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Show Journal of Neuro- Ophlhalmology 20( 1): 32- 34, 2000. 2000 Lippincott Williams & Wilkins, Inc., Philadelphia Visual Loss and Central Venous Catheterization: Cortical Blindness and Hemianopsia After Inadvertent Subclavian Artery Entry Robert C. Wang, MD, Steven E. Katz, MD, and Martin Lubow, MD A case of presumed embolic transient ischemic episodes and multifocal infarcts to the occipital and parietal cortices and the cerebellum of a young woman with ulcerative colitis is reported. These episodes were manifested by multifocal neurologic deficits including cortical blindness, visual hallucinations, and homonymous hemianopsia. They correlated with parenteral nutrition via a central line, presumed venous, but found to be in the subclavian artery. The complications of central venous lines are reviewed. The need for attention to neighborhood structures and unexpected symptoms, in view of the less well- recognized arterial embolic complications is emphasized. Key Words: Central venous catheterization ( adverse reactions)- Cortical blindness- Thromboembolic disease- Total parenteral nutrition- Ulcerative colitis. Central venous catheterization ( CVC), a technique to allow direct catheter access to a major vein adjacent to the heart, allows venous monitoring and parenteral access in seriously ill patients. In 1945, both Myers ( 1) and Zimmerman ( 2) described the use of plastic catheters for continuous vascular access. In 1969, English et al. ( 3) reported the use of CVC to provide parenteral nutrition in a patient with diarrhea. Ulcerative colitis ( UC) is an idiopathic inflammatory disease of the colon frequently causing diffuse mucosal friability, erosions, and bleeding. Because UC may lead to impaired nutrition with severe anemia and hypovolemia, CVC is often required. We present a case in which a young woman with active UC had focal neurologic symptoms and signs shortly after installation of a right subclavian CVC. CASE REPORT A 31- year- old woman was transferred from an outside hospital with an exacerbation of UC. The day after ad- Manuscript received February 18, 1999; accepted November 4, 1999. From the William H. Havener Eye Center, The Ohio State University, Columbus, Ohio. Address correspondence to Steven E. Katz, MD, 5717 University Hospitals Clinic, 456 West 10th Avenue, Columbus, OH 43210. mission, a right subclavian central venous access line was placed for total parenteral nutrition ( TPN). When the pump was started, the patient noted acute vertigo and a sudden loss of vision in both eyes. She could only perceive light and was unable to see any other details in her room. This gradually improved after several minutes. Mild confusion was attributable to narcotics given for the CVC procedure. She also noted light flashes each time the central line was flushed with normal saline. The following morning she had nausea, vomiting, and persistent confusion. She described numbers on the clock face as " appearing backwards." These symptoms waxed and waned throughout the day. Intermittently, while looking directly at her mother, her father to the left appeared blurry. On the fourth hospital day, during ward rounds, the staff noted that the patient had slurred speech and left arm weakness lasting 30 minutes. A neurologic consultant found no abnormalities beyond her variable symptoms and considered transient ischemic attacks or multiple sclerosis as diagnostic possibilities. A neurooph-thalmology consultation was requested. Her medical history was significant in that ulcerative colitis had been diagnosed in 1984. Review of systems was of interest in that " migraine" headaches had appeared 8 months earlier, after her last pregnancy. There was no history of uveitis. She was on no medications at the time of admission and had no known drug allergies. Her family history was positive for ulcerative colitis, Crohn disease, diabetes, coronary artery disease, and atrial fibrillation. She denied tobacco or significant alcohol use. Her hospital treatment included sulfasalazine, methylprednisolone, and azathioprine. Visual acuity was 20/ 20 in each eye and the pupil reactions were brisk with no relative afferent pupillary defect. Sensorimotor, slit- lamp, and dilated funduscopic evaluations were unremarkable. No retinal emboli were noted. Automated visual fields showed a left homonymous hemianopsia ( Fig. 1). Because of the arterial embolic flavor of the symptoms and signs, an arterial embolic source was sought. No further use of the CVC was strongly recommended, pending investigation of her neurovascular studies. A magnetic resonance imaging/ arteriogram later that 32 VISUAL LOSS AND CENTRAL VENOUS CATHETERIZATION 33 FIG. 1. Humphrey visual field testing confirms a left homonymous hemianopsia. day showed a right cerebellar hemispheric infarct ( Fig. 2A) