Neurological emergencies Flashcards
Causes of primary brain injury
Contusion
Haematoma
Laceration
Vasogenic oedema as a result of traumatic injury
Secondary brain injury
Associated with excitatory neurotransmitter release, inflammation, and increased intracranial pressure
Central perfusion pressure (CPP)
CPP = Mean arterial pressure (MAP) - Intracranial pressure (ICP)
Obtunded
Depressed responses to normal stimulation.
Stuporous
Basically asleep but rousable with noxious stimulus e.g. pinching toe.
Comatose
Non-responsive even to noxious stimulus.
Decerebellate posture
Opisthotonos, thoracic limb extension and pelvic limb (hip) flexion, normal mentation.
Indicates damage to cerebellum.
May slip in and out of this posture.
Decerebrate posture
Similar but pelvic limbs extended, and mentation reduced.
Indicates more severe damage at level of forebrain.
Usually stuporous or comatose.
Effect of increasing intracranial pressure on pupils
Initial miosis (constricted pupil/s), followed by mydriasis (dilated pupil/s).
Anisocoria (different size pupils) may result from changes occurring assymetrically.
Signs of elevated intracranial pressure
Reduced level of mentation: compression of brainstem and ascending reticular activating system (ARAS) leads to obtundation, stupor, and eventually coma.
Brainstem reflexes: compression of midbrain may cause anisocoria: miosis (initially).
Altered pupil function: miosis progressing to mydriasis, +/- anisocoria
Mydriasis (later stages); fixed miotic or mydriatic pupils mean prognosis guarded.
Loss of vestibulo-ocular reflex
Loss of motor function.
Cushing response: Increased MAP and bradycardia occurring simultaneously.
Cushing response
an end-stage response to persistent and life-threatening elevations of intracranial pressure.
It results from autoregulatory mechanisms causing increased MAP, in order to try to maintain cerebral perfusion pressure.
This systemic hypertension then leads to a reflex bradycardia, as the rest of the body tries to deal with a systemic hypertension.
Do not over-interpret bradycardia as evidence of raised ICP.
Treatment of head trauma
Maintenance of cerebral blood flow
- elevate head 30 degrees
- ensure no occlusion of jugular veins
Ensure normovolaemia achieved and maintained - IV fluids
- Mild trauma: crystalloid aliquots
- More severe trauma: hypertonic saline bolus, or mannitol
Oxygenation - aim for 80mmHg partital pressure of oxygen
Hyperventilation - emergency method of reducing ICP
Adjunctive treatments for head trauma
Anti-seizure medication - prophylactically??
Analgesia - can use opioids but be careful of resp depression
Hypothermia - may have neuroprotective effects but not recommended therapeuticaly
Corticosteroids - contraindicated (increased mortality)
Nutritional support
Diagnosis of intoxications
Can be very difficult! Diagnosis is usually presumptive based on signs and suspected history.
Acute onset of rapidly progressive neurological signs
Neurological signs in the presence of other body system signs especially gastrointestinal
Multifocal neurological signs e.g. seizures plus cranial nerve deficits
Usually don’t know what the toxin is
Common toxins
Mouldy food poisoning (mycotoxins, aflatoxicosis)
Organophosphates, permethrins, hexachlorophene, bromethalin
Metaldehyde, strychnine
Avermectins
Chocolate, amphetamines, caffeine
Recreational drugs
Xylitol
(grapes and raisins)
Clinical tip: toxin ingestion may present as acute SE, but is also a common cause of non-SE tremor
Differential diagnoses for acute generalised tremor in adult dogs and cats
Intoxication
Idiopathic tremor (‘little white shaker disease’)
Hypocalcaemia
Basic investigation for intoxication and tremor
Biochemistry (glucose, urea/creatinine, albumen, liver enzymes)
Electrolytes (Ca, Na, K)
Complete Blood Count (anaemia, polycythaemia, leucocytosis)
Acute phase protein (serum amyloid A, C reactive protein)
Urinalysis
Bile acids (portosystemic shunt)
Managament strategies for intoxication
Initiate life support
- body temp
- active cooling or warming
- correct any hypoglycaemia
- maintain systemic blood pressure
- monitor urinary output
- oxygenation
Reduce toxin absorption
- induction of emesis
- administration of activated charcoal
- administration of intravenous lipid solution
Metaldehyde intoxication (Slug pellets)
Commonly used by gardeners
Rarely ingested by cats and dogs
Common signs include seizures, tremor, tachycardia and hyperthermia
Symptomatic treatment plus fluid therapy to control acidosis
Prognosis guarded, but if they survive 24hrs they are likely to get over it.
