematode
➡ Equine stomach worm

Hosts

FH = Equids

• Stomach, Skin, Eyes, Genitalia, Lungs

IH = Musca flies 🪰

🔄 Life Cycle

🐴 Horse feces containing eggs/larvae → Flies ingest them → Develop → L3 → Fly feeds on ocular/nasal discharge → Deposits L3 on horse → Larvae normally migrate to stomach → Mature into adult worms

But larvae deposited around wounds/eyes can cause cutaneous/ocular habronemiasis.

🩺 Clinical Signs

Cutaneous / ocular form

• Conjunctivitis, Thickening of eyelid

• Granuloma formation in skin, Severe itching, Self-inflicted injuries

💊 Treatment

• Ivermectin, Topical corticosteroids

🧠 PARASITE QUICK MEMORY

🪰 THELAZIA

FLY → EYE → visible worms
➡ Lacrimation + conjunctivitis
➡ Pull worms out + ivermectin

🪱 ONCHOCERCA

Ligaments → microfilariae → eye
➡ Keratitis + granulomas
➡ Ivermectin + corticosteroids

🪰 HABRONEMA

Stomach worm + fly
➡ Fly deposits larvae around eye/wounds
➡ Granulomatous lesions + itching
➡ Ivermectin + corticosteroids

⭐ EXAM ESSENTIALS

Uveitis = inflammation of iris + ciliary body + choroid

Acute uveitis:
➡ Pain + miosis + ↓ IOP

Chronic uveitis:
➡ Cataract/cloudy eye

ERU:
➡ Autoimmune + recurrent episodes
➡ Most important cause of blindness

ERU treatment:
➡ Vitrectomy / cyclosporine implant

Prognosis:
➡ Guarded to poor

Equine hoof diseases

HOOF ANATOMY

Outer Structures:

Hoof Wall

• Covers the front and sides of the coffin bone.

Parts:

• Toe = front

• Quarters = sides

• Heel

➡ Continually growing keratinous material
➡ No nerves or blood vessels

3 Layers of the Hoof Wall

1⃣ Outer layer → Periople

2⃣ Middle layer → Bulk of wall

3⃣ Inner layer → Laminae

⭐ Laminae attach the coffin bone to the inside of the hoof wall and bear much of the weight.

Coronary Band

Located at the top of hoof where hairline meets hoof.

➡ Primary growth + nutritional source for hoof wall.

⚖ Weight-Bearing Structures:

Sole

Protects internal structures of hoof.

Designed to bear internal weight transferred through border of sole, rather than weight directly from ground.

White Line

➡ Junction between hoof wall + sole

Frog 🐸

Tough V-shaped structure pointing down from heels.

➡ Protects digital cushion beneath it.

🦴 Inner Structures:

Digital Cushion

• Located below coffin bone toward back of hoof. Cartilaginous cushion and a major shock absorber

Coffin Bone (“hovbeinet”)

= Pedal bone / distal phalanx

➡ Largest bone in hoof, Helps shape hoof wall, Surrounded by tissues forming the laminae

Navicular Bone

= Distal sesamoid bone (Small bone behind coffin bone)

➡ Helps stabilize coffin bone and is associated with deep digital flexor tendon apparatus

🔥 1. LAMINITIS (“Forfangenhet”)

Definition

Laminitis = inflammation of the laminae.

⭐ Zert definition: “Laminitis is a disconnection of the epidermal and dermal lamella, connected with failure of the suspensory apparatus.”

🔬 Lamellae

Laminae = sensitive tissues connecting hoof wall → coffin bone.

Lamellae = villi-like structures.

Two components:

1. Dermal lamellae

• Originate from corium. Sensitive

2. Epidermal lamellae

• Originate from the deepest layers of the hoof wall. Insensitive

They normally:

➡ Interlock with each other
➡ Suspend coffin bone inside hoof capsule

🔍 Etiology – MULTIFACTORIAL

⭐ Most common cause is obesity

🦠 Systemic infections

• Enterocolitis, Endotoxemia, Septicemia

• Pleuropneumonia, Metritis, Retention

🍞 Overfeeding carbohydrates

➡ Dysbacteriosis, Endotoxicosis

🌱 Lush grass (rapidly growing spring grass with high amount of sugars and starch)

➡ Hindgut fermentation, Lactic acid production

🦵 Mechanical causes

• Contralateral limb overload, Chronic overload, Hard work on hard surface, Poor hoof trimming

🧬 Endocrinopathy / Metabolic

• Insulin resistance, Diabetes mellitus, Hyperlipemia, Cushing, Hypothyroidism

⚙ Pathogenesis

Exact mechanism largely unknown.

Believed to involve:

Hypoperfusion → Ischemia → Necrosis of lamellae → Dermal–epidermal junction becomes edematous + weakened → Loss of interlaminar bond → Failure of suspensory apparatus → Coffin bone displacement

🔄 ROTATION vs SINKING ⭐⭐⭐

🔄 Rotation

Damage extends over large area
⬇
Suspensory support of distal phalanx lost
⬇
Body weight + pull of DDFT + dorsal soft-tissue pressure
⬇
Mechanical separation of distal phalanx from hoof wall
⬇
🦴 Coffin bone rotates away from dorsal hoof wall

➡ Palmar rotation

Heel remains suspended by laminar attachment.

🧠 Think:

TOE attachment fails → DDFT pulls → bone ROTATES

⬇ Sinking

More severe.

ALL suspensory support of laminae lost → Entire distal phalanx drops distally inside hoof → Without obvious rotation.

🧠 Difference

ROTATION 🔄
➡ Part of support remains and Coffin bone tilts

SINKING ⬇
➡ All support fails and Whole coffin bone drops → much worse prognosis.

🌍 Systemic Changes

• Cardiovascular: Tachycardia, Hypertension

• Endocrine:↑ Catecholamines, ↑ Cortisol

• Renal: Glomerulonephritis

• Liver damage

🩺 Clinical Signs of Laminitis

Systemic

• ↑ Heart rate, Tachypnea, Fever

Hoof

• 💥 Pounding digital pulse, 🔥 Warm hoof wall

• Lameness, Pain, Reluctance to move

⭐ Typical Laminitis Stance:

Forelimbs stretched forward + Hindlimbs underneath body (Horse tries to remove weight from painful forefeet/toes)

🔎 Diagnosis

• Clinical signs

• ⭐ X-ray

X-ray:

• Degree of coffin bone rotation and Hoof wall thickness

🚨 ACUTE LAMINITIS = EMERGENCY

1. Cryotherapy

➡ Hoof in ice bath / ice packs

⭐ Especially important early.

💊 2. Stop Pain ➡ NSAIDs

🎯 3. Remove Initiating Cause

Examples:

• Remove from pasture, ATB for infection, Anti-endotoxin medication

🩸 4. Reduce Vasoconstriction / Hypertension

• Acepromazine, Potassium chloride, Topical nitroglycerin

🦶 5. Mechanical Support

• Deep soft bedding, Pre-shaped frog pads

🚨 AVOID:

• ❌ Perineural analgesia

• ❌ Forced exercise

🕐 CHRONIC LAMINITIS

General

• Limit carbohydrates, Potassium chloride, Biotin

✂ Corrective Foot Trimming

• Remove excess horn, Trim heels

👞 Therapeutic Shoeing

Wide-webbed / seated-out bar shoe of thick steel

➡ Increase support, Minimize pressure on sole

📊 LAMINITIS GRADING

Grade	Clinical sign
1	Shifting weight
2	Typical stiff, stilted laminitis gait
3	Reluctance to walk + typical gait
4	Recumbency

🧠 1 shift → 2 stiff → 3 reluctant → 4 down

❄ PREVENTION

Subacute / Preclinical Stage

Example:

Horse with colic + suspected endotoxemia

➡ Put hooves in ICE ❄

Also Support frog, Elevate heel

➡ Decreases pulling force of DDFT

General Prevention

➡ Correct feeding (Especially control glucose/carbohydrate intake)

📈 Prognosis

🟢 Good

• No rotation by 10 days

• Recovered by approximately day 60 (2months)

🔴 Unfavorable

• Acute phase >10 days

• Recumbency, High BP, Secondary infection, Displacement of distal phalanx

⚫ Hopeless

• Sinking of distal phalanx >20 mm founder distance

• Exungulation of hoof

💔 2. HOOF CRACKS

Deep cracks often accompanied by localized infection of the dermis.

Can be:

• Partial or Complete

Etiology

• Overgrown hoof wall, Poor-quality horn, Poor foot balance, Tearing, Breed predisposition

Clinical Signs

• Lameness, Visible cracks

Diagnosis

• Clinical signs, Hoof tester

• Uni-axial analgesia → determine clinical significance

Treatment

• Oil, Biotin, Methionine, Adequate immobilization

• Partial hoof-wall resection

Prevention

➡ Regular good foot care
➡ Oils, biotin etc.

⚪ 3. WHITE LINE DISEASE= Horny Capsule Disease

Dermal + epidermal layers become separated at toe → Visible at white line → Dermal region exposed →🦠 Ascending infection

Etiology

• Focal hemorrhage

• Seroma

• Chronic untreated bacterial infection

• Mycotic infection of corium

• Chronic pododermatitis

Pathogenesis

• Persistent infection → Cavity formation → Damaged laminae fail to produce keratin → Abnormal/empty hoof wall region

Clinical Signs

• Brown, crumbly horn-like material along white line

• Non-keratinized void extending from white line

• Lameness

Diagnosis

• Clinical signs

• 🔨 Percussion → hollow sound

• X-ray → gas shadow in soft tissue

Treatment

• Regular cleansing

• Wide-webbed flat shoes

• Severe cases → remove affected horn

• Dress exposed laminae

• Allow newly formed horn to grow normally

• Antifungal foot soaks

📌 4. PENETRATING WOUNDS OF THE SOLE

Puncture wound through sole or frog

➡ Can involve dermis or deeper structures.

