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Basics ⬇

Outline

BASICS

Definition!!navigator!!

Laminitis is failure of the hoof–distal phalanx attachment apparatus.

Pathophysiology!!navigator!!

  • The lamellae suspend P3 within the hoof capsule—epidermal lamellae extend like sheets from the stratum medium of the inner hoof wall, interdigitating with dermal lamellae that are ultimately connected to P3. Each primary lamella has multiple secondary lamellae, increasing surface area and strength of attachment. The basement membrane separates the epidermal and dermal lamellae and is a key structural component. Collagen bundles, arranged in linear rows, connect the basement membrane to P3, forming the “suspensory apparatus of the distal phalanx”
  • Although the pathophysiology remains unclear, loss of normal epidermal basal cell adhesions/cytoskeletal integrity appears to be a key early event regardless of cause. Altered growth factor signaling, inflammation, and changes in perfusion and/or energy balance appear to trigger these events, leading to loss of structural integrity, with the distractive forces of weight-bearing then contributing to further to damage
  • There are 3 distinct major forms of laminitis based on the underlying cause and mechanisms—laminitis associated with severe systemic disease (sepsis associated); laminitis associated with insulin dysregulation (endocrinopathic laminitis); and laminitis associated with excessive weight-bearing on a foot (supporting limb laminitis)
  • Endocrinopathic laminitis is intrinsically linked to insulin dysregulation in horses/ponies and encompasses laminitis associated with EMS, PPID, and exogenous corticosteroid administration. Current evidence suggests that excess insulin overstimulates growth factor receptor IGF-1R, which triggers a response in lamellar epidermal cells that involves disruption of normal cell adhesions
  • Sepsis-associated laminitis occurs with severe systemic inflammation, usually as a result of infection (e.g. pneumonia) or the absorption of bacterial products (particularly endotoxin) from the gastrointestinal tract (e.g. colitis, natural/experimental alimentary carbohydrate overload). Marked local inflammation including infiltration of the lamellae with neutrophils is characteristic
  • Supporting limb laminitis appears to be the result of ischemia due to reduced lamellar perfusion due to both increased load and reduced unweighting/load cycling on a limb
  • Pasture-associated laminitis may involve pathophysiologic elements of both endocrinopathic and sepsis-associated forms
  • Once the lamellar attachments are weakened, the nature and severity of the resultant pathology are determined by the extent of lamellar damage. Severe, wholesale acute lamellar detachment can result in downward P3 “sinking” within the hoof capsule. In less severe cases, deep flexor tendon tension and lamellar epidermis proliferation result in palmar rotation of P3 away from dorsal hoof wall and formation of the “lamellar wedge.” Loss of the suspensory function of the lamellae leads to compression of the sole corium by the distal surface of P3, a considerable source of pain in chronic cases. With displacement of P3, growth of the hoof wall becomes disrupted, and vascular structures may be compressed
  • In many endocrinopathic cases chronic laminitis pathology is very slowly progressive and substantial pathology is often already present by the time clinical signs are first recognized
  • In many acute cases damage is mild and there is no resultant detectable displacement of P3

Systems Affected!!navigator!!

Musculoskeletal—foot.

Genetics!!navigator!!

N/A

Incidence/Prevalence!!navigator!!

N/A

Geographic Distribution!!navigator!!

N/A

Signalment!!navigator!!

  • Rare (absent?) in foals or weanlings
  • Pony breeds more susceptible to the endocrinopathic form
  • Chronic laminitis is common in broodmares

Signs!!navigator!!

