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268 Cards in this Set
- Front
- Back
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Epilepsy |
-Common disorder in dogs and humans |
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Seizure |
-Clinical manifestation of a paroxysmal even |
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Epilepsy
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-Chronic condition, characterized by recurrent seizures
-Need to have multiple seizures -Idiopathic epilepsy -Symptomatic epilepsy -Probable symptomatic/cryptogenic epilepsy -Reactive seizures |
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Idiopathic Epilepsy
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-Recurrent seizures for which no structural cause is found
-histopathologic slicing does not show any abnormalities --may still have biochemical abnormalities -Known or suspected genetic basis -“True” seizures, primary epilepsy |
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Symptomatic Epilepsy
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-Recurrent seizures that has a structural cause
-Secondary epilepsy -Most commonly idiopathic -Brain malformations that cause epilepsy |
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Probably symptomatic/Cryptogenic/Hidden epilepsy
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-Recurrent seizures that are thought to be symptomatic but cannot find a reason |
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Reactive Seizures
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-Seizure due to metabolic or toxic causes
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Causes of Seizures
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-No one really knows!
-Imbalance between excitation (glutamate and aspartate NT) and inhibition (GABA) -Synchronous firing of neurons --decreased or increased synchrony pre-ictally --Increased synchrony ictally -Altered expression on receptor sub-types (GABA and glutamate), can be genetic -Everyone has the potential to have a seizure, depending on conditions |
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Characterization of Seizures in dogs
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-Where the seizure starts in the brain determines how the seizure will “look”
-Self-limiting: --focal: sensory, motor, elementary, automatisms --generalized: tonic-clonic, clonc, myoclonic, atonic -Clustered or continuous: --focal: motor, sensory --generalized: reflexive |
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Self-limiting Sensory focal seizure
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-One part of the brain starts to fire synchronously
-can be specific music in head, taste in mouth |
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Self-limiting motor focal seizure
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-“tic”
-Animal usually stays conscious -can be simple, or can be automatisms --whole body part moves --“chewing seizure” |
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Generalized self-limiting seizures
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-Can start focal and move to involve all of the brain
-Loss of consciousness -Can be tonic-clonic: stiff muscles and spasms -Myoclonic: “thunderbolt” to the body -Atonic: no movement at all |
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Clustered/continuous Seizures
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-“Status Epilepticus”
-Seizures that do not stop -Can be generalized, muscle activity that just continues |
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Aura continua Seizure
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-Clustered/continuous seizure that is focal
-Song plays in head over and over for hours on end, taste in mouth for long period of time |
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Secondary common seizure categorization scheme
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-Partial seizures vs. generalized seizures |
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Information needed about seizures
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-Was it a seizure?
-Was it an idiopathic or symptomatic seizure? -Characteristics of the event -Patient characteristics -Diagnostic testing |
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How to know an event was a seizure
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-Sudden (paroxysmal)
-Stereotypical, look the same each time -Alteration in behavior -Characterized by: --derangement in consciousness --alterations in muscle tone and movement, urination and defecation --disturbances in autonomic function --abnormalities on EEG (MAIN SIGN) |
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Ictal state
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-During the seizure
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Post-ictal state
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-Brain is no longer seizuring, but is still not in the normal state
-Animal may be blind, may have difficulty walking -Can last 1-2 hours before return to normal |
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EEG for seizures
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-Gold standard for seizure analysis and diagnosis
-Assesses cerebral cortex and electrical activity -Stimulatory and inhibitory impulses in brain are set at certain level to prevent seizures |
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Stages of a seizure
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1. Prodrome: behavior changes, occurs hours or days before the seizure
2. Aura: immediately before the seizure and is part of the seizure -characterized by sensory, psychosensory, or experiential symptoms -May suggest seizure has focal onset -If not followed by generalized seizures, Is a simple focal sensory seizure 3. Ictus: seizure event, generalized seizure 4. Post-ictal phase: behavior changes hours or days after the seizure |
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DDx for Seizures
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-Syncope (fainting, no post-ictal phase)
-Narcolepsy (usually has inciting cause due to high activity, no post-ictal phase) -Cataplexy -Episodic Weakness -Muscle tremors -Vestibular event -Anaphylactic episode -Scratching episode |
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Non-epileptic Electroencephalogram (EEG)
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-EEG is recorded by placing electrodes over the scalp
-Measure of the summed extracellular current flow of the brain under the electrode --Record the difference in current flow between electrodes -Alpha waves: high frequency 8-13 Hz -Beta waves: higher frequency 13-30 Hz -Delta and Theta waves: lower frequency --need to boost gain to get recorded stimulus |
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Sedation for EEG
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-Need to give drug that sedates animal but does not wipe out the brain waves
-No iso! Intended to remember nothing! -Medetomidine puts animal in a state that is similar to slow-wave sleep |
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Epileptic EEG
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-Abnormal synchrony of discharges of neuronal ensemble
-Synchronous discharges result in stereotyped and involuntary paroxysmal alterations in behavior -“Spike” characterizes a seizure -Spike and wave pattern generalizes during generalized seizure, all leads throughout all recording of brain waves |
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Relationship between EEG and intracellular/extracellular activity
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-EEG: intermittent high voltage, negative waves appear on EEG
-Surface EEG shows summed activity, abnormal activity |
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Idiopathic Epilepsy
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-No structural cause identified
-Generalized seizures are most common -Animal appears normal during interictal period -Animal is between 6 months and 5 years of age at first seizure -Brain looks normal -Neurologic exam, CBC, chem, MRI, and CSF are all normal -Hereditary bases has been identified in many different dog breeds |
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Symptomatic Epilepsy
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-Seizures occur due to lesions of the cerebral cortex or diencephalon
-Degenerative conditions -Anomalous conditions (hydrocephalus, lissencephaly) -Neoplasia -Infection/inflammation -Trauma -Vascular issues -May be focal or generalized seizures -Usually have asymmetrical neurologic dysfunction -Neurologic exam is not normal, postural deficits -Animals are often less than 1 year or more than 7 years old --very young or very old dogs |
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Probable symptomatic/Cryptogenic Epilepsy
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-Previous head trauma
-Previous encephalitis -Presumed previous hypoxic episode |
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Reactive Seizures
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-Due to metabolic disorder
-Glucose, electrolytes, oxygenation, acid/base balance, osnolarity -Renal function -Hepatic function (portosystemic shunt, hepatic dysfunction or failure) -Blood viscosity -Toxins --lead, organophosphates, metaldehyde, strychnine, molds |
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Toxins that can cause seizures
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-Mold!
-Lead -Organophosphates -Metaldehyde (snail bait) -Strychnine |
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Reactive Seizure Characteristics
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-Generalized seizure
-dog is abnormal, may have signs of systemic disease -Signs of diffuse neurologic dysfunction may be present -Signs of systemic disease may be present |
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How to decide origin of Seizure
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-Idiopathic, symptomatic, or reactive
-Age of animal -Inter-ictal state -Symmetry of clinical signs during a seizure --focal or generalized -Presence of metabolic toxins -Structural causes |
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Symmetry of Clinical signs during a Seizure
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-Some individuals have specific pre-ictal activity that occurs before seizure
-Due to focal locus of onset? -Gives hint that maybe there are some structural abnormalities that causes seizure to occur |
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Characteristics of Idiopathic Epilepsy
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-Onset of generalized seizures between 1-5 years of age
-Normal interictal period -Normal interictal neurologic examination -No history of toxin exposure -Normal bloodwork, CEF analysis, and brain imaging |
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MRI or CSF tap of an epileptic patient
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-Seizure is asymmetric
--turns to one side, lifts one limb -Patient is younger than 1 year or older than 5 years -No metabolic or toxic cause can be found -Patient is abnormal interictally, between seizures -Patient is a breed which is commonly affected by certain disease processes -Patient is a cat! |
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Caring for a patient with Seizures
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-Assess the patient
--observe and characterize the seizure if possible -Get a good history -Place catheter and draw blood -Decide if anti-convulsant agents is a good approach |
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History for Seizuring Patients
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-What did the seizure look like?
-Could the animal stand, or did it fall down? -was the animal alert, aware, or conscious? -Was there movement of the limbs or body? -Did the animal salivate, urinate, vomit, or defecate? -What did the eyes look like? --dilated, constricted, nystagmus? -Asymmetrical signs? -What did the animal look like immediately before and after the seizure? -how long did the seizure last? -If the animal has had seizures in the past, were they identical? |
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Questions to ask to figure out what kind of seizure happened
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-How old is the animal?
-Is the animal vaccinated? -Any exposure to toxins? -Does the animal have any other metabolic problems or other problems? -Other related animals having seizures? -has the animal had seizures in the past? -When did the seizures occur? -Is there anything that can induce a seizure? -Is the animal normal between seizures? |
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CBC and blood smear for Seizure analysis
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-CBC and blood smear
-Serum chemistry analysis --electrolytes, glucpse, ALT, BUN, Creatinine, ammonia, cholesterol, bile acids -Refrigerate or freeze blood and urine for future analysis -Blood gas if available |
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Anticonvulsant medication for Single Seizures
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- hard to know if seizure will happen again
-usually do not give drugs -Give if non-cardiogenic pulmonary edema develops -Give if single seizure is status epilepticus and lasts for a long time -Can also try to control if dog has done damage to the house |
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Anti-convulsant medication for Recurrent seizures
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-Treat with anti-convulsants if the dog continues to have seizures
--frequency, severity, ictal and post-ictal status, and size of animal may affect anti-convulsant treatment decision -Phenobarbital -Potassium bromide |
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Mechanism of Action for Anti-epileptic Drugs
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-Block voltage-gated Na channels
--phenytoin, carbamazepine, lamotrigine, valproic acid, topiramate -Enhance GABA-ergic transmission --benzodiazepines, barbiturates, tiagabine -Inhibit excitatory glutamatergic transmission --topiramate -Modulate Ca ion channels --ethosuximide, topiramate, gabapentin |
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Phenobarbital
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-Seizure maintenance medication
-Works on Cl channel and makes it harder to depolarize neuron -3-5mg/kg every 12 hours --check serum levels in 14 days and every 6 months after giving --Want serum concentration to be 15-35 ug/ml -Check liver function every 12 months -Side effects: sedation/ataxia, PU/PD, polyphagia, induction of hepatic enzymes, hepatotoxicity |
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Potassium Bromide
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-Seizure Maintenance medication in Dogs
-Works on Cl channels and makes it harder to depolarize neuron -oldest anti-convulsant known -30mg/kg given once per day -Check serum levels in 4 months, takes a long time to build up --serum concentration should be 1-3 ug/ml -Side effects: sedation/ataxia, PU/PD, polyphagia, eosinophilic bronchitis in cats -Very salty solution, has to be given with food -Cannot be given chronically to cats, develop chronic pneumonitis and eosinophilic bronchitis |
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Gabapentin
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-Can be used as anti-convulsant for seizures, but does not work well
-Hardly ever used |
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Zonisamide
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-Anti-convulsant used during seizures
-Better for small dogs, work well with few side-effects -Mechanism of action is unknown -Mild side effects: ataxia, vomiting, lethargy, some hepatic metabolism -5-10mg/kg PO twice daily |
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Keppra/Leveetiracetam
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-Anti-convulsant used during seizures
-No hepatic metabolism -must be given 3x daily, every 8 hours -Has almost no side effects! |
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Benzodiazepine as maintenance anticonvulsant
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-Tolerance develops, works for 2-3 weeks and then stops working
-Works for longer in cats, but can result in hepatotoxicity -Valium, Clonazepam, Chlorazepate |
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Cluster of Seizures Treatment
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-Two or more seizures in 24-hour time period or status epilepticus
-“Load” the dog, loading dose for dogs not on phenobarbital -Give more phenobarbital to dogs already on low doses of phenobarbital -Can load with Potassium bromide, but cannot give PO --rectally or via stomach tube are options --Can give IV as sodium bromide to protect cardiac function |
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Combination therapy for Seizure Control
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-Hard to figure out!
-Can add drugs, and each time will get a few more dogs to stop seizuring regularly, but not clear why or how it works -Combinations of drugs with different mechanisms does not work as well as expected --can’t mix and match -Similar to NSAID use and avoidance of side effects |
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Status Epilepticus Pharmacological Treatment
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-Talk to the dog!
-IV diazepam: 0.5mg/kg --give 3-5x to stop the seizure --can give as CRI -If alone, double dose and give rectally -Give Phenobarbital to stop future seizures 16mg/kg --works in about 20 min -If diazepam/midazolam does not work, can try: --propofol, with or without iso --Thiopental --pentobarbital to effect --Fos-phenytoin --Keppra |
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Status Epilepticus Supportive Care Treatment
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-Support patient with IV catheter, fluids, ventilation
-Check blood glucose (usually increased because patient is stressed) -Monitor temp, blood pressure, and blood gas -continue to treat seizure with drugs -Give mannitol to reduce swelling in the brain (giving mannitol once will not hurt the animal) |
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Changes in the brain during Status Epilepticus
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-Increased cerebral blood flow
-Increased central venous pressure -Increased cerebrospinal fluid pressure -increased ICP |
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Systemic complication of Status Epilepticus
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-Cardiovascular: arrhythmias
-Respiratory: erratic intercostal and diaphragmatic muscle contractions --abnormal brain stem electrical activity -Bronchial constriction -Increased bronchial secretions -Neurogenic pulmonary edema |
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Systemic complications of Seizures
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-Changes in blood glucose
-Hyperthermia -Rhabdomyolysis -Acid-Base imbalances |
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Supportive Care for Seizures
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-Maintain normothermia
-Elevate head at 30 degree angle -Avoid jugular compression -Monitor: --temp --EKG --signs of increased ICP --Cardiovascular and respiratory signs |
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Common side effects of anti-epileptic drugs |
-Sedation |
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Questions when presented with animal showing possible neurologic signs
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-Is Neurologic dysfunction present?
-If yes, what part of the nervous system is malfunctioning? -What diseases may be responsible for malfunction of this region? |
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What diseases may be responsible for malfunction of cerebrum?
