Lecture 14- Disease of equine muscle 3

Myopathy vs rhabdomyolysis

Myopathy = subtle signs, normal CK; Rhabdomyolysis = muscle integrity disruption, pain, weakness, myoglobinuria, ↑ CK, AKI risk

Sporadic vs chronic ER

Sporadic = no prior ER; Chronic = repeated ER; Myopathy = repeated stiffness/reluctance, normal CK

Genetic exertional myopathies

MYHM, MH, PSSM1 (validated tests)

Non‑genetic exertional myopathies

RER, PSSM2‑ER, MFM‑ER, MFM‑WB (no validated genetic tests)

SER etiology

Overexertion; dietary imbalance; underlying disease; all breeds affected

SER clinical signs

Muscle pain; stiffness → recumbency; unwilling to move; urination posture; resembles colic; sweating; tachycardia; tachypnea; pigmenturia

SER diagnosis

CK/AST ↑ (1,000–100,000+); hyperkalemia; dehydration; acidosis; pigmenturia; casts; rule‑outs

SER treatment

Minimize movement; sedation; fluids/electrolytes; NSAIDs; furosemide; methocarbamol/dantrolene; rest; gradual return to work

ER causes overview

Sporadic ER (extrinsic); Chronic ER (intrinsic: MH, RER, PSSM1, PSSM2‑ER, MFM‑ER)

RER etiology

Genetic predisposition (unknown mutation); abnormal intracellular Ca regulation; TB/STB/Arabians; young, fit, nervous; females; recurrent episodes

RER triggers

Excitement; stress; high‑starch diet; rest before exercise; environmental changes

RER clinical signs

Muscle cramps; stiffness; pain; migrating lameness; sweating; tachypnea; refusal to move; pain on palpation; ↑ HR/RR

RER CK testing

Draw CK 4–6h post‑exercise; expect 3–4× baseline; more fluctuation in 2‑year‑olds

RER diagnosis

History + signs; CK/AST; biopsy for difficult cases; fractional excretion; Vit E/Se; exercise testing for subclinical cases

RER treatment

Treat rhabdo; reduce triggers; pharmacologic + management; high‑fat low‑starch diet; electrolytes

RER diet

Forage: high‑quality grass/oat hay 1.5–2% BW; NSC <20% DE; fat 20–25% DE; complete feeds: Re‑Leve, Ultium

Comparative diet: RER

NSC low‑moderate (<20%); fat high (20–25%); protein standard; supplements: electrolytes

Comparative diet: PSSM

NSC strictly low (<12%); fat high; protein standard; supplement: acetyl‑L‑carnitine

Comparative diet: MFM

NSC moderate (20–30% concentrate); fat low‑moderate (6–8%); protein very high (12% CP); supplements: CoQ10, NAC

PSSM overview

Glycogen storage disease; abnormal polysaccharide accumulation; energy deficit

PSSM1 etiology

Autosomal dominant GYS1 mutation; validated genetic test

PSSM1 breeds

QH + related; European draft breeds; >20 breeds

PSSM1 triggers

Rest before exercise; diet; exercise level; environmental factors; other genes

PSSM1 clinical signs

Young horses; ER with little exercise; tucked abdomen; camped‑out stance; lazy; shifting lameness; fasciculations; sweating; hindlimb stiffness; colic‑like signs

PSSM1 draft horse signs

Classic ER OR progressive weakness, muscle loss, recumbency

PSSM1 diagnosis

Genetic test; interpret cautiously in drafts; biopsy for polysaccharide aggregates

PSSM1 treatment

See SER; horses remain susceptible; avoid rest; turnout; regular incremental exercise; low NSC (<12%); high fat; commercial diet

PSSM2‑ER etiology

No identified mutation; abnormal glycogen/polysaccharide (less than PSSM1); higher glycogen concentrations

PSSM2‑ER breeds

QH (barrel, working, reining >> halter); others

PSSM2‑ER clinical signs

Pain; sweating; firm muscles; stiffness; reluctance after light exercise; low‑grade lameness; fasciculations; occasional pasture rhabdo

PSSM2‑ER diagnosis

No validated genetic test; compatible signs + ↑ CK after exercise; muscle biopsy

PSSM2‑ER treatment

Same as PSSM1/PSSM management; diet/exercise program

MFM overview

Myofibrillar disarray + desmin aggregation; structural myopathy; mitochondrial complex I involvement; low cysteine antioxidants

MFM lesions

Myofibrillar disarray; ectopic desmin accumulation

MFM phenotypes

MFM‑ER (Arabians); MFM‑WB (Warmbloods)

MFM‑ER (Arabians) signs

Older endurance horses; ER at end of long rides; stiffness; pain; CK >10,000; biopsy: desmin aggregates

MFM‑WB signs

Young promising horses → issues at 6–8y; lack stamina; unwilling to go forward; poor collection; abnormal canter transitions; stiffness; mild pain; mild shifting lameness; mild‑moderate atrophy; rarely ER; CK normal

MFM‑WB diagnosis

Rule out tack, training, ulcers, asthma, eNAD/VEM, orthopedic; CK 4h post‑exercise; biopsy (gluteal/SM)

MFM‑WB treatment

Diet; supplements; rest/exercise program; MFM Pellet (KER)

MFM diagnostic workflow

Tack fit → physical exam → neuro exam → lameness exam + 4h CK → Vit E/Se → gastroscopy → biopsy

Malignant hyperthermia etiology

Autosomal dominant RYR1 mutation; Ca release channel dysfunction

MH triggers

Halothane anesthesia; succinylcholine; stress; excitement; exercise

MH breeds

QH + related

MH clinical signs anesthesia

Tachycardia; hyperthermia; muscle rigidity; severe lactic acidosis; ↑ CK; electrolyte derangements

MH clinical signs exertional

Excessive sweating; tachycardia; tachypnea; hyperthermia; rigidity; sudden death

MH association

May occur with PSSM1; PSSM horses respond poorly to typical MH treatment

MH diagnosis

Genetic test (validated)

MH treatment

Dantrolene; supportive care; avoid triggers

Validated genetic tests

MYHM; MH; PSSM1

No validated genetic tests

RER; PSSM2‑ER; MFM‑ER; MFM‑WB