General Comments

  • Wide range of clinical presentations, from severe lameness and recumbency to poor performance in an athletic horse that is not overtly lame
  • Laminitis is divided into 3 phases—developmental, acute, and chronic

Historical Findings

  • Acute or recurrent lameness of variable severity in 1 or more limbs
  • Reluctance to move ± more frequent recumbency
  • Lameness worse when circling or on hard ground
  • Recent systemic disease or access to excess grain or lush pasture
  • ±Severe, prolonged contralateral limb lameness

Physical Examination Findings

  • Developmental phase
    • No clinical signs; however, primary disease and pathologic processes that lead to lamellar damage are under way
  • Acute laminitis
    • Increased digital pulse amplitude and hoof wall/coronary band temperature
    • ±Distal limb edema
    • Incessant shifting weight in fore- and hindlimbs
    • In mild cases, subtle lameness
    • With increasing severity, obvious lameness at the walk; worse circling on a hard surface
    • Most often, 1 or both front feet are affected; less severe in the hindlimbs
    • Characteristic stance—forelimbs extended forward and hindlimbs underneath the body
    • In severe cases, unwillingness to move and recumbency
    • ±Difficulty lifting limbs due to reluctance to bear weight on opposite limb
    • Tachycardia, tachypnea, and sweating may be profound
    • Highly variable response to hoof testing. ± Generalized hoof pain or focal pain in toe region. ± Reaction to tapping the hoof wall
  • Chronic laminitis
    • Defined by ≥48 h of clinical laminitis and/or radiographic displacement of P3 within the hoof capsule
    • Increased digital pulse amplitude
    • Variable lameness
    • ±Prolonged periods in recumbency
    • Palpable coronary band cleft
    • Prolapse of the sole in the toe; ± P3 penetration through the sole
    • ±Uneven hoof growth rings, wider in quarters/heels, narrower in dorsal hoof wall
    • Characteristic “dished” appearance to dorsal hoof wall
    • ±White line separation, seedy toe, and abscess
    • ±Persistent tachycardia and hypertension
    • Weight loss in moderate to severe cases

Causes!!navigator!!

  • Systemic septic diseases including colitis (bacterial, Potomac horse fever, grain overload), anterior enteritis, colonic volvulus, septic peritonitis, pneumonia, metritis/retained fetal membranes
  • Insulin dysregulation due to EMS or PPID
  • Pastures rich in nonstructural carbohydrate, particularly in combination with EMS or PPID
  • Excessive weight-bearing on a limb due to pain or dysfunction of the opposite limb
  • Exertional rhabdomyolysis
  • Exposure to black walnut (Juglans nigra) heartwood shavings
  • Ingestion of the toxic plant hoary alyssum (Berteroa incana) in hay or pasture
  • Excessive work on hard surfaces
  • Corticosteroid administration
  • Excessive intake of cold water (empirical reports only)

Risk Factors!!navigator!!

See Causes.

Diagnosis ⬆ ⬇

Outline

DIAGNOSIS

Differential Diagnosis!!navigator!!

  • Other painful conditions such as rhabdomyolysis, tetanus, or pleurodynia secondary to pleuropneumonia. Rule out by absence of increased digital pulse amplitude and digital hyperthermia
  • Unilateral limb laminitis or laminitis that is more severe in 1 digit must be differentiated from hoof abscess or P3 fracture. Rule out by hoof testing and radiographs

CBC/Biochemistry/Urinalysis!!navigator!!

  • Abnormalities due to inciting cause(s)
  • ±Stress leukogram

Other Laboratory Tests!!navigator!!

  • Testing of the pituitary adrenal axis in cases of suspected PPID (Cushing disease). Baseline adrenocorticotropic hormone concentration or thyrotropin-releasing hormone response test preferred to dexamethasone suppression test

  • Baseline insulin concentration or preferably dynamic testing (oral sugar test) for the diagnosis of insulin dysregulation of PPID or EMS.
  • Plasma creatinine and albumin concentrations with NSAID use to monitor for toxicity

Imaging!!navigator!!