Alphachoralose intoxication (rodenticide)
May affect dogs and cats consuming poisoned rodents or poison directly
Seizures, coma, severe hypothermia
Seizure control with diazepam, symptomatic treatment with active warming
Prognosis generally good
Organophosphate and carbamate insecticide intoxication
Inhibitors of acetyl cholinesterase
Hypersalivation, vomiting and diarrhoea
Neurological signs including tremors, seizures, miosis
Atropine to control muscarinic (GI) effects
Treatment can be given with specific cholinesterase reactivators eg Pralidoxime
Prognosis guarded and dependent on dose
Permethrin parasiticide intoxication
Commercially available spot-on flea treatments - easy to overdose cats
Cats appear susceptible to toxic effects of prolonged neuronal sodium channel binding
Tremors, seizures, hypersalivation
Diazepam often poor at controlling seizures
Methocarbamol works best.
Prognosis fair but effects may last 24-48 hours
Consider intravenous lipid therapy
Cannabinoid and marijuana intoxication
Signs develop within 1-3 hours of ingestion
Ataxia, depression, urinary incontinence, sometimes agitation and vocalisation
Symptomatic treatment, diazepam if severe agitation
Intravenous lipids may be helpful
Prognosis generally good, recovery often within 24 hours
Caffeine and chocolate intoxication
Significant doses required for clinical signs to develop
Dosage and toxic effects charts available online
Signs may include restlessness, tremors, seizures plus GI effects (often the only signs)
Treatment is supportive and prognosis generally good
Tremorogenic mycotoxin intoxication
Mouldy food poisoning; spaghetti, cottage cheese, nuts, bread commonly involved
Acute onset of severe and persistent whole body tremor which may progress to seizures
Signs often last 1-2 days, and can be very difficult to control.
Tremor does not disappear when animal is at rest, and can be confused with status epilepticus - benzodiazepines do not work with the mycotoxins, whereas they would with status epilepticus.
Symptomatic and supportive treatment only, although intravenous lipids have been shown to be of value in some cases
Prognosis can be really quite guarded if they have had enough mouldy food.
Spinal cord injury
Acute severe spinal cord injury may be caused by a variety of mechanisms.
As well as the obvious external trauma e.g. road traffic accident (vertebral fracture/luxation), vascular processes (fibrocartilaginous embolism), inflammatory processes (acute myelitis) and degenerative processes (acute intervertebral disc extrusion) can all lead to severe and sometimes irreversible spinal cord injury.
Types of spinal cord injury
Contusion
Compression
Laceration
Iscaemia
Contusion spinal cord injury
primary injury associated with disruption of blood supply, and secondary cell damage due to disruption of blood vessels leading to inflammation and secondary changes including vasogenic and cytotoxic oedema as already described for brain injury
Compression spinal cord curgery
caused by extruded intervertebral disc material of disrupted bone.
Chronic compression may lead to demyelination and eventual axonal loss
Laceration spinal cord injury
axonal transection, disruption of blood supply
Iscaemic spinal cord injury
disruption of blood supply caused by trauma or thrombosis / embolism, as well as the effects of contusion already described, lead to ischaemia which may be a major cause of primary and secondary cell damage
Primary spinal cord injury
The immediate, direct effects of the trauma including laceration, compressimn, contusion and ischaemia.
Little chance to influence this in most cases.
The damage is done by the time the patient is seen.
Secondary spinal cord injury
a cascade of secondary effects which may continue for weeks or months following the initial injury.