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-Degenerative: focal, multifocal, diffuse, symmetric
--insidious and progressive -Anomalous: focal asymmetric or symmetric --static -Metabolic: diffuse, symmetric --waxes and wanes, episodic, progressive -Neoplastic: focal or multifocal, asymmetric --insidious or acute, progressive -Inflammatory: Focal, multifocal, or diffuse, symmetric or asymmetric --Insidious or acute, progressive, may improve on own -Infarct: focal asymmetric --acute, improves -Trauma: focal asymmetric or symmetric --acute, improves -Toxin: focal or diffuse symmetric --acute, improves |
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Diagnostic testing to confirm DDx for cerebral disease
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-CBC, chem
-Organ function tests -Endocrine tests -Titers for infectious disease -CSF analysis -EKG or EEG -Imaging -Biopsy -Observe clinical progression of signs |
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CBC/Chem for cerebral diseases
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-Useful for metabolic disease and some infectious/inflammatory diseases
-Lymphopenia in CDV -Thrombocytopenia in RMSF |
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Tests for infectious/inflammatory diseases of cerebrum
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-Available tests:
--Viral: CDV, FIV, FIP --Protozoal: toxoplasma, neospora --Rickettsial: RMSF, Ehrlichia --Bacterial: culture --fungal: Cryptococcus, blastomyces, aspergillus, others -Unavailable ante-mortem tests: --viral: rabies --parasitic migration: cuterebra --Non-infectious: Granulomatous meningoencephalitis (GME), Necrotizing encephalitis (pug encephalitis) |
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CSF fluid analysis
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-Spinal tap near the back of the head, into cistern
-Normal values: --Protein should be less than or equal to 25 mg/dl -Less than 5 WBC, few white cells -Less than 30 RBC -Increased protein, increased cells is abnormal -Humans May have headache after spinal tap due to dripping and pulling on meninges --not seen in dogs and cats |
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Cat anti-epileptic drugs
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-NO potassium bromide! Causes pneumonitis
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Electrophysiology for diagnosis of cerebral disease
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-Demyelinating disease
-Myasthenia gravis -Denervation |
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Other diagnostics for cerebral disease
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-Brainstem auditory evoked response testing
-Electroretinogram for diagnosis of cerebral disease -Spinal cord evoked potential -Somatosensory evoked potentials -Electroencephalogram -MRI and radiographs |
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Radiographs for cerebral disease
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-Meningioma: cause calcification
-Only thing you can really identify! -Can do pneumo-contrast study by injecting air into the brain -Positive contrast agents injected into the ventricles can “image” ventricles -Subarachnoid injection to image spinal cord -All contrast agents cause seizures! |
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Cerebral Angiography
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-Inject dye into the arteries
-Cerebral vasculature lights up -Increased blood supply to tumors or other areas of disease --don’t actually see tumor, just vasculature associated with tumor |
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Radionucleotide studies
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-Inject radioactive glucose into brain
-neoplastic tissue will take up more glucose |
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Computerized Tomography
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-Planes of the body at different angles
-Radiographs in transverse sections of the brain -Can look at different planes of the brain -Allowed for better visualization of brain tumors -Allowed for 3-dimensional re-building of radiograph images, reconstructed images |
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Magnetic Resonance Imaging
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-High sensitivity, can clearly see if a lesion is present
-Also specific, increased contrast allows for better diagnosis -Contrast is based on how long you wait for protons to re-align -Can lead to a specific diagnosis very quickly |
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T1 weighted image
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-Lots of anatomical images
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T2 weighted image
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-Can see fluid well
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Proton Density weighted image
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-Can tell difference between gray matter, white matter, and ventricles
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Brain Biopsy
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-Ante-mortem diagnosis
-Kind of a last-chance option -Primarily for intraparenchymal lesions -Can use CT-guided stereotactic systems, free-hand CT guided biopsy, or ultrasound guided biopsy -Gives quick definitive diagnostic of what is going on |
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Paralysis
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-Complete loss of voluntary motor ability
--cannot get body to move -Does not mean loss of reflexes -Loss of voluntary control |
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Paresis
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-Partial loss of voluntary motor ability
-Animal tremors when trying to stand or move -“Weakness” |
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Spastic vs. Flaccid
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-Spastic: Increased tone to limbs
-Flaccid: decreased tone to limbs |
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Ataxia
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-Incoordination
-Inability to predict where the food will land -Spinal ataxia is characterized by crossing over of limbs, longer stride length, abduction, circumduction, scuffing toes -Classic for sensory dysfunction -Spinal disease |
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Vestibular Ataxia
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-Loss of Balance
-Brainstem or inner ear disease |
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Cerebellar Ataxia
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-“Dysmetria”
-Abnormal range of motion -Goose-stepping gait with late onset of voluntary motion -Cerebellar disease |
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Disease of motor nerve, endplate, or muscle and gait analysis
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-Normal mental status
-Gait: no ataxia, short-strided, flaccid paresis or paralysos --Lower Motor neuron paresis/paralysis -Ipsilateral deficits -Normal sensation -Ipsilateral hyporeflexia, small or diminished reflexes -Weak dog that is trying to stand, tremoring when walking, taking very short steps |
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L4-S1 disease and gait analysis
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-Mental status is normal
-Pelvic limbs will have Lower motor neuron issues --short-strided gait, flaccid paresis or paralysis -Thoracic limbs are normal -Ipsilateral deficits -Depressed sensation below the lesion or limb -Reflexes are small in the back limbs --ilsilateral, hyporeflexia in the pelvic limb -Can look like orthopedic disease, but dog will not right a flipped foot |
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T3-L3 Disease and gait analysis
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-Normal mental status
-Pelvic limbs: upper motor neuron signs --big reflexes, crossed-extension, increased tone, spastic paresis/paralysis --ataxia develops because spinal tracts are affected, causes long-strided gait -Thoracic limb: normal -Ipsilateral deficits -Sensation is depressed below the lesion -Ipsilateral hyperreflexia in pelvic limb |
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C6-T2 Disease and gait analysis
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-Normal mentation
-Pelvic limbs: upper motor neuron disease --ipsilateral spastic paresis/paralysis, long-strided gait -Thoracic limbs: lower-motor neuron disease --short-strided gait, flaccid paralysis or paresis -2-engine gait -Ipsilateral postural deficits -Sensation is depressed below the lesion -Ipsilateral hyperreflexia in pelvic limb, hyporeflexia in thoracic limb |
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C1-C5 disease and gait analysis
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-Normal mentation
-Spinal ataxia, long-strided in hindlimbs and forelimbs, ipsilateral spastic paresis or paralysis -Ipsilateral deficits -Sensation is depressed below the lesion -Ipsilateral hyperreflexia in all limbs |
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Midbrain/Pons/Medulla gait analysis
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-Altered mental status
-Spinal or vestibular ataxia, spastic tetraparesis or paralysis -Sloppy, incoordinated gait, animal can’t tell where their limbs are -Ipsilateral deficits -May get spinal and vestibular ataxia -Decreased sensation caudal to the lesion -Ipsilateral hyperreflexia in all limbs -Cranial nerves V-XII deficits |
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Cerebellum disease and gait analysis
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-Normal mental status
-Cerebellar ataxia or dysmetria -Ipsilateral deficits --“goose-stepping” -Normal sensation -Normal segmental reflexes -No cranial nerve deficits -May have menace deficits or intention tremors |
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Cerebral Hemisphere Disease and gait analysis
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-Altered mental status |
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Equine Neurologic Exam
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-Cannot do a lot of postural reflex tests
-Look at mental status --can depend on breed and “job” -Cranial nerves -Gait and posture with postural reactions -Spinal reflexes and muscle evaluation |
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Mental status of a horse
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-Observe the animal in the stall, outside, and with people
-Appropriate behavior varies with age, breed, use, prior experiences |
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Levels of Consciousness
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-Hyperesthetic
-Alert and responsive -Dull -Obtunded: usually there is a problem in the brian -Stuporous: respond to painful stimuli -Comatose: non-responsive -Significant changes indicate intracranial disease |
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Cranial nerve Exam in horses
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-Similar to that for small animals
-Eyes: --slow PLR but brisk palpebral reflexes -Angle of the eyelash is telling -Head elevation should result in ventral strabismus -Do not try to gag a horse! -Abnormal cranial nerve exam indicates brainstem problem or peripheral neuropathy |
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Gait and Posture analysis of Horses
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-Evaluate posture in the stall
-Need to take horse out to do a proper gait analysis --Unless horse is severely ataxic! -Postural reactions and proprioception are evaluated during gait exam --Hopping or knucking horses is difficult and potentially dangerous! |
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Gait exam in horses
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-Walk in a straight line
-Trot in a straight line -Walk in serpentine -Walk with head elevated -Walk while pulling tail -Small circles in both directions -Walk backwards -Walk over uneven terrain (hills, curbs, etc.) |
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Cerebellar Ataxia
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-Spastic, burst-y gait, Hypermetric
-Strength is maintained -Head/neck intention tremors -Loss of menace response --coordination is lost -Tendency to rear |
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Vestibular Ataxia
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-Peripheral vs. central
-Head tilt -Loss of balance, leaning/falling/drifting/rolling to one side -Nystagmus in acute stage |
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General Proprioceptive, Spinal ataxia
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-Proprioceptive tracts in brainstem and spinal cord are involved