Etiology

➡ Standing/kicking against sharp objects

⚠ Secondary infection common.

🚨 Most Dangerous Area:

⭐ Middle → palmar/plantar third of frog + sulci

Why? Deep penetration here can damage:

• DDFT, Navicular bursa, Ligaments, Digital flexor tendon sheath

🩺 Clinical Signs

• Acute onset lameness

• May improve after foreign body removal

• Non-weight-bearing lameness with secondary infection

• Purulent discharge

• Systemic signs of infection

• Occasionally stringhalt-like gait

🔎 Diagnosis

• Observation

  • Foreign body may still be embedded

• Hoof tester

• Synoviocentesis + fluid analysis

• Plain radiography

• Contrast radiography

• Positive contrast arthrography

• Sonography

💊 Treatment

• ATB, Tetanus antitoxin, Cleaning, Drainage, Antiseptic drainage

🚨 Emergency surgical debridement when indicated.

If Synovial Penetration:

Navicular bursa
➡ Navicular bursoscopy
➡ Focal debridement

DIP joint
➡ Arthroscopic lavage

Aftercare ➡ Daily antiseptic dressing under sterile bandage

🦴 5. NAVICULAR SYNDROME = Palmar Heel Pain / Podotrochlosis

⭐ One of the most common causes of chronic forelimb lameness in athletic horses.

Chronic degenerative condition involving the navicular bone and associated structures.

⚙ Pathological Changes

1⃣ Medullary Changes

➡ Focal loss of medullary architecture
➡ Subsequent synovial invagination

2⃣ Sclerosis

➡ Medullary sclerosis + Damage to fibrocartilage on flexor surface

3⃣ DDFT Damage

Damaged navicular flexor surface → DDFT repeatedly contacts it → Traumatic fibrillation of DDFT → Adhesions between tendon + bone

4⃣ Enthesiophytes

➡ Bone spurs (osteophytes) at proximal + distal borders of navicular bone

🔍 Etiology

Unknown → multifactorial / complex

Important:

• Distal limb conformation

• Degree/type of athletic loading

Genetic/hereditary predisposition

• Thoroughbred

• Quarter Horse

• Warmblood

🩺 Clinical Signs

Early ➡ Intermittent, progressive lameness

REST → improves
WORK → returns

⬇

Eventually becomes consistent.

⭐ Usually bilateral

Horse tries to avoid loading heels:

➡ Short stride, Choppy gait, Pointing hoof

🔎 Diagnosis

Clinical

• History

• Hoof tester

  • Sensitive over center of frog

• Flexion test

• Hoof shape:

  • Contracted heel

  • Atrophy of frog

💉 Nerve Blocks

Palmar digital nerve block or Navicular bursa block → ⭐ Lameness disappears/improves

🩻 X-ray

May show:

• Enthesiophytes on wings of navicular bone

• Cystic lesions

• Calcification of DDFT

💊 Treatment of Navicular Syndrome

👞 1. Shoeing

⭐ Foot must be kept balanced.

Options:

• Rolled toe, Egg-bar shoe, Adequate heel support

➡ Goal = improve mechanics and reduce stress on heel/navicular apparatus.

🔪 2. Surgery

• Desmotomy of suspensory ligament ➡ Alters loading of navicular bone

• Palmar digital neurotomy ➡ Removes pain sensation from affected region

💊 3. Anti-inflammatory Treatment

• Aspirin, Banamine, PBZ, Polysulphated glycosaminoglycans

🧠 QUICK MEMORY

🔥 LAMINITIS

Laminae fail → coffin bone loses suspension

Two major consequences:

🔄 ROTATION
= coffin bone tilts

⬇ SINKING
= whole coffin bone drops

Classic signs:
➡ 🔥 Hot feet
➡ 💥 Pounding digital pulse
➡ 😣 Severe pain
➡ 🐴 Forelegs forward

🚨 Acute = ICE + NSAIDs + treat cause + support hoof

⚪ WHITE LINE DISEASE

White line separates → Infection moves upward → Brown crumbly horn + cavity

📌 PENETRATING WOUND

Especially dangerous through:

⭐ Middle/palmar frog

Frog → DDFT → Navicular bursa/navicular region → DIP region → Deep penetration = 🚨 possible synovial infection

🦴 NAVICULAR SYNDROME

Think:

ATHLETIC HORSE + CHRONIC BILATERAL FORELIMB LAMENESS + HEEL PAIN

➡ Short/choppy stride
➡ Worse with work
➡ Palmar digital block improves lameness
➡ Balance hoof + support heel

⭐ EXAM DIFFERENTIATION

Laminitis
➡ Laminae
➡ Acute painful feet
➡ Rotation/sinking of coffin bone

White line disease
➡ Separation at white line
➡ Brown crumbly horn + hollow cavity

Penetrating sole wound
➡ Foreign body through sole/frog
➡ Risk DDFT/navicular bursa/DIP infection

Navicular syndrome
➡ Chronic palmar heel pain
➡ Athletic horse
➡ Usually bilateral forelimbs

Equine fractures

A fracture = break in the continuity of a bone.

On X-ray: Discontinuity of cortex, Radiolucent fracture line

🔍 Etiology

⭐ Common in racing horses

Typical:

• Stress fractures of carpal joint and fetlock joint

Other causes:

• Direct external trauma, Kicks, Collisions

📚 Classification

1⃣ Open / Closed

Closed fracture
➡ Skin intact

Open fracture
➡ Skin communicates with fracture → High infection risk

2⃣ Simple / Complicated

Simple
➡ Single uncomplicated fracture

Complicated
➡ Associated damage to soft tissues, joints, vessels, infection etc.

3⃣ According to Fracture Line / Location

• Transverse, Oblique, Longitudinal, Spiral, Comminuted, Diaphyseal, Metaphyseal

• Physeal → Salter-Harris

• Articular

• Long-bone fractures, Short-bone fractures

4⃣ Fragment Position

• Dislocation / displacement

• Compression

🩺 Clinical Signs

• Pain, Swelling, Lameness

• Abnormal mobility

• Loss of function

  • Often non-weight-bearing

• Crepitus

🔎 Diagnosis

⭐ X-ray

• Minimum 2 planes

• Often multiple oblique views

Also:

• CT, Scintigraphy, Ultrasonography

🦴 FRACTURE HEALING

There are two major types:

1⃣ PRIMARY BONE HEALING = Direct healing

Requires:
➡ Rigid stabilization ± compression of bone ends

The bone ends are held in very close/direct contact.

Important consequence → Little/no callus formation

Osteoblasts fill and remodel the fracture directly.

Divided into:

• Contact healing and Gap healing

⭐ Best especially in intra-articular fractures

Why? Because large callus formation inside/around a joint would interfere with joint function.

2⃣ SECONDARY BONE HEALING= Indirect healing

Spontaneous fracture healing when there is no completely rigid fixation.

➡ Callus formation occurs.

There are 3 phases:

🔥 Phase 1 – Inflammatory Phase

Starts immediately.

Fracture → Bleeding → Hematoma formation → Inflammatory cells invade

• Clinical → Pain and Swelling

🛠 Phase 2 – Repair Phase

Begins within a few days, before inflammation completely subsides.

Lasts weeks.

Important cells:

• Chondroblasts, Fibroblasts, Osteoblasts

Sequence

1⃣ Granulation tissue forms → Soft callus → 2⃣ Cartilage formation → 3⃣ Fibrous tissue formation → 4⃣ Calcium deposited → 🦴 Hard callus

🔄 Phase 3 – Remodeling

Final phase.

Woven bone → replaced by → Lamellar bone

At the same time:
➡ Excess callus is resorbed

Result:
➡ Bone gradually regains more normal structure and strength.

🧠 PRIMARY vs SECONDARY HEALING

PRIMARY

Rigid fixation + compression
➡ Bone ends directly together, Minimal callus

SECONDARY

Some movement / indirect contact
➡ Hematoma, Soft callus, Hard callus, Remodeling

🚑 INITIAL TREATMENT OF FRACTURES

Main goals:

• Minimize damage to soft tissues

• Minimize further damage to bone ends

• Allow horse to regain control of limb

• Provide pain relief

• Limit soft-tissue swelling

🚨 If Skin is Penetrated

Open fracture:

1. Clean wound

2. Water-soluble ATB ointment

3. Sterile dressing

4. Then immobilize

🔧 STABILIZATION METHODS

External Fixation

• Splint

• Robert Jones bandage

• Cast

• Transfixation cast

• Pinless fixation

Internal Fixation

• Lag screws

• Plates

• Ligatures

Major displaced fractures usually require internal fixation.

🔩 LAG SCREWS

⭐ Give contact healing / primary healing

Principle

Screw compresses the fracture fragments together.

➡ Pressure across fracture line
➡ Rigid contact
➡ Minimal movement
➡ 🚫 Avoid callus formation

Used especially in:

• Transverse fractures

• Oblique fractures

• Metacarpal/tarsal fractures

Technique:

Small stab incision → Drill gliding hole through near cortex → Measure → Smaller drill bit into far cortex → Insert screw → Fragments compressed together

🧠 Why does a lag screw compress?

The screw threads engage only the far fragment.

When the screw is tightened:

Far fragment is pulled toward Near fragment ➡ Fracture ends are compressed.

🧱 PLATES

Used:

• To stabilize fractures

• Especially long bones

Types:

DCP ➡ Dynamic compression plate

LCP ⭐ ➡ Locking compression plate

LC ➡ Low-contact plate

⭐ LCP – Most Used

The screw head locks into the plate.

➡ Screw cannot move within plate
➡ Very stable fixation
➡ Better healing

Used especially in simple fractures.

🦾 TRANSFIXATION CAST

Principle:

➡ Pins/nails pass through bone

Cast → pin → bone → pin → cast

This transfers weight through pins and cast rather than through the fractured distal limb.

➡ Reduces compression/loading of fracture fragments.

👞 SHOEING

For some hoof-bone fractures:

➡ Bar shoe

Especially:

• Pedal/coffin bone fractures

• Navicular bone fractures

Plus:
➡ Box rest

🩺 AFTERCARE

• External support

  • Bandage, Splint, Cast

• Antibiotics, Analgesia

• Box rest

🚫 Never use corticosteroids with intra-articular fractures

⚠ COMPLICATIONS OF FRACTURE HEALING

1. 🦠 Infection

Especially:

• Open fractures

• Internal fixation

2. 🦴 “Fracture Disease”

Due to prolonged immobilization:

• Muscle atrophy

• Soft-tissue adhesions

• Joint stiffness

• Osteoporosis

3. ❌ Healing Problems

Delayed union

➡ Fracture heals too slowly

Malunion

➡ Fracture heals in wrong position

Non-union

➡ Fracture fails to unite

Foals

Prolonged immobilization can cause:

• Laxity of supporting soft tissues

• Growth disturbance

• Angular limb deformities in contralateral limb

Adult Horses

🚨 Contralateral limb laminitis

Horse avoids loading fractured limb → Overloads opposite limb → Laminitis

✅ TREATABLE FRACTURES

🏇 Stress Fractures

Mostly:

• Fetlock, Carpus

• Racing horses

Treatment:
➡ Primary healing
➡ Lag screw fixation

🧩 Chip Fractures

Locations:

• Fetlock, Carpus

Treatment:
➡ Arthroscopic removal

🦴 Proximal Phalanx Fractures

Sagittal/frontal plane fractures:

➡ Lag screws

🦴 Proximal Sesamoid Bone Fractures

Apical / mid-body fractures

➡ Lag screws
or
➡ Circumferential wiring

🦵 Condylar Fractures

Distal 3rd metacarpal/metatarsal bone:

➡ Lag screws

🦴 Third Metacarpal/Tarsal Bone

Transverse / oblique fractures:

➡ Compression plate

💪 Olecranon Fractures

➡ Compression plate

Long-Bone Fractures

Generally treated mainly in young foals.

➡ Compression plates can be used.

In adult horses:
➡ Prognosis often poor
➡ Euthanasia frequently advised for severe long-bone fractures.

🚫 Femoral Head Fracture

➡ Euthanasia

🧠 QUICK FRACTURE-TREATMENT TABLE

Fracture	Typical Treatment
Stress fracture – fetlock/carpus	Lag screw
Chip fracture – carpus/fetlock	Arthroscopic removal
Proximal phalanx sagittal/frontal	Lag screw
Proximal sesamoid apical/mid-body	Lag screw / wiring
Condylar MCIII/MTIII	Lag screw
Transverse/oblique MCIII/MTIII	Compression plate
Olecranon	Compression plate
Pedal/navicular bone	Bar shoe + box rest
Severe adult long-bone fracture	Often euthanasia
Femoral head	Euthanasia

⭐ EXAM ESSENTIALS

Fracture diagnosis
➡ X-ray in 2 planes + oblique views

Primary healing
➡ Rigid fixation
➡ Minimal/no callus
➡ Best for intra-articular fractures

Secondary healing
➡ Inflammation → repair/callus → remodeling

Lag screw
➡ Compresses fragments

LCP
➡ Screw locks into plate → high stability

Transfixation cast
➡ Pins transfer load from bone into cast

Adult long-bone fractures
➡ Often poor prognosis/euthanasia

Major complication in adults
➡ Contralateral limb laminitis

Developmental Anomalies of Bones

1⃣ ANGULAR LIMB DEFORMITY – ALD

ALD = skeletal defect where a portion of the limb is bent inward or outward at an abnormal angle from the midline of the body.

⭐ Relatively common in newborn and young foals.

Most commonly affects:

• Carpus, Sometimes tarsus, Fetlock

↔ VALGUS vs VARUS ⭐

When viewed FROM THE FRONT:

VALGUS: OUTWARD bending

Can be normal immediately after birth → foal may grow out of it.

VARUS: INWARD bending (⚠ Usually more severe)

🔍 Etiology

Most foals are born with some degree of limb deviation.

• Often due to: Ligament laxity, Muscle weakness

• Usually corrects itself as foal exercises.

Perinatal Factors:

• Premature birth, Twin pregnancy, Placentitis, Perinatal soft-tissue trauma, Flaccidity/laxity of soft tissues surrounding joints, Poorly calcified bone

Developmental Factors:

• Unbalanced nutrition, Excessive exercise, Trauma, Inappropriate growth, Hypothyroid hormone deficiency

🩺 Clinical Signs

• Presence of valgus or varus

• Swelling, Lameness

• Excessive hoof wear on:

  • Medial side or Lateral side

🔎 Diagnosis

• Clinical signs, Degree of deviation

• ⭐ X-ray

💊 TREATMENT OF ALD

Conservative Treatment:

For young foals with mild deviation:

• Stall rest, Splints, Cast placement, Corrective hoof trimming, Glue-on shoes → Dalric type, Inside/outside hoof extensions

VALGUS

➡ Trim lateral side and Preserve medial side

VARUS

➡ Opposite:

• Trim medial side and Preserve lateral side

🔪 Surgical Treatment:

Used for:

• Older foals

• Severe deviations

• No response to conservative treatment

The principle is to alter growth on the two sides of the growth plate.

VALGUS

➡ Enhance growth on lateral side

Needle into growth plate:

• 4 sites

• Approximately 1.5 cm

• Foals a few weeks old

VARUS

⚠ Correction should start within 2 weeks.

• Hoof extension on lateral side

• Enhance growth on medial side

• Slow growth on lateral side with screw

🔧 More Invasive Techniques

• Periosteal stripping of radius

• Transphyseal bridging

• Transphyseal screw placement

• Corrective osteotomy or ostectomy 🇺🇸 = “American way” (❌ Zert doesn't like this)

🧠 PRINCIPLE OF GROWTH CORRECTION

The limb is bent because the two sides are not growing equally.

To straighten it:

OPTION 1:
➡ Enhance growth on the short/slow side

OR

OPTION 2:
➡ Slow growth on the long/fast side with a screw/bridge

⬇

Foal continues growing

⬇

🦵 Limb gradually straightens.

📈 Prognosis

Without treatment ➡ Severe deformity → poor recovery

Early detection + appropriate treatment/surgery ➡ ⭐ Favorable

🦴 PHYSEAL FUSION AGE IN HORSE

Important because treatment must occur while the growth plate is still active.

Bone	Physis	Fusion
Humerus	Proximal	18–30 months
Humerus	Distal	15–21 months
Radius	Proximal	15–21 months
Radius	Distal	6–9 months
Metacarpus	Distal	8–12 months
Phalanx 1	Proximal	6–9 months
Femur	Distal	24–30 months
Tibia	Proximal	25–30 months
Tibia	Distal	18–24 months

🧠 Young foal = more growth remaining = more opportunity to correct ALD.

2⃣ PHYSITIS

What is the Physis?

Growth plate / physis = cartilage disc separating epiphysis from metaphysis

➡ Responsible for longitudinal growth of long bones.

Physitis = inflammation + swelling of a growth plate, occurs most commonly in fast-growing, well-muscled foals and weanlings between 3 and 6 months of age

The condition affects the ends of long bones near major joints—most frequently above the knee (distal radius), fetlock (distal cannon bone), or hock (distal tibia)

Common Locations:

Nursing foals:
➡ Often P1

After weaning:
➡ Often radius

Also:

• Radius, Metacarpus, Metatarsus

🔍 Etiology

• Trauma, Overfeeding, Obesity

• Mineral imbalances:

  • Vitamin D

  • Calcium

  • Phosphorus

• Genetic predisposition

• Salter-Harris fractures

⚙ Pathogenesis

➡ Disturbance of endochondral ossification

Normally:

Growth-plate cartilage
⬇
Gradually replaced by bone

In physitis:

❌ Process is disturbed
⬇
Growth plate becomes swollen/inflamed

🩺 Clinical Signs

• Swelling and warm at physis (often joint), Variable lameness, Choppy gait

🔎 Diagnosis

• ⭐ X-ray

• Calcium : phosphorus → approximately 1:1

• ↑ Alkaline phosphatase

💊 Treatment

Main goal:

⭐ REDUCE EXCESSIVE GROWTH RATE + CORRECT NUTRITION

• Reduce food intake

• Reduce body weight

• Reduce growth rate

• Limit exercise

• Box rest

• Soft bedding/surface

• Correct dietary imbalances

• Keep off pasture temporarily

3⃣ PHYSEAL FRACTURES = Salter-Harris Fractures

Fractures involving the growth plate.

Typically occur in foals.

Common cause:
➡ Mare stepping on foal in stable.

⚠ Important because damage to the growth plate can disturb future bone growth.

🦴 SALTER-HARRIS CLASSIFICATION ⭐⭐⭐

1. Type I

➡ Through physis only

2. Type II ⭐ MOST COMMON

➡ Through physis + metaphysis, “Above the growth plate”

3. Type III

➡ Through physis + epiphysis ➡ Extends toward/into joint

4. Type IV

➡ Through all three: Metaphysis → Physis → Epiphysis

5. Type V

➡ Compression/crushing of physis

🔧 Treatment of Physeal Fractures

Important to use a locking technique.

• ⭐ Locking compression plate – LCP

  • Especially for long bones

• Lag screws

• Cast

➡ Metal plates and screws stabilize the fracture.

Goal

• Stable fixation, Correct alignment, Protect growth plate, Minimize future growth deformity

⚠ Why Are Physeal Fractures Important?

Growth plate damaged → Growth may stop/become unequal → One side grows differently → Angular limb deformity / growth disturbance

4⃣ DEFECTS OF THE SPINE

Uncommon in horses.

1. Scoliosis

➡ S-shaped / lateral curvature of spine

2. Lordosis

= Sway-back ➡ Downward curvature of spine

3. Kyphosis

➡ Upward curvature of spine

4. Synostosis

➡ Fusion of one vertebra with the next vertebra

5⃣ DIGIT MALFORMATION 🦶

➡ 2nd or 4th splint bone develops into a complete lower limb and foot.

Normally the splint bones are reduced structures.

With this developmental anomaly:

Splint bone → Develops excessively → Formation of an additional digit/foo

6⃣ RICKETS ☀🦴

⭐ Rare in horses.

Etiology

➡ Nutritional deficiency of vitamin D

⚙ Consequence

Vitamin D deficiency → Abnormal bone mineralization → Metaphyseal flaring → Bowing of extremities

⭐ EXAM ESSENTIALS

ALD
➡ Newborn/young foals
➡ Carpus most common
➡ Valgus = outward
➡ Varus = inward

Treatment of ALD
➡ Mild/young = conservative
➡ Severe/older = manipulate physeal growth

Physitis
➡ Inflammation/swelling of physis
➡ Disturbed endochondral ossification

Salter-Harris
➡ Fracture involving growth plate
➡ Type II most common in your notes

Main danger of physeal damage
➡ Growth disturbance → angular limb deformity

Spine
➡ Scoliosis / lordosis / kyphosis / synostosis

Rickets
➡ Vitamin D deficiency → metaphyseal flaring + bowed limbs

Tendinosis and Tendon Ruptures

ANATOMY – TENDONS & LIGAMENTS

Tendons (sener) = bands of dense connective tissue connecting muscle to bone/cartilage (produce/transmits movement)

Ligaments (leddbånd) = connect bone to bone (provides stability)

FLEXOR SIDE – palmar/plantar

• Superficial digital flexor tendon (SDFT)

• Deep digital flexor tendon (DDFT)

• Check ligaments

• Suspensory ligament

EXTENSOR SIDE – cranial/dorsal

• Common digital extensor

• Lateral digital extensor

• Long digital extensor

1⃣ SUPERFICIAL DIGITAL FLEXOR TENDON – SDFT

🐴 Forelimb

Origin: Medial humeral epicondyle

→ Runs caudally/palmarly down forelimb

Insertion: Middle / 2nd phalanx (P2)

Function

• Flexes proximal and middle phalangeal joints and Stabilizes metacarpophalangeal (fetlock) joint

🐴 Hindlimb

Origin: Proximal tibia

Insertion: Middle / 2nd phalanx (P2)

Functions:

• Extends the digit, Assists in extending the hock, and Flexes the stifle

2⃣ DEEP DIGITAL FLEXOR TENDON – DDFT

Main function:
➡ Flexes distal phalanx/digit

Forelimb: Medial humeral epicondyle → Runs caudally/palmarly → Distal / 3rd phalanx – P3

Hindlimb: Deep digital flexor muscle → Passes distal to tarsus → Distal / 3rd phalanx – P3

CHECK LIGAMENTS

Both SDFT and DDFT have accessory/check ligaments connecting them to bone.

• Proximal Check Ligament: Belongs to SDFT → Attaches to radius

• Distal Check Ligament: Belongs to DDFT → Attaches to MCIII

3⃣ EXTENSOR TENDONS

Extensors are not primarily responsible for producing extension.

➡ Their important role is to limit/reduce excessive flexion.

Therefore:
⭐ Extensor injuries are generally less critical than flexor/suspensory injuries.

Common Digital Extensor Tendon

Lateral humeral epicondyle → Runs cranially → P3

Lateral Digital Extensor Tendon – Forelimb

Lateral humeral epicondyle → P1

Long Digital Extensor Tendon – Hindlimb

Proximal tarsal region → P3

Lateral Digital Extensor – Hindlimb

Proximal tarsal region → Fuses with extensor apparatus → Associated with P3

🏗 STAY / SUSPENSORY APPARATUS ⭐⭐⭐

The suspensory apparatus:

➡ Supports the pastern (kronleddet) + fetlock (kodeleddet)

➡ Prevents excessive extension/hyperextension of the fetlock

Main components:

1. Suspensory ligament

2. DDFT

3. SDFT

4. Proximal sesamoid bones

5. Extensor branches

6. Sesamoid ligaments:

   • Straight

   • Oblique

   • Cruciate

   • Short sesamoid ligaments

🔗 SUSPENSORY LIGAMENT “Gaffelbåndet/Fesseltreget”

Origin: Proximal MCIII/MTIII → Runs down palmar/plantar surface of cannon bone → Divides into:
➡ Medial branch
➡ Lateral branch

→ Passes around/attaches to proximal sesamoid bones

→ Extensor branches continue dorsally into the extensor apparatus.

⭐ Main function:
➡ Prevent excessive fetlock extension

⚠ Severe disruption of the entire suspensory apparatus can be catastrophic and may require euthanasia.

BACK OF LEG = structures preventing fetlock from collapsing downward.

4⃣ TENDINOSIS / TENDINITIS

Tendinosis = Strain injury acquired from excessive training.

Tendinitis = Inflammatory reaction to the strain injury.

Severity ranges from: Mild inflammation → Fiber disruption / tendon rupture

🏇 Occurrence

Very common, especially in:
➡ Racing horses

Most commonly affected:

🥇 SDFT ⭐⭐⭐

Also:

• DDFT

• Accessory ligament of DDFT – ALDDFT (distal check ligament)

• Suspensory ligament (gaffelbåndet)

More common in forelimb than hindlimb

🔍 Etiology

• Overextension

• Poor conditioning

• Fatigue

• Poor racetrack conditions

• Persistent training despite inflammation

⚙ PATHOGENESIS

Especially affects digital flexor tendons.

In racehorses:
⭐ SDFT most commonly affected.

Primary lesion: Excessive strain → Central rupture of tendon fibers → Hemorrhage → Edema → Inflammation

The most frequently injured tendons/ligaments are on ➡ Palmar/plantar aspect of distal limb

🩺 CLINICAL SIGNS

🔥 Acute → Classic inflammation: Severe lameness, Heat, Pain, Swelling

⏳ Chronic → Lameness during hard work, Fibrosis, Thickened tendon, Adhesions in peritendinous area

🔎 DIAGNOSIS

⭐ ULTRASOUND – USG

Can show:

• Fluid/effusion around tendon

• Fiber disruption

• ⭐ Central core lesion

Also: MRI

Clinical examination:

• Pain, Heat, Swelling, Lameness

• Palpation of affected structure

💊 TREATMENT OF TENDINOSIS/TENDINITIS

⚠ Very long treatment

➡ Up to 18 months (1,5y)

🧊 Acute Phase First ~3 days

• Ice packs / prolonged cooling

• NSAIDs

Purpose: reduce swelling, inflammation and pain

🚶 Rehabilitation: ⭐ Controlled movement

➡ Gradually increasing controlled exercise, 🚫 No uncontrolled pasture exercise.

🩸 REGENERATIVE TREATMENT

Platelet-rich plasma– PRP ⭐⭐⭐ Zert's favorite!

• Injected intratendinously under USG guidance.

• PRP contains growth factors.

➡ Intended to improve tendon healing and quality of repair.

Other Growth Factors

• Insulin-like growth factor – IGF

Stem Cells

• Usually obtained from Bone marrow

• ❌ Impractical, Zert doesn't like it

Laser Therapy

• Can be used as part of treatment/rehabilitation.

🧬 TENDON REPAIR

A major problem with tendon healing:

Normal tendon → Injury → Scar formation → Healed tendon becomes stiffer → Functionally inferior to original tendon → Predisposed to reinjury

⭐ Important concept: A healed tendon is not the same as the original tendon!

🕸 SCAFFOLD

Example: Urinary bladder matrix

Basically a graft/scaffold placed on/in the damaged tendon.

Think of it as: Skeleton/framework/template for healing cells

Normal scar tissue has: Less elasticity

Scaffold aims to: Improve organization/quality of repaired tissue.

🔪 TENDON SURGERY

1⃣ Proximal Check Ligament Desmotomy (Desmotomy = cutting a ligament)

Scarred tendon → Tendon becomes stiff / less elastic → Cut proximal accessory/check ligament → Allows more movement/extension → Compensates for reduced tendon elasticity

🧠 Cut check ligament → give tendon more freedom

2⃣ Annular Ligament Desmotomy

➡ Transection of proximal or distal annular ligament

Why?

Scar formation → Tendon becomes thick → Annular ligament restricts tendon expansion/movement → Cut annular ligament → More space for tendon

3⃣ Fasciotomy

➡ Cutting/opening fascia to reduce restriction and improve healing.

Locations:

Forelimb ➡ Carpal region

Hindlimb ➡ Plantar tarsal region

5⃣ TENDON RUPTURE / TRANSECTION

Traumatic rupture can involve the suspensory apparatus, with or without fractures of both proximal sesamoid bones.

➡ Loss of support of fetlock.

Common:
🏇 Racing injury

Often:
➡ Not completely ruptured
➡ Some connection remains between proximal and distal portions.

🔍 Etiology

• Racing injury, Excessive weight bearing/loading, Kicks, Wire cuts

🩺 Clinical Signs

• Severe acute lameness after racing/exercise, Severe pain

• Abnormal limb position depending on structure damaged

⭐ The position of the limb can tell you which tendon is ruptured.

💥 SDFT RUPTURE

➡ Hyperextension of fetlock
➡ Heel drop

Why?

SDFT normally helps support the fetlock.

Rupture → Less support → Fetlock extends excessively → Heel drops

🧠 SDFT → Sinking heel

💥 DDFT RUPTURE

➡ Overextension
➡ Elevation of toe

DDFT normally flexes/supports distal digit.

Rupture → Loss of flexor pull on P3 → Toe becomes elevated

🧠 DDFT → toe UP

💥 SUSPENSORY LIGAMENT RUPTURE

• Overextension of fetlock + Subluxation of pastern region

Because:
⭐ Suspensory ligament is a major anti-hyperextension structure.

🚨 WHOLE SUSPENSORY APPARATUS RUPTURE

Catastrophic.

➡ Complete loss of fetlock support

Horse may:

⚠ Step on the palmar/plantar surface of the fetlock

The limb appears essentially “broken down.”

➡ Very poor prognosis
➡ Euthanasia often indicated

💥 EXTENSOR TENDON RUPTURE

➡ Dorsal knuckling of fetlock

Why?

Loss of extensor function → Horse cannot adequately oppose flexion → Knuckling

⭐ Usually less catastrophic than flexor/suspensory rupture.

💥 PERONEUS TERTIUS RUPTURE

➡ Stifle joint is flexed

This structure is part of the hindlimb reciprocal apparatus.

🧠 RUPTURE = LOOK AT THE LIMB POSITION

Ruptured structure	Typical appearance
SDFT	Hyperextended fetlock + heel drop
DDFT	Overextension + toe elevation
Suspensory ligament	Hyperextension + pastern subluxation
Whole suspensory apparatus	Fetlock collapses → horse may step on palmar surface
Extensor tendon	Dorsal knuckling
Peroneus tertius	Abnormal reciprocal apparatus; stifle-related abnormality

🔎 DIAGNOSIS OF RUPTURE

Palpation

Look for:

• Swelling, Heat, Pain, Loss of normal tendon continuity

Always Compare with contralateral limb

🩻 X-ray

Minimum 4 views:

1. Dorsopalmar

2. Lateromedial

3. Oblique

4. Opposite oblique

Important to identify:
➡ Proximal sesamoid bone fractures

💊 TREATMENT OF RUPTURE

Depends on severity.

If NOT Completely Ruptured:

Conservative

Immediate stabilization to prevent further damage:

• Cast + splint

• Fixation/support bandage

• Wound care

Goal:

➡ Prevent continued hyperextension
➡ Protect remaining tendon fibers

🔪 Debridement ➡ Remove damaged/devitalized tissue

BUT:

⭐ Save as much remaining viable tendon as possible
🚫 Do not suture tendon

🦴 Surgical – Severe Suspensory Apparatus Injury

If the whole suspensory apparatus is disrupted:

➡ Arthrodesis

Arthrodesis = Surgical immobilization of a joint by fusion of adjacent bones

Joint surfaces → Surgically fused → No joint movement → Provides structural stability

⚠ Expensive.

⚠ EUTHANASIA

Indicated in catastrophic injuries where functional support cannot realistically be restored.

Especially:
➡ Complete catastrophic suspensory apparatus failure.

⭐ EXAM ESSENTIALS

Tendon
➡ Muscle → bone → movement

Ligament
➡ Bone → bone → stability

Most common tendon injured in racehorses
➡ ⭐ SDFT

Most common location
➡ Palmar/plantar distal limb

Primary lesion
➡ Central rupture of tendon fibers + hemorrhage + edema

Best diagnostic method
➡ ⭐ USG → central core lesion

Healing
➡ Long, up to 18 months
➡ Healed tendon is stiffer and functionally inferior
➡ High reinjury risk

Zert's favorite regenerative treatment
➡ ⭐ PRP under USG guidance

Proximal check ligament desmotomy
➡ Increases functional elasticity/movement of scarred tendon unit

Complete suspensory apparatus rupture
➡ Catastrophic loss of fetlock support → arthrodesis or euthanasia

Developmental Anomalies of Tendons

There are 2 main types:

1⃣ FLEXURAL LAXITY

➡ Tendons/supporting structures are too long / weak / flaccid
➡ Joint hyperextends

2⃣ FLEXURAL DEFORMITY

➡ Flexor structures are too short / contracted
➡ Joint remains flexed / knuckles

🧠 MOST IMPORTANT DIFFERENCE

	LAXITY	FLEXURAL DEFORMITY
Tendon	Too long / weak	Too short / tight
Joint	Hyperextension	Flexion
Limb appearance	Drops backward/down	Knuckles forward
Think	⬇ LOOSE	↪ TIGHT

🧠 LAX = loose and long
🧠 FLEXURAL = flexed because tendon is short

1⃣ FLEXURAL LAXITY= Weak / Flaccid Tendons

Laxity = deformity where joints are hyperextended because of loss/weakness of supporting structures.

Weak/long flexor structures
⬇
Cannot adequately support joints
⬇
Joint hyperextends
⬇
Fetlock drops toward ground

🔍 Etiology

Quite frequent in premature foals.

Causes:

• Prematurity ⭐, Intrauterine infection, Infection/disease of mare

Older horses:

Can occur due to:

• Previous injuries/diseases, Nutritional deficiencies, Lack of exercise, Normal aging

🩺 Clinical Signs

General

➡ Overextension / hyperextension

DDFT laxity

➡ Toe elevation

Because the DDFT is not providing normal flexor tension.

Severe laxity

Fetlock drops further and further:

Normal
⬇
Hyperextension
⬇
Fetlock approaches ground
⬇
Foal may walk on palmar/plantar surface of phalanges

This causes:

• Skin abrasions, Pastern trauma, Fetlock trauma

🔎 Diagnosis

X-ray ⭐

Especially used to check:
➡ Skeletal maturity

Premature foal may show:

• Insufficient mineralization, Delayed long-bone development

💊 Treatment

Most cases are treated conservatively.

• Box stay/rest

• Moderate controlled exercise

• Light bandaging

👞 Shoeing

If the foal has difficulty standing:

➡ Heel extensions

Purpose:

Heel extension → Provides more support → Allows full contact between solear surface and ground

🚫 Usually Contraindicated

• Cast

• Surgery

Because many cases improve naturally as the foal becomes stronger.

• Severe insufficient mineralization ➡ Euthanasia may be necessary.

🛡 Prevention

Foals

➡ Proper care of pregnant mare
➡ Prevent premature delivery

⚠ A severely premature/immature foal should not be encouraged to stand prematurely, particularly if skeletal mineralization is inadequate.

Older Horses

• Treat tendon injuries promptly, Good nutrition, Sufficient exercise

2⃣ FLEXURAL DEFORMITY= Tendon/soft-tissue shortening

Flexural deformity = limb deviates from normal vertical alignment because structures on the flexor side are too short/tight or because of abnormalities of the extensor apparatus.

Can be congential or acquired

🐣 CONGENITAL FLEXURAL DEFORMITIES

Two important forms:

1. Shortening of flexor tendons

➡ Digital and/or carpal joints remain flexed

2. Elongation/rupture of common digital extensor tendon

➡ Cannot adequately extend digit

3⃣ CONGENITAL FLEXOR TENDON SHORTENING

Mainly affects:
➡ Forelimbs

Flexor tendons are too short → Pull joints into flexion → Foal cannot straighten limbs

🔍 Etiology

Often unknown.

Possible:

• Infection of mare, Intrauterine malpositioning, Other developmental factors

🩺 Clinical Signs

• Unable to stand normally

• Unable to nurse if severe

• Flexion of carpal joints

• Contracted appearance

🔎 Diagnosis

• Clinical signs

• X-ray

💊 Treatment

Conservative

• Stretch limbs

• Bandages

• Cast

💉 Oxytetracycline ⭐

According to your course notes:

➡ Oxytetracycline binds calcium
➡ Produces relaxation/lengthening of contracted flexor structures

Used in:
⭐ Congenital flexural deformity

🔪 Surgery

Severe/persistent cases ➡ Surgical release/cutting of contracted tendon or accessory ligament depending on the structure involved.

4⃣ RUPTURE / ELONGATION OF COMMON DIGITAL EXTENSOR TENDON

Occasionally seen in foals.

Usually affects:
➡ Dorsal extensor tendon
➡ Mainly around carpal region

Tendon is:

• Elongated or Ruptured

🔍 Etiology

Often unknown.

Can be associated with Large foals

⚙ What Happens?

Extensor normally helps prevent excessive flexion.

Extensor elongated/ruptured
⬇
Cannot extend digit properly
⬇
Digit flexes excessively
⬇
🐴 Over-knuckling

🩺 Clinical Signs

• Inability to extend digit

• Difficulty stepping normally on hoof

• Over-knuckling

• Swelling of tendon sheath

🔎 Diagnosis

• Clinical signs

• ⭐ USG

💊 Treatment

• Cast / splint for prolonged support

• Controlled standing

➡ Standing helps improve extensor function.

