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CASE PRESENTATION

01/05/09
Dr Suparna Gangopadhyay

Spinal Fellow

Hampstead Rehabilitation Centre


Profile
 28 year old male

 From Port Augusta

 Dependant in most ADLs, full time carer

 Under Work Cover Insurance


Diagnosis

 C5 Incomplete tetraplegia (ASIA B)


secondary to MBA

 06/04/2000
Past Medical History
 UTI : treated conservatively

 AD in Dec 2008

 CT abdomen : long standing bladder


calculi
Past Surgical History
 25/11/08 : L arm tendon transfer surgery
Posterior Deltoid to Triceps
BR to Wrist extensors and FPL
EPL split with K-wire to thumb IP joint

 April 2008 : Skin flap to R leg/thigh


Personal History
 Heavy Smoker

 Drinks Alcohol

 Illicit drug abuse


Present Admission
 Seating Program

 23/03/09: Myocutaneous flap for R sacral


pressure sore
Complication
 22/04/09, 20:10 :

SPC change, poor urine outflow

pressure on the bladder

urinary flow improved

sudden rise in BP

flushing, headache

abdominal spasms
Contd…
GTN patch and tablets

fall in BP

GTN patch removed

patient repositioned, BP shoot further

bowel empty, urine sample – nitrite highly positive

transferred to RAH for Urology referral

readmitted after BP stabilised


Diagnosis
 Autonomic Dysreflexia (AD) secondary to :
Bladder distension ?
Sudden pressure on the bladder ?
UTI ?
Renal calculi ?
DSD ?
Background
 Massiveimbalanced reflex sympathetic
discharge in SCI patients above
splanchnic sympathetic outflow (T5-T6)

 Anthony Bowlby first recognized in 1890,


profuse sweating/erythematous rash of
head/neck initiated by catheterization in an
18-year-old SCI patient
Pathophysiology
 After spinal shock phase

 Below injury: intact PNS transmit impulses (bladder/bowel) through


STT/PC to stimulate thoracolumbar sympathetic neurons in IML
gray matter

 Inhibitory outflow from cerebral VMCs increased, but unable to pass


below the block

 Large sympathetic outflow: release of NTs (NE, DA-b-hydroxylase,


DA): piloerection, pallor, severe vasoconstriction; sudden rise in BP
and vasodilation above level of injury

 Headache: vasodilation of pain sensitive IC vessels

 VMRs attempt to lower BP: bradycardia, but can’t counter severe


vasoconstriction

 Parasympathetic nerves above level of injury: profuse sweating,


vasodilation, flushing
Summary
 Sympathetics prevail below and
parasympathetic nerves prevail above the
level of injury

 Once the inciting stimulus is removed,


reflex hypertension resolves
Causes
Most Common:

 Bladder distension / DSD / Bowel impaction / Pressure ulcers /


Ingrown toenail

Less Common:
 UTI (SCI patients may have positive urine culture)
 Bowel distension / Haemorrhoids
 Gallstones / Appendicitis or other abdominal pathology
 Menstruation / Pregnancy, especially labor and delivery
 Sexual intercourse / Ejaculation
 DVT / PE
 Burns or sunburn / Blisters
 Insect bites
 Temperature fluctuations
 Constrictive clothing, shoes, or appliances
 HO
 Fractures or other trauma
 Pain
History
 Blurry vision

 Headache

 Senseof apprehension/anxiety over an


impending physical problem
Physical
 Sudden significant rise in SBP & DBP
 Bradycardia (may be a relative slowing)

 N SBP above T6: 90-110 mm Hg


 BP 20-40 mm Hg above reference range: sign of AD (in children: 15
more, in adolescents:15-20 more)
 Cardiac arrhythmias, AF, VTs

 Profuse sweating/Flushing over face, neck and shoulders


 Goose bumps above/possibly below the level

 Blurred vision
 Spots in the visual fields

 Nasal congestion

 No symptoms, despite elevated blood pressure (Silent AD)


D/D

 Essential hypertension

 Pheochromocytoma
Complications

 Directly from severe peripheral HTn:

