chronic autonomic dysfunction in sci
DESCRIPTION
Chronic Autonomic Dysfunction in SCI. Aims of this Session. Describe autonomic dysfunction: physiology, pathophysiology in SCI Discuss lasting effects of autonomic dysfunction in SCI Describe severe autonomic dysreflexia, its recognition, treatment and prevention. - PowerPoint PPT PresentationTRANSCRIPT
Chronic Autonomic Dysfunction in SCI
Aims of this Session
• Describe autonomic dysfunction: physiology, pathophysiology in SCI
• Discuss lasting effects of autonomic dysfunction in SCI
• Describe severe autonomic dysreflexia, its recognition, treatment and prevention
• SCI affects the somatic (i.e. the sensory and motor pathways we are aware of and can control) nervous system below the level of the injury
• However the autonomic (i.e. ‘self-regulating’) nervous system is also affected, and, like the somatic central nervous system, the severity and extent of the damage is largely related to the level and neurological completeness of the injury
Autonomic Dysfunction: Physiology & Pathophysiology of SCI
What is the Autonomic Nervous System?
• The ANS maintains many body systems that need to run constantly without conscious effort: for example breathing, digestion, secretion and storage of urine, thermoregulation, circulation of blood.
• The ANS can be viewed as two systems, the sympathetic and parasympathetic, which respond to each other and the external environment in order to maintain an internal equilibrium while facilitating conscious response to challenges (‘flight or fight’)
Parasympathetic
Sympathetic
What is the Autonomic Nervous System?
• It is important to realise that the primary mode of action of the autonomic nervous system is the reflex: stimulus-response.
• As we have seen the parasympathetic and sympathetic tend to involve distinct levels of the spinal cord
• This means that the nature of the autonomic dysfunction in an individual is heavily influenced by the location and extent of the SCI
Autonomic Dysfunction: Physiology & Pathophysiology of SCI
Autonomic Dysfunction Landmarks
brain
C1-C7
T1-T6
T7-T12
L1-L5
S1-S5coccyx
sympathetic cardioaccelerator supply T6Profound spinal shockRisk of severe autonomic dysreflexia
LMN lesionNo spasmAreflexic NBDSevere erectile dysfunction
UMN lesion
Spasm
Reflex NBD
Reflex erection
Neurological Completeness of Injury: Risk of Severe Autonomic Episodes
24 5 63 0
119 28 48201 32
0%10%20%30%40%50%60%70%80%90%
100%
A B C D E
ASIA score
No AD
AD
High Risk Group: AIS ‘A’ Tetraplegics
• After spinal shock has subsided, there will be a persistent autonomic dyssynergy, again relative to level and density of lesion
• The parasympathetic and sympathetic systems will not be properly moderated or inhibited by each other, which will often result in hyperreflexia, particularly of the sympathetic system
• This will often have evident functional physiological consequences
Chronic Autonomic Dysfunction in SCI
Cardiovascular System
Signs Mechanism EffectHypotension
(postural)
Passive dilatation of blood vessels below injury (sympathetic inactivity)
Syncope (dizziness, fainting, visual disturbance) when sitting up suddenly
The BP is often very labile
Bradycardia Unopposed vagal stimulation(sympathetic inactivity)
Tetraplegics may often have a labile HR with a low resting pulse. This can lead to misdiagnosis
Poikilothermia Passive dilatation of blood vessels below injury(sympathetic inactivity)
Potential hypothermia
Respiratory systemMechanism Effect
respiration,
PO2
Diaphragmatic respiration
Nasal blockage, stuffiness
Vasodilation of face and air passages(compensatory sympathetic overactivity)
Often becomes interpreted that bladder or bowels are about to empty
Inability to expectorate effectively
Absent intercostals and auxiliary respiratory muscles
Chest infection
Gastrointestinal System
Signs MechanismNausea, vomiting, bloating
Slow gastrocolonic transit (sympathetic inactivity)
Constipation, faecal incontinence
Neurogenic bowel dysfunctions
‘Silent’ autonomic dysreflexia(sympathetic/parasympathetic dyssenergy with no somatic influence)
Skin
Signs Mechanism EffectMarks easily
Sweating, gooseflesh, flushing (often in response to sympathetic stimulation rather than heat or cold)
(sympathetic hyperreflexia)
Increased risk of pressure ulcers, discomfort
Poikilothermia (sympathetic dyssynergy)
Danger of causing burns to anaesthetic skin when attempting to correct hypothermia
Genitourinary System
Signs Mechanism EffectIntermittent oligouria
Poor renal perfusion when sitting due to postural hypotension
(sympathetic inactivity)
Reduced urine output when mobilising, with compensatory polyuria overnight
Dependent oedema of lower limbs
Retention of urine
Bladder reflexes absent/ineffective
Blocked urinary catheter
(sympathetic and parasympathetic dyssynergy)
Damage to upper urinary tract, infection and haematuria
Autonomic dysreflexia
Erectile and ejaculatory dysfunction
Disruption of reflex pathways Treatment required for erectile and ejaculatory dysfunctions
Amenorrhea Secondary to nutritional and metabolic deficits
Tends to resolve within 6/12, with resultant normal fertility
Chronic Autonomic Dysfunction in SCI
• Autonomic symptoms can be many and various
• Many of these can be distressing
• In the absence of normal somatic sensation these can be a useful aid to diagnosis
• Many SCI individuals ‘learn’ to interpret autonomic signs usefully
• Distressing autonomic symptoms can often be addressed rationally. For example:– Sweating often responds to
sympatheticomimetics (oxybutynin etc)– Postural hypotension is treated by gradual
mobilisation, and use of elastic stockings and abdominal binder. Sometimes ephedrine is used
• However attention must be given to any underlying cause- particularly bladder and bowel management
Chronic Autonomic Dysfunction in SCI
What is Autonomic Dysreflexia?
• Severe autonomic dysflexia is a sudden rise in blood pressure in response to a harmful stimulus (usually the increase in pressure in a body cavity caused by the collection of fluid)
• Untreated, this rise in blood pressure may continue and result in cerebrovascular events or even death
• The noxious stimulus triggers unmediated sympathetic reflex activity which causes massive vasoconstriction below the level of injury.
• This in turn causes a rise in central blood pressure which causes an alarming headache
• The area above the lesion tries to compensate with vasodilation, causing flushing and sweating
What is Autonomic Dysreflexia?
• In most cases the noxious stimulus is urine in the bladder (probably above 90% of new dysreflexia)
• In practice (outside of SCI Centres) this is usually due to a blocked catheter
What is Autonomic Dysreflexia?
• Bowel triggers are constipation, anal fissure, bleeding haemorrhoids etc
• Other (rarer) primary causes include infected pressure sores and abscesses, pus from an ingrowing toenail collecting behind the nail, and DVT
What is Autonomic Dysreflexia?
Recognition of Severe Autonomic Dysreflexia
• Non- drainage of urine
• Severe headache
• (raised BP)
• (sweating and flushed above lesion)
• Change catheter (do not attempt washout)
• (Give chemical vasodilator eg: GTN)
• Reassure
• (Elevate head)
Treatment of Severe Autonomic Dysreflexia
• Good bladder and bowel management:
– Regular catheter change
– Avoid constipation
Prevention of severe Autonomic Dysreflexia