Sodium chloride, ammoniated feed and gossypol-2 (1)
Page 1: Introduction to Sodium Chloride
ROSS UNIVERSITY ROYAL UNIVERSITY SCHOOL OF VETERINARY MEDICINE
Focus on Sodium Chloride
Page 2: Learning Objectives
General characteristics, sources, and exposure mode of sodium chloride
Distinction between indirect and direct sodium ion toxicosis
Toxicokinetics and mechanisms of action of sodium chloride
Toxicity, clinical signs, and lesions caused by sodium chloride
Diagnosis protocol for sodium chloride poisoning
Therapeutic protocol for sodium chloride poisoning
Page 3: Conditions Related to Sodium Chloride
Excess salt can result in:
Salt poisoning
Hypernatremia
Sodium ion toxicosis
Water deprivation-sodium ion intoxication
Most descriptive term: Water deprivation-sodium ion intoxication
Page 4: Sodium Chloride Functions in the Body
Sodium (main cation) and chloride (main anion) crucial for regulating osmotic balance in extracellular fluid (ECF)
Homeostatic mechanisms control serum sodium concentration and osmolarity through:
Thirst
Antidiuretic hormone
Renal reabsorption of sodium
Page 5: Sources of Sodium Chloride
Normal dietary presence: 0.5–1% salt
Production animals often receive free access to salt blocks or mineral mixes
Additional salt sources:
High-saline groundwater
Brine or seawater
Improperly mixed feed
Page 6: Companion Animal Exposures
Exposures include:
Use of salt as an emetic (outdated practice)
Consumption of salt-containing items (rock salt, dough-salt)
Improperly mixed oral electrolyte solutions
Feeding brine, whey, or garbage
Page 7: Salt Tolerance
Animals can generally tolerate high salt levels if fresh water is freely available
Page 8: Direct Sodium Ion Toxicosis
Acute ingestion of excess sodium leads to hypernatremia, termed:
Direct sodium ion toxicosis
Acute sodium ion toxicosis or acute hypernatremia
Clinical signs develop within 1–2 days
Page 9: Indirect Sodium Ion Toxicosis
More common hypernatremia form due to restricted water intake, termed:
Indirect sodium ion toxicosis
Chronic sodium ion toxicosis or chronic hypernatremia
Clinical signs may emerge over 4–7 days; early changes may be overlooked
Page 10: Causes of Restricted Water Intake
Common causes include:
Frozen water sources
Unpalatable water
Mechanical failure
Overcrowding or naïve animals
Owner neglect
Page 12: Mechanism of Sodium Toxicity
Increased sodium causes rapid serum sodium rise and distribution throughout the body
Osmolarity monitored by hypothalamus; responses include:
Stimulating thirst
Antidiuretic hormone release
Renal sodium reabsorption
Page 13: Brain Sodium Levels
Sodium enters the brain by passive diffusion; removed by active transport
Rapid diffusion across the blood-brain barrier raises sodium in cerebral spinal fluid above normal (135-150 mmol/l)
Brain cells increase intracellular osmolarity to prevent water loss, preventing cell shrinkage
Page 14: Risks of Rapid Hypernatremia Development
Rapid hypernatremia may cause significant brain cell shrinkage
This can lead to blood supply disruption and possible hemorrhages
Severe dehydration may induce seizure-like activity and death
Page 15: Brain Response and Edema
Continued sodium level rise might inhibit glycolysis, reducing cellular energy
Rapid decreases in serum sodium can cause water influx into the brain, leading to swelling and clinical signs
Page 16: Acute Toxic Dose of Sodium Chloride
Approximate acute toxic dose:
2.2 g/kg for swine, equine, bovine
6 g/kg for ovine
4 g/kg for dogs
Swine most sensitive with highest clinical reports
Page 17: Tolerance in Animals
Swine/poultry can be severely affected with restricted water or high-salt diets
Animals can tolerate over 10% salt in feed with adequate water access
Horses rarely affected
Page 18: Clinical Signs in Swine
Initial signs:
Loss of appetite
Thirst
Restlessness
Pruritus and constipation
Progression to aimless wandering, head pressing, circling, seizure-like activity, and lateral recumbency
Page 21: Clinical Signs in Cattle
Acute excess intake:
Gastroenteritis
Weakness
Dehydration, tremors, ataxia
Possible blindness and seizure-like activity
Rapid deterioration and death within 24 hours post severe signs
Page 22: Clinical Signs in Other Animals
Poultry and birds:
Depression, weakness, dyspnea, sudden death
Dogs:
Vomiting, diarrhea, muscle tremors, seizures
Increased severity above 180 mEq/l serum sodium
Page 23: Postmortem Findings
Findings may include:
Gastric irritation, ulceration, hemorrhages
Abnormally dry gastrointestinal contents
Histopathologic lesions like cerebral edema and inflammation of meninges
Page 28: Diagnosis Criteria
Diagnostic sodium concentrations:
Serum and CSF sodium levels of 160 mEq/L or more
Brain sodium concentrations above 2000 ppm diagnostic in cattle/swine
Upper normal for cattle (1600 ppm) and swine (1800 ppm, wet weight)
Page 29: Treatment Prior to Clinical Signs
Before clinical signs appear, treatment includes:
Full water access and close observation for several hours
Page 30: Treatment Concept
Aim to gradually restore normal water and electrolyte balance over 2–3 days
Rapid serum sodium reduction may cause cerebral edema
Page 31: Herd-Specific Treatment
In large animals, limit water intake to 0.5% body weight hourly until hydration normalizes
Page 32: Individual Animal Treatment