  • Standard lateromedial radiographs to assess P3 position relative to the hoof capsule. Radiopaque marker placed on dorsal hoof wall at the coronary band aids in measurements. A steel rod of known length can be used to correct for magnification
  • Radiographs obtained at onset of clinical signs to document progression
  • P3 rotation, dorsal hoof wall to P3 distance, and coronary band to the extensor process of P3 distance can guide progression and prognosis
  • Digital venograms may be useful in chronic cases to determine vascular compression or thrombosis. ± Guide hoof wall resection or coronary grooving. Adhere to published descriptions of this technique to avoid common artifacts

Other Diagnostic Procedures!!navigator!!

Avoid perineural anesthesia unless there is difficulty isolating lameness to the foot.

Pathologic Findings!!navigator!!

  • Chronic—sagittal sectioning of the feet reveals characteristic formation of lamellar wedge and palmar rotation of P3
  • Acute—lamellar histopathology recommended, gross changes may not be obvious

Treatment ⬆ ⬇

Outline

TREATMENT

Aims!!navigator!!

  • Treat underlying cause(s)
  • Acute—limit mechanical damage, control inflammation
  • Chronic—provide mechanical support, encourage normal hoof growth
  • Provide adequate analgesia and supportive care

Appropriate Health Care!!navigator!!

Developmental Phase

  • Laminitis is irreversible; focus is prevention during the developmental phase and minimizing progression in the early acute phase
  • With septic disease/endotoxemia, aggressive systemic treatment with anti-inflammatory and antiendotoxic therapy as well as continuous cooling of the feet. Ideally, an ice and water mixture is applied from the proximal metacarpal/metatarsal region to (and including) the hooves and is regularly replenished. Maintain ice boots for up to 7 days
  • Preemptive shoe removal and application of frog/sole support

Acute Phase

  • Once clinical signs are apparent, limit mechanical damage
  • Strict stall confinement
  • Continuous cooling of the feet after the onset of lameness in sepsis-associated cases
  • Light sedation may encourage recumbency
  • In less painful horses, shoe removal, excessive toe conservatively trimmed
  • Bed on sand or apply silicone impression material or Styrofoam padding to the sole
  • Styrofoam pads custom sized to the foot and taped on overnight. Once crushed down, remove pad and cut off the toe portion. Reapply pad with an additional second pad underneath to preferentially load the caudal foot
  • ±Heel elevation (10–20°) to reduce deep flexor tendon tension and redistribute distracting forces from the dorsal wall to quarters/heels
  • Judicial NSAID use; excessive analgesia may encourage locomotion and increase mechanical damage
  • ±Sling support during standing periods especially with rapid P3 sinking

Chronic Phase

  • Medical management of underlying endocrinopathy (EMS or PPID), diet management, restrict nonstructural carbohydrate consumption (soaked hay, commercially formulated feeds)
  • Ongoing farriery and a close client–veterinarian–farrier relationship are required for successful management
  • Avoid radical trimming or shoeing. Gradual changes over >1 shoeing interval to avoid destabilizing the foot and worsening of clinical signs
  • Shoe/pad/trim or other farrier techniques that redistribute weight from hoof wall to frog and caudal sole, minimize breakover forces, and reduce deep flexor tendon tension
  • Radiographs should be used as a guide for trimming and shoeing

Nursing Care!!navigator!!

  • Deep bedding, particularly if recumbent for prolonged periods
  • Sling support may facilitate trimming and shoeing

Activity!!navigator!!

  • In acute phase, absolute strict stall confinement
  • Stall rest for at least 1 month, and up to ≥6 months, after an acute laminitis; depends on severity
  • Very, very gradual reintroduction to exercise

Diet!!navigator!!

  • Avoid excessive carbohydrate in grain, hay, and pasture
  • Obese and/or EMS horses benefit from controlled, gradual weight loss

Client Education!!navigator!!

  • Clients should be made aware of the potentially life-threatening nature of the disease
  • Client compliance with management of restricted turnout and diet (including access to pasture) is vitally important to treatment success

Surgical Considerations!!navigator!!

