27 – Salt and Sulfur Flashcards
(19 cards)
1
Q
*How do animals get salt poisoning?
A
- Prolonged water deprivation
- Excess salt intake
a. High salt poisoning
b. Formulation errors
c. Drinking saline water
d. Oil field brine, butcher shop brine - Administration of sodium containing fluids to an animal w/o access to water
**MOST COMMON=WATER DEPRIVATION
2
Q
*Salt poisoning: species
A
- All species susceptible
- SWINE more sensitive
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)
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
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
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
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
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
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
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
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
12
Q
Sulfur
A
- Necessary dietary nutrient
- Excess ingestion
o High sulfur in DIET
o High sulfates in WATER
o Excessive fertilizer
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
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
15
Q
Sulfur toxicosis: clinical features
A
- Polioenecphalomalacia
o Head pressing
o Blind
o Circling
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