-Proprioceptive deficits --scuffing, knuckling, crossing over, delayed protraction, excessive pivoting, irregular stride -Accompanied by weakness |
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Paresis
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-Deficiency in generation of gait or ability to support weight
-UMN: long stride with exaggerated proprioceptive deficits --scuffing, delayed protraction, pivoting --signs similar to general proprioceptive ataxia -LMN: short, choppy stride, weakness, muscle tremors |
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Spinal reflexes and muscle evaluation in horses
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-If horse is ambulatory, do not need to perform tendon or withdrawal reflexes
-Cervicofacial -Cutaneous trunci -Perineal -Muscle tone, size, symmetry -Skin sensation -Sweating |
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Important questions in Equine neurologic exam
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-Normal vs. abnormal
-Neuroanatomical diagnosis --prosencephalon --cerebellum --brainstem --C1-C5/6 --C6-T2 --T3-L3 --L4-S1/5 --Neuromuscular (LMN) |
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Cervical Myelopathy DDx
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-Cervical vertebral stenotic myelopathy/ Cervical vertebral malformation (Wobbler’s)
-Trauma -Equine Protozoal Myeloencephalitis -Equine degenerative myeloencephalopathy -West nile virus -Equine Herpes Virus-1 -Eastern Equine Encephalitis -Rabies |
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Cervical Vertebral Stenotic Myelopathy/ Cervical Vertebral Myelopathy
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-“Wobbler’s”
-Vertebral canal is not big enough for the spinal cord -Bones may not line up correctly, there may be arthritis, may have soft tissue inflammation and hypertrophy -Multifactorial disease (genes, diet, trauma) -Type 1: young, rapidly growing horses --usually male --vertebral malformation or dynamic instability in middle part of the neck --May even be a CJD-like lesion -Type 2: Older horses --static compression at C5-6 or C6-7 -Same signs for both forms --symmetric or asymmetric ataxia and upper motor neuron paresis in all 4 limbs --Pelvic limbs may be more severely affected --Neck pain is inconsistent |
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Diagnosis of Cervical vertebral stenotic myelopathy
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-Radiographs: intravertebral or intervertebral sagittal ratios
-Myelogram to look for more than 50% compression of dorsal column -MRI would be ideal, but impossible due to size -Post-mortem exam is definitive |
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Intravertebral Ratio
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-Assess whether there is enough room in the vertebral column for the spinal cord
-Diagonostic for wobbler’s -Spinal cord should be at least 52% of the widest part of cranial vertebral body --caudally should be at least 56% --If less than 50%, canal may be too small for horse |
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Intervertebral Ratio
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-Caudal aspect of dorsal lamina of cranial vertebrae to cranial aspect of the vertebral body of caudal vertebrae
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Myelogram in Horses
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-Needle goes into atlanto-occipital space, into dorsal sub-arachnoid space
-Inject contrast into sub-arachnoid space -Can see a bump over disc spaces in ventral spinal cord -For compression need thinning of both dorsal and ventral contrast columns |
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Post-mortem lesions of Cervical Vertebral Stenotic Myelopathy
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-Expect to see neuronal degeneration cranial and caudal to the lesion
-New bone formation in vertebral canal -Soft tissue impinges laterally on spinal cord |
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Cervical Vertebral Stenotic Myelopathy Treatment
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-Restrict diet in young animals
--“Paced” diet, feed young animal 75% of caloric requirements --Slows growth, allows vertebral canal to “catch up” -Ventral cervical interbody fusion, fuse vertebral bodies -Dexamethasone provide transient improvement |
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Equine Degenerative Myelopathy
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-Cervical spinal ataxia in young horses
-Forelimbs are often as severely affected as hind limbs -Degenerative condition, not infectious or traumatic -Multifactorial etiology --genetics, diet, environment --linked to vitamin E deficiency? -Diagnosis of exclusion, definitive diagnosis on histopathology -No effective treatment, supplement with vitamin E |
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Equine Degenerative Myeloencephalopathy Lesions
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-Causes very specific lesions on post-mortem
-Spheroids inbrainstem but no cranial nerve deficits -Axonal degeneration --symmetrical axonal loss and secondary demyelination |
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Equine Protozoal Myeloencephalitis EPM
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-Common disease, seen often
-Sarcocystis neurona (or Neospora hughesii) -Opossum is the definitive host --LOTs of intermediate hosts (cats, skunks, armadillos) -Horse is not the normal host, aberrant host -Any horse can be affected, and lots of horses are exposed, but rare occurrence --less than 1% of all exposed horses become diseased --most horses mount immune response and clear infection -Variable signs, protozoa can affect any part of CNS, can be multiple areas or focal areas -Often see spinal or general proprioceptive ataxia -Mixed UMN and LMN signs, often asymmetrical muscle atrophy -Can be treated! |
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Equine Protozoal Myeloencephalitis EPM Acquisition
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-horse eats opossum manure
-Cysts develop in muscle |
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EPM diagnosis
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-Sarcocystis neurona
-Lots of horses are exposed and few have clinical signs, makes diagnosis difficult -Diagnosis is always presumptive without post-mortem exam -3 principles of diagnosis: --Compatible clinical signs (atrophy, ataxia, asymmetry) --Exclusion of other diseases, rule out all other diseases --Prove exposure via antibody production in blood or CSF (only do if other signs are also present) |
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Difficulties of EPM diagnosis
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-Over-diagnosis is a problem!
--Rarely causes chronic lameness, but causes gait that mimics lameness --If animal gets better with NSAIDs, not EPM -Many horses are exposed to parasite and are positive for serum antibodies, only a small % develop clinical signs --both groups will have antibody in the blood, few will have antibody in CSF -Serum tests are considered to have high sensitivity and low specificity --cannot differentiate between occult and current infection -CSF testing increases specificity, false positives are still possible --Antibodies diffuse from blood to spinal fluid at constant rate --look at relative proportion of antibodies in blood and CSF |
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Ante-mortem tests for EPM
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-Western Blot
-Indirect Fluorescent antibody test -Surface antigen 1,5,6 ELISA -Surface antigen 2,3,4 ELISA (current preferred test) -Less common tests include PCR, direct antigen test, stall-side ELISA test -All tests can be performed on CSF or serum -No tests is considered to be the gold standard -Only necropsy is definitive! |
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EPM post-mortem lesions
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-Dark, patchy lesions in spinal cord
-Can be small lesions or large lesions -Inflammatory lesions -Random foci of hemorrhage, necrosis, and inflammation |
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FDA-approved EPM Treatment
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-Rebalance: pyrimethamine sulfadiazine
--mix of 2 antimicrobial folate inhibitors --oldest treatment -Marquis: ponazuril, anti-protozoal --most popular choice at the moment -Protazil: diclazuril --similar to ponazuril -Success of treatment is consistent with all treatments --60% of horses will improve with treatment, will not go back to “normal” --only 15% return to normal, even with treatment |
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EHV-1
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-Alpha herpesvirus
-Ubiquitous, almost all horses over 2 years have been exposed -Causes latent infections, T-lymphocytes in trigeminal ganglia or lymph nodes --reactivated after stress --50% of horses are latently infected -Mainly a respiratory pathogen, causes fever, inappetence, serous nasal discharge -Also associated with abortions, neonatal death, and neurologic disease/Myeloencephalopathy -T3-L3 Lesion -Less common than EPM -Very contagious -EHV-1 itself is not reportable, EHV-1 with neurologic signs IS reportable - |
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EHV-1 Strains
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-“Wild type”, non-neuropathogenic
-“Mutant”, neuropathogenic -Both strains cause paralytic outbreaks -Most of outbreaks are associated with the mutant strain -Both strains cause respiratory disease and abortions |
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Neuropathogenic EHV-1
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-Mutation is a single nucleotide polymorphism within gene encoding viral DNA
polymerase --Makes DNA polymerase more effective, more copies of virus produced --more virus in blood stream -Associated with higher level of viremia and neuropathogenicity --higher attack rate and neurologic mortality rate -PCR can differentiate mutant from wild-type |
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EHV-1 Transmission
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-Contagious infection!
-Aerosol -Fomites -Horse shedding virus can have reactivated latent virus or could have been horizontally infected --no way to know where strain came from |
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EHV-1 Pathogenesis
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-Virus enters respiratory epithelial cells
-Transported to regional lymph nodes in 1-2 days --replicates in respiratory epithelium for up to 14 days -Virus enters PBM cells and circulates for up to 21 days -Endotheliotropic virus, not neurotropic -Causes vasculitis with hemorrhage and thrombosis --leads to hypoxia and ischemia in adjacent CNS tissue -Hemorrhage, hypoxia, ischemia of endothelium cause clinical signs |
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EHV-1 Clinical Signs
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-Fever, usually precedes other signs and can occur at same time as neurologic signs
--fever and neurologic signs at the same time -Pelvic limbs will be more severely affected than the thoracic limbs -Paresis and ataxia -Decreased tail and anal tone -Recumbency -Vestibular signs are rare, other cranial nerve signs are less common |
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EHV-1 CSF analysis
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-Changes look like vasculopathy
-Normal to mildly elevated nucleated cell count -Yellow discoloration from bleeding into nervous system -Increased protein levels because blood vessels are leaky -Albuminocytologic dissociation with xanthochromia |
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EHV-1 Diagnosis
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-PCR assay is best way
--submit nasal swabs and whole EDTA blood -Post-mortem histopathology and immunohistochemistry |
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EHV-1 Treatment
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-Valacyclovir anti-viral
--most effective during early stages -Supportive care -Maintain comfort, hydration, nutrition -Bladder care (Catheterization and antimicrobials) -Anti-thormbotics? No proof that they help -Anti-inflammatory drugs are used if horse is about to become recumbent |
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EHV-1 prognosis
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-Variable prognosis
-Animal either gets better or dies quickly -Clinical signs usually worsen for 24-48 hours, then stabilize or improve -Mildly affected horses have fair to goof chance for full recovery -Recumbent horses have poor prognosis, unikely to return to normal function |
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Vaccination for EHV-1
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-DO not protect against neurologic form!