Major instigator is thought to be disruption of blood supply, ischaemia and reperfusion injury which leads to changes in vascular permeability.
This in turn results in the release of inflammatory mediators and neurotoxins which further exacerbate the ischaemic effects as well as having direct toxic effects on nervous tissue, both neuronal and glial.
Much research is focussed on trying to mitigate and intervene in the processes of secondary spinal cord injury.
Cervical spinal injury
Highly unusual for a patient to be presented alive, with an injury severe enough to cause loss of deep pain perception.
Assessment involves checking for asymmetry, presence/absence of spinal reflexes such as pedal withdrawal in order to localise as accurately as possible.
Prognostic information not possible from the neurological examination if deep pain perception preserved.
Tetraparesis: prognosis excellent
Tetraplegia: prognosis guarded, especially if respiratory function compromised
Tetraplegia with absent deep pain sensation: rare presentation due to severity of injury, usually grave prognosis
Thoracic/lumbar spinal injury
Localisation again usually possible with a combination of spinal reflexes especially including cutaneous trunci.
Be careful of spinal shock (temporary loss of spinal reflexes in pelvic limbs associated with acute severe thoracolumbar injury) and Schiff-Sherrington phenomenon.
Paraparesis or plegia: excellent
Paraplegia with loss of deep pain perception: 55% recovery with surgical treatment in intervertebral disc extrusion, but probably <5% recovery in traumatic fracture/luxation injury
Thoracolumbar spinal cord injury
Grade 0 = Normal
Grade 1 = Painful
Grade 2 = Ambulatory paraparetic
Grade 3 = Non-ambulatory paraparetic
Grade 4 = Paraplegic with deep pain present
Grade 5 = Paraplegic with deep pain absent
Spinal cord injury of the lumbosacral area
Perineal, lateral digit and tail sensation preserved: prognosis excellent
Perineal, lateral digit and/or tail sensation lost; prognosis guarded with significant risk permanent incontinence.
The major prognostic indicator is presence/absence of deep pain perception in pelvic limbs.
In cases of intervertebral disc extrusion, absent deep pain perception implies a prognosis for recovery of ambulation of 55% with surgical treatment.
For traumatic spinal cord injury this is thought to be significantly lower, and consideration should be given to early euthanasia of dogs and cats presenting with absent pelvic limb dep pain perception and evidence of traumatic thoracolumbar spinal cord injury, due to the very small chance of recovery.
Initial treatment and assessent of spinal injury
Correct hypovolaemia and ensure adequate systemic blood pressure is maintained to preserve adequate blood flow to injured spinal cord
Provide Oxygen to maintain adequate blood oxygen saturation
Corticosteroids: NO evidence of a benefit
Other neuroprotective agents: lack of evidence currently
Once stable, take lateral radiographs of affected region; if no fracture identified consider ventrodorsal
Care with sedation and movement / positioning
Survey radiography: always take orthogonal radiographs to avoid missing a subluxation which may only be visible in one plane.
Where available CT scanning is more sensitive and allows 3D image evaluation, especially where surgical intervention is planned. CT if available may be faster and give more detail of injuries
Medical management of vertebral fracture/luxation
Where deep pain perception is preserved, and the injury is deemed inherently stable, this can be successful.
A combination of cage confinement with or without external splinting may lead to a good outcome in many cases, especially lower lumbar injuries where the cauda equina may be affected rather than the spinal cord.
A three compartment model has been developed for assessing vertebral column stability.
If only one compartment is affected, stability should be preserved. If more than 1 it is not impossible but you have to be aware that the situation is unstable.
Medical management in acute severe spinal cord trauma
Neuroprotection: ensure adequate Oxygenation and mean arterial pressure (as with brain injury)
Corticosteroids: no evidence for efficacy in veterinary medicine; controversial in human spinal cord injury with a recent meta-analysis finding no conclusive evidence for efficacy. Potential gastrointestinal side-effects in high dose use in spinal cord injury mean their use is contraindicated.
Other neuroprotective agents: lack of evidence currently.
