LAM: Exam 3

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<p><span style="background-color: transparent;"><strong>Neurological Localization of PNS and Spinal Cord Disease</strong></span></p>

Neurological Localization of PNS and Spinal Cord Disease

  • Spinal cord: Gait abnormalities w/ absence of intracranial signs

    • gait deficits, spastic paresis, ataxia, Flaccid paresis & muscle atrophy, proprioceptive deficits

  • Cervical: Head normal, both fore & hindlimbs abnormal

  • Below T2: Head/neck/forelimbs normal, hindlimbs abnormal

    • If tetraparesis w/o brain signs → lesion localizes to C1–T2

  • White matter lesions (long tracts): spastic paresis, ataxia caudal to lesion

    • sensory information from the body to the brain (ascending tracts) and motor commands from the brain to the muscles and glands (descending tracts). 

  • Gray matter lesions (LMN): flaccid paresis, muscle atrophy (focal/segmental)

  • Peripheral n.: flaccid paresis, focal atrophy, sensory loss in one limb

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<p>Motor unit</p>

Motor unit

  • consisting of a single motor neuron (nerve cell) and all the individual skeletal muscle fibers it innervates

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Localization of Brain Disease

  • Cerebrum- Forebrain: depression, disorientation, nervousness, hyperexcitability, compulsive walking/circling, head pressing, maniacal behavior, seizures, cortical blindness

    • Consciousness, awareness, behavior change, intellect, voluntary motor control (UMN)

  • Brainstem: Alterations in consciousness & arousal - no brain signs

    • obtunded, stupor, coma, cranial nerve deficits, head tilt, leaning/listing, resting nystagmus, spastic paresis, ataxia, vestibular ataxia

      • motion, vestibular input

  • Cerebellum: attention tremor, coordination & motor activity(rate/range/speed/force)

    • Dysmetria/hypermetria(all 4 legs), Truncal sway, Intention tremor of head, Loss of menace response, Disequilibrium or paradoxical vestibular syndrome

      • motor activity, arousal (RAS), aranial nerve nuclei, vestibular & somatic motor integration

  • Cranial N.: Head abnormal, limbs/trunk normal

  • Diffuse Brain: Head + limbs abnormal

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Cerebrospinal Fluid Analysis

  • Collection sites:

    • Lumbosacral: Standing horse

      • Needle enters ventral subarachnoid space through conus medullaris (S4–S5)

      • Collect from dorsal subarachnoid space

    • Atlanto-occipital: Recumbent under GA

      • Midline insertion between atlas wings and nuchal crest

    • Atlanto-axial: Standing, lateral approach

  • Evaluation:

    • Colour: Clear, colorless

    • WBC: 0–4, mononuclear

      • IgG index = (CSF IgG / serum IgG) × (serum albumin / CSF albumin) → intrathecal IgG production

    • Total protein: < 90 mg/dL

      • Albumin quotient = (CSF albumin / serum albumin) × 100 → BBB integrity

    • Ab testing: 

      • Viral: EHV-1, WNV, EEV, WEV

      • Protozoal: EPM

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Diagnostic Imaging of the Nervous System

  • Radiography/myelography: vertebral alignment, compression

  • CT/MRI: brain, cervical spine

  • Electromyography: LMN dz vs myopathy

  • Electroencephalography: cerebral electrical activity

  • Auditory brainstem evoked response: hearing & brainstem lesions

    • Cell bodies: ventral gray horn (spinal cord) or brainstem nuclei

    • Axons: form ventral spinal roots & motor cranial nerves

    • Why: directly cause muscle contraction (motor unit)

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what are the clinical signs of peripheral nerve injuries or neuropathies in a horse?

  • lameness, poor coordination (ataxia), and weakness, which can be severe enough to prevent weight bearing.

  • muscle wasting (atrophy), drooping or paralysis of facial features like the lip or ear, gait abnormalities like goose-stepping or toe-dragging, and a lack of sensation in affected areas. 

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Cranial Nerves

  • I Olfactory: Smell (sensory)

  • II Optic: Vision (sensory)

  • III Oculomotor: Eye movement, parasympathetic to ciliary muscle

  • IV Trochlear: Dorsal oblique muscle

  • V Trigeminal: Mastication, facial sensation

  • VI Abducens: Lateral rectus & retractor bulbi

  • VII Facial: Facial expression, salivation, lacrimation, taste

  • VIII Vestibulocochlear: Balance & hearing, head position

  • IX Glossopharyngeal: Pharynx, salivation, taste

  • X Vagus: Pharynx, larynx, parasympathetic to thorax & abdomen

  • XI Spinal Accessory: Neck & pharyngeal muscles

  • XII Hypoglossal: Tongue movement

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Adult Seizures

  • Et: Uncontrolled synchronous discharge of cerebral cortical neurons

    • CS Specific to cerebral cortex

  • Types:

    • Primary: trauma, infection, toxins, developmental

    • Secondary: hepatic/renal, glucose/Na/Ca disturbances, hyperthermia, hypoxia/ischemia

    • Idiopathic: Sporadic adult idiopathic epilepsy (all breeds)

  • Cs: 

    • Focal(partial/localized/absence): facial/limb twitching, compulsive circling, self-mutilation

    • Gen: loss of consciousness, recumbency, tonic-clonic activity, post-ictal blindness/depression

    • Epilepsy: recurrent seizures, non-progressive cerebral cortical disease

  • Tx: Diagnosis & treatment of underlying dz #1!!! protect the head, Padding, Diazepam (short/ER), Phenobarbital (Long term) Levetiracetam (Keppra), Bromides, Gaba

    • Management: Loading dose, maintenance dose, daily dose for recurrent seizures

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Juvenile Idiopathic Epilepsy

  • inheritable

  • Sig: Arabian foal syndrome, start ~ <6m

  • Cs: post-ictal depression: most common, disorientation, blindness, trauma

  • Dx: CS, history and breeding

  • Tx: Diazepam acutely, phenobarbital 1y (maintenance), supportive care, self limiting with age, don’t breed

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Lavender Foal Syndrome

  • coat color dilution lethal

  • Et: Autosomal recessive, lethal

  • Sig: Egyptian Arabians w/ color dilution (lavender/pink/purple)

  • Cs: inability to stand @ birth, seizures,  CNS signs, death

  • Tx: Euthanasia

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Cerebellar Abiotrophy

  • inheritable

  • Et: Autosomal recessive

  • Sig: Arabians, 6m

  • Cs: symmetric hypermetria/dysmetria(4 limbs), spasticity, truncal sway, intention tremor, absent menace

  • Dt: genetic testing

  • Tx: euthanasia, no treatment

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Seizure Disorders in Foals

  • Neonatal encephalopathy; due to perinatal oxygen

    deprivation = most common!!!!

    • metabolite/electrolyte disturbances, bacterial meningitis, congenital defects(Arabians), older foals: trauma

  • Cerebellar Abiotrophy, Lavender Foal Syndrome,Juvenile Idiopathic Epilepsy

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<p><span style="background-color: transparent;"><strong>Cranial Trauma</strong></span></p>

Cranial Trauma

  • Common injury: direct impact

  • Et: edema #1!!**, ↑ ICP, herniation

    • severe/uncontrolled edema: cerebral and/or cerebellar herniation

  • Cs: Depression, recumbency w/ stupor or coma, vestibular signs, blood/CSF from ears/nose = fracture, abnormal pupils, head tilt

    • Frontal/parietal/orbital: concussion, contusion, hemorrhage, brain parenchyma disruption

    • Petrous temporal/occipital: very common - young by flipping over backwards

      • vestibular dysfunction, facial paralysis, bleeding from ears, optic nerve damage

    • Poll injuries: hyperextension of neck,  basilar fractures = fractures/b-sphenoid & b-occipital bone separation = intracranial hemorrhage & severe brain injury, guttural pouch hemorrhage, tearing optic nerve: blindness

      • Rupture/avulsion of ventral straight mm &/or fracture at base of brain

  • Dt: rads, CT, MRI, endoscopy

  • Tx: Stabilize airway / padding, IV catheter, Mannitol/furosemide (not w/ hemorrhage), hypertonic saline, hyperventilation (foals), Sx for fragments, monitor BP

    • poor prognosis → hemorrhage in CSF, recumbence, seizures, coma, fixed pupils, erratic breathing

<ul><li><p><strong><u>Common injury: direct impact</u></strong></p></li><li><p><span style="background-color: transparent;"><strong><span>Et: </span></strong></span><span style="background-color: transparent; color: red;"><strong><u><span>edema #1!!**</span></u></strong></span><span style="background-color: transparent;"><span>, ↑ ICP, herniation</span></span></p><ul><li><p><u>severe/uncontrolled edema</u>: cerebral and/or cerebellar herniation</p></li></ul></li><li><p><span style="background-color: transparent;"><strong><span>Cs: </span></strong><span>Depression, recumbency w/ stupor or coma, </span></span><span style="background-color: transparent; color: red;"><span>vestibular signs,</span></span><span style="background-color: transparent;"><span> </span></span><span style="background-color: transparent; color: red;"><span>blood/CSF from ears/nose = fracture</span></span><span style="background-color: transparent;"><span>, abnormal pupils, head tilt</span></span></p><ul><li><p><span style="background-color: transparent;"><strong><span>Frontal/parietal/orbital: </span></strong></span><span style="background-color: transparent; color: red;"><span>concussion, contusion, hemorrhage</span></span><span style="background-color: transparent;"><span>, brain parenchyma disruption</span></span></p></li><li><p><span style="background-color: transparent;"><strong><span>Petrous temporal/occipital: very common - young by flipping over backwards</span></strong></span></p><ul><li><p><span style="background-color: transparent;"><span>vestibular dysfunction, facial paralysis, bleeding from ears, optic nerve damage</span></span></p></li></ul></li><li><p><span style="background-color: transparent;"><strong><span>Poll injuries:</span></strong><span> </span></span><span style="background-color: transparent; color: red;"><span>hyperextension of neck,</span></span><span style="background-color: transparent;"><span>&nbsp; basilar fractures = fractures/b-sphenoid &amp; b-occipital bone separation = </span></span><span style="background-color: transparent; color: red;"><span>intracranial hemorrhage &amp; severe brain injury,</span></span><span style="background-color: transparent;"><span> </span><u><span>guttural pouch hemorrhage, </span></u></span><span style="background-color: transparent; color: red;"><u><span>tearing optic nerve: </span></u><span>blindness</span></span></p><ul><li><p> Rupture/avulsion of ventral straight mm &amp;/or fracture at base of brain</p></li></ul></li></ul></li><li><p><span style="background-color: transparent;"><strong><span>Dt: </span></strong><span>rads, CT, MRI, endoscopy</span></span></p></li><li><p><span style="background-color: transparent;"><strong><span>Tx: </span></strong></span><span style="background-color: transparent; color: red;"><span>Stabilize airway / padding</span></span><span style="background-color: transparent;"><span>, IV catheter, </span><u><span>Mannitol/furosemide (not w/ hemorrhage), hypertonic saline</span></u><span>, hyperventilation (foals), Sx for fragments, monitor BP</span></span></p><ul><li><p><strong>poor prognosis →</strong><u> hemorrhage in CSF, recumbence, seizures, coma, fixed pupils, erratic breathing</u></p></li></ul></li></ul><p></p>
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Metabolic and Hepatic Encephalopathy

  • Very common!

  • Et: hepatic failure, hyperammonemia, renal failure, uremia(head pressing), glucose/Na/Ca imbalance, hypercalcemia, Theiler’s dz, hyperlipemia, Plant Alkaloids toxicity, cholangiohepatitis, chronic hepatitis, mycotoxins

  • Cs: behavior changes, seizures

  • Tx: dextrose fluids, dietary modifications, lactulose, neomycin, metronidazole

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<p><span style="background-color: transparent;"><span>Nigropallidal encephalomalacia</span></span></p>

Nigropallidal encephalomalacia

  • Neuro toxins

  • Et: Repin toxin in Yellow Star Thistle & Russian Knapweed

    • necrosis of substantia nigra & globus pallidus: UMN → throat, tongue

    • Cs: facial dystonia, “sardonic grin,” inability to eat/swallow, dunks head into bucket for water

      • necropsy: neuronal cell bodies in midbrain

    • Tx: Euthanasia 

<ul><li><p><span style="background-color: transparent;"><strong><span>Neuro toxins</span></strong></span></p></li><li><p><span style="background-color: transparent;"><strong><span>Et: </span></strong><u><span>Repin</span></u><span> toxin in </span><strong><u><span>Yellow Star Thistle &amp; Russian Knapweed</span></u></strong></span></p><ul><li><p><span style="background-color: transparent; color: green;"><strong><u><span>necrosis of substantia nigra &amp; globus pallidus: UMN → throat, tongue</span></u></strong></span></p></li><li><p><span style="background-color: transparent; color: red;"><strong><span>Cs: facial dystonia, </span><u><span>“sardonic grin,” inability to eat/swallow, dunks head into bucket for water</span></u></strong></span></p><ul><li><p>necropsy: neuronal cell bodies in midbrain</p></li></ul></li><li><p><span style="background-color: transparent;"><strong><span>Tx:</span></strong><span> </span><u><span>Euthanasia&nbsp;</span></u></span></p></li></ul></li></ul><img src="https://knowt-user-attachments.s3.amazonaws.com/7c270f8e-0dd2-452c-87e4-adcd9748e34a.png" data-width="50%" data-align="center"><p></p>
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<p><span style="background-color: transparent;"><span>Locoism: acquired polysaccharide storage disease</span></span></p>

Locoism: acquired polysaccharide storage disease

  • Neuro toxins

  • Et: Oxytropis/Astragalus spp 

    • endophytic fungus produces → Swainsonine causes lysosomal storage dz

      • Intracytoplasmic vacuolization of cells

  • Cs: ataxia, alternating somnolence/excitability, intention tremor, flaccid lips, dysphagia

    • young, herd problem

  • Px: permanent deficits, ill thrift

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<p><span style="background-color: transparent;"><span>Leukoencephalomalacia: mycotoxin Moldy Corn Poisoning</span></span></p>

Leukoencephalomalacia: mycotoxin Moldy Corn Poisoning

  • Neuro toxins

  • Et: Fusarium verticilloides (fumonisin B1),

    • liquefactive necrosis of cerebral hemispheres and liver damage

    • Cs: rapid progressive signs, ataxia, blindness, seizures, agitation, death

    • Dt: toxin in feed

    • Tx: Euthanasia 

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Sorghum Toxicosis

  • Neuro toxins

  • Et: Sudan/Johnson grasses, sorghum hybrids

    • cyanide compounds or lathyrogens

    • Axonal degeneration in spinal tracts, dorsal roots, cerebellar peduncles

    • Cs: Hindlimb ataxia, urinary retention, cystitis

      • Often outbreaks/herd problem

    • Tx: remove source, manage bladder/cystitis

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Bacterial Infections of the Nervous System

  • Brain Abscess: young horses

    • Et: head trauma, hematogenous spread (S equi zooepidemicus/equi), extension from sinus/middle ear & tooth abscess

    • Cs: brain signs, depression, circling, blindness, seizures, CN deficits, head pressing

    • Dt: inflammlatory leukogram, CSF (↑ neutrophils, protein), imaging

    • Tx: high-dose antibiotics (penicillin, sulfa), NSAIDs, DMSO, drain, seizure (phenobarbital)

    • Px: guarded-poor

  • Spinal Abscess:

    • Et: Strangles (Strep equi), septicemia in foals

      • extradural, vertebral body

    • Cs: spinal cord compression, progressive paresis/ataxia

  • Meningitis

    • Et: rare complication of neonatal septicemia or local extension

      • neuroborelliosis(lyme)

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Sleeping sickness

  • Alpha Virus Encephalidities

  • Et: Mosquito-borne→birds, seasonal, viral

  • Horses dead end host

    • EEE: SE US, severe, high mortality, poor Px

      • very common

    • WEE: western US, rare

      • less common

    • VEE: FAD→regulated, South/Central America, zoonotic, severe

      • horses = major amplifiers

  • Cs: high fever, rapid progressive encephalopathy→ recumbence

    • incubation 1-3w

  • Dt: IgM ELISA (MAC-ELISA), CSF neutrophilia

  • Tx: supportive, core vax → prevention

    • x3 in 1st year, then annually 

    • Combo w/ tetanus

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West Nile Virus

  • mosquito-borne encephalomyelitis virus, seasonal

  • Et: Endemic in north america, polioencephalomyelitis

    • gray matter of brainstem, spinal cord

  • Cs: weakness, stumbling, recumbence, muscle fasciculations, CN deficits, blinking, twitching muzzle

  • Dt: IgM ELISA

  • Tx: supportive, sling support, core inactivated vax: protective

  • Px: 30% mortality, worse if recumbent

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Rabies

  • fatal viral encephalomyelitis → saliva

  • DDX MUST be considered for any undiagnosed encephalopathy

  • Et: zoonotic, raccoon(#1), skunk, fox, bat

    • bite causes virus ascends nerves, varies from days to long incubation

      • typical bites: muzzle/face/distal limbs

  • Cs: paralytic (ascending paraparesis), encephalopathic (“furious/dumb”), terminal hyperesthesia, self-mutilation, recumbency → death

  • Dt: DFA on brain postmortem(brainstem & cerebellum), limit exposure: gloves/wash hands

    • no antemortem test

    • NOTIFY PUBLIC HEALTH OFFICALS!!

  • Tx: Euthanasia, core killed vax → x2 @ 6/7m & annual

    • prevention is key!

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<p><span style="background-color: transparent;"><strong><span>Equine Protozoal Myeloencephalitis (EPM)</span></strong></span></p>

Equine Protozoal Myeloencephalitis (EPM)

  • The most common infectious equine CNS disease

    • brainstem & spinal cord most common

  • Et: Sarcocystis neurona, opossum** → horse dead end host

    • sporocysts in contaminated feed/water

    • focal/multifocal gray + white lesions → hemorrhage, and necrosis

  • Cs: asymmetrical ataxia(side of lesion), focal muscle atrophy w/ ±  cranial nerve defects: facial paralysis, dysphagia, LMN signs(spastic hind limbs), CN 5(facial paralysis)

  • Dt: rule-outs, serology, CSF ELISA, necropsy (definitive)

    • + serum titer = exposure

    • S neurona antibodies in serum & CSF: both positive = EPM

  • Tx: ponazuril, diclazuril, sulfadiazine/pyrimethamine(cheap)

    • best outcome when tx early!

  • Px: 60% improve, 20% full recovery, relapses common

<ul><li><p><span style="color: red;"><strong><u>The most common infectious equine CNS disease</u></strong></span></p><ul><li><p>brainstem &amp; spinal cord most common</p></li></ul></li><li><p><span style="background-color: transparent;"><strong><span>Et: </span></strong></span><span style="background-color: transparent; color: green;"><u><span>Sarcocystis neurona</span></u></span><span style="background-color: transparent;"><u><span>, </span></u><strong><u><span>opossum** → horse dead end host</span></u></strong></span></p><ul><li><p><span style="background-color: transparent;"><span>sporocysts in </span></span><span style="background-color: transparent; color: green;"><span>contaminated feed/water</span></span></p></li><li><p><span style="background-color: transparent;"><strong><span>focal/multifocal gray + white lesions →&nbsp;hemorrhage, and necrosis </span></strong></span></p></li></ul></li><li><p><span style="background-color: transparent;"><strong><span>Cs:</span></strong><span> </span></span><span style="background-color: transparent; color: red;"><strong><u><span>asymmetrical ataxia(side of lesion)</span></u><span>, focal muscle atrophy w/ ±&nbsp; cranial nerve defects:</span></strong></span><span style="background-color: transparent;"><span>&nbsp;</span></span><span style="background-color: transparent; color: red;"><strong><span>facial paralysis</span></strong></span><span style="background-color: transparent;"><span>, dysphagia, LMN signs(spastic hind limbs), </span></span><span style="background-color: transparent; color: red;"><span>CN 5(facial paralysis)</span></span></p></li><li><p><span style="background-color: transparent;"><strong><span>Dt: </span></strong><span>rule-outs, serology, CSF ELISA, necropsy (definitive)</span></span></p><ul><li><p><span style="color: green;">+ serum titer = exposure</span></p></li><li><p><span style="color: green;">S neurona antibodies in serum <strong>&amp;</strong> CSF: both&nbsp;<strong>positive = EPM</strong></span></p></li></ul></li><li><p><span style="background-color: transparent;"><strong><span>Tx:</span></strong><span> ponazuril, diclazuril, sulfadiazine/pyrimethamine(cheap)</span></span></p><ul><li><p>best outcome when tx early! </p></li></ul></li><li><p><span style="background-color: transparent;"><strong><span>Px:</span></strong><span> 60% improve, 20% full recovery, relapses common</span></span></p></li></ul><p></p>
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<p><span style="background-color: transparent;"><strong>Spinal Cord Trauma</strong></span></p>

Spinal Cord Trauma

  • White matter (long tracts): spastic paresis & ataxia behind lesion

  • Gray matter (LMNs): flaccid paresis & atrophy, focal/segmental

  • Et: edema, vertebral fracture, cord impingement

    • cervical spine from young horses → flipping over, pulling back

      • dens/atlas & thoracolumbar fractures: young

  • Cs: paresis, ataxia(disrupts long tracts)*, hypalgesia: diminished sensitivity or response to normally painful stimuli

  • Stable = standing Unstable= down 

  • no brain signs, tetraparesis localizes to C1-T2

  • Tx: Non fracture/stable: DMSO, corticosteroids, NSAIDs, stall rest, Sx(unstable fractures)

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<p><span style="background-color: transparent;"><strong><span>Cervical Stenotic Myelopathy (CSM)</span></strong></span></p>

Cervical Stenotic Myelopathy (CSM)

  • “Wobbler Syndrome” → young, rapidly growing foals

    • OC: Developmental disease of growing cartilage

  • Et: Abnormal vertebral growth/development (osteochondrosis OC), Instability/malformation with cord compression

    • Most common non-infectious neuro dz of horses!!

      • Abnormal growth & development = cervical cord compression & tetraparesis & spastic ataxia

    • cervical: Osteochondritis dissecans (OCD) of facet joints &/or Physeal dysplasia

  • Types:

    • Type I (Dynamic instability/high): C3-C6, intermittent, young horses

    • Type II (Static compression/low): C5-T1, constant, older horses

      • present @ 2-5 yrs

  • Cs: young Clumsy → BAR, stumbling, falling, poor performance, UMN + proprioception defects, spastic tetraparesis, hindlib ataxia(more severe)

  • Dt: rads, sagittal ratios, myelography, CT/MRI

  • Tx: reduce growth rate, Vit E supp, steroids, DMSO, Interbody fusion Sx “bagby”(type I), Dorsal laminectomy (type II)

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Occipito-Atlanto-Axial Malformations (OAAM)

  • Stenosis/cervical spinal cord compression!

  • Et: Congenital defect 

    • Cord compression at birth

  • Sig: Arabians, QH, Drafts

  • Cs: spastic tetraparesis & ataxia: from birth some a bit older, limited cervical ROM (cannot extend neck)

  • Dt: imaging(cervical), history, PE

  • Tx: euthanasia 

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Equine Neuroaxonal Dystrophy (eNAD) and Equine Degenerative Myelopathy (EDM)

  • Et: Dev degenerative dz of spinal proprioceptive tracts( ALL 4 limbs)

    • Vit E deficiency (mare or foal)

      • had no access to green grass/quality hay

  • Sig: 6-24m, QH

  • Cs: Symmetric ataxia @ 6-24m , clumsy young horse

    • Generally no CS(eNAD), CS showing (EDM)

  • Dt: exclusion, history of Vit. E deficiency, histopathology postmortem

    • Normal vitals, labs, CSF, cervical imaging

  • Tx: Vit E supp (prevents progression, not reversal)

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Equine Herpesvirus-1 Myeloencephalopathy (EHM)

  • Herpes, reportable!, effects white matter

  • Et: Neurotropic EHV-1 strains → acute ataxia & sacral signs & abortion

    • Latent virus: resp dz, cell-associated viremia in CNS, endothelial infection

      • Vasculitis in thoracolumbar & sacral cord: edema, hemorrhage, infarction

  • Sig: Adults >3y, event/comingling/stress outbreaks

  • Cs: Acute onset hindlimb ataxia, urinary retention, bladder paralysis, tail/anal tone loss, penile prolapse, fever

    • RARE: encephalopathy/brainstem/CN signs

  • Dx: ↑ protein, pleocytosis, xanthochromia-yellow (CSF tap); PCR(nasal/blood), paired sera (4x titer rise), IHC(necropsy)

  • Tx: NSAIDs, steroids, DMSO, antivirals (valacyclovir @ risk), biosecurity, quarantine, vax (resp only; not protective for CNS dz)

  • Px: 40% mortality, residual deficits

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Post-Anesthetic Myelomalacia

  • Et: dorsal recumbent anesthesia

    • ischemic injury to lumbosacral spinal cord gray matter

  • Sig: young draft horses after Sx

  • Cs: Fail to rise, bilateral hindlimb paresis, paralysis

  • Ddx: Type I PSSM (draft breeds), Post-anesthetic myopathies/neuropathies (treatable)

  • Px: poor, don’t recover

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 Vestibular Disease

  • Vest. system: Maintain posture, muscle tone & equilibrium, Orientation of head

  • Et: trauma, infection, petrosal fractures, temporohyoid osteoarthropathy, otitis media-interna

    • Central: medulla, pons, cerebellum

    • Peripheral: CN VIII; common in horses → temporal bone

      • CN VII & VIII run close together, lesions may effect both

        • Facial paralysis very common

  • Cs: Head tilt, leaning, falling, rolling, resting horizontal fast nystagmus

    • Signs ipsilateral(same side) to lesion

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<p><span style="background-color: transparent;"><strong>Temporohyoid Osteoarthropathy</strong></span></p>

Temporohyoid Osteoarthropathy

  • Et: otitis media, guttural pouch dz, cribbing, idiopathic degen

    • Bony proliferation, sclerosis, fusion of temporohyoid articulation

    • Stenosis of ear canal, obliteration of tympanic bulla

  • Cs: mastication pain, head rubbing, head shaking

    • spontaneous fracture(due to fusion): acute vestibular signs + facial paralysis

  • Dt: endoscopy, radios, CT

  • Tx: anti-inflam, antibiotics, protect cornea, ceratohyoidectomy Sx→ prevent fracture 

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Otitis Media–Interna

  • Cs: vestibular dz, facial paralysis,

    • Extension beyond inner ear: osteomyelitis calivrium, subdural abscess, meningitis → lead to CNS signs

  • Dt: tympanocentesis, cytology/culture, rads/CT/MRI

  • Tx: aggressive antibiotics, anti-inflammation → less severe

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Pharyngeal & Laryngeal Neuropathies

  • Pharyngeal:

    • Et: guttural pouch mycosis, trauma (surgery, fractures), neoplasia

    • Cs: dysphagia, feed in nostrils, weight loss

  • Laryngeal:

    • Et: Idiopathic left laryngeal hemiplegia, recurrent laryngeal nerve injury: (perivascular injection of NSAIDS) or lead poisoning (polyneuritis)

    • Cs: abnormal whinny, inspiratory noise, obx

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<p><span style="background-color: transparent;"><strong>Horner Syndrome</strong></span></p>

Horner Syndrome

  • Et: cranial trauma, guttural pouch disease, cervical injections, SC injury, brachial plexus injury, thoracic trauma/mass

    • disruption of Sympathetic pathway dz to head/neck

  • Cs: Ptosis, enophthalmos, 3rd eyelid prolapse, miosis, focal sweating (distribution helps localize lesion)

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Neuropathic (Photic) Head Shaking

  • Et: trigeminal (CN V ophthalmic branch) hyperesthesia

    • exposure to light or environmental stimuli

  • Cs: head shaking, sneezing, rubbing, snorting

    • progressive

  • Dx: r/o other head shaking issues

  • Tx: Nose nets, UV masks, cyproheptadine, carbamazepine, euthanasia(many cases are debilitating)

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Polyneuritis Equi (Cauda Equina Neuritis)

  • Et: Immune-mediated

    • chronic granulomatous inflam, fibrosis of cauda equina nerve roots

  • Cs: hyperesthesia around rump/tail, tail rubbing!!, flaccid bladder (overflow incontinence), urine scald, fecal retention, tail paralysis/atrophy, perineal anesthesia, penile prolapse/anesthesia

  • Tx: no cure, corticosteroids(temp effect), catheterization, manual rectal emptying, nursing care, euthanasia

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Stringhalt

  • characteristic gait abnormality spasmodic hyper-flexion of one or both hind limbs!

  • Et: peripheral axonal degeneration of peroneal nerve

    • Sporadic: usually unilateral, often after hock injury

    • Epidemic: herd outbreaks, bilateral, Plant tox: flatweed, false dandelion, cheeseweed

  • Cs: spasmodic hyperflexion of hindlimbs

  • Tx: tenectomy of lateral digital extensor → sporadic

    • remove from pasture → epidemic 

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Dysautonomia (Equine Grass Sickness)

  • generalized GI motility disorder

  • Et: enteric nervous system, ANS ganglia degeneration

    • idiopathic, C botulinum type C toxin

  • Sig: pastured horses, UK

  • Cs: Dysphagia, gastric dilation, reflux, impaction, SI ileus, colonic impaction, death

  • Px: fatal

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<p><span style="background-color: transparent;"><strong>Traumatic Peripheral Nerve Injuries</strong></span></p>

Traumatic Peripheral Nerve Injuries

  • Et:

    • Facial nerve: base of ear or halter injury under anesthesia

    • Suprascapular nerve: harness/collar injury

      • Sweeney

    • Radial nerve: trauma, fracture, anesthesia

    • Brachial plexus: root avulsion, limb paralysis

    • Femoral nerve: anesthesia, pelvic/femur fracture

    • Obturator nerve: dystocia, pelvic fracture

    • Sciatic/peroneal nerve: IM injection in foals, pelvic trauma, anesthesia

  • Tx: Sx, time, anti-inflam, corticosteroids, slings/splints, hydrotherapy, eye care (lubricants, tarsorrhaphy)

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<p><span style="background-color: transparent;"><strong>Equine Motor Neuron Disease</strong></span></p>

Equine Motor Neuron Disease

  • Et: Vit E deficiency, poor hay, no pasture, stabled

    • degeneration of LMNs in cord & brainstem

  • Cs: weakness, trembling, recumbency, weight loss, muscle atrophy, base-narrow stance, dropped head, elevated tailhead

  • Dt: low serum Vit E, muscle biopsy (sacrocaudalis), retinal lesions

  • Tx: Vit E supp, pasture access

  • Px: guarded

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Botulism

  • Et: C botulinum toxin (types B, A, C) blocks NMJ

    • Forage: ingested contaminated feed, silage, carcasses

      • many horses effected/herd issue

    • Wound: rare

    • Toxoinfectious: foals ingest spores and toxin produced in gut

      • “Shaker foal” → endemic areas

  • Cs: weakness, dysphagia, generalized paresis, recumbency, resp failure, flaccid paralysis!

    • signs occur 1-17d after ingestion/exposure!!

  • Dt: toxin ID (mouse bioassay on feed/poop)

  • Tx: Antitoxin, toxoid vax → prevention

    • good if remain standing 

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Tetanus

  • Clostridium tetani in wounds/conditions that favor anaerobic growth

    • spinal cord and brainstem, UMN w/ renshaw cells

    • CS: generalized muscle rigidity, vague stiffness, muscle spasms “sawhorse”, prolapsed 3rd eyelid, sensitive to touch/sound

      • End stage: respiratory failure

    • TX: wound debridement & antibiotics, antitoxin, acepromazine, quite place w/ low light, supportive care

      • Core vax: tetanus, revaccinate w/ injury or sx if vaccine was >6m ago

        • give toxoid and antitoxin together

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UA

  • Looks like Beer

  • Consistency: Turbid/viscous 

    • Ca carbonate & mucus

  • Colour: Yellow–brown color

    • Pigments: hemoglobin, myoglobin, bilirubin, plant pigments, drugs

    • Bld: kidney, bladder, urethra

    • Dz: NSAID injury, neoplasia, cystitis, idiopathic hemorrhage

  • USG: 1.025–1.060

    • Isosthenuria = 1.008–1.017

  • pH: alkaline 

    • 7.5–9

  • Absent: glucose, protein, bacteria, casts

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Acute Renal Failure

  • Et: >70–80% nephron loss & Isosthenuria in the face of azotemia!!

    • Pre-renal: ↓ renal perfusion from hypovolemia/fluid defect, shock, dehydration

      • Physiologic oliguria, reversible

    • Renal (intrinsic): ischemic injury =Hypoxia, toxic injury 

      • Commonly acute tubular nephrosis

      • shock, SIRS/endotoxemia, sepsis, NSAIDs, aminoglycosides, tetracyclines, myoglobin (rhabdomyolysis), hemoglobin, cantharidin (blister beetles), vit D/K3, acorns, heavy metals

      • renal ischemia is a major predisposition for

        toxic injury

  • Cs: Depression, edema, encephalopathy

  • Dt: azotemia, ↓ Na, ↓ Cl, ↑ K, isosthenuria, aciduria, ↑ GGT:Cr, casts

  • Tx: Fluids!! (until Cr stabilizes), diuretics (furosemide) until CK drop

    • Monitor: urine output, lytes, creatinine, PU/PD will persist during recovery

    • Goal: convert oliguria → polyuria

  • can’t concentrate urine, &/or creatinine

    remains elevated, there is chronic renal disease

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<p><span style="background-color: transparent;"><strong>Chronic Kidney Disease</strong></span></p>

Chronic Kidney Disease

  • Irreversible, progressive

  • Et: >70–80% nephron loss = renal failure and compensatory hypertrophy, reduced nephrotic mass

    • Congenital: agenesis, dysplasia, polycystic kidney

      • Sig: Young horses (1–5 yrs) @ birth, poor BCS, rough coat

    • Acquired: chronic interstitial nephritis (#1), infiltrative diseases (LSA, neoplasia), glomerulonephropathy →  hypoalbuminemia and edema

  • Cs: Gradual weight loss, poor appetite, rough coat, PU/PD, edema, dental tartar

  • Dt: azotemia, isosthenuria,↓ Na, ↓ Cl, ↑ K, metabolic acidosis, small fibrotic kidneys, ± ↑ Ca

  • Tx: Hydration, salt, grass hay (↓ Ca), palatable concentrate, add fat, lyte balance, tx acidosis

  • Px: poor

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Renal Tubular Acidosis

  • Et: Tubular dysfunction → bicarb loss → hyperchloremic metabolic acidosis

  • Cs: depression, weakness, inappetence

    • No azotemia 

  • Tx: bicarb + KCl

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Pyelonephritis

  • Et: ascending or hematogenous: Uncommon

    • R equi, strangles, lepto, septic foals

  • Cs: fever, depression, pyuria, bacteriuria, hematuria

  • Dt: leukocytosis, fibrinogen,

    • UA, culture, US, endoscopy, lepto PCR

  • Tx: antibiotics based on culture

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Cystitis (Lower UTI)

  • Et: secondary to bladder stones, paralysis, incompetent sphincter (mares), catheter, abnormal flow

    • mares more prone, iatrogenic w/ catheters

  • Cs: stranguria, pollakiuria, incontinence, hematuria

  • Dt: >10 WBC/hpf or >20 bacteria/hpf, culture, endoscopy

  • Tx: based on culture: TMS, ampicillin, ceftiofur, penicillin

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Urolithiasis

  • Types:

    • Ca carbonate: #1, yellow spiculated

    • Ca phosphate: Grey-white, smooth

  • Sites: kidney, ureter, bladder, urethra

    • some: spontaneous develop in bladder, CKD

    • Renal Calculi: originates from renal pelvis → hydronephrosis, abdominal pain

  • Sig: males > females

  • Cs: pain, hematuria, obstruction, CKD

  • Dt: US, rectal, endoscopy

  • Tx: lithotripsy, cystotomy, nephrectomy if unilateral,

    • ↑ water, add salt, avoid alfalfa, reduce calcium intake

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Control of Bladder Micturition

  • Pontine micturition center in brainstem controls:

    • Filling/storage: inhibits detrusor, parasympathetic LMNs, closes sphincters

    • Voiding: contracts detrusor, relaxes sphincters

  • Ascending: sensory

  • Descending: UMN

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<p><span style="background-color: transparent;"><strong>Neurogenic Bladder</strong></span></p>

Neurogenic Bladder

  • Et: Polyneuritis equi, EHV-1, sorghum toxicity, EPM, neoplasia, spinal trauma

    • UMN spastic bladder long tracts: lesion above sacral segments 

      • Cs: spastic bladder, open internal sphincter, and spastic urethralis → dysynergia(detrussor & urethralis), intermittent incontinence 

    • LMN Flaccid bladder: lesion in sacral cord/nerves 

      • Cs: flaccid, distended bladder, overflow incontinence,  loss of perineal reflex

  • Tx: Manual evacuation, catheter, Bethanechol (stimulate detrusor), Phenoxybenzamine (relax sphincter), Dantrolene (relax urethralis), Phenazopyridine (mucosal analgesic)

  • Px: risk of sabulous cystitis from Ca carbonate buildup

    • sabulous cystitisaccumulation of sediment in floor of bladder

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Detrusor Atony & Idiopathic Sabulous Cystitis

  • Mares, idiopathic 

    • retention of urine & accumulation of sabulous debris = ultimately resulting in detrussor atony

    Et: neuro dysfunction, pain = urine retention , idiopathic in geldings w/ sabulous cystitis

  • Cs: Flaccid bladder

  • Tx: flush bladder, antibiotics, Bethanechol (stimulate detrusor), Phenoxybenzamine (relax sphincter)

  • Px: fair, chronic

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<p><span style="background-color: transparent;"><strong>Uroperitoneum</strong></span></p>

Uroperitoneum

  • Et: 

    • Foals: Ruptured bladder(most common), urachal tear(dorsal), ureter, hospital aquirred

    • Adults RARE: trauma, dystocia, obstruction(males)

      • Sm: dorsal tears: medically managed, LG: SX repair

  • Dt: azotemia, ↓ Na, ↓ Cl, K, met. acidosisperitoneal Cr > serum Cr, US, abdominocentesis

  • Tx: 09% NaCl + dextrose/bicarb (#1), Sx→ stabilize first

    • avoid K fluids

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<p><span style="background-color: transparent;"><strong>Omphalitis</strong></span></p>

Omphalitis

  • infection of the umbilical stump, the remnant of the umbilical cord left after birth

  • Et: failure passive transfer, ascending infection through urachus, arteries, vein

  • Cs: umbilical inflam, patent urachus, abscess, uroperitoneum

  • Dt: palpation + US for signs of infection!

  • Tx: antibiotics, Sx removal of infected/leaky remnants

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Parturient & Urethral Injuries

  • Et: bladder rupture, urethral incompetence/laceration, detrusor injury, bladder prolapse→ urethra or cervical tear

  • Sig: Mares

  • Tx: catheter, Sx, Bethanechol (stimulate detrusor),

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Male Dorsal Urethral Hemorrhage

  • Et: Defect in dorsal urethral mucosa communicating with corpus spongiosum

  • Cs: hemospermia &/or expulsion of blood at end of urination

    • blood staining on canon/pasterns

  • Tx: perineal urethrotomy/transect bulbospongiosum

    • heals by 2° intention, relieves pressure 

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Polyuria & Polydipsia

  • Et: renal failure, PPID(cushings), psychogenic(wet stall), corticosteroids, α2 agonists, diuretics

  • Cs: r/o renal issues 1st

    • PU: >25 L/day urine

    • PD: >50 L/day water

  • Dt: water deprivation test (psychogenic: primary) very common

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Urinary Neoplasia

  • Et: 

    • Kidney: renal cell carcinoma (old), nephroblastoma (young)

    • Bladder: SCC, TCC, adenoma

    • Urethra/external genitalia: SCC, sarcoid, melanoma

  • Dt: rectal exam, US, biopsy

  • Tx: nephrectomy if unilateral

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Castration Surgical Planning Considerations

  • Why: Stop stud behaviour, genetic soft cull, Dz of testis or spermatic cord

  • When: 1.5–2 years

    • Sx at 1.5–2 years allows MS dev under testosterone

    • Older stallions have learned behaviour persists + more complications

  • Risks: Hemorrhage, preputial/scrotal swelling, septic funiculitis, schirrhous cord, septic peritonitis, hydrocele, omental prolapse, visceration or eventration

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<p><span style="background-color: transparent;"><strong>Pre and Post Op Considerations for Castration</strong></span></p>

Pre and Post Op Considerations for Castration

  • Pre-Op: make sure you have the RIGHT horse

    • Tetanus Vax: Must be current 

      • Give tetanus toxoid if uncertain

    • Confirm two testes in scrotum; no inguinal hernia

    • Rx: ± Penicillin(clostridial), flunixin

  • Ventral scrotum incision, no ligatures

    • Nut to nut : emasculators 

  • Op: 

    • Closed: Young with small cords

    • Open: Most common

    • Recombinant R lateral: xylazine (sedation), ketamine (induction)

      • Better control, safety, hemostasis BUT risk & $$ of GA

    • Standing: alpha-2 + butorphanol (sedation), local to testicles & cords

      • Avoids GA, cheaper BUT bad for movement, bleeding, poor behaviour, ponies, donkeys, mules, small testes

  • Post-Op: 

    • Incisions left open for drainage

    • Confine 24 hrs, then exercise twice daily for 2w

      • reduce edema and promote drainage

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Routine Castration

  • Position: 

    • R Lateral recumbency: upper hindlimb pulled forward & secured

      • Remove halter, pad, cover eyes

    • Standing: Wrap tail

  • Insise: 

    • Compress testes into scrotum

    • 10 cm incision over each testis, parallel to median raphe, 2 cm from midline

  • Exteriorize: via ventral scrotal incisions

    • Closed: Tunic not opened and strip fascia around cord proximally

    • Open: Open vaginal tunic, split mesorchium

  • Cut: Apply emasculator “nut to nut”