--does protect against respiratory form and abortions -Can decrease risk of shedding and spreading to other horses --allows herd immunity -Vaccinating is still important! |
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EHV-1 Outbreak control
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-contact the state vet!
-Stop horse movement, quarantine animal -Monitor, take temperature 2x daily --fever is early sign of infection -PCR test to identify positive horses -Move affected horses into strict isolation, restrict personnel, and use barrier precautions -Consider valacyclovir for horses early in fever progression -Disinfect facilities! |
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West Nile Virus
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-Most common equine viral encephalitis
-Flavivirus with mosquito vector -Cases appear in late summer or fall |
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West Nile Virus Clinical Signs
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-Spinal ataxia, intracranial disease
--affects brain and spinal cord -Hyperesthesia and fine motor fasciculations are common --“twitchy” animal -Spinal cord signs are usually more pronounced than cerebral signs -Fever is less consistent than with EHV-1 |
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West Nile Virus Diagnosis
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-IgM capture ELISA is best test
--Vaccines produce IgG antibodies, do not want to test for IgG antibodies --IgM indicates recent infection -Often see mononuclear pleocytosis on CSF analysis |
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West Nile Virus Treatment and Prognosis
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-Treat with hyper-immune plasma and supportive care
-Prognosis is fair to good --60% of animals have complete recovery -Vaccinate! Vaccine is highly effective! |
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Eastern Equine Encephalitis
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-Alphavirus with mosquito vector
-Similar to WEE, VEE -Most cases occur in late summer or fall -Clinical signs: fever, depression, diffuse or multifocal spinal cord and intracranial disease --brain signs usually predominate -Rapidly progressive, highly fatal -IgM ELISA capture -CSF will have neutrophilic pleocytosis -No specific treatment -Vaccination is key! Very protective! -Poor prognosis |
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Rabies in horses
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-Lyssavirus, rhabdoviridae
-Uniformly fatal, cases deteriorate quickly and animal usually dies within 10 days -No ante-mortem test available, post-mortem exam is definitive for diagnosis --will see negri bodies in neurons (pathognomonic, but not always present) -CSF shows lymphocytic pleocytosis -SUBMIT SAMPLES! All undiagnosed neurologic diseases! |
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Hepatic Encephalopathy in horses |
-Most common cause of equine encephalopathy? Intestinal encephalopathy may be more common |
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Neurologic Exam in Small Ruminants
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-Similar to small animal neurologic exam
-Mentation/behavior -Cranial nerve exam -Gait and posture -Postural reflexes -Spinal reflexes and muscle evaluation |
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Goals for neurologic exam in Small Ruminants
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-Decide if animal is normal or abnormal
-Localize the lesion -Formulate DDx list -Formulate diagnostic plan -Formulate therapeutic plan |
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Diagnostic aids in Small Ruminant Neurology
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-CSF analysis
-Imaging: --radiography --myelography --CT/MRI -Electrodiagnostics: EEG and EMG -Limiting factor is financial constraints and equipment availability |
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CSF analysis in Small Ruminants
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-Important to rule in or out DDx
-Know landmarks! Lumbosacral space is ideal -Manual restraint with or without sedation in sternal recumbency -Clip, sterile prep -Lidocaine block (not totally necessary) -3.5” 18 or 20 g spinal needle -3cc slip-lock syringes -Remove less than 1cc/kg! -EDTA and no-additive tubes should be used |
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Diseases causing intracranial signs in Small Ruminants
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-Polioencephalomalacia
-Listeriosis -Parelaphostrongylosis (less common presentation) -Bacterial meningoencephalitis or brain abscess/empyema -Thermal injury post-disbudding -Viral encephalitides can also occur (EEE, WNV, EHV-1) |
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Diseases causing spinal cord signs in small ruminants
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-P.tenuis, P. tenuis, P. tenuis!!
-Spinal fractures or subluxations -Diskospondylitis, vertebral body abscess -Enzootic ataxia or copper deficiency -Caprine Arthritis Encephalitis virus |
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Polioencephalomalacia in small ruminants
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-Softening or necrosis of the gray matter of the brain
-Causes necrosis of the cerebral cortex -All causes have the same send result -Diffuse metabolic encephalopathy --more common than hepatic encephalopathy in large animals -Historically attributed to thiamin deficiency -Can be after grain overload -Sulfur toxicity -Salt poisoning or water deprivation -Lead toxicity |
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Central blindness
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-No menace response bilaterally
-Normal PLR bilaterally |
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Thiamine deficiency and Polioencephalomalacia
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-Thiamine is needed for pentose phosphate pathway, glucose pathway
-Brain needs glucose -Thiamine may be low due to grain overload --grain overload changes pH, results in bacterial population change --thiaminase-producing bacterial grow and break down thiamine |
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Polioencephalomalacia Clinical Diagnosis
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-More common in younger animals than older animals
-Forebrain signs predominate --behavior changes, cortical blindness, dullness or obtundation, head-pressing, seizures -In severe cases, may start to see hind-brain signs --brain swells and herniates, puts pressure on the hindbrain --Strabismus, nystagmus, tremors, ataxia, miosis opisthotonous |
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Polioencephalomalacia Thiamin Treatment
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-Response to thiamine can give diagnosis
-10 mg/kg, any route --go slowly if giving IV -Give lots! Give repeatedly! -Thiamine will not hurt, just B vitamins and will be excreted in urine -Even cases without low thiamine levels may respond |
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Polioencephalomalacia Lab Diagnosis
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-Analyze blood thiamine status
--Thiamine is important co-factor for RBC transketolase activity -CSF is often normal, not specific --may see milk pleocytosis or increased protein -Gross post-mortem exam shows yellowish cortex, purple under UV light -Post-mortem histopathology is definitive, shows laminar necrosis of the cortex |
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Polioencepahlomalacia treatment
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-Thiamine! 10mg/kg
-IN severe cases can try to control brain swelling and prevent herniation --dexamethasone, manitol -Prognosis is good if treated early -Prognosis is guarded if severe --blindness may be permanent, takes longest time to resolve |
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Listeriosis in Small Ruminants
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-Meningoencephalitis due to listeria monocytogenes
-“Circling disease,” “silage disease” -Usually comes from soil contamination in small ruminants -Can cause septicemia and abortions -Theoretically zoonotic, but uncommon |
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Listeriosis pathogenesis
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-Bacteria enter abrasions in oral mucosa
-bacteria ascend sensory branches of trigeminal nerve to brainstem --seed the rest of the brainstem -Form micro-abscesses in brainstem -Brainstem signs predominate |
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Listeriosis Clinical diagnosis
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-Brainstem signs predominate
-Deficits in cranial nerves 5-12 -Spnial or vestibular ataxia -Changes in mentation due to interference with reticular activating system -Normally does not cause blindness, does not get to optic nerve -Lose menace response due to facial paralysis -Can show forebrain signs (seizures) when meningitis spreads |
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Listeriosis lab diagnosis
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-CSF analysis
-Usually shows non-suppurative inflammation -Mononuclear pleocytosis with increased total protein -May also see neutrophils or bacteria -Hard to culture bacteria from CSF -Definitive diagnosis is made at necropsy --microabscesses in brainstem with meningoencephalitis --Immunohistochemistry --culture |
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Listeriosis treatment
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-Low case attack rate, but high fatality rate
-treatment is possible, easier to cure in cattle than small ruminants -Antibiotics are main therapy --Penicillin, oxytetracycline, florfenicol -Consider steroid treatment as anti-inflammatory |
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Parelaphostrongylus tenuis
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-Protostrongylid nematode
-Deer release L1 in manure, L1 jump into snail or slug and molt -Deer eats snail, slug, or slime containing L3 --Larva migrates across stomach lining, migrates into spinal cord -Larva makes deer protein so deer immune system does not attack --parasite can live in spinal cord or deer --molts into L4 and adult stage during migration -Adults lay eggs in venous sinuses of the brain -Egg emboli are in the blood, get lodged in the lungs and hatch -crawl into airways, migrate into trachea, are brought into pharynx (tracheal migration) -In aberrant host, parasite tried to do normal lifecycle but host immune system attacks larva --does not make it to brain, causes damage as it moves along --life cycle is not completed in aberrant host |
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P. tenuis diagnosis
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-Will see eosinophils on CSF analysis and increased protein
-Vertebral radiographs -Signs progress if left untreated, until the animal is recumbent -Can mimic other diseases -Definitive diagnosis on post-mortem exam |
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P. tenuis treatment
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-Ivermectin
-Fenbendazole -Dexamethasone -Physical Therapy |
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Parelaphostrongylosis
