Autonomic Complication

Dysreflexia of Voiding

in Patients with Cystourethrography

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ZORAN

weeks after the surgery the patient was referred to the radiology department for a loopogram to check the patency of the right ureter. The loopogram was performed using a Foley catheter with the balloon inflated in the distal end of the loop with 20 ml of normal saline connected to a drip infusion bottle placed 30 cm above the level of the loop. After receiving 50 ml of contrast, the patient complained of facial flushing and sweating, pounding headache, and nausea. The loop was immediately drained. Physical examination revealed profuse sweating of the face and elevation of the blood pressure from a baseline of 1 00/70 mm Hg to 1 90/1 00 mm Hg. The pulse rate decreased from baseline 72 to 65/ mm. The blood pressure and pulse rate returned to normal within 5 mm after emptying of the loop ; at the same time the patient’s subjective symptoms disappeared. At a later date the examination was repeated without recurrence of dysreflexia.

Many radiologists are unfamiliar with potentially life threatening complications that may occur during the perfonmance of cystourethrography or loopography in patients with spinal cord lesions above T7. The most pronounced manifestation of this complication is uncontrollable hyperwhich,

if unrecognized,

may

lead

Discussion

to convulsions,

Autonomic

cerebral hemorrhage, retinal hemorrhage, renal failure, and even death. Autonomic dysreflexia is quite unpredictable. It need not recur during the second examination, or it might occur during the second examination even if the first examination was uneventful. The purpose of this paper is to familiarize radiologists since it is not mentioned

enon

of the

Reports

Case C. G. (89-31-02) was an 18-year-old quadriplegic male with spinal injury at the level of C2 and with recurrent urinary tract infections. He was evaluated in the radiology department for possible vesicounetenic reflux and for the cause of unacceptable bladder residuum. A no. 12 Foley catheter was placed in the navicular fossa, and the urethra and the bladder were filled in a retrograde fashion. After introduction of 1 20 ml of contrast material, the patient complained of stuftiness of the nasal passages. profuse sweating of the face and neck, and sudden onset of severe headache. On physical examination he had a flushed, red face and profuse sweating over the forehead. There was sudden increase in the blood pressure from a baseline of 1 00/70 mm Hg to 21 0/1 00 mm Hg. Pulse rate changed from baseline 75 to 60/mm. The bladder was immediately

emptied.

The

blood

pressure

next 5 mm and gradually returned mm. At the same time the patient’s sided.

remained

to normal subjective

high

for

Am

J Roentgenol

University

1 27 : 293-295,

1976

is a peculiar in patients

neurologic

with

phenom-

a spinal

cord

lesion

face

and

neck,

and

blockage

of the

nasal

passages

sometimes symptoms pronounced

associated with difficulty in breathing. These are not always present and some may be more than others. Physical findings include increase

in systolic

and

diastolic

the

within the next 30 symptoms also sub-

200

mm Hg and 50-i

the

interomedial

This

results

blood

nic

vascular

lateral

horns

in vasoconstniction, bed,

kidney,

pressure

(as

of the vasoconstniction

marked

increase

in the

in

the

much

spinal

particularly skin,

a result

wall.

of Radiology,

only

as 100-

systemic

and

legs

occurring blood

grey

matter.

in the splanch[4]

below

(fig.

1

).

T7, there

As is

pressure.

