27. Head and spinal trauma. Emergency and critical care. Diseases of the peripheral nerves on the fore and hind limbs.

What are the key initial steps in managing an emergency patient?

1. Ensuring ABCs (Airway, Breathing, Circulation)

2. Oxygen administration (mask, hyperbaric chamber)

3. Glucose control (avoid hyperglycaemia → nerve damage)

4. Anti-oedema drugs (Mannitol, NSAIDs)

How can CNS injuries be classified?

1. Primary

2. Secondary

What is a primary CNS injury?

Direct physical damage from the traumatic event (contusion, laceration, haemorrhage, haematoma, vasogenic oedema, unstable fractures)

What is a secondary CNS injury?

Complex cascade of biochemical, vascular, and systemic changes occurring minutes to days after the primary injury → depletion of ATP, influx of Na & Ca into cells → increase in excitatory neurotransmitters → cytotoxic oedema, failure of membrane pumps, neuronal damage and death → local tissue acidosis, hypoperfusion, reactive oxygen radicals, inflammatory cytokines activating arachidonic acid & coagulation cascades, thus damaging the blood-brain barrier (BBB)

How does inflammation contribute to secondary CNS injury?

Release of nitric oxide → excessive vasodilation, loss of pressure autoregulation → neuronal death

What systemic changes can compromise cerebral perfusion?

Hypotension, hypoxia, inflammation, glucose changes, hyperthermia, electrolyte abnormalities, acid-base abnormalities, hypercapnia/hypocapnia

What are the types of pathogenesis of CNS trauma?

1. Acute compression

2. Slow/chronic compression

What are the two types of acute compression in CNS trauma?

Impact/shock and hypoperfusion

What is the effect of vasospasm in acute compression?

Activation of AMPA (glutamate) receptors → intracellular Ca build-up, free radicals → lipid peroxidation, fluid/protein/electrolyte/erythrocyte leakage → haemorrhagic necrosis in grey matter.

Which is more susceptible to ischaemia, grey or white matter?

Grey matter

What are the effects of slow compression in CNS trauma?

Chronic mass pressure → increased intraparenchymal pressure → white matter damage: gliosis, demyelination, axonal oedema, vacuolization → impaired proprioception, motor skills, skin sensitivity, deep pain (grey matter is relatively preserved)

What happens with critical compression in slow compression?

Vasculature collapse, vasogenic oedema, rapid symptom progression

What are some common causes of brain/head trauma?

Traffic accidents, falls, dog fights

What are some types of brain/head injury?

Concussion, contusion, coup-contrecoup, diffuse axonal injury

What are the pathological changes after brain/head trauma?

Damage to brain tissue or vessels in brain → brain herniation, brain oedema → astrocyte swelling → cytotoxic oedema

What are some clinical signs of brain/head trauma?

Bleeding from nose/ears, confusion, disorientation, lethargy, pale gums, loss of consciousness, head pressing, pupil dilation (mydriasis)/differences (anisocoria), nystagmus, stumbling, seizures, shock, weakness, paralysis, coma, death

How is brain/head trauma diagnosed?

History, clinical signs, X-ray, MRI, CT, intracranial pressure measurement

Check reflexes: corneal, pupillary light, palpebral

What are the key treatments for brain/head trauma?

1. ABC therapy: correct hypoxia and hypotension (>90 mmHg) → supply O2 to maintain pO2 >90%.

2. IV fluids – lactated ringer (shock dose) +/- glucose (avoid hyperglycemia)

   1. Hypertonic saline – over 10-15 min to expand IV volume + draw fluid from ECS → corrects BP

3. Mannitol – control brain edema and decrease ICP 0.5-1 mg/kg IV over 15 min

4. Seizure = diazepam, 0.1-0.5 mg/kg/h (phenobarbital if not effective enough)

5. Keep head elevated - prevent gravity from causing blood to go to the head.

6. Craniotomy - opening of skull for decompression - poor prognosis

Why are glucocorticoids and narcotics contraindicated in brain/head trauma?