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-Does not cause disease in white-tailed deer
--Molecular mimicry to evade immunological detection in competent host -Migration in aberrant host causes variety of signs --does not complete life cycle |
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Parelaphostrongylosis clinical diagnosis
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-Clinical signs
-Most common in llamas and alpacas, then goats, then sheep in fall or winter -Asymmetric, progressive spinal cord signs --paresis and ataxia -Often signs progress until animal is recumbent -Can mimic other diseases |
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Parelaphostrongylosis Treatment
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-Anthelmintics (Ivermectin, fenbendazole) |
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Parelaphostrongylosis prevention
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-Avoid exposure to deer or gastropods |
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Lesions in Cerebrum
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-Change in behavior
-Change in mentation --depression, obtunded, comatose -Head pressing -Blindness --no PLR indicates cortical blindness -Seizures |
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DDx for lesions in Cerebrum
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-Trauma (associated with acute onset)
-Metabolic derangements --hepatic encephalopathy, liver is not detoxifying blood --Ketosis: fat mobilization derangements --Thiamin deficiency: problem with metabolism of carbohydrates, causes polioencephalomalacia -Infectious: --rabies --BSE -Toxins: --Pb poisoning --Salt toxicity: young calves or adults deprived of water |
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Lead poisoning in Cattle
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-Toxin causing cerebral dernagements
-Changes carbohydrate metabolism -Causes central blindness and seizures |
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Lesions in Cerebellum
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-Hypermetria
-Intention tremors -BVD is main DDx --teratogenic, can result in cerebellar hypoplasia --causes wide forelimb stance --viral particles will not be in the calf, infection will be cleared already |
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CN II: Optic
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-PLR
-Blindness -Fundic exam of optic nerve |
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CN III: Oculomotor
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-Parasympathetic fibers cause PLR
-Allows for movement of the eye and strabismus |
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CN IV: Trochlear
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-Movement of the eye, strabismus
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CN V: Trigeminal
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-Motor innervation to muscles of mastication
-Sensory innervation to the face |
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CN VI: Abducens
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-Responsible for eye movement
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CN VII: Facial
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-Motor innervation to muscles of facial expression
--lip droop, ear droop, ptosis |
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CN VIII: Vestibulocochlear
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-Balance and orientation with the horizon
-Head tilt towards the side of the lesion -Ataxia, circling, leaning -Nystagmus -Peripheral vs. central damage: --look for other cranial nerve deficits --Look for reticular activating system involvement |
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CN IX: Glossopharyngeal
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-Swallowing, gag reflex
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CN X: Vagus
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-Swallowing
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CN XI: Spinal accessory
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-Trapezius muscle innervation
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CN XII: Hypoglossal
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-Tongue tone
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Brainstem lesions
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-Cranial nerves can be damaged in brainstem
-Facial and vestibular nerves can be damaged in the inner ear |
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DDx for Brainstem disease
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-head trauma
-Listeriosis (top DDx) --in silage, bacteria travels up trigeminal nerve to brainstem from cuts in mouth -CN VII and VIII affected only: inner ear infection --usually ascending |
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Spinal cord lesion
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-Everything cranial to lesion will be normal
-Reflexes stay intact -Localization of lesion is important for imaging and DDx |
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Caudal sacral lesions
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-Front and hind legs are normal
-Loss of innervation to the tail --limp tail --decreased anal tone --decreased sensation to perineum |
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Deep pain
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-One of last things to go away with nerve damage
-Indicates extensive damage |
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L4-S2 lesion, lumbosacral intumescence
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-Front legs will be normal
-Motor neurons to hind limbs are damaged --Paresis if partial, paralysis if total --Flaccid tone in hind limbs -Loss of voluntary motion to hind limbs -Denervation atrophy will occur in hind limbs after 7-10 days |
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Hind limb reflexes
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-Cannot test if the animal is standing
-Femoral nerve: innervates quadriceps muscles --patellar reflex, tap patellar tendon -Sciatic nerve: --limb withdrawal, pinch toe and see if animal pulls back --check for nociception/deep pain sensation |
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T3-L2 lesion
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-Front legs are not affected
-Hind legs have decreased voluntary motion, paresis/paralysis, decreased proprioception -Look at gait changes -Motor neurons are still intact to hind limb, will have muscle tone -May have increased tone or spasticity -UMN is damaged to hind limb, LMN are intact -No atrophy in hind legs -Reflexes in hind limb are normal or hyper-reflexive due to loss of fine motor control from UMN |
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C7-T2 lesion
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-Front and hind limbs are both affected
-Hind legs: paresis/paralysis --motor and proprioceptive tracts are affected --have muscle tone, muscles may be spastic --reflexes will be intact, maybe hyper-reflexive -Forelimbs will show paresis/paralysis --decreased muscle tone, LMN is affected --muscles become atrophied --reflexes will be decreased or absent -Test withdrawal and triceps tendon reflex |
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C1-C6 lesion
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-Disruption of tracts going up and down spinal cord
-Hindlegs and front legs have same signs, all limbs are affected -Paresis/paralysis -decreased proprioception -No atrophy -Reflexes will be normal or increased |
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DDx for spinal cord lesions
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-Trauma
-Vertebral abscess, osteomyelitis, abscess causing spinal cord compression -Neoplasia causing spinal cord compression --lymphosarcoma in cows |
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Cow Age and spinal cord lesions
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-Older cows: Lymphosarcoma
--caused by bovine leucosis virus -Younger cows: vertebral abscess or osteomyelitis --hematogenous spread of bacteria --older animals usually have robust enough immune system to prevent infection -Trauma can occur at any age --more likely to occur in calves --hard to cause a vertebral fracture in ALL cows --usually due to osteopenia and pathologic fracture, look for decreased Ca in diet |
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Location of Spinal lesion
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-Adult: lumbosacral is common from mounting
-Lymphosarcoma is almost always lumbar -Abscesses or osteomyelitis is usually thoracolumbar |
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CSF analysis for cows with spinal lesions
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-Trauma: may see RBCs
-Osteomyelitis/abscesses: increased protein, increased WBCs (neutrophils) -Lymphosarcoma: neoplastic lymphocytes --present in 50% of cases |
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Treatment for spinal cord injuries in cows
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-Lymphosarcoma: can give steroids for temporary regression
--no great treatment -Trauma: nothing -Osteomyelitis or abscess: usually no successful treatment, disease has already progressed |
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Neurologic cows and rabies
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-Treat all neurologic cases as rabies potential!
-especially if animal is bellowing, foaming at the mouth, acting “crazy” |
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Polioencephalomalacia in Calves
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-Stargazing
-Blindness with intact PLR -No menace response |
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Head turn vs head tilt
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-Head turn is animal looking consistently to one side |
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Biliary Tract Anatomy
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-Gallbladder between quadrate and right medial liver lobes
-Cystic duct joins with hepatic ducts to become common bile duct --Dogs have 2-7 hepatic ducts --cats have 1-5 hepatic ducts |
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Dog Bile Duct anatomy
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-Major duodenal papilla:
--exit for common bile duct and pancreatic duct --separate exits -Minor duodenal papilla: --exit for accessory pancreatic duct |
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Cat Bile Duct Anatomy
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-Major duodenal papilla:
--exit for conjoined common bile duct and pancreatic duct --ducts are JOINED when they enter the papilla -Minor duodenal papilla: |
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Surgical Syndromes of Bile Duct
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-Extra-hepatic biliary obstruction (EHBO)
-Bile peritonitis -Gall bladder mucocele -All present with similar, non-specific clinical signs |
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Clinical signs of bile duct pathology
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-Non-specific!
