CNS: head trauma, metabolic, lysosomal storage diseases Flashcards
describe head trauma
- primary injury: biomechanical secondary to forces at impact
-penetrating injury, skull fracture, hemorrhage/hematoma, all directly damage brain parenchyma - secondary injury: series of cellular reactions mediated by oxygen free radicals, excitatory amino acids, nitric oxide that result in
- cerebral edema: most severe 24-48 hours
- hematoma and edema increase intracranial pressure!!
what are the consequences of increased intracranial pressure?
- transtentorial herniation: compression of midbrain, loss of consciousness, mydriatic unresponsive pupils, often starts asymmetrically and can lead to death
- foramenal herniation: compresses respiratory centers in medulla, frequently fatal
- miosis: acute, diffuse brain disorder, not helpful in localization; sympathetic innervation to the eye begins in the hypothalamus (UMN)
- mydriasis: may indicate transtentorial herniation/progression of severity (worse than miosis); if bilateral, death is imminent
won’t be tested on specifics on exam!
increased intracranial pressure leads to brain herniation!!!
how does intracranial presure/head trauam affect postural reactions?
- decerebrate rigidity:
-rostral brainstem lesion; stupor or coma; all limbs extended, opisthotonos, abnormal PLR
-due to loss of communication between cerebrum and brainstem (loss of descending UMN input from cerebrum to medulla for flexion of limbs) - decerebellate rigidity:
-cerebellar lesions;
-thoracic limbs extended, pelvic limbs flexed, opisthotonos, can have NORMAL mentation!! - most severely: not tested on specifics of this
-cushing reflex
-must be stupor/coma
-likely bilateral mydriatic pupils
-hypertensive and bradycardic
what does the brain need to prevent neuronal death?
a normal blood supply!!
- brain receives 25% of cardiac output and has a high metabolic rate
- needs adequate blood flow for oxygen, glucose, etc.; driven by systemic arterial pressure (blood pressure) and affected by metabolism (O2, CO2)
- monro kellie doctrine: the total volume of the brain, CSF, and blood within the cranium is constant
-to maintain cerebral blood flow, you MUST maintain normal arterial blood pressure
describe evaluation of a clinical patient with head trauma
immediate:
1. ABC
2. thoracic rads for concurrent trauma
3. minimum database
4. BLOOD PRESSURE: maintain normal MAP!!!
evaluate neuro status: eval 3 categories; each receives 1-6 and total possible score is 18 (3-8=grave prog, 9-14 = guarded, 15-18 great)
1. level of consciousness
2. motor activity
3. brainstem reflexes
additional diagnostics:
1. radiographs/CT/MRI
-helpful for ID fractures, compression fx may need surgery, helpful to rule out concurrent spinal trauma
2. MRI or CT for hematoma
describe evaluation of neuro status
eval 3 categories; each receives 1-6 and total possible score is 18 (3-8=grave prog, 9-14 = guarded, 15-18 great)
- level of consciousness: assesses functional capabilities
-brainstem (ARAS)
-cerebral cortex
-can be obtunded, semi-coma/stupor, or coma - motor activity:
-may be affected by level of consciousness
-spinal reflexes should be normal to exaggerated if no concurrent spinal cord injury
–if depressed, indicates severe lesion/close to death - brainstem reflexes:
-assessment of pupils: mydriatic, miosis (see above for prognosis)
-occulocephalic reflex: VIII in, 3, 4, 6 out (should move eyes when you move their head)
describe treatment of patients with head trauma
level 1: patient resuscitation
1. fluid management!!
-establish and maintain euvolemia and MAP to maintain cerebral blood flow
-typically crytalloids, can give hypertonic saline for resuscitation
2. oxygenation!!!! (prevent secondary brain injury)
3. elevate head: improve venous drainage, decrease ICP
-head at 30 degrees and no jugular restriction
-if still bad, move to level 2
level 2: resuscitated patients with progressive signs of elevated ICP
1. osmotic diuretics to reduce ICP and cerebral edema to improve cerebral blood flow
-mannitol or hypertonic saline
2. sedation and pain meds:
-if agitated or painful, minimize effects on blood pressure
-titrate to effect
3. corticosteroids ONLY if desperate, typically have negative impact
if still bad, move to level 3
level 3: failure of level 2 therapy (refractory head trauma)
1. surgery
-indications: depressed skull fracture, hematoma, reduce ICP by opening skull (rare)
what is the big sign of metabolic disorder?