• Glucocorticoids: hyperglycaemia, immunosuppression;

• Narcotics: increased intracranial pressure

How can the prognosis of brain/head trauma be monitored?

1. Repeated neurological examination

2. Neurological score (0 = normal, 5 = plegia with loss of voluntary function and loss of deep pain)

3. Progression

4. Deep pain assessment (may be able to walk with spinal walk - learned behaviour, but not urinate/defecate)

5. Cranial nerve assessment (more cranial nerves affected → worse prognosis)

How is prognosis affected according to the size of the fibres effected?

The smaller the fibres, the worse the prognosis. The smallest fibres do not have a myelin sheath → no protection → do not regenerate.

A. Proprioceptive deficits (good)

B. Paresis/paralysis (fair)

C. Loss of cutaneous sensation (fair)

D. Loss of deep pain (poor)

What are some common causes of spinal trauma?

1. External trauma e.g. concussion, compression, laceration → IVD protrusion, fractures, dislocations, subluxation

2. Infarction (FibroCartilaginous Embolism)

3. Pathological luxation of the the spine

What is pathological luxation of the spine?

Hereditary ligament instability → decreased spinal support

What is the difference between a pathological and traumatic fracture of the spine?

Pathological: bone disease;

Traumatic: force (hyperextension/hyperflexion of vertebral junctions)

How can external traumatic injuries of the spine be divided?

1. Ventral compartment injuries

2. Dorsal compartment injuries

Which structures may be affected in ventral compartment injuries?

1. Vertebral body

2. IV disc

3. Dorsal/ventral longitudinal ligaments

4. Inter-transverse ligaments

Which structures may be affected in dorsal compartment injuries?

1. Lamina

2. Pedicles

3. Spinal processes

4. Articular processes

5. Ligaments (supraspinosus, interspinosus, interarcuate)

What does primary spinal cord injury refer to?

Injury immediately after impact

What does secondary spinal cord injury refer to?

Biochemical processes potentiating further damage (can be prevented)

What are some clinical signs of spinal trauma?

Depends on location of injury.

Loss of function, ataxia, pain/loss of deep pain, neurological deficits, spasms, weakness, paralysis, urinary/faecal incontinence

How is spinal trauma diagnosed?

History, clinical signs, neurological examination, X-ray (2 views), myelography, MRI, CT

What does treatment of spinal injuries depend on?

Location and type of trauma. Non-surgical management is generally recommended for most injuries.

What are some conservative treatments for spinal trauma?

IV fluids, mannitol, diazepam, head elevation, strict cage rest, rehabilitation, NSAIDs, weight reduction

What are some surgical treatments for spinal trauma?

Decompression (laminectomy), removal of compressive disc material (fenestration), stabilisation of vertebrae

What are the ABCs of emergency and critical care?

• Airway: Clear obstruction if present; intubate or perform tracheostomy for oxygen delivery.

• Breathing: Monitor breathing pattern; if not breathing, perform CPR. Dull lung sounds indicate fluid/air in pleural space – perform thoracocentesis.

• Circulation: Monitor heart rate, mucous membrane colour, capillary refill time, pulse. White gums = possible shock/blood loss. If no heartbeat, start CPR.

• Drugs

What are some signs of shock?

Rapid heart rate, pale mucous membranes, low BP, weak pulse

What are some emergency drugs and their uses?

1. Adrenaline: ↑BP, peripheral vasodilation, bronchodilation.

2. Atropine: ↑HR, antispasmodic, avoid bradycardia, mydriatic.

3. Diazepam: Seizure control.

4. Dopamine: ↑BP, ↑HR.

5. Doxapram: Respiratory stimulant.

What are peripheral nerves?

Nerves outside the brain and spinal cord

What is a characteristic of peripheral nerve disease (compared to CNS disease)?

Usually unilateral

What are the components of the peripheral nervous system?

