Transcript No Slide Title

Objectives for NS 2:
You should be able to define, describe pathogenesis,
list lesions and know how to diagnose the following
conditions:
• Cytotoxic, osmotic and vasogenic brain edema)
• Thiamine-responsive polioencephalomalacia of
ruminants
• Thiamine deficiency in carnivores
• Lead poisoning
• Salt poisoning
• Toxin-induced vasogenic brain edema
Response to injury - Brain edema
Brain swelling (cerebral edema)
Increased intracranial pressure
E. Simko WCVM
Response to injury - Brain edema
Brain swelling (edema)
Intracranial
pressure
Blood
perfusion
pressure
Ischemic
necrosis
E. Simko WCVM
Response to injury - Brain edema
Brain edema
• Cytotoxic (intracellular)
• Extra cellular edema
Osmotic
Vasogenic
E. Simko WCVM
Response to injury - Brain edema
Diagnosis:
• Gross:
cerebellar coning (herniation)
cerebral herniation
flattened gyri
• Microscopically
neuronal necrosis
edema is not evident in most cases
E. Simko WCVM
Polioencephalomalacia (PEM)
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Thiamine-responsive PEM of ruminants
Lead poisoning in ruminants
Salt poisoning in pigs & occ. in rumin.
Hypoxia
Response to injury - Brain edema
Cytotoxic edema (cellular degeneration)
Thiamine-responsive polioencephalomalacia
in ruminants
Etiology
• Disturbance of thiamine production/absorption
concentrate ruminal pH
change in flora
Bacterial thiaminase
• [sulfur, sulfates, sulfides] in diet or water
E. Simko WCVM
Cytotoxic edema - Thiamine deficiency
Pathogenesis
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Thiamine interferes with glucose
metabolism and Krebs cycle in CNS
ATP production
Na/K transport is impaired
Intacellular H2O (hydropic degeneration)
Cellular swelling (Cytototoxic edema)
Energy exhaustion
Intacranial pressure & blood perfusion
Ischemic necrosis
E. Simko WCVM
Cytotoxic edema - Thiamine deficiency
Lesions
• Brain swelling
(flattened gyri, cerebellar coning)
• Yellow cortical discoloration
(autofluorescence under UV light)
• Cortical liquefaction and cavitation
Histology
Laminar cortical necrosis
E. Simko WCVM
Cytotoxic edema - Thiamine deficiency
Diagnosis
• History
• Response to thiamine
• Gross and histologic lesions
• Rule out the other causes of PEM
E. Simko WCVM
Cytotoxic edema - Thiamine deficiency
Dietary thiamine deficiency in carnivores
• Dog, cat, mink (Human – Wernicke’s encephalopathy)
• Depend on exogenous source of vitamin
• Pathogenesis: diet with thiaminase, sulfur
preservatives or exposed to high temperature
Lesions:
Symmetrical necrosis of thalamic and
mid-brain nuclei
E. Simko WCVM
Brain edema
Lead poisoning
Source:
Lesions:
Old batteries
and paint
Polioencephalomalacia
similar to thiamine resp.
Lead shotgun
Waterfowl
pellets
PNS degeneration
(Esophageal/crop dilation
and impaction)
Cattle
E. Simko WCVM
Brain edema - Lead poisoning
Pathogenesis in cattle
• Direct endothelial injury
• Damaged metabolism
vasogenic edema
cellular swelling
• Energy exhaustion
• Increased intracranial pressure
• Failure of blood perfusion
• Ischemic necrosis
E. Simko WCVM
Brain edema - Lead poisoning
Diagnosis
• Gross and histologic lesions
• Lead particles in the rumen
• Lead level in liver and kidney
E. Simko WCVM
Osmosis and semi-permeable cellular membrane
Swelling
Hypo Os
Hypo Os
Shrinkage
Hyper Os
Hyper Os
Brain edema
Osmotic brain edema
H2O
BRAIN
H2O
Dehydr.
N
Dehydr.
N
IV H2O, behavioral, ADH)
Edema
Edema
Water intoxication (
PLASMA
BRAIN
PLASMA
E. Simko WCVM
Osmotic brain edema - Salt toxicity
Edema
NaCl
H
O
2
t = 0 hr
ClNa+
BRAIN
Na+
Na+
Cl-
Cl-
PLASMA
Dehydr.
N
N
Dehydr.
Edema
Water deprivation +/- high salt
Cl-
Na+
ClNa+
Na+ Cl- Cl- Na+
Cl
+
Na+
Na
+
Cl- Na
Na+ Cl-
BRAIN
NormoNa
NormoOs
Dehydration
PLASMA
HyperNa
HyperOs
Dehydration
Osmotic brain edema - Salt toxicity
Equilibration of CNS hyperNa
Edema
Edema
t = > 36 hr
Dehydr.
N
ClClNa+
Na+
BRAIN
HyperNa
HyperOs
Dehydration
ClNa+
Na+ Cl- Cl+
Na
Cl
+
Na
+
Cl- Na
PLASMA
HyperNa
HyperOs
Dehydration
Dehydr.
N
AA
ClAA
Na+
BRAIN
NormoNa
HyperOs
Dehydration
ClNa+
Na+ Cl- Cl+
Cl- Na
+
Na
+
Cl- Na
PLASMA
HyperNa
HyperOs
Dehydration
Osmotic brain edema - Salt toxicity
Dehydr.
AA
ClAA
Na+
Na+
BRAIN
NormoNa
HyperOs
Dehydration
H2O
ClNa+
Na+ Cl- Cl+
Cl- Na
+
Na
+
Cl- Na
Edema
N
Water access
N
Dehydr.
Edema
t = > 36 hr
AA
ClAA
Na+
PLASMA
HyperNa
BRAIN
NormoNa
HyperOs
Dehydration
HyperOs
Edema
Na+
Na+
Cl-
Cl-
PLASMA
NormoNa
NormalOs
Normal hydr.
Osmotic brain edema - Salt toxicity
Lesions
• Brain swelling
• Cerebrocortical necrosis (occ)
Histology
• Laminar cerebrocortical necrosis
• Perivascular eosinophilic infiltrate (Po)
E. Simko WCVM
Osmotic brain edema - Salt toxicity
Diagnosis
• History
• Gross and histologic lesions
• Na level in the brain
E. Simko WCVM
Vasogenic brain edema
Vasogenic brain edema
The most common type of brain edema
Pathogenesis: damaged BBB
Examples:
Toxins
Inflammatory processes (H. somnus)
E. Simko WCVM
White matter
Grey matter
E. Simko WCVM
Vasogenic brain edema - Salt toxicity
Toxins
Toxin-induced
• Shigella toxin type II (Edema disease) Po
Fibrinoid vasculitis
• Epsilon toxin (C. perfringens D enterotoxemia) Ov
Symmetrical encephalomalacia
• Fumonisin B1 (Fusarium momiliforme) Moldy corn
Equine leucoencephalomalacia
E. Simko WCVM
Response to injury - Necrosis
Necrosis
Trauma
Thiamine deficiency
Lead poisoning
Salt poisoning
Edema disease
Clostridial eterotoxemia
Equine leucoencephalomalacia
Infarction
Infarction