The normal individual would control the blood pressure rise through the baroceptons in the carotid sinus and aortic

W. W. (70-81 -06) was a 23-year-old spinal injury at the level of C4. Urinary an ileal conduit was performed several ureteral calculus causing obstruction Department

dysneflexia occurs

00 mm Hg, respectively) ; bradycardia; and redness and sweating of the face and neck along with paleness of the skin of the abdomen and the lower extremities. The pathologic reflex begins during the distension of the bladder, urethra, rectum, or intestine, and the afferent pathways lead to the spinothalamic tracts and dorsal columns of the spinal cord. While traversing the spinal cord, the afferent impulses excite the sympathetic motor neurons of

Case 2

I

that

at T7 or above [1-3]. Pathologic autonomic reflexes are triggered by distension of the bladder, urethra, and rectum and, to a lesser extent, by distension of the small and large bowel. The patient’s subjective symptoms will usually include sudden onset of severe headache, flushing and sweating

with this peculiar complication, in basic uroradiologic textbooks. Case

Cord Lesions: Ileal Loopography

L. BARBARIC1

Autonomic dysreflexia is a pathologic reflex which occurs in patients with a spinal cord lesion above Ti. The most dangerous manifestation of this reflex is marked increase in systolic and diastolic blood pressure. The trigger is the distension of the urinary bladder, urethra, rectum, or intestine. it can and does occur during radiological examinations such as cystourethrography, loopography, and probably during the barium enema. Because of possible deleterious consequences of marked hypertension. blood pressures in these patients should be continuously monitored during the examinations and appropriate measures immediately instituted should the reaction occur.

tension

Spinal and

male quadriplegic with a tract diversion by means of years ago. Recently a right was removed, and several

of Rochester

School

of Medicine

These

would

send

affenent

impulses

to the

vasomotor

center in the medulla. The inhibitory impulses from the vasomotor center decrease the blood pressure in two ways: (1 by slowing the heart rate and mildly decreasing myo)

and

Dentistry,

293

Rochester,

New

York

14642.

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294

BARBARIC

Fig. 1 -A and B, Afferent pathways from the bladder ; C. efferent pathway to the bladder ; 0, dorsal column ; E, spinothalamic tract ; F, sympathetic efferent pathways to splanchnic vascular bed (17-Li). Transection at T7 or

above.

cardial contractility via efferent vagal impulses, and (2) by dilating the splanchnic and skin vasculature through the sympathetic pathways of the cord. These impulses would effectively

balance

the sympathetic

bladder distension. However, in the

patient

excitation

with

high

caused

spinal

cord

by the

lesion,

the

uncontrolled.

available blood

for

In

the

pressure

such

vasomotor

is to decrease

According

to

Poiseuille’s

a patient, center the

the

to

heart

formula,

only

combat rate

(fig.

pressure

flow

due to the slowed

affect the high impulses above

heart

blood pressure. the transsection

rate will only

The will

procedure completely pressure,

2). is

the

minimally

the

of

norepinephnine from sympathetic nerve endings and epinephnine from adrenal medulla during dysreflexia [5]. The radiologist must be aware of this complication since it could have a potentially deleterious effect on the patient. Generally, the higher the spinal cord lesion above T7, the more

apt

more

severe

questioned

sodes during

the

patient

the prior

is to experience

manifestations. to the

of dysneflexia. the examination

procedure

dysreflexia

The

patient

regarding

Constant blood is mandatory.

pressure

and

the

should previous

be epi-

monitoring

still

blocking

agent,

tnimethaphan

can be administered

remain

45’.

[4,

high,

optic

in autonomic ganglion cells

(Arfonad,

membranes

liberated

against

from

presynoptic

a direct

peripheral

pharmacological

diazoxide

or hydralazine iv.). Prior

that

Schering

hydrochloride

to and

at the

action

time

desired blocks receptor postsyn-

acetylcholine

In addition, effect.

be

are

weight

CIBA;

of the examination

useful

instead

body

(Apresoline,

it may

Other

used

; 5 mg/kg

of

intraveThe rate

the agent

of

endings. can

posi-

(1 mg/mI)

by occupying stabilizing the

vasodilaton

agents

(Hyperstat,

the nerve

Roche),

in a semisitting

is administered of 60 drops/mm.

ganglia and by

more

ganglionic

concentration

in 5% dextrose solution starting at an average rate

thereby 7].