    • Open: Crush vessels, then vas deferens, cremaster, tunic separately

  • Close: Incisions left open for drainage 

    • second intention healing

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Testicular Descent

  • Normally occurs by 1m 

  • Testis initially behind kidneys

  • Gubernaculum testis: connects testis to scrotum

  • Testis enlarges → regresses → descends via inguinal canal

  • Gubernaculum contracts, pulling testis into scrotum

  • Inguinal extension of GT

    • becomes proper lig of testis, lig of tail of epididymis, scrotal lig

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<p><span style="background-color: transparent;"><strong>Cryptorchidism</strong></span></p>

Cryptorchidism

  • Et: Failure of, one > both, testicles to descend into scrotum

    • Inguinal: testis in inguinal canal

    • Incomplete abdominal: epididymis in canal, testis just inside internal ring

    • Complete abdominal: both epididymis & testis retained in abdomen

  • Sig: Percherons, Saddlebreds, QH

    • TB are RARE

  • Cs: late descent at 2-3y, absent testes, stallion-like behavior, unclear castration history

    • produce testosterone, no sperm from retained testes

  • Dt: Palpation, US, high testosterone/estrogen, hCG stim, Laparoscopy (definitive)

  • Tx: castration: inguinal (most common)

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Cryptorchid Castration

  • Inguinal approach (#1):

    • GA, dorsal recumbency

    • Incise over superficial ring

    • Locate inverted vaginal process and exteriorize

  • Para-inguinal: incomplete abdominal retention

    • Considered safer than inguinal

  • Abdominal: complete abdominal retention

  • Laparoscopic: Minimally invasive option

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Parturition in Mares

  • Gestation: 320-365 days 

    • avg 340, generally are constant year to year

    • premature if <320d

  • Stage 1: 4-24h

    • Discomfort, restlessness 

  • Stage 2: delivery within 20 min

    • Rupture of chorioallantois (water breaks)

    • Prolonged = dystocia and birth asphyxia risk

  • Stage 3: <3 hrs

    • Expulsion of fetal membranes

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Neonatal Behavior and Vitals

  • Behavior: precocious, BAR, teat seeking

    • Sternal in 10 min

      • Abnormal = Not sternal by 10 min

    • Standing by 1 hr

      • Abnormal = Not attempting to rise by 20 min or standing by 1 hr

    • Suckling by 2 hrs

      • Abnormal = Weak suckle reflex at 10 min

    • Sleep ~50% of time, stretches then teat seeks

  • HR: 80–120

  • RR: 40–60

    • Abnormal = not breathing in 30 sec

  • Temp: 99–102°F

  • Diet: Consume 25%+ BW in milk/day

  • Feces: Pass meconium at 12–24 hrs

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Neonatal Septicemia

  • Et: FPT → bacterial dissemination

    • Bacti enter umbilicus, MM, GIT, lack of colostrum

  • Cs: neonatal weakness, organ failure, sepsis, dropped ears, fever Prolonged CRT, weak pilse, cold limbs 

    • major cause of neonatal death

  • Tx: Correct FPT, Antibiotics, Resp Support, Cardio Support, Nutrition, Seizure Management, Umbilical Care, Enviro Management 

    • Treat ASAP

  • Px:Poor

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Peripartum Asphyxia (Hypoxic-Ischemic Encephalopathy)

  • Et: oxygen deprivation “dummy foals”

    • Prenatal: placental insufficiency, fescue tox, bacterial, torsion

    • Parturient: birth asphyxia 

    • Postnatal: immature lungs, aspiration, rib fractures

  • Cs: neonatal weakness, disoriented, no suckle reflex, seizures, coma, brain edema

  • Tx: Correct FPT, Antibiotics, Resp Support, Cardio Support, Nutrition, Seizure Management, Umbilical Care, Enviro Management 

  • Px: Good if full-term

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Prematurity/Dysmaturity

  • Et: Placental insufficiency, placentitis, fescue toxicosis late pregnancy(placenta edema), late abortion

    • Premature: < 320 days

    • Dysmature: signs of immaturity despite normal gestation

  • Cs: neonatal weakness, abnormal ossification (carpal/cuboidal bones), tendon laxity, respiratory issues, domed head, floppy ears, silky hair coat

  • Tx: Correct FPT, Antibiotics, Resp Support, Cardio Support, Nutrition, Seizure Management, Umbilical Care, Enviro Management 

  • Px: Fair to Poor

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Placentitis

  • Ascending bacterial infection in 3rd trimester

    • Mare not very sick

  • CS: Vaginal discharge, premature udder development, premature lactation(colostrum lost)

    • death, abortion, premature, Premature placental detachment, prenatal septicemia

  • Foals hypoxemic in utero, high rish for asphyxia : small weak foals

  • high risk for FPT

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Fescue toxicosis

  • Mares ingest tall fescue pasture in late pregnancy 

    • Ergots Alkaloids induce the endocrine dysfunction and negative effects on preg/lactation

  • CS: placental edema and insufficiency, hypogalactia(low milk supply) & lack of udder development!

  • Take mare off pasture >30d before gestation 

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Supportive & Intensive Care for Neonates

  • Correcting FPT: colostrum within 12hrs (15–2L in divided feedings), plasma transfusion after 12hrs (gut closure)

    • Goal is IgG >800 mg/dL by 24 hrs

    • Measure plasma IgG w/in 24h, test colostrum

  • Antibiotics: Ceftiofur (mild), beta-lactam + aminoglycoside (severe)

    • Broad spectrum (G-) for E coli, streptococci, anaerobes

  • Resp Support: insufflation (septic/recumbent), continuous (premature/asphyxiated) 

  • Cardiovascular Support: use arterial blood gas analysis 

    • Fluids: boluses (20 ml/kg), maintenance 100 ml/kg/day

      • Correct electrolytes & glucose

    • Pressors (dopamine/dobutamine): hypotensive

  • Nutrition: Mare’s milk (#1), goat’s milk, replacer, pan feed, NG tube, TPN

    • Goal is 15–25% BW milk/day, gain 1–3 lbs/day

    • Dextrose, AA, lipids 

  • Seizure Management: diazepam/midazolam, phenobarbital, mannitol/furosemide (cerebral edema)

  • Umbilical Care: palpate, US; daily antibiotics or Sx removal

    • Omphalitis/omphalophlebitis common in weak foals

  • Enviro: padded stall, keep sternal and rotate hourly, ophthalmic care to prevent corneal ulcers