Presentation is loading. Please wait.

Presentation is loading. Please wait.

Chronic Autonomic Dysfunction in SCI. Aims of this Session Describe autonomic dysfunction: physiology, pathophysiology in SCI Discuss lasting effects.

Similar presentations


Presentation on theme: "Chronic Autonomic Dysfunction in SCI. Aims of this Session Describe autonomic dysfunction: physiology, pathophysiology in SCI Discuss lasting effects."— Presentation transcript:

1 Chronic Autonomic Dysfunction in SCI

2 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

3 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

4 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’)

5 Parasympathetic

6 Sympathetic

7 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.

8 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

9 Autonomic Dysfunction Landmarks brain C1-C7 T1-T6 T7-T12 L1-L5 S1-S5 coccyx sympathetic cardioaccelerator supply T6 Profound spinal shock Risk of severe autonomic dysreflexia LMN lesion No spasm Areflexic NBD Severe erectile dysfunction UMN lesion Spasm Reflex NBD Reflex erection

10 Neurological Completeness of Injury: Risk of Severe Autonomic Episodes

11 High Risk Group: AIS ‘A’ Tetraplegics

12 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

13 Cardiovascular System SignsMechanismEffect Hypotension (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 BradycardiaUnopposed vagal stimulation (sympathetic inactivity) Tetraplegics may often have a labile HR with a low resting pulse. This can lead to misdiagnosis PoikilothermiaPassive dilatation of blood vessels below injury (sympathetic inactivity) Potential hypothermia

14 Respiratory system MechanismEffect  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

15 Gastrointestinal System SignsMechanism Nausea, vomiting, bloating Slow gastrocolonic transit (sympathetic inactivity) Constipation, faecal incontinence Neurogenic bowel dysfunctions ‘Silent’ autonomic dysreflexia (sympathetic/parasympathetic dyssenergy with no somatic influence)

16 Skin SignsMechanismEffect Marks 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

17 Genitourinary System SignsMechanismEffect Intermittent 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 pathwaysTreatment required for erectile and ejaculatory dysfunctions AmenorrheaSecondary to nutritional and metabolic deficits Tends to resolve within 6/12, with resultant normal fertility

18 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 usefull y

19 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

20 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

21 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?

22 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?

23 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?

24 Recognition of Severe Autonomic Dysreflexia Non- drainage of urine Severe headache (raised BP) (sweating and flushed above lesion)

25 Change catheter (do not attempt washout) (Give chemical vasodilator eg: GTN) Reassure (Elevate head) Treatment of Severe Autonomic Dysreflexia

26 Good bladder and bowel management: –Regular catheter change –Avoid constipation Prevention of severe Autonomic Dysreflexia


Download ppt "Chronic Autonomic Dysfunction in SCI. Aims of this Session Describe autonomic dysfunction: physiology, pathophysiology in SCI Discuss lasting effects."

Similar presentations


Ads by Google