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Kardiologia Polska 2012; 70, 5: 499–500 ISSN 0022–9032

CASE REPORT

Address for correspondence:

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Gonenc Kocabay, MD, Hurriyet Mahallesi, Uzmanlar Caddesi, Reyhan Sokak, Burcu Temel Sitesi, E Blok Kat 5 Daire 12 Yakacik, Kartal, Istanbul, Turkey, tel: 00 90 532 518 00 35, fax: 00 90 532 518 00 35, e-mail: gonenckocabay@yahoo.com

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Received: 28.04.2011 Accepted:Accepted:Accepted:Accepted:Accepted: 01.06.2011 Copyright © Polskie Towarzystwo Kardiologiczne

Contrast−induced monoplegia following coronary angioplasty with iopromide

Monoplegia wywołana kontrastem po angioplastyce wieńcowej z zastosowaniem jopromidu

Ahmet Aykan, Regayip Zehir, Can Yucel Karabay, Gonenc Kocabay

Department of Cardiology, Kartal Kosuyolu Heart Education and Research Hospital, Istanbul, Turkey

A b s t r a c t

Seizures, alterations in mental and cerebral functions, and ophthalmoplegia are known side effects of contrast agents. Here we report a case of self-limiting monoplegia in a patient after the administration of intracoronary iopromide after coronary angiography which emphasises that, although benign, contrast-induced monoplegia is a neurological disease which requires careful evaluation and accurate management.

Key words: iopromide, contrast agent, encephalopathy, monoplegia, coronary angiography

Kardiol Pol 2012; 70, 5: 499–500

coronaries. Within four hours, the patient complained of na- usea and an inability to move his left lower extremity with a loss of sensation in the lower extremity, and then he beca- me confused. Babinski sign was present in the left lower extre- mity with loss of motor function and sensation. A computeri- sed tomography (CT) scan of the brain was performed which revealed extravascular localised contrast media in the sagittal sinus and occipital lobe. After 12 hours, he recovered com- pletely without any neurologic deficits by use of supportive medications and adequate hydration. Cranial diffusion magnetic resonance imaging (MRI) was performed after 36 hours. This revealed normal findings and the contrast agent was reabsor- bed from the subarachnoid space (Fig. 1).

Non-ionic contrast agents usually have several side ef- fects including seizure, alteration of cerebral function, confu- sion, short-term memory loss, mental aberrations and oph- thalmoplegia [1, 2]. Also encephalopathy after administration of non-ionic contrast agents has been reported in the litera- ture [4–7]. The blood brain barrier mostly prevents the entry of contrast agent into the central nervous system (CNS), but cerebral angiography and aortography may alter the barrier and increase the amount of contrast agent entering the CNS [3].

Contrast agents have been shown to have side effects such as seizure, alteration of cerebral function, confusion, short-term memory loss, mental aberrations and ophthalmo- plegia [1, 2] although non-ionic agents are far less neurotoxic [1, 3]. In this report, we present the case of a patient who developed contrast-induced monoplegia following coronary angioplasty with the non-ionic contrast agent, iopromide (Ultravist®).

A 68 year-old male patient was admitted to our emer- gency department with new onset, squeezing type, chest pain.

His physical examination was normal. Electrocardiography revealed ST segment depression in anterior precordial leads with T wave inversion. He had hypertension and hyperlipida- emia for seven years. Heparin 5,000 U intravenous, 300 mg acetylsalicylic acid, and 600 mg clopidogrel was administe- red to the patient, who was then transferred to the catheter laboratory for coronary angiography because of unstable an- gina pectoris. Coronary angiography revealed 90% stenosis in the mid segment of the left anterior desending artery, and a 2.75 ¥ 25 mm sirolimus-eluting stent implantation was performed in the same session. Full coverage was achieved with TIMI-3 flow. A total dose of 250 mL was injected to the

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Ahmet Aykan et al.

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But encephalopathy after coronary intervention is very rare and has been reported only on a few occasions [7–10].

The clinical scenario in this patient was consistent with intracranial haemorrhage, but there must be a sign in the cra- nial CT. It may be postulated that early radiologic evaluation in intracranial haemorrhage is not always 100% accurate, but we performed cranial MRI to the patient 36 hours after the situation. Furthermore, the symptoms were resolved sponta- neously. Another possible explanation may be transient ischa- emic attack, but this was clearly exluded in the cranial MRI.

The patient was free from any metabolic disease or abnor- mality which could be a contributory cause of monoplegia and confusion.

So the only remaining explanation in this scenario was that monoplegia was induced by the contrast agent, which was iopromide. Unfortunately, we could not perform an electro- encephalography because of the short duration of symptoms.

There is a debate about the mechanism and causes of neurotoxicity. In high concentrations, hypertonic contrast agents can disrupt the blood brain barrier and facilitate their entry into the CNS. Repeated injections of contrast agents may result in neurotoxic effects within several minutes [3, 6].

The leakage of the contrast into the cerebrospinal fluid and electrolyte imbalance may cause an encephalopathy [3]. Extra- vasation of contrast agent usually affects the posterior circula- tion and causes cortical blindness. The presented case did not have any visual problems. Clearance of the contrast agent from CNS may be achieved via backward washing of this agent and sink action of cerebrospinal fluid. Sustained high con- centrations of the agent in the CNS may be observed in pa- tients with renal failure [3]. Our case is the first in the literatu- re to describe iopromide-induced monoplegia.

Although it is rare, contrast-induced monoplegia and encephalopathy may occur during coronary intervention wi- thout a particular predisposition. Despite the benign nature of contrast encephalopathy, it may be an early warning sign of future nervous system disease. Thus, close follow up of these patients is necessary.

This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.

Conflict of interest: none declared References

1. Hershkowitz N, Bryan RN. Neurotoxic effects of water-soluble contrast agents on rat hippocampus: extracellular recordings.

Invest Radiol, 1982; 17: 271–275.

2. Kocabay G, Bayram T. Unilateral isolated partial occulomotor nerve paralysis after percutaneous intervention. Angiology, 2009; 60: 385–386.

3. Junck L, Marshall WH. Neurotoxicity of radiological contrast agents. Ann Neurol, 1983; 13: 469–484.

4. Ito N, Nishio R, Ozuki T et al. A state of delirium (confusion) following cerebral angiography with ioxilan: a case report. Nip- pon Igaku Hoshasen Gakkai Zasshi, 2002; 62: 370–371.

5. Onizuka K, Bun M. A state of confusion following cerebral an- giography with iopamidol: a case report. No Shinkei Geka, 1999;

27: 1027–1029.

6. Dangas G, Monsein LH, Laureno R et al. Transient contrast encephalopathy after carotid artery stenting. J Endovasc Ther, 2001; 8: 111–113.

7. Kocabay G, Karabay CY. Iopromide-induced encephalopathy following coronary angioplasty. Perfusion, 2011; 26: 67–70.

8. Sawaya RA, Hammoud R, Arnaout S et al. Contrast-induced encephalopathy following coronary angioplasty with iohexol.

South Med J, 2007; 100: 1054–1055.

9. Sharp S, Stone J, Beach R. Contrast agent neurotoxicity pre- senting as subarachnoid hemorrhage. Neurology, 1999; 52:

1503–1505.

10. Foltys H, Krings T, Block F. Cerebral contrast medium extrava- sation after coronary angioplasty. Nervenarzt, 2003; 74: 892–895.

Figure 1.

Figure 1.

Figure 1.

Figure 1.

Figure 1. A, B.A, B.A, B.A, B.A, B. Cranial diffusion magnetic resonance imaging

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