Friday, May 12, 2006

Post cord transection

Sangram Patil

Spinal cord anatomy

Physiology

Blood supply-
Single ASA, 2 small PSAs
Essentially no collateral supply between the two
Segmental vessels, large distance between them- watershed area between upper thoracic and lumbar region. Artery of Adamkiewicz (T8-L3).
Regulation of SC blood flow
SC perfusion pressure
Auto regulation- abolished by trauma

Pathophysiology of acute cord injury (ASCI)
Primary injury
Original impact and compression of SC.
No treatment

Secondary injury
Ischemia triggered by primary injury, and other mechanisms.
Systemic effects of ASCI
CVS, R/S, GIT, GUT, Temperature, CNS, Skin.
CNS- Central/ Anterior/Posterior/ Hemi section/ complete transection

Chronic cord injury/ transection
Spinal Shock

Autonomic dysreflexia

Other CVS changes

Blood Volume
Abnormal Valsalva response- no plateau, no overshoot.
Orthostatic hypotension- gradual adaptation d/t autoreg.
Increased renin-angiotensin response- salt-water retention.

Continued..

Respiratory system

C1/2, C3/4, lower cervical- intercostal.
Reduced VC- might recover to some extent;
Increased WOB, reduced ERV/FVC (better in head up position).
Abdominal muscle paralysis- cough, atelectasis, V/Q mismatch.

Muscles

Increased Ach receptors, K changes with suxamethonium.
Spasticity- due to intact spinal reflex arc below the level of lesion.

Bones

Reduced density below the level.
Temperature- perception, regulation.

Continued..
Skin-
decubitus ulcers, common reason for operations in them.
Blood-
Anaemia, DVT.
GUT-
emptying, shock-reflex phase (detrusor-sphinctor dyssynergia), predisposed to Renal Failure.
GIT- emptying delayed

Chronic Pain- 60% of them.

Anaesthetic implications:
Pre-anaesthetic checklist
Anaesthesia

Standby anaesthesia
Risk of AD- cervical injury, history of AD, urological procedures.
Spasm- proprioceptive/ cutaneous stimuli cause spasm of muscles.
Patient wish- IV sedation is a choice.
Previous procedures done as standby anaesthesia.

General anaesthesia
Premedication
Sedatives, nifedipine 10 mg S/L.
Monitoring- routine, CVP/PAC.
Drugs-reduced circulating BV, small VOD for anaesthetics, more sensitive to IV agents, reduced ability to tolerate CVS effects, reduced renal clearance.
Propofol is well established now, ketamine- spasm, NDMR single dose usually sufficient.
Sux- avoid 3days to 9months.

Induction- large vein, preload, RSI not routine.
Maintenance- IPPV, risk of more drop in CO with IPPV.
Positioning- pressure points
Fluids- preload, meticulous attention to balance.
Anticholinergics at induction for low HR.
Temperature

Autonomic dysreflexia- Halothane, enflurane/ isoflurane equally well. Increase the depth under GA.
Spasm- increase depth, relaxants rarely.
Penile erections- metaraminaol, increase depth.

Recovery- temperature, respiration. AD may occur in recovery.

Pregnancy- Increased changes of SCI, reduced CVS/RS reserve when there is increased demand

Regional anaesthesia..
Reliable prevention of AD with spinal.
Difficult to decide level of block
Dose-response relationship is not well established.
Epidural not very satisfactory blockade.

Procedures usually needing anaesthesia

Spine fixation
Intrathecal baclofen infusion apparatus
Ant sacral root stimulators, phrenic nerve pacing.
Urological procedures
Limbs, ulcers.
Other procedures.

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