Prognosis

⭐ Good

🚫 IMPORTANT

Oxytetracycline is CONTRAINDICATED!

Why remember this?

The problem is already:

Extensor tendon = too long / elongated

You do NOT want treatment aimed at further relaxing/lengthening soft tissues.

🧠

Short flexors → oxytetracycline ✅

Elongated extensor → oxytetracycline ❌

🌱 ACQUIRED FLEXURAL DEFORMITIES

Two major forms:

EARLY – suckling foal

➡ Club foot

LATE – weaned foal

➡ Flexural deformity of metacarpophalangeal joint

5⃣ CLUB FOOT

Early – Suckling Foal

Also called:
🩰 Ballerina conformation

The foal walks on its toe tip.

Main problem:
⭐ DDFT is functionally too short/tight relative to the bones

⚙ Pathogenesis

Rapid bone growth
+
DDFT doesn't lengthen enough
⬇
DDFT becomes relatively too short
⬇
Pulls strongly on P3
⬇
Changes/rotates coffin-bone orientation
⬇
Heel becomes high
⬇
Foal stands on toe

🩰 = BALLERINA

🔍 Etiology

• Overfeeding

  • Excess energy, Excess protein

• Bone grows faster than tendon

• Mineral imbalance:

  • P, Ca

• Sudden changes in feed intake

• Secondary hyperparathyroidism

• Exercise

• Trauma, Overload, Deep bedding, “Grass hoof”

🌱 What is “Grass Hoof”?

Foal repeatedly stands in the same position while grazing.

For example:
➡ Same limb repeatedly placed forward/backward

⬇

Unequal loading/growth

⬇

Can contribute to abnormal hoof conformation.

🩺 Clinical Signs – Club Foot

• High heels

• Stands on toes

• Sole does not contact ground normally

• Over-knuckling

• Upright/steep hoof

🧠 Club foot = HIGH HEEL + TOE TIP

🔎 Diagnosis

• Clinical appearance

• X-ray

• Sole elevation

💊 Treatment

👞 Hoof Correction / Shoeing

• Plastic shoe

• Instant shoe

• Dallmer shoe

Used approximately:
➡ 2–3 months

Purpose:
➡ Improve hoof-ground relationship/support during correction.

🔪 Surgical Treatment

• Accessory Ligament of DDFT Desmotomy ⭐

➡ Transect accessory/check ligament of DDFT

• Elongation Tenotomy

Can be performed:

• Middle metacarpal region
  and/or

• Tendon sheath region

➡ Used to release severe contracture.

🛡 Prevention of Club Foot

• Remove from pasture temporarily if needed

• Reduce excessive energy intake

• Reduce excessive protein intake

• Correct mineral balance

• Harder ground

• Correct hoof trimming

6⃣ LATE FLEXURAL DEFORMITY

Metacarpophalangeal / Fetlock Joint

• Occurs in older foals after weaning.

Associated with shortening/contracture of multiple supporting structures:

• Suspensory ligament

• Distal sesamoid ligaments

• DDFT

• Accessory ligament of DDFT

• SDFT

➡ Essentially the whole supporting/flexor apparatus becomes too tight/short.

🔍 Etiology

• Poor ossification

• Overfeeding

• Sudden nutritional changes

• Mineral imbalance

• Overload

• Trauma

🩺 Clinical Signs

Steep fetlock conformation

Normally fetlock/pastern:
➡ approximately 135° according to your notes

With deformity:
➡ Becomes very steep / almost straight

Also:
➡ Over-knuckling

🔎 Diagnosis

Primarily:
➡ Clinical signs

💊 Treatment

👞 Heel Support

➡ Elevate heel with wedge

Heel elevation
⬇
Changes tension/loading of DDFT
⬇
Helps correction/elongation of flexor unit

🔪 Surgery

Transect accessory ligaments of:

• DDFT

• SDFT

➡ Reduces restriction from contracted flexor structures.

🧠 THE WHOLE QUESTION IN ONE PICTURE

                    TENDON ANOMALIES
                          │
             ┌────────────┴────────────┐
             │                         │
          LAXITY                 FLEXURAL DEFORMITY
        TOO LONG                     TOO SHORT
        / WEAK                        / TIGHT
             │                         │
             ↓                         ↓
       HYPEREXTENSION               FLEXION
             │                      / KNUCKLING
             │
       Fetlock DOWN
       Toe may UP
                               ┌─────────┴─────────┐
                               │                   │
                          CONGENITAL            ACQUIRED
                               │                   │
                       Short flexors       ┌───────┴───────┐
                       → can't stand       │               │
                       → oxytetra        EARLY           LATE
                                         │               │
                                      CLUB FOOT      FETLOCK
                                         │          DEFORMITY
                                      DDFT short     whole apparatus
                                         │            tight
                                      🩰 TOE         knuckling

🧠 SUPER-QUICK DIFFERENTIATION ⭐⭐⭐

Condition	Main problem	Appearance
Flexural laxity	Flexors weak/long	⬇️ Fetlock hyperextends
Congenital flexor shortening	Flexors too short	↪ Limb remains flexed
Extensor elongation/rupture	Extensor too long/damaged	↪ Knuckling
Club foot	DDFT relatively too short	🩰 High heel + toe-tip
Late fetlock deformity	Supporting/flexor apparatus too short	↪ Steep fetlock + knuckling

⭐ EXAM ESSENTIALS

Two types of developmental tendon anomalies:

1. Laxity = LENGTHENING
➡ Weak/long structures
➡ Hyperextension
➡ Severe = fetlock on ground

2. Flexural deformity = SHORTENING
➡ Tight/short structures
➡ Flexion/knuckling

Premature foal + fetlock dropping down

➡ Flexural laxity

Newborn + flexed limbs + cannot stand

➡ Congenital flexural deformity
➡ Stretch/bandage/cast
➡ Oxytetracycline

Newborn + extensor rupture

➡ Knuckling
➡ Cast/splint
➡ ❌ NO oxytetracycline
➡ Good prognosis

Suckling foal + high heel + walks on toe

➡ Club foot
➡ DDFT too short
➡ 🩰 Ballerina conformation

Weaned foal + very steep/straight fetlock

➡ Late flexural deformity
➡ Multiple flexor/suspensory structures contracted

Osteoarthritis

Osteoarthritis (OA) = progressive destruction of articular cartilage, accompanied by changes in:

🦴 Bone

• Osteophyte formation, Degeneration/remodeling

Soft tissues

• Capsular fibrosis

⭐ Very frequent problem in horses, especially in high-motion joints.

1⃣ CLASSIFICATION

PRIMARY OA

Develops mainly due to:

➡ Chronic repetitive trauma
➡ Repetitive overloading

Risk factors depend on:

• Breed, Age, Sex, Conformation

Think:

🏇 Repeated loading → Small cartilage damage → More loading → Progressive OA

SECONDARY OA

OA develops as a consequence of another joint disease.

Examples:

• Traumatic arthritis

• Articular fracture

• Osteochondrosis

• Septic arthritis

🧠 Difference

PRIMARY
➡ Repetitive wear/overload itself starts OA

SECONDARY
➡ Another joint disease starts OA

2⃣ PATHOGENESIS ⭐⭐⭐

OA involves BOTH:

🔨 Mechanical destruction

🔥 Chemical/inflammatory destruction

These processes reinforce each other.

🔨 MECHANICAL DAMAGE:

Repeated abnormal loading/instability → cartilage damaged → Cartilage becomes less able to tolerate loading → More mechanical damage

🔥 CHEMICAL / INFLAMMATORY DAMAGE

Damaged joint tissues activate inflammatory pathways.

Important substances include:

• Cytokines (TNF, Interleukins) ➡ Promote synovitis and cartilage catabolism.

• Enzymes (Collagenase, Lysosomal enzymes, Proteoglycan-degrading enzymes) ➡ Break down components of cartilage matrix.

• Inflammatory Mediators (Prostaglandins, Leukotrienes, Histamine, Nitric oxide

• Other Factors: Free radicals, Antibodies

🔄 OA VICIOUS CYCLE ⭐⭐ ⭐

This is the main sequence to understand:

Mechanical injury / overload
⬇
💥 Cartilage damage
⬇
🔥 Inflammatory mediators released
⬇
Synovitis + capsulitis
⬇
Enzymes/cytokines damage cartilage
⬇
Loss of proteoglycans ⭐
⬇
Cartilage becomes soft and weak
⬇
More susceptible to mechanical damage
⬇
💥 MORE CARTILAGE DAMAGE
⬇
🦴 Subchondral bone changes
⬇
OA progresses

🔄 And the cycle continues.

🧠 WHY ARE PROTEOGLYCANS IMPORTANT?

Proteoglycans help cartilage:

💧 Retain water + Resist compression

OA
⬇
Proteoglycans lost
⬇
Cartilage becomes soft
⬇
Cannot tolerate normal forces
⬇
More mechanical damage

⭐ Initial important change = breakdown/loss of proteoglycans!!

3⃣ PATHOLOGY

OA affects:

BONE + CARTILAGE + SOFT TISSUES

🦴 BONE

Changes include:

• Osteophytes, Remodeling, Subchondral sclerosis, Subchondral lysis, Fractures

Osteophyte = new bone formation around joint margins (“Bone spurs”)

CARTILAGE

Normal cartilage:
➡ Smooth and Firm

OA cartilage becomes:

• Soft, Yellow, Surface fibrillation, Eroded, Disrupted/lost

🧵 What is Fibrillation?