  • With significant P3 rotation (>15°) or where the dorsal tip of P3 is penetrating the sole or causing solar prolapse, deep flexor tenotomy may be beneficial
  • In chronic cases, coronary grooving or dorsal hoof wall resection can relieve tension on the coronary band, reduce sublamellar venous compression, and facilitate better quality hoof wall regrowth

Medications ⬆ ⬇

Outline

MEDICATIONS

Drug(s) of Choice!!navigator!!

  • NSAIDs—phenylbutazone (2.2–4.4 mg/kg every 12 h) tends to provide superior analgesia to flunixin meglumine (1 mg/kg every 12 h)
  • Acepromazine (0.02–0.04 mg/kg IV or IM every 6 h) during the acute phase

Contraindications!!navigator!!

Avoid corticosteroid administration.

Precautions!!navigator!!

Monitor for signs of toxicity with long-term NSAID use.

Possible Interactions!!navigator!!

N/A

Alternative Drugs!!navigator!!

  • Constant rate infusion of lidocaine, ketamine, and morphine, alone or in combination, can provide potent short-term analgesia
  • Gabapentin (20 mg/kg orally every 12 h) in severe acute or chronic cases
  • Metformin and pergolide should be restricted to patients with confirmed insulin dysregulation or PPID, respectively

Follow-up ⬆ ⬇

Outline

FOLLOW-UP

Patient Monitoring!!navigator!!

  • Daily monitoring of acute cases
  • Chronic cases require consistent monitoring; the frequency depends on the experience of the owner/trainer and disease severity
  • Initially, repeat radiographs obtained at each trimming/shoeing interval (2 weeks) and subsequently at 4 week intervals
  • Repeat endocrine testing for EMS and PPID as appropriate

Prevention/Avoidance!!navigator!!

  • Aggressive and early treatment of primary disease in systemically ill horses
  • Identify horses with EMS/PPID or insulin dysregulation and strict dietary control to avoid hay/grain and pasture high in soluble carbohydrate; maintain an ideal body weight
  • For high-risk horses, avoid pasture turnout when nonstructural carbohydrate levels are likely to be highest—midmorning to late afternoon, spring and fall, during flowering and early seeding or after frosts
  • Use a grazing muzzle during high-risk periods

Possible Complications!!navigator!!

  • Detachment and sloughing of hoof wall in severe acute/subacute cases
  • Progressive rotation, sinking, and sole penetration of P3 followed by necrosis and osteomyelitis in chronic disease
  • ±Persistent hypertension with cardiac hypertrophy in chronic disease
  • ±Renal failure and right dorsal colitis from long-term NSAID use

Expected Course and Prognosis!!navigator!!

  • Depends entirely on extent of the lamellar damage; however, lameness severity is always the most useful prognostic indicator regardless of other factors
  • “Sinking” of P3 results in a poor prognosis for survival
  • Sole penetration by P3 significantly worsens prognosis
  • Chronic cases with >15° of P3 rotation have a guarded prognosis for survival and grave prognosis for soundness
  • Return to athletic activity is highly variable; horses with >5° of P3 rotation or sinking of P3 are unlikely to return to athletic activity

Miscellaneous ⬆ ⬇

Outline

MISCELLANEOUS

Associated Conditions!!navigator!!

N/A

Age-Related Factors!!navigator!!

N/A

Zoonotic Potential!!navigator!!

N/A

Pregnancy/Fertility/Breeding!!navigator!!

N/A

Synonyms!!navigator!!

Founder

Abbreviations!!navigator!!

  • EMS = equine metabolic syndrome
  • NSAID = nonsteroidal anti-inflammatory drug
  • PPID = pituitary pars intermedia dysfunction
  • P3 = third phalanx

Suggested Reading ⬆ ⬇

Belknap JK, Geor R, eds. Equine Laminitis. Ames, IA: Wiley Blackwell, 2017.

Author(s) ⬆

Author: Andrew W. van Eps

Consulting Editor: Elizabeth J. Davidson