27 – Salt and Sulfur Flashcards

(19 cards)

1
Q

*How do animals get salt poisoning?

A
  1. Prolonged water deprivation
  2. Excess salt intake
    a. High salt poisoning
    b. Formulation errors
    c. Drinking saline water
    d. Oil field brine, butcher shop brine
  3. Administration of sodium containing fluids to an animal w/o access to water
    **MOST COMMON=WATER DEPRIVATION
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2
Q

*Salt poisoning: species

A
  • All species susceptible
  • SWINE more sensitive
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3
Q

What are 6 areas to consider with water deprivation?

A
  • Environment (ex. hot weather)
  • Availability
  • Accessibility (ex. competition)
  • Palatability (ex. medication, minerals)
  • Welfare
  • Physiology (ex. pregnant, lactating)
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4
Q

What are some examples of high salt intake in livestock?

A
  • High salt diets in poultry and swine with some water restriction
  • High salt in milk replacer of dairy calves (ex. whey)
  • Excessive electrolyte supplementation of dairy calves
  • Consumption of brine/process water from oil drilling sites
  • Free choice to salt following period of no access
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5
Q

What are some examples of salt poisoning in companion animals?

A
  • Prolonged water deprivation
  • Excessive salt intake
    o Homemade playdough
    o Paintball ingestion
    o Bread dough ingestion
    o Drinking ocean water
    o Salt as an emetic
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6
Q

Salt poisoning: mechanism

A
  • Hypernatremia
    o High brain [Na] impairs neuronal energy metabolism
     Failure to pump Na from CNS
  • Access to water restored: water moves along osmotic gradient into brain
    o CEREBRAL EDEMA
    o TARGET: CNS
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7
Q

Salt poisoning: clinical features

A
  • GI: anorexia, thirst, restlessness, watery diarrhea
  • **CNS: ACUTE ONSET OF NEUROLOGICAL SIGNS THAT PROGRESSIVELY WORSEN
    o Wandering, circling, head pressing
    o Tetraparesis, ataxia, hyperesthesia
    o “dog sitting”
    o Recumbency
    o Fasciculations
    o Death due to respiratory failure
    o *PIGS: PRURITUS, CONSTIPATION
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8
Q

Salt poisoning: clin path and gross necropsy

A
  • Clin path
    o Hypernatremia
    o High sodium in CSF
    o Pigs: eosinopenia
  • Gross
    o Non-specific: GI irritation
    o Dry ingesta
    o Recent rehydration
    o Poultry: anasarca
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9
Q

*Salt poisoning: management

A
  • NO decontamination
    1. *SLOW REHYDRATION
    2. Closely monitor patient’s neurological status
  • If worsens after fluid therapy: likely worsening of cerebral edema (ex. give mannitol?)
  • Frequent measurement of serum NA
  • Large animals: intermittent access to water, or HYPERTONIC saline to effect
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10
Q

*Salt poisoning: diagnosis

A
  • HISTORY OF WATER DEPRIVATION AND/OR HIGH SALT INTAKE
  • Antemortem
    o Chem panel: hypernatremia
    o CSF [Na]
  • Postmortem: FRESH brain for [Na+]
    o Alternative: ocular fluid
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11
Q

Salt poisoning: prevention

A
  • Always ensure ab libitum access to fresh water
  • Mitigate other causes of water loss
  • Shade, housing, bedding, ventilation
  • Check sulfate and salt concentration of water sources
  • Management: avoid overstocking, make sure they know where water is, check water systems are working
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12
Q

Sulfur

A
  • Necessary dietary nutrient
  • Excess ingestion
    o High sulfur in DIET
    o High sulfates in WATER
    o Excessive fertilizer
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13
Q

What are some high sulfur feeds?

A
  • Sulfur accumulating weeds
  • High protein feed: alfalfa
  • Distiller’s grain
  • Molasses
  • Brassica species: kale, radishes, turnips, canola, cabbage, broccoli, mustard
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14
Q

Sulfur mechanism

A
  • *RUMINANT PROBLEM
  • Sulfur in rumen=H2S production=detoxification overwhelmed eructated and inhaled=brain
    o H2S=inhibits cytochrome oxidase in mitochondrial ETC (inhibition of aerobic respiration)
  • Takes TIME
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15
Q

Sulfur toxicosis: clinical features

A
  • Polioenecphalomalacia
    o Head pressing
    o Blind
    o Circling
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16
Q

Sulfur toxicosis: diagnosis

A
  • History
  • Suspicion of polio corroborated by FEED AND WATER TESTING RESULTS
  • NO tissue test available
  • Gross necropsy: rumenitis, alveolitits
  • Histo: cerebrocortical necrosis
17
Q

Sulfur toxicosis: management

A
  • Remove animals from suspect feed
  • Lack of thiamine therapy
  • Symptomatic and supportive care
  • Prognosis: variable based on severity
18
Q

Sulfur: prevention

A
  • test diet and water for total dietary sulfur
  • restrict access to high sulfur plants (ex. Brassica)
19
Q

Diagnostic approach to polioencephalomalacia (PEM)

A
  • ETIOLOGIES IN RUMINANTS: lead, salt, sulfur, thiamine deficiency
    1. Lead: recent pasture turnout, batteries, time of year
     Live: whole blood
     Dead: liver and kidney
    2. Salt: water deprivation
     Live: hypernatremia
     Dead: fresh brain for Na+
    3. Sulfur: high in ration or water
     Test feed and water (no sulfur tissue test)
    4. Thiamine: response to thiamine therapy