Normal cartilage:

──────── smooth

OA:

≋≋≋≋ frayed/rough

➡ Surface starts splitting into small fibers/fissures.

🧱 SOFT TISSUES / SYNOVIUM

• Congestion

• Thickening

• Mononuclear inflammatory infiltration

• Villous hypertrophy

• Capsular edema

• Eventually capsular fibrosis

4⃣ CLINICAL SIGNS

Can include:

• Lameness, Pain on palpation, Positive joint flexion test

• Joint thickening, Reduced range of movement

• Crepitus

⚠ Many horses can be relatively asymptomatic.

➡ Radiographic OA does not necessarily mean the horse is obviously painful.

5⃣ DIAGNOSIS

💉 Local Analgesia ⭐

Local/intra-articular diagnostic analgesia can be used to identify the painful region/joint.

Block joint
⬇
Lameness disappears/improves
⬇
➡ Joint is implicated as pain source

🩻 RADIOGRAPHY

Can show:

• Osteophytes, Lysis

• Narrowed joint space, Subchondral bone changes/remodeling

⚠ Important:

X-ray changes occur relatively LATE.

So:

Early OA
➡ Cartilage damage may already exist but X-ray may still look relatively normal.

☢ SCINTIGRAPHY

➡ Increased radionuclide uptake

Indicates:
➡ Increased bone turnover/activity

🧲 MRI

Good for detecting:

• Subchondral bone abnormalities

• Cartilage abnormalities

• Soft-tissue abnormalities

📷 ARTHROSCOPY

Allows direct visualization inside joint.

Can identify:

• Cartilage softening, Fibrillation

• Cartilage loss, Osteophytosis / osteophytes

⭐ Advantage:
➡ Actually see the articular cartilage directly.

6⃣ TREATMENT

⚠ Important principle:

Articular cartilage has extremely limited regenerative capacity.

➡ Once significantly damaged, it does not simply regenerate back to normal cartilage.

Therefore treatment aims to:

• Reduce inflammation

• Reduce pain

• Slow further destruction

• Improve joint environment

• Correct instability/loading

• Maintain function

🟢 CONSERVATIVE TREATMENT

• Light/controlled exercise

• Correct overweight

• Pain management

• Minimize micro-instability of joint

🧠 Complete inactivity isn't necessarily the goal:

Controlled movement → maintain joint function

💉 INTRA-ARTICULAR MEDICATION

1⃣ CORTICOSTEROIDS

Strong anti-inflammatory drugs.

• Used when Joint is inflamed

But according to Zert:
⚠ Not always ideal because some inflammation is part of normal healing.

Avoid/inappropriate especially when there are:

• Severe lesions or Subchondral fractures

1. 💊 Methylprednisolone Acetate

Has relatively large crystals and can be more damaging to cartilage.

➡ Therefore, use mainly in LOW-MOTION JOINTS.

Examples:

• Pastern, Tarsal joints

🧠 Methylpred = LOW motion

2. 💊 Betamethasone + Triamcinolone

Used in HIGH-MOTION JOINTS.

Examples: Coffin, Carpal, Fetlock

🧠 Beta/Triam = HIGH motion

💧 2⃣ HYALURONIC ACID – HA ⭐

Important component of normal synovial fluid/cartilage environment.

Typically used:

➡ Together with corticosteroids in mild synovitis

Can also be used:

• IV after arthroscopy

• Prophylactically

⭐ Zert believes in this

💉 3⃣ POLYSULFATED GLYCOSAMINOGLYCANS – PSGAGs

⭐ First choice in severe chronic arthritis

Aim → Support/protect cartilage matrix and joint environment.

🩸 4⃣ PLATELET-RICH PLASMA – PRP

⭐ Very good

Contains platelets and growth factors.

➡ Used to modify inflammation and promote a more favorable healing environment.

🧬 5⃣ IRAP (Interleukin-1 Receptor Antagonist Protein)

IL-1: binds receptor on synovial/joint cells → promotes inflammation and cartilage destruction

IRAP blocks IL-1 receptor → IL-1 cannot exert as much effect → Less inflammatory signaling

🔪 6⃣ SURGICAL ARTHRODESIS

Arthrodesis = surgical fusion of a joint

Joint surfaces are fused → Joint no longer moves → Painful movement eliminated / stability restored

Used in selected cases such as:

• Intra-articular fractures, OCD, Ligament instability

Most useful where the loss of motion can be tolerated!

🏊 7⃣ PHYSICAL THERAPY

Examples:

• Swimming, Underwater treadmill

• Shock-wave therapy

Purpose:
➡ Maintain controlled movement/function while limiting excessive joint loading.

🧠 OA TREATMENT OVERVIEW

                    OSTEOARTHRITIS
                         │
        ┌────────────────┼────────────────┐
        │                │                │
   CONSERVATIVE     MEDICATION         SURGERY
        │                │                │
 Light exercise      Steroids         Arthrodesis
 Weight control         HA
 Pain control         PSGAG
 Stability             PRP
                       IRAP
        │
        ↓
 PHYSIOTHERAPY
 Swimming
 Underwater treadmill
 Shock wave

🧠 QUICK DIFFERENTIATION OF DRUGS

Treatment	Remember
Methylprednisolone	Corticosteroid → LOW-motion joints
Betamethasone	Corticosteroid → HIGH-motion joints
Triamcinolone	Corticosteroid → HIGH-motion joints
Hyaluronic acid	Mild synovitis, often + corticosteroid ⭐ Zert likes
PSGAG	Severe chronic arthritis
PRP	Growth factors / biologic treatment
IRAP	🚫 Blocks IL-1 receptor

🧠 OA IN ONE SEQUENCE ⭐⭐⭐

OVERLOAD / JOINT DISEASE
⬇
💥 CARTILAGE DAMAGE
⬇
🔥 INFLAMMATION
⬇
TNF + IL + prostaglandins + enzymes
⬇
PROTEOGLYCAN LOSS
⬇
🟡 CARTILAGE SOFTENS
⬇
FIBRILLATION + EROSION
⬇
🦴 SUBCHONDRAL BONE CHANGES
⬇
🦴 OSTEOPHYTES
⬇
PROGRESSIVE OA

🔄 Mechanical damage and inflammation continue to promote each other.

⭐ EXAM ESSENTIALS

Definition

OA = progressive cartilage destruction + bone and soft-tissue changes.

Primary OA

➡ Chronic repetitive trauma / overload

Secondary OA

➡ Consequence of another joint disease

Pathogenesis

➡ Mechanical + inflammatory/chemical destruction

Important early cartilage change

➡ Loss of proteoglycans → cartilage softens

Bone

➡ Osteophytes + remodeling + sclerosis/lysis

Cartilage

➡ Soft → fibrillation → erosion → loss

Clinical signs

➡ Lameness + reduced ROM + joint thickening + crepitus

⚠ But OA can be asymptomatic.

Diagnosis

💉 Local analgesia → localize pain
🩻 X-ray → relatively late changes
🧲 MRI → cartilage/subchondral bone
📷 Arthroscopy → directly visualize cartilage

Treatment

➡ Controlled exercise + weight management + pain control
➡ IA medication / biologics
➡ Correct instability
➡ Arthrodesis in selected cases

Developmental Anomalies of Joints

Joint disorders can involve:

• Synovial membrane, Surrounding tendons, Subchondral bone, Articular cartilage, Bursae, Synovial fluid

Main conditions:

1⃣ Septic arthritis – Joint ill in foals
2⃣ Osteochondrosis dissecans – OCD
3⃣ Subchondral bone cysts
4⃣ Spavin

1⃣ 🦠 SEPTIC ARTHRITIS/Joint ill

Septic arthritis = infection and inflammation of a synovial joint.

🚨 EMERGENCY

Can rapidly cause:
➡ Cartilage destruction, Secondary osteoarthritis, Permanent joint damage

Particularly important in foals.

🔍 Etiology

Main cause:
🦠 Bacterial infection

Important bacteria:

• Coliforms, Staphylococcus aureus, Streptococcus, Salmonella, Rhodococcus, Actinobacillus

🐴 ADULT HORSES

In adults, infection usually enters the joint directly.

Common causes:

💥 Penetrating wound into joint, or extension from nearby infection

Examples:

• Kick wound near hock, Kick wound near elbow

Can also be:

💉 Iatrogenic, following

• Arthrocentesis

• Intra-articular injection

• Surgery

FOALS ⭐⭐⭐

In foals, infection commonly reaches joints through:

🩸 HEMATOGENOUS SPREAD

Bacteria enter bloodstream → Travel through circulation → Reach synovial structures → Septic arthritis

Therefore:
➡ Multiple joints may be involved (septic polyarthritis)

🚪 Where Does Infection Start in Foals?

Possible primary sources:

• Umbilicus / urachus → Blood → Joint

• Pneumonia

• Enteritis

• Maternal placentitis ➡ Infection associated with pregnancy/perinatal period

• ⭐ Insufficient colostrum: Failure of passive transfer → Insufficient maternal antibodies → Foal highly susceptible to septicemia → Bacteria spread hematogenously → Joint ill

🩺 Clinical Signs

Local signs: Severe lameness, Joint swelling, Heat, Pain, Joint effusion

Systemic signs may include: 🌡 Pyrexia/fever

Especially in foals:
➡ May have systemic septicemia.

🔎 DIAGNOSIS

1.💉 SYNOVIAL FLUID ANALYSIS ⭐⭐⭐

One of the most important diagnostic methods.