Retinal/Cerebral hemorrhage
MI
Seizures
Management**
 Check BP: If elevated, sit up immediately (if possible,
lower the legs as well) and loosen any clothing or
constrictive devices (Sitting leads to pooling of blood in
the LEs and may reduce BP)

 Monitor BP/Pulse every 2-5 minutes until they have


stabilized (BP may fluctuate from impaired autonomic
regulation)

 Survey for precipitating causes, beginning with the


urinary system, the most common cause of AD

**The Consortium for Spinal Cord Medicine, 1997


Bladder Management
 2% lidocaine jelly (to decrease sensory input and relax
sphincter) and IDC

 If patient has IDC, check for kinks, folds, constrictions, or


obstructions and for correct placement of IDC

 If catheter appears to be blocked, gently irrigate the


bladder with 10-15 cc NS at room temperature

 Avoid manually compressing or tapping on the bladder

 If IDC is draining and BP remains elevated, suspect fecal


impaction, the second most common cause of AD
Bowel Management
 If SBP is at or above 150 mm Hg, consider drug
management without causing hypotension prior to check

 When SBP is <150 mm Hg, check the rectum for stool


using lidocaine jelly as lubricant

 If present, gently remove, if possible

 If AD becomes worse, stop

 Instill additional jelly and recheck after 20mins


Antihypertensives
 Agents with rapid onset and short duration administered
while investigating causes if SBP is at or above 150 mm
Hg

 The most commonly used agents are nifedipine and


nitrates. Other agents are mecamylamine, diazoxide,
and phenoxybenzamine

 Use with extreme caution in older persons, people with


CAD or patients with history of cardiac side effects with
Sildenafil

 Patients with past experiences are treated with


antihypertensives prior to procedures known to cause
AD episodes
Nifedipine (Procardia)
 Calcium ion influx inhibitor (slow-channel blocker
or calcium ion antagonist)
 Inhibits transmembrane influx of calcium ions
into cardiac and smooth muscle
 Reduces arterial pressure at rest and at a given
level of exercise by dilating peripheral arterioles
and reducing afterload

 Adult

10 mg cap, bite and swallow (not sublingual)


Nitroglycerine (Depo-Nit, Nitrostat,
Nitrol, Nitro-Bid)
 Relaxation of vascular smooth muscle, producing
vasodilator effect on both peripheral arteries and veins

 Dilation of postcapillary vessels reducing preload

 Arteriolar relaxation reduces after-load

 Adult
0.4 mg per metered spray for SL use or 2% ointment
Start with 0.5-in strip to chest wall and titrate
Alternatively, 0.15-0.6 mg tab SL or 5 mcg/min IV
Investigate further
 Ifprecipitating cause is still not clear, check for
less frequent causes

 Hospitalisation /Transfer to ED:


Poor response to tx
Cause not yet identified
Monitoring to maintain BP control on drugs
Cystoscopy/Urodynamic/Advanced studies
Suspicion of an obstetrical complication
Post episode
 Monitor symptoms, Pulse and BP for at least 2
hours after resolution of the episode coz AD may
resolve from medication

 BP restoration to N (90-110 SBP for a tetraplegic


in sitting position)

 Pulse rate restoration to N

 Individual comfortable with no signs/symptoms


Follow-up
 Adjusting
the tx plan to ensure future
episodes are recognised and treated to
prevent medical crisis or, ideally, are
avoided altogether
Prevention
 Goodbladder and bowel care are
mainstays in preventing episodes of AD

 Education
IMPERATIVE
 OT/ PT / Recreation therapists / Rehab
Nurse / Medical Professionals should
educate patient & family members about
AD

 Ensure that they are familiar with


prevention strategies, signs and
symptoms, and proper management
Medicolegal Pitfalls
 Failureto have a high index of suspicion and
recognize the problem quickly could present
medical and legal problems for the physician

A physician who assumes that headache and


anxiety in a person with complete C6 tetraplegia
is a manifestation of depression, without
checking vital signs, is at medical/legal risk

 Document the episode


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