Neurological emergencies

Question 1

Causes of primary brain injury

Answer 1

Contusion
Haematoma
Laceration
Vasogenic oedema as a result of traumatic injury

Question 2

Secondary brain injury

Answer 2

Associated with excitatory neurotransmitter release, inflammation, and increased intracranial pressure

Question 3

Central perfusion pressure (CPP)

Answer 3

CPP = Mean arterial pressure (MAP) - Intracranial pressure (ICP)

Question 4

Obtunded

Answer 4

Depressed responses to normal stimulation.

Question 5

Stuporous

Answer 5

Basically asleep but rousable with noxious stimulus e.g. pinching toe.

Question 6

Comatose

Answer 6

Non-responsive even to noxious stimulus.

Question 7

Decerebellate posture

Answer 7

Opisthotonos, thoracic limb extension and pelvic limb (hip) flexion, normal mentation.

Indicates damage to cerebellum.

May slip in and out of this posture.

Question 8

Decerebrate posture

Answer 8

Similar but pelvic limbs extended, and mentation reduced.

Indicates more severe damage at level of forebrain.

Usually stuporous or comatose.

Question 9

Effect of increasing intracranial pressure on pupils

Answer 9

Initial miosis (constricted pupil/s), followed by mydriasis (dilated pupil/s).

Anisocoria (different size pupils) may result from changes occurring assymetrically.

Question 10

Signs of elevated intracranial pressure

Answer 10

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.

Question 11

Cushing response

Answer 11

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.

Question 12

Treatment of head trauma

Answer 12

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

Question 13

Adjunctive treatments for head trauma

Answer 13

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

Question 14

Diagnosis of intoxications

Answer 14

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

Question 15

Common toxins

Answer 15

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

Question 16

Differential diagnoses for acute generalised tremor in adult dogs and cats

Answer 16

Intoxication

Idiopathic tremor (‘little white shaker disease’)

Hypocalcaemia

Question 17

Basic investigation for intoxication and tremor

Answer 17

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)

Question 18

Managament strategies for intoxication

Answer 18

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

Question 19

Metaldehyde intoxication (Slug pellets)

Answer 19

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.

Question 20

Alphachoralose intoxication (rodenticide)

Answer 20

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

Question 21

Organophosphate and carbamate insecticide intoxication

Answer 21

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

Question 22

Permethrin parasiticide intoxication

Answer 22

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

Question 23

Cannabinoid and marijuana intoxication

Answer 23

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

Question 24

Caffeine and chocolate intoxication

Answer 24

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

Question 25

Tremorogenic mycotoxin intoxication

Answer 25

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.

Question 26

Spinal cord injury

Answer 26

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.

Question 27

Types of spinal cord injury

Answer 27

Contusion Compression Laceration Iscaemia

Question 28

Contusion spinal cord injury

Answer 28

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

Question 29

Compression spinal cord curgery

Answer 29

caused by extruded intervertebral disc material of disrupted bone. Chronic compression may lead to demyelination and eventual axonal loss

Question 30

Laceration spinal cord injury

Answer 30

axonal transection, disruption of blood supply

Question 31

Iscaemic spinal cord injury

Answer 31

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

Question 32

Primary spinal cord injury

Answer 32

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.

Question 33

Secondary spinal cord injury

Answer 33

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.

Question 34

Cervical spinal injury

Answer 34

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

Question 35

Thoracic/lumbar spinal injury

Answer 35

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

Question 36

Thoracolumbar spinal cord injury

Answer 36

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

Question 37

Spinal cord injury of the lumbosacral area

Answer 37

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.

Question 38

Initial treatment and assessent of spinal injury

Answer 38

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

Question 39

Medical management of vertebral fracture/luxation

Answer 39

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.

Question 40

Medical management in acute severe spinal cord trauma

Answer 40

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.