1. Cranial nerves

2. Spinal nerve roots

3. Dorsal root ganglia

4. Peripheral nerve trunks

5. Motor neuron branches

6. Peripheral autonomic nervous system

How can neuropathies be classified according to lesion severity?

1. Neuropraxia: mildest form of nerve injury. Interruption of transmission, no atrophy

2. Axonotmesis: higher degree of injury. Damage to axons, loss of function

3. Neurotmesis: complete severance of peripheral nerve trunk. All function lost

What is a mononeuropathy?

Disease affecting a single nerve

What are some causes of mononeuropathies?

Trauma (car crash, bites), intramuscular injections

What types of clinical signs are associated with mononeuropathies?

Lower motor neuron signs: Gait abnormalities, rapid atrophy, dysmetria, ataxia

What is a polyneuropathy?

Disease affecting multiple nerves

What are some causes of polyneuropathies?

Demyelination, axonal degeneration, lysosomal storage disease, Coonhound paralysis, myasthenia gravis, Cushing's disease, thrombosis

What are some signs of polyneuropathies?

LMN: Paresis, paralysis, hypotonia, hyperaesthesia, ataxia, loss of tone and reflexes

Autonomic signs (rare): Cranial nerves, bladder control and panniculus reflex usually intact

How are peripheral nerve diseases diagnosed?

1. History, clinical signs, neurological exam, X-ray, biopsy, electromyography

2. Evaluate muscles innervated by injured nerves by palpation and electromyography (needle inserted into muscles to record electrical impulse).

3. Evaluate grade of spinal cord weakness – ataxia, arched back, paresis, paralysis, deep pain.

What factors affect nerve regeneration?

Lesion severity, tissue loss, time since injury, patient age, surgical technique

What is primary nerve repair?

Immediate repair (8-12 hours) for clean, sharp wounds e.g. glass

What is secondary nerve repair?

Delayed repair (2-6 weeks) for major trauma and contamination

Does primary or secondary repair of nerve damage have better nerve regeneration, and why?

Secondary because contamination/inflammation has resolved

What are some additional treatments for peripheral nerve injuries?

Corticosteroids (oedema), Vitamin B1, bandaging, electrostimulation, arthrodesis

Which nerves are involved in thoracic limb paralysis?

1. Brachial plexus (C6-T2)

2. Suprascapular (C6-T2)

3. Axillary (C6-C7)

4. Musculocutaneous (C6-C7)

5. Radial (C8-T2)

6. Median and ulnar (C7-T2)

What are the signs of supracapsular nerve injury?

Supra/infraspinatus atrophy, prominent scapula

What are the signs of axillary nerve injury?

No significant signs. Affects flexors of shoulder (teres major/minor, deltoideus)

What are the signs of musculocutaneous nerve injury?

Biceps brachii and brachialis atrophy

What are the signs of radial nerve injury?

Extensor atrophy, flexed leg/paw dragging

What are the signs of median and ulnar nerve injury?

Carpal and digital flexor atrophy, absent cutaneous palmar sensation

Which nerves are involved in pelvic limb paralysis?

1. Lumbosacral plexus (L4-S2)

2. Obturator (L4-L6)

3. Femoral (L3-L6)

4. Sciatic/Ischiatic (L5-S2)

5. Tibial (L4-S3)

6. Pudendal (S1-S3)

What are the signs of obturator nerve injury?

Adduction weakness, slipping, external sphincter dysfunction

What are the signs of femoral nerve injury?

Stifle extensor weakness, no weight bearing

What are the signs of ischiatic/sciatic nerve injury?

Plantigrade stance, paw dragging, no withdrawal reflex

What are the signs of common peroneal nerve injury?

Lateral and long digital extensor weakness, cranial tibial reflex loss

What are the signs of tibial nerve injury?

Gastrocnemius, popliteus, digital flexor weakness

What are the signs of pudendal nerve injury?

Anal reflex and urethral sphincter dysfunction

What is Dancing Doberman Syndrome?

Distal polyneuropathy of hindlimbs in Dobermans, causing involuntary flexion