objectives for ns 2: cytotoxic, osmotic and vasogenic brain edema) thiamine-responsive...
TRANSCRIPT
Objectives for NS 2:
• Cytotoxic, osmotic and vasogenic brain edema)• Thiamine-responsive polioencephalomalacia of
ruminants
• Thiamine deficiency in carnivores
• Lead poisoning
• Salt poisoning
• Toxin-induced vasogenic brain edema
You should be able to define, describe pathogenesis,
list lesions and know how to diagnose the following
conditions:
Increased intracranial pressure
Brain swelling (cerebral edema)
E. Simko WCVM
Response to injury - Brain edema
Brain swelling (edema)
Intracranial pressure
Blood perfusion pressure
Ischemicnecrosis
E. Simko WCVM
Response to injury - Brain edema
Brain edema
• Cytotoxic (intracellular)
• Extra cellular edemaOsmotic Vasogenic
E. Simko WCVM
Response to injury - Brain edema
• Gross: cerebellar coning (herniation)cerebral herniationflattened gyri
• Microscopicallyneuronal necrosisedema is not evident in most cases
Diagnosis:
E. Simko WCVM
Response to injury - Brain edema
Polioencephalomalacia (PEM)
• Thiamine-responsive PEM of ruminants• Lead poisoning in ruminants• Salt poisoning in pigs & occ. in rumin.• Hypoxia
Cytotoxic edema (cellular degeneration)
Thiamine-responsive polioencephalomalaciain ruminants
• Disturbance of thiamine production/absorption
concentrate ruminal pH change in flora
Bacterial thiaminase
• [sulfur, sulfates, sulfides] in diet or water
Etiology
E. Simko WCVM
Response to injury - Brain edema
PathogenesisCytotoxic edema - Thiamine deficiency
• 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
Lesions
• Brain swelling (flattened gyri, cerebellar coning)
• Yellow cortical discoloration(autofluorescence under UV light)
• Cortical liquefaction and cavitation
HistologyLaminar cortical
necrosisE. 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 andmid-brain nuclei
E. Simko WCVM
Cytotoxic edema - Thiamine deficiency
Lead poisoning
Cattle
Waterfowl
Source:
Old batteries and paint
Lead shotgun pellets
Lesions:
Polioencephalomalaciasimilar to thiamine resp.
PNS degeneration(Esophageal/crop dilation
and impaction)
E. Simko WCVM
Brain edema
Pathogenesis in cattle
• Direct endothelial injury vasogenic edema
• Damaged metabolism cellular swelling
• Energy exhaustion
• Increased intracranial pressure
• Failure of blood perfusion
• Ischemic necrosis
Brain edema - Lead poisoning
E. Simko WCVM
Diagnosis
• Gross and histologic lesions
• Lead particles in the rumen
• Lead level in liver and kidney
E. Simko WCVM
Brain edema - Lead poisoning
Osmosis and semi-permeable cellular membrane
Hypo Os
Hyper Os
Hypo Os
Hyper Os
Swelling
Shrinkage
Osmotic brain edema
H2O
E. Simko WCVM
Water intoxication ( IV H2O, behavioral, ADH)
N
Ed
ema
Deh
ydr.
Brain edema
BRAIN PLASMA BRAIN PLASMA
H2O
N
Ed
ema
Deh
ydr.
Water deprivation +/- high salt
Dehydration
t = 0 hr
HyperNa
Osmotic brain edema - Salt toxicity
BRAIN
N
Ed
ema
Deh
ydr.
BRAIN PLASMA
NaCl
N
Ed
ema
Deh
ydr.
PLASMA
Na+Cl-Na+
Na+
Cl-
Na+
Na+
Cl-
Cl-
Cl-
Na+
Na+
Cl- Na+
Cl-
Na+
Cl-
H2O
Cl-
Cl-Na+
Na+
Dehydration
NormoNaNormoOs HyperOs
Equilibration of CNS hyperNa
PLASMAHyperNa
t = > 36 hr
HyperNa
Osmotic brain edema - Salt toxicity
N
Ed
ema
Deh
ydr.
BRAIN
Cl-
Na+ Na+Cl-Na+
Na+
Cl-
Na+
Na+
Cl-
Cl-
Cl-
Na+
Cl-
Dehydration Dehydration
PLASMANormoNa HyperNa
N
Ed
ema
Deh
ydr.
BRAIN
AA
AA Na+Cl-Na+
Na+
Cl-
Na+
Na+
Cl-
Cl-
Cl-
Na+
Cl-
Dehydration Dehydration
HyperOsHyperOs HyperOs
HyperOs
Water accesst = > 36 hrH2O
Osmotic brain edema - Salt toxicity
PLASMANormoNa NormoNa
N
Ed
ema
Deh
ydr.
BRAIN
AA
AANa+
Cl-
Edema Normal hydr.
HyperOs NormalOs
PLASMANormoNa HyperNa
N
Ed
ema
Deh
ydr.
BRAIN
AA
AA Na+Cl-Na+
Na+
Cl-
Na+
Na+
Cl-
Cl-
Cl-
Na+
Cl-
Dehydration Dehydration
HyperOs HyperOs
Na+
Na+
Cl-
Na+
Cl-
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
Osmotic brain edema - Salt toxicity
Vasogenic brain edema
The most common type of brain edema
Pathogenesis: damaged BBB
Examples:
Toxins
Inflammatory processes (H. somnus)
E. Simko WCVM
Vasogenic brain edema
White matter Grey matterE. Simko WCVM
• 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
Toxins
E. Simko WCVM
Vasogenic brain edema - Salt toxicity
Toxin-induced
Necrosis
TraumaThiamine deficiencyLead poisoningSalt poisoningEdema diseaseClostridial eterotoxemiaEquine leucoencephalomalaciaInfarction
Response to injury - Necrosis
Infarction