-Lethargy -Anorexia -Vomiting -Diarrhea -Icterus -May or may not have abdominal pain |
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Extra-hepatic biliary obstruction (EHBO) in dogs
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-Obstruction of common Bile Duct that is due to something outside of the liver
-Extraluminal: pancreatitis, neoplasia -Intraluminal: Cholelithiasis, foreign body, neoplasia -Intramural: neoplasia in the wall of the bile duct |
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Extra-helatic Biliary Obstruction (EHBO) in cats
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-Inflammatory cause (68%)
--cholangiohepatitis --Cholecystitis --cholelithiasis --Pancreatitis --Hepatic lipidosis -Neoplasia (32%) --Pancreatic adenocarcinoma --Biliary adenocarcinoma --Lymphoma -Occasionally can be due to diaphragmatic hernia, fluke, or foreign body -Can be a combination of inflammatory factors, hard to know which one is the initial/primary cause |
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Feline EHBO Inflammatory complex
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-Many different factors work together, interact with each other
-IBD may be a component -Cholangiohepatitis, Cholelithiasis, Cholecystitis, and pancreatitis |
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Endotoxemia and EHBO
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-Endotoxemia is a consequence of EHBO
-Absence of bile salts in the intestine leads to bacterial overgrowth --bacteria produce endotoxins in cell walls --Endotoxins can be absorbed across the intestine -Impaired hepatic clearance contributes to absorption |
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Physiological effects of EHBO
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-Decreased myocardial contractility
-Hypotension -Decreased vasopressor response -Acute renal failure -Coagulopathies (including DIC) -gastro-intestinal hemorrhage -Delayed wound healing -Most effects are related to endotoxemia |
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EHBO diagnostic tests
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-Hyperbilirubinemia
-increased serum ALP, ALT, GGT --indicates hepatocellular damage -Leucocytosis -Hypoalbuminemia -Urinalysis: bilirubinuria or bilirubin crystals -Coagulation profile: prolonged PT, PTT, PIVKA --due to vitamin K deficiency -Fecal examination: acholic feces due to trematode eggs (cats) |
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EHBO Radiographs
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-cranial organomegaly, liver enlargement
-cholelithiasis, most opaque -Peritonitis and loss of serosal detail |
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Abdominal Ultrasound for EHBO
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-Common bile duct and gallbladder distention
-Distension does NOT confirm obstruction -Choleliths, neoplastic lesions, mucoceles --structures that cause obstruction, may be visible |
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EHBO Scintigraphy
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-Injection of radiopharmaceutical agent
-If there is no intestinal visualization of agent at 3 hours, EHB obstruction is likely |
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Bile Peritonitis
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-Usually due to underlying cause
-Trauma, laceration of common bile duct or gallbladder -Necrotizing cholecystitis or ruptured mucocele -Bile peritonitis can occur secondary to all causes of EHBO |
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Diagnosis of Bile Peritonitis
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-Hyperbilirubinemia
-Radiographs -Abdominal ultrasound -Bile pigments in effusion on cytology -Abdominocentesis gives definitive diagnosis --if bilirubin in effusion is more than 2x serum, indicates bile peritonitis |
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Bile peritonitis pathophysiology and treatment
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-Bile is adjuvant in peritonitis, makes peritonitis worse
--irritates serosal layer -Imperative to treat the underlying leakage! -Thorough abdominal lavage -Bile peritonitis is a surgical emergency! |
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Biliary Mucoceles
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-Cystic mucinous hyperplasia of gallbladder is underlying lesion
--lesion of the wall of the gallbladder -Gallbladder is filled with thick gel-like shiny green/black congealed bile --should be liquid, not congealed gross thick stuff --lamellar striations --obstructs flow though biliary system -Pressure necrosis of gallbladder wall can lead to rupture -Can be incidental finding -Cholecystectomy is treatment of choice, remove gallbladder |
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Biliary mucocele Imaging
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-Ultrasound is most useful and sensitive diagnostic test
-Bile sludge accumulation acts as early lesion -Later lesion is “stellate appearance” or “kiwi gallbladder” |
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Surgical Access to Biliary structures
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-Laparotomy from xiphoid to pubis
-Need good retraction and excellent surgical lighting -Packing of sponges between the liver and diaphragm can be helpful --moves biliary tract caudally |
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Surgical procedures of the Biliary Tract
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-Cholecystectomy
-Choledochotomy -Cholecystoenterostomy --re-routing bile duct to empty into intestine directly --Cholecystoduodenostomy --Cholecystojejunostomy -Bile duct trauma --primary repair --bile stenting with primary repair --Cholecystostomy |
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Exploratory laparotomy for bile duct surgery
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-Diagnostic and therapeutic
-Look at everything in the abdomen -Make antimesenteric duodenotomy 3-5cm aboral to the pylorus -Flush gallbladder, always look for patency of the common bile duct |
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Cholecystotomy
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-Incision into gall bladder to remove gallstones
-Removing gallbladder stones and suturing gallbladder back together -Rarely performed --gallbladder has limited blood supply, does not heal well |
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Choledochotomy
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-Incision into the bile duct to remove stones from the biliary system
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Cholecystectomy
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-Removal of the gallbladder altogether
-need to dissect gallbladder out from hepatic fossa -remove all material above all hepatic ducts --ligate proximal to where the hepatic ducts empty -Use non-absorbable suture, want a permanent closure |
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Cholecystoenterostomy
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-Connecting the gallbladder to the intestine somewhere besides duodenal papilla
-Diversion of bile from gallbladder to intestine at duodenum or jejunum -Gallbladder needs to be healthy for procedure to be successful -Can be done when a pancreatic tumor is causing biliary tract obstruction |
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Cholecystoenterostomy
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-Gallbladder is incised from base to apex
-Opening is sutured to antimesenteric duodenum or jejunum --duodenotomy or jejunotomy -Maximize the size of the anastomosis, needs to be more than 2.5cm -Large opening could cause colangehepatitis from bacteria in intestinal tract, but needs to be sufficiently large |
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Choledochal Tube Stenting
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-Place tube stent within bile duct
-treats Obstructions proximal to or at sphincter, caused by compression or blockage at the sphincter -Maintains patency of duct after primary repair -Stent keeps bile duct open until pancreatitis resolves -Eventually tube is pooped out |
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Lacerations or Rupture of GallBladder or bile ducts
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-Primary repair can be tough, ducts are very small!