Monitoring serum sodium concentration is the first treatment step
Help determine free water deficit (FWD) replacement
Replace not more than 50% of FWD in the first 24 hours
Page 33: Sodium Reduction Rates
Serum sodium levels should decrease at 0.5-1.0 mEq/l/hour, slower rate for chronic hypernatremia
In acute cases without clinical dehydration, 5% dextrose solution may aid in decreasing sodium
Page 34: Diuretics Usage
Diuretics like furosemide may help prevent pulmonary edema during fluid therapy
Use slightly hypertonic IV fluids to reduce cerebral edema risk
Page 35: Brain Edema Management
If brain edema is suspected, consider:
Mannitol
Dexamethasone
Dimethyl sulfoxide
Page 36: Case Study Overview
Incident on a small broiler unit using home-mixed feed
Two flocks affected w/ signs: watery diarrhea, thirst, weakness
High mortality observed
Page 37: Descriptions of Affected Birds
Most dead birds had fluid in the pericardial sac, edematous lungs, pale swollen kidneys
Cystic dilation of testes noted in young birds (indicative of sodium toxicity)
Page 39: Testing Results
Liver sodium levels: 4 g/kg wet weight
Broiler feed had >7% sodium (specifications 0.4%)
Brain samples showed high sodium levels (8,810 ppm to 14,300 ppm)
Page 40: Case Presentation 2 Overview
12 pigs (80 kg) showed severe diarrhea, muscle tremors
Clinical signs appeared 6 days after diet change with fatalities
Page 41: Clinical Signs in Pigs
Symptoms included:
Weakness, especially in hind limbs
Circling, normal body temp, slight tachycardia
Conjunctival congestion, diarrhea
Page 42: History of Pigs
8 days prior, pigs fed 100 kg of Vegeta (high in salt)
Limited access to water during the period
Page 43: Lesions in Dead Pigs
Found lesions included:
Gastric and intestinal irritations
Cerebral hemorrhages in one pig
Cerebral edema
Page 44: Ammoniated Feed Introduction
Overview of learning objectives related to ammoniated feed
Page 45: Ammoniated Feed Symptoms
Bovine bonkers syndrome and hyperexcitability syndrome linked to ammoniated hay and liquid molasses
Page 46: Ammoniation Process
Ammoniation increases protein content via treatment with ammonia
Injection can lead to uneven ammoniation depending on bale conditions
Page 47: Ammoniation Timing
Ammoniation time varies with temperature:
80°F: less than 1 week
<40°F: over 8 weeks
Page 48: Ammoniation Benefits
Increases feed digestibility, palatability, and efficiency
Can replace up to 40% of protein-derived nitrogen
Page 49: Quality of Feeds
"Bovine bonkers" linked to ammoniation of high-quality forages with higher soluble sugar content
Page 50: Route of Exposure for Ammoniated Feed
Oral ingestion of toxic feeds or via milk from nursing calves
Page 51: Imidazoles Formation
Imidazoles, formed via ammoniation, are convulsive agents due to Maillard reaction
Page 52: Risk Factors for Ammoniated Feed
Conditions leading to increased toxicity:
High pH, temperature, water content
Excess ammonia application
Page 53: Clinical Signs of Bovine Bonkers
Symptoms include:
Trembling, stampeding, rapid blinking, and behavior inconsistencies
Page 54: Trauma Risks from Hyperexcitability
Lesions arise from physical traumas following hyperexcitability episodes
Page 55: Diagnosis of Ammoniated Feed Poisoning
Diagnosis based on access history and clinical signs
Requires chemical analysis of milk/serum/feed
Page 56: Treatment Protocol
Key treatments involve removing suspect feed and managing stress and self-harm risks
Good prognosis if promptly addressed
Page 57: Introduction to Gossypol
Overview of learning objectives regarding gossypol
Page 58: Gossypol From Cottonseeds
Whole cottonseed, a significant protein and fiber source, releases gossypol during oil extraction
Page 59: Gossypol Structure
Gossypol is a polyphenolic binaphthalene pigment concentrated in cottonseed glands
Page 60: Exposure and Resistance
Gossypol primarily ingested orally; ruminants show more resistance than monogastrics
Page 61: Toxicokinetics of Gossypol
Accumulates in organs (heart, liver, kidney) but not in milk
Excretion primarily via biliary pathways
Page 62: Mechanisms of Gossypol Toxicosis
Cardiovascular tissue damage and reproductive issues, including sperm motility disruptions
Page 63: Gossypol Effects on Nutritional Content
Alters yolk color and may cause visible changes in poultry products due to gossypol reactions
Page 64: Gossypol Toxicity Guidelines
Poultry/swine feed limits: 100 ppm for young; >1000 ppm for mature ruminants
Page 65: Clinical Signs of Gossypol Poisoning
Ruminants may exhibit cardiac failure; swine show cardiac insufficiency
Page 66: Clinical Pathology Findings
Increased erythrocyte fragility leads to lower packed cell volume and elevated liver enzymes
Page 67: Lesion Findings
Thoracic and peritoneal cavity fluid, edema, and primary histopathological findings in hearts and lungs
Page 68: Diagnosis of Gossypol Poisoning
Based on long-term exposure history and free gossypol levels in feed
Page 69: Differential Diagnoses
Includes other ionophores, nutritional deficiencies, and various plant toxicities
Page 70: Treatment for Gossypol Poisoning
Immediate removal of gossypol-containing feeds
Recovery is possible but may take weeks to months
Page 71: References
Cited works and texts related to veterinary toxicology
Page 72: Conclusion
Thank you for attention!