Normal synovial fluid:
➡ Clear
➡ Viscous
➡ Low cellularity

Septic joint:

• ↑ Volume

• Turbid/cloudy

• Clots

• ↓ Viscosity

• ↑ Cell count

• Leukocytosis / high neutrophils

• ↑ Protein

🧠 Memory: SEPTIC FLUID = CLOUDY + WATERY + CELLS + PROTEIN

2.🧫 Microbiology

Culture synovial fluid.

⚠ Approximately 50% may be culture-negative

Possible reason:
➡ Neutrophils may have killed/removed bacteria
➡ Previous antibiotic treatment may also reduce recovery

So:

❌ Negative culture does NOT necessarily exclude septic arthritis.

3.🩻 X-RAY

⚠ Almost useless EARLY

Significant radiographic bone changes may not appear until approximately ➡ 7–10 days after infection

But septic joint is an emergency. 🚨 You cannot wait 7–10 days.

4.📡 ULTRASOUND

Useful.

Normal synovial fluid:
➡ Anechoic / black

Septic joint:
➡ Fibrin/clots/debris can become echogenic/hyperechoic

5.📷 ARTHROSCOPY ⭐

Very useful for:

Diagnosis (➡ Direct visualization of joint)

AND

Treatment ➡ Lavage, Remove fibrin/debris, Evaluate cartilage

⭐ Diagnosis + treatment at the same time

💊 TREATMENT – SEPTIC ARTHRITIS

🚨 Treat aggressively and immediately.

Main goals:

REMOVE INFECTION + REMOVE INFLAMMATORY MATERIAL + ANTIBIOTICS

💦 1. Joint Drainage & Lavage ⭐⭐⭐

Use several liters of sterile fluid.

Example:
➡ Hartmann's solution

Often performed during:
➡ Arthroscopy

Purpose: Bacteria + Inflammatory mediators + Fibrin + Debris → 💦 WASH THEM OUT

💉 2. Antibiotics

Prolonged and intensive treatment.

Can be:

• Systemic, Intra-articular

Common aminoglycosides:

• Gentamicin, Amikacin

Can be combined with: ➡ Procaine benzylpenicillin IM

💊 3. NSAIDs

Example:
➡ Flunixin

Purpose:

• Reduce inflammation, Reduce pain

🔪 4. Synovectomy / Debridement

➡ Remove fibrin clots and abnormal synovial material.

🧠 SEPTIC ARTHRITIS IN ONE LINE

BACTERIA → JOINT → SYNOVITIS → CARTILAGE DAMAGE → OA

Treatment:

💦 LAVAGE + ANTIBIOTICS + NSAIDs + REMOVE FIBRIN/DEBRIS

2⃣ OSTEOCHONDROSIS – OC

First, understand the difference:

Osteochondrosis = underlying developmental disorder

OCD = Osteochondrosis dissecans ➡ Clinical manifestation where abnormal cartilage develops fissures/flaps/fragments at the articular surface.

🦴 NORMAL ENDOCHONDRAL OSSIFICATION

Growing foal:

Cartilage → matures → is replaced by → BONE

This is:

⭐ Endochondral ossification

❌ OSTEOCHONDROSIS = disturbance of endochondral ossification

Parts of:

• Physeal growth cartilage

• Articular-epiphyseal cartilage

fail to convert normally into bone.

This can contribute to:

• Angular deformities, Valgus deformities, Osteochondrosis dissecans – OCD

3⃣ OSTEOCHONDROSIS DISSECANS – OCD ⭐⭐⭐

OCD is the clinically important articular form of osteochondrosis.

➡ Abnormal cartilage remains at the joint surface
➡ May fissure
➡ May form a flap
➡ May become an osteochondral fragment

🔍 Etiology

⭐ Multifactorial

Important factors:

• Rapid Growth: Growth spurts followed by growth setbacks.

• Mineral Imbalance: High phosphorus, Copper deficiency, High zinc

• Mechanical Trauma: Site-specific loading/trauma.

• Hormonal Factors: Growth hormone, Insulin, Thyroid hormones, Sex hormones ➡ More common in males

⚙ PATHOGENESIS OF OCD ⭐⭐⭐

This is the important sequence:

Normal cartilage should be converted into bone

BUT:

❌ Endochondral ossification fails → Deep cartilage is not converted to bone → Cartilage becomes abnormally thick → Deep chondrocytes become farther from nutrition → Poor nutrition to deep cartilage → Chondrocytes die → Cartilage necrosis → Fissures form → Fissure extends toward articular surface → CARTILAGE FLAP → May partially ossify → OSTEOCHONDRAL FRAGMENT

AGE

Clinical signs/lesions arise from:

➡️ Birth to approximately 2–3 years

Epiphyseal osseous development is not complete until approximately:
➡ 9–10 months

Therefore in young horses:

⭐ Some early lesions may resolve spontaneously during development.

🩺 Clinical Signs – OCD

• Lameness, Stiffness

• Positive flexion test

• Joint effusion

Joint effusion is especially noticeable in:

• Stifle, Hock

🔎 Diagnosis

🩻 X-ray ⭐

➡ Subchondral defects
➡ Osteochondral fragments

📷 Arthroscopy

➡ Direct visualization

Also:

• MRI, CT

💊 Treatment – OCD

Conservative

For selected young/mild lesions:

• Rest, Correct dietary intake, Correct mineral/nutritional imbalance

🔪 Surgical

➡ Arthroscopic debridement

Remove:

• Separated osteochondral fragments, Abnormal cartilage, Abnormal subchondral bone

🩸 PRP

➡ Platelet-rich plasma. Used to improve the healing environment.

💧 Hyaluronic Acid

⭐ Best. Used to improve joint environment and manage synovitis.

4⃣ SUBCHONDRAL BONE CYSTS = Osseous Cyst-Like Lesions

Cyst-like lesions occur in the subchondral bone, directly beneath articular cartilage.

Reported locations include:

• Medial femorotibial joint (medial femoral condyle of stifle joint)⭐, Carpus, Pastern, Coffin joint, Fetlock, Elbow, Shoulder, Hock

🔍 Etiology + Pathogenesis

Can be associated with:

Osteochondrosis

➡ Abnormal cartilage/endochondral ossification persists as localized defect within subchondral bone

OR

Trauma

➡ Localized trauma to:

• Articular cartilage, Underlying subchondral bone

• → Cyst-like lesion develops (fluid filled cavity in bone just beneath articular cartilage)

🩺 Clinical Signs

• Lameness localized to joint, Joint effusion

🔎 Diagnosis

• Flexion test

• 🩻 X-ray, CT, MRI

💊 Treatment

Conservative: Rest

Surgical / Interventional:

• Corticosteroid injection into cyst

• Debridement

• Grafts

• Cartilage resurfacing

5⃣ SPAVIN

Degenerative, Non-Septic Arthritis

⭐ Seen in LOW-MOTION JOINTS

Frequently affects:
➡ Distal tarsal/hock joints

Mostly seen in:
➡ Adult horses

📌 What Is Spavin?

Spavin = chronic degenerative non-septic arthritis of low-motion hock joints.

Joint degeneration → Pain + inflammation → Progressive degeneration → Bone proliferation
⬇
Eventually:
🦴 ANKYLOSIS / FUSION

🔗 ANKYLOSIS

Ankylosis = pathological fusion/stiffening of a joint.

In spavin:

Joint gradually degenerates → Joint space disappears → Bones fuse → Joint no longer moves

Because these are low-motion joints, complete fusion may eventually reduce pain from movement.

🔍 Etiology

• Overloading, Conformation problems

🩺 Clinical Signs

• Pain, Lameness, Stiffness

💊 Treatment

Tildren IV ➡ Tiludronate

Purpose: Reduces osteolysis / excessive bone resorption

🧠 THE FOUR CONDITIONS – DON'T MIX THEM UP ⭐⭐⭐

Condition	Main problem	Typical patient	Key clue
🦠 Septic arthritis	Bacterial joint infection	Foal or adult	Hot, swollen painful joint
🦴 OCD	Failed endochondral ossification	Young horse	Thick cartilage → flap/fragment
🕳 Subchondral cyst	Cyst-like lesion beneath cartilage	Young horse	Subchondral defect
🦵 Spavin	Degenerative non-septic arthritis	Adult horse	Low-motion hock → eventual fusion

⭐ EXAM ESSENTIALS

SEPTIC ARTHRITIS

➡ Bacterial infection = emergency
➡ Adults: penetrating wound/iatrogenic/local spread
➡ Foals: hematogenous, often due to failure of passive transfer/septicemia
➡ Multiple joints possible
➡ Synovial fluid: turbid, ↓ viscosity, ↑ cells, ↑ protein
➡ Culture can be negative
➡ X-ray changes delayed 7–10 days
➡ USG → fibrin/debris
➡ Arthroscopy = diagnosis + treatment
➡ Lavage + antibiotics + NSAID

OCD

➡ Failure of endochondral ossification
➡ Rapid growth + minerals + trauma + hormones
➡ Thick cartilage → necrosis → fissure → flap → fragment
➡ Young horses
➡ Some early lesions can resolve
➡ X-ray + arthroscopy
➡ Rest/diet or surgical debridement

SUBCHONDRAL CYST

➡ Lesion beneath cartilage
➡ OC or trauma
➡ Lameness + effusion
➡ X-ray/CT/MRI
➡ Rest or cyst treatment/debridement/grafts

SPAVIN

➡ Degenerative, non-septic arthritis
➡ Adult horse
➡ Low-motion tarsal joints
➡ Pain + lameness + stiffness
➡ Final result = ankylosis/fusion
➡ Tildren IV → ↓ osteolysis