BILATERALLY SYMMETRICAL!!
usually affect prosencephalon more than anything else
describe hepatic encephalopathy
- liver is diseased so numerous neurotoxins that would be metabolized by the liver reach the brain unmetabolized
-AMMONIA: can directly test for
-gamma-aminobutyric acid
-glutamate
-mercaptans
-aromatic amino acid
-benzodiazepine-like compounds
all go to the brain and cause a sedative effect
- portosystemic shunt: cause small liver
-congenital: most common! can be occult
-acquired: liver failure, systemically ill!!!
describe portosystemic shunt
- cause small liver
-congenital: most common! can be occult
-acquired: liver failure, systemically ill!!! - portosystemic shunt from an anomalous vessel diverts blood to systemic circulation via vena cava instead of going to the liver first
describe congenital PSS signalment and clinical signs
- majority diagnosed <1 year of age
-can be occult and diagnosed in middle aged dogs - yorkshire terrier most common (40x more than other breeds)
-also maltese, mini schnauzer, etc. - clinical signs:
-often wax and wane, worse post-prandial
-GI signs: anorexia, vomiting, diarrhea, ptyalism
-dysuria, stranguria, pollakuria, haematurie
-cats: copper colored irises, ptyalism - NEURO SIGNS:
-wax and wane, worse post-prandial
-seziures
-abnormal mental status (dull to coma)
-abnormal behavior: pacing, circling, head pressing
-blindness with normal PLR
describe congenital PSS diagnosis
- fasting and 2hr post-prandial bile acids
-shunting of reabsorbed bile acids to systemic circulation
-elevated bile acids nearly 100% sensitive but not 100% specific
-ONLY ABOVE relevant for neuro exam - serum ammonia
- +/- abnormal markers of liver function
-albumin, urea, protein, glucose, cholesterol
-erythrocyte microcytosis - +/- elevated liver enzymes
- +/- ammonium urate cyrstals in urine
- imaging to ID protsosystemic shunt versus liver biopsy
describe treatment of congenital PSS
- treat underlying cause (sx to repair shunt)
- reduce serum levels of neurotoxic metabolites
-high quality, low protein diet - lactulose! increase GI transit time, alter gut flora reducing colonic ammonia production
- antibiotics to reduce urease-producing bacteria
- anti-seizure meds: ideally without hepatic metabolism
-potassium bromide
-levetiracetam - prognosis: depends on ability to treat underlying disease
-a low protein diet helps!
what are causes of hypoglycemia?
- iatrogenic (insulin overdose)
- neoplasia: insulinoma!!
- HYPOADRENOCORTICISM
- liver disease
- glycogen storage disease
- sepsis
- xylitol toxicity
- transient in toy and mini breed and hunting dogs
describe clinical signs and diagnosis of hypoglycemia
- SEIZURES
- altered mentation
- visual deficits
- weakness/ataxia
- coma progressing to death
diagnosis is bloodwork!
describe treatment of hypoglycemia
oral glucose syrup and ID underlying cause
what is the bottom line with electrolyte disturbances?
can cause neuro signs; do a minimum database and check electrolytes on ALL sick animals
-cause symmetrical abnormalities (for EXAM, barber said don’t memorize specifics)
hyernatremia: rapid changes = clinical signs
-seizures, mentation changes, blindness, tremors, gait deficits resulting in coma
-if chronic, safer to slowly correct
hyponatremia: also correct slowly, similar signs to hypernatremia
hypercalcemia: depressed
hypocalcemia: weakness, inense facial rubbing
describe polycythemia
- too many red cells! diagnose with blood work
-elevated HCT - more common in cats than dogs
-can be primary or secondary to cancer - neuro signs and PU/PD (body trying to drink more to dilute)
-dull mentation
-seizures - treat with fluid therapy, repeated phlebotomy, +/- hydroxyurea
describe thiamine (vitamin B1) deficiency
- thiamine: essential in carbohydrate, amino acid, and fatty acid synthesis and metabolism
-destroyed by heat, sulphur preservatives, and diets with high thiaminase activity (like raw fish) and has been reported in commercial diets - more common in cats than dogs
-impaired vision, mydriasis!!, vestibular signs!!, ventroflexion, dull mentation!!, seizures - treat: thiamine supplementation 50mg/day IM for 3-5 days
- good prognosis if caught early
-not wrong to give thiamine to any cat that is bilterally symmetrical with mentation change, ventroflexion where you don’t have a definitive diagnosis (won’t hurt)
what can cause cervical flexion/ventroflexion in cats? (NOT tested on)
- hypokalemia: CKD, hyperaldosteronism
- thiamine deficiency
- hyperthyroidism
- neuromuscular disease (myasthenia gravis, polymyositis)
- also CKD, electrolyte abnormalities, toxicosis
NOT tested on