ultrafast

camsylate

A 0.1%

viscus,

dangerously An

the patient

the

ml of 1% lidocape the

dysreflexia

needed.

with

up to at least

exert

release

pressure

exami-

intestine,

and the structure effect on the blood up in a sitting posi-

into

of the

are

tensive

accelerated

limb

or

of administration is then adjusted to maintain level of hypotension. This pharmacologic

inhibitory sympathetic result in vasodilatation

indicates

afferent

measures

Arfonad nously

nadiologic

loop,

5-10

Astra)

drastic

tion

during ileal

is to instill

(Xylocamne,

Should

means

occurs urethra,

procedure

transmission sites on the

This

bladder,

Another

in the head and neck, explaining the stuffy nose, flushing of the face and neck, and marked perspiration in these regions. In addition, there is significant increase of the catecholamine metabolites in the urine after the hypenepisode.

dysreflexia

the

should be stopped immediately emptied [6]. If this has no the patient should be propped

breaking

increased in tubes

of

hydrochloride

only linearly affected by rate of flow but is affected to the fourth power by the diameter of the tube. Thus the decreased

If autonomic

nation

tion.

inhibiting impulses from the vasomoton center are unable to reach the splanchnic circulation due to the cord lesion. Hence the sympathetic excitation below the lesion continues

Fig. 2.-A, Afferent pathways from carotid sinus via Hering’s and glossopharyngeal nerves. B, Afferent pathways from baroreceptors in aortic wall via vagus. C, Vasomotor center in medulla. 0. Efferent pathways carrying inhibitory impulses to heart via vagus. E, Efferent sympathetic pathways from vasomotor center carrying inhibitory impulses to thoracolumbar spinal cord and splanchnic vasculature; these pathways are ineffective below transection. F, Efferent sympathetic pathways to upper half of body carrying inhibitory sympathetic impulses causing vasodilatation and sweating. Transection at T7 or above.

some

iv.) 15

mg

patients

may already be on some form of medication, most likely phenoxybenzamine, an alpha-adrenergic blocking agent. This the

is likely

to reduce

examination The examining

the

[8, 9]. physician

incidence should

of dysreflexia be

thoroughly

during familiar

AUTONOMIC

with

the

drugs

described

and

approach

these

patients

with

due care and diligence.

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REFERENCES 1 . Guttmann L Whittenidge D : Effects of bladder distension on autonomic mechanisms after spinal cord injuries. Brain 70 : 361 404, 1947 2. Kurnick ND : Autonomic hyperreflexia and its control in patients with spinal cord lesions. Ann Intern Med 44 : 678-686, 1956 3. Lapides J : Autonomic hyperreflexia, in Urology, edited by Campbell MF, Harrison JH, Philadelphia, Saunders, 1971, pp 1361

-1 362

4. Roussan matic and complete 450-456,

MS. Abramson AS, Lippmann HI, D’Oronzio G : Soautonomic responses to bladder filling in patients with transvere myelopathy. Arch Phys Med Rehab 47: 1966

295

DYSREFLEXIA

5. Sell HG, Naftchi NE, Lowman EW, Ausk HA : Autonomic hyperreflexia and catecholamine metabolites in spinal cord injury. Arch Phys MedRehab 53:415-417, 1972 6. McCallum RW : The radiologic assessment of the lower urinary tract in paraplegics-a new method. J Can Assoc Radiol 25: 34-38, 1974 7. Bors E, French JD : Management of paroxysmal hypertension following injuries to cervical and upper thoracic segments of the spinal cord. Arch Surg 64 :803-81 2, 1952 8. Sizemore GW, Winternitz WW: Autonomic hyper-reflexiaSuppression with alpha-adrenergic blocking agents. N EngI J Med2:795, 1970 9. Krane AJ, Olsson CA : Phenoxybenzamine in neurogenic bladder dysfunction. 1973

II. Clinical

considerations.

J Urol

110:653-656,