-Anastomosis and tube stenting is common solution -Duct sutured primarily, can be stented to reduce chance of stricture |
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Cholecystostomy tube
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-Tube from gallbladder out of body through body wall
-Can be placed surgically or percutaneously -Can be a primary treatment or adjunct treatment -Provides temporary relief of obstruction -Tube releases pressure on gallbladder |
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Decision making in Surgical procedures of the Bile Duct
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-Cannot demonstrate patency of common bile duct:
--re-route bile duct, connect bile duct to intestines (cholecystoenterostomy) -Functional EHBO: Biliary stenting, cholecystostomy, or choledochotomy --incision into bile duct to remove stone -Biliary mucocele/cholelithiasis, Gallbladder neoplasia or trauma: --Cholecystectomy, remove gallbladder -Traumatic injury to common bile duct: primary closure or biliary re-routing |
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Adjunctive Surgical Procedures for bile duct pathology
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-Culture and sensitivity of abdominal effusion or gallbladder and bile
-Liver biopsy -Consider feeding tube, animals are very sick |
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Post-operative management of Bile system surgery
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-Continued fluid therapy
-Maintain Electrolyte balance and acid-base balance -Nutrition -Antibiotic therapy -Open abdominal drainage of needed -Patient is usually in ICU post surgery |
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Post-operative complications of Bile system surgery
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-Leakage of bile due to poor healing of gallbladder
--can lead to pancreatitis -Peritonitis -Hemorrhage due to endotoxemia and reduced vitamin K absorption -Pancreatitis -Re-obstruction of biliary tree -Ascending cholangiohepatitis with re-routing procedures -Sepsis |
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Canine mortality in Biliary surgery
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-high complication and mortality rate
-39% death from Necrotizing cholecystitis -Cholelithiasis (48%) -EHBD (41%) -Bile peritonitis (50%) |
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Feline mortality in biliary surgery
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-EHBO: 57%
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Biliary pathology prognosis
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-Overall survival rate is 50% |
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Normal Esophagus
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-Mucosa
-Submucosa -Muscularis -Adventitia/serosa -Usually not seen on radiographs, may see some gas patterns --silhouettes with other mediastinal structures -Normally sits dorsally to the trachea on radiographs |
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Dog esophagus vs. cat esophagus
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-Dogs: entire esophagus has skeletal muscle
--longitudinal -Cats: distal 1/3 is smooth muscle --oblique orientation |
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Lower Esophageal Sphincter
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-Circular layer of muscularis tissue
-Rugal folds, diaphragmatic crus, and oblique angle of entry of esophagus into stomach help prevent reflux |
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Barium Esophagogram
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-Used to see if there are any abnormalities in the esophagus
-Take different frames at different times to look for abnormalities -Stricture, foreign bodies, masses, fistulas, hernias, etc. -Iodinated contrast is used instead of barium if perforation is suspected |
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Upper Esophageal Sphincter
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-Cranial portion of esophagus
-Looks like a soft-tissue thickened area at upper esophageal sphincter --cricopharyngeus and thyropharyngeus muscles attach to dorsal larynx -Looks like a mass, is not |
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Gas in normal esophagus
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-Pockets of gas can be seen in normal locations
-Thoracic inlet, dorsal to the heart/heart base areas tend to accumulate gas -Fluid accumulation in caudal mediastinum is normal |
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Tracheal Stripe Sign
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-Indicator for gas in the esophagus
-Gas acts as negative contrast agent -Apparent thick wall between esophagus and trachea -Line looks thick due to summation of ventral wall of esophagus and dorsal wall of the trachea -Evaluate entire esophagus to figure out if it is dilated |
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Esophageal Diseases
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-Hiatal hernia
-Megaesophagus -Vascular stricture -Foreign Body -Perforation -Fistula -Diverticulum -Stricture -Tumors -Gastro-intestinal intussusception |
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Hiatal Hernia
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-Protrusion of abdominal structures through esophageal hiatus
-Sliding hiatal hernia is most common -Lower esophageal sphincter area moves into thoracic cavity --portion of the stomach ends up in the thoracic cavity -Predisposes animal to reflux which predisposes to esophagitis --esophagitis can lead to strictures etc. |
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Causes of Hiatal hernia
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-Abnormal esophageal hiatus
-Abnormally decreased intra-thoracic pressure, due to upper airway obstruction or airway disease -Increased abdominal pressure --peritoneal effusion, abdominal mass, organomegaly |
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Gastro-esophageal Reflux Disease
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-Esophagitis
-Motility disorders |
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Hiatal Hernia on radiograph
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-Caudo-dorsal round to oval
-Soft-tissue opacity between and cranial to crus -Need orthogonal views to make sure it is a hiatal hernia |
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DDx for Hiatal Hernias
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-Foreign body
-Granuloma -Diverticula -Pulmonary mass -Caudal mediastinal mass |
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Para-esophageal hernia
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-Uncommon
-Usually occur secondary to bad hiatal hernia -Stomach and esophagus are side-by-side in caudal mediastinum -Lower esophageal sphincter stays in place, stomach sneaks out -Diagnose via contrast study or abdominal CT |
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Megaesophagus
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-“Big esophagus”
-Can be primary (idiopathic) or secondary --CNS disease, neuromuscular disorders, endocrine disorders, Mechanical esophageal lesions -Neuromuscular disorders causing megaesophagus --myasthenia gravis, polymyositis, dysautonomia |
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Megaesophagus radiographic signs
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-Gas dilation
-Fluid or food accumulation -Widened mediastinum -Ventral displacement of the trachea and heart -Cranio-ventral alveolar pulmonary pattern -Widened cranial mediastinum on VD projection -Contrast study can show dilation well |
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Vascular Ring Anomalies
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-Abnormal vessel at the base of the heart causes esophageal narrowing
-“Hugs” esophagus and makes passage of food difficult -congenital situation, animal is born with condition |
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Aortic Arches
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-4th forms aortic arch
-6th forms pulmonary trunk, ductus arteriosis, and right pulmonary artery |
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Persistent Right Aortic Arch
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-Vascular ring anomaly
-Vascular ring consists of right aortic arch, ligamentum arteriosum from main pulmonary artery to right aorta -Aorta is on the right side --ductus arteriosus has to go around the esophagus to connect aorta to pulmonary artery |
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Radiographic signs of Persistent Right Aortic Arch
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-Sacular dilation of the esophagus cranial to the heart base
-Lefward deviation of the trachea cranial at the heart base -Ventral deviation of the trachea -Right-sided aortic arch |
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Double Aortic Arch
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-Vascular ring anomaly, vascular stricture
-Right and left 4th aortic arches are present -Causes more severe respiratory signs --due to constriction of the trachea AND esophagus -No space for the trachea |
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Persistent Right Ductus Arteriosus
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-Mirror image of persistent right aortic arch
-Right 6th arch instead of left persists as ductus arteriosus --compresses esophagus from the right side |
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Aberrant left subclavian artery
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-Vascular ring anomaly
-Partial compression -Artery arises from persistent right aortic arch, compresses esophagus as it travels from right to left |
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Aberrant Right subclavian artery
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-Right subclavian artery arises from left aortic arch
-Travels to right and compresses esophagus dorsally |
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Esophageal foreign bodies
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-Common in dogs and cats
-Common locations: --thoracic inlet --heart base --esophageal hiatus -Esophagus is very sensitive and delicate, perforates quickly --needs to be removed ASAP |
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Esophageal Perforation
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-Results from rupture of the esophageal wall
-Direct trauma from foreign body -Can be secondary necrosis |
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Radiographic signs of Esophageal Perforation
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-Pneumomediastinum
-Mediastinal widening due to inflammation -Pneumothorax -Pleural effusion -If perforation is expected, use iodinated contrast instead of barium |
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Esophageal fistula
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-Communication between esophagus and airways
-Not common -Congenital or acquired --acquired from foreign body trauma -Chronic fistulas are hard to diagnose --may be small or fill with granulation tissue |
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Radiographic signs of Esophageal fistula
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-Foreign body
-Pneumomediastinum -Interstitial or alveolar pattern -Tracheal or bronchial contrast material after positive contrast esophagogram |
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Esophageal Diverticulum
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-Localized outward expansion of the esophageal wall, forming a pouch
-Can be congenital or acquired -Increased esophageal pressure from vascular ring anomaly -Mediastinal diseases leading to fibrosis |
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Esophageal Stricture
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-Mural constriction of the esophagus
-Whole wall is narrow, cannot dilate normally -Rarely congenital -Acquired is much more common, can be due to trauma or chronic inflammation -Does not show up on radiographs --unless focal distention of the esophagus --fluid or gas dilation orad to the stricture area |
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Esophageal Tumors
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-Rare
-May be associated with Spirocerca lupi infection --leads to fibrosarcoma or osteosarcoma -Spontaneous tumors --leiomyomas, carcinomas, papillomas, lymphosarcoma -Metastatic neoplasia |
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Radiographic signs of Esophageal Neoplasia
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-Soft tissue mass anywhere in the esophagus
-Displacement of other organs due to mass effect -Dilation of the esophagus around the mass -Need additional imaging to confirm --contrast study, CT, MRI, Ultrasound |
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Gastroesophageal Intussusception
|
-Involution of all or part of the stomach into the esophageal lumen
-Stomach hangs out inside caudal esophagus -Associated with young age and german shephardism -Often preceded by megaesophagus -More often occurs in young dogs |
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Gastro-esophageal intussusception on Radiographs
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-Dilation of intra-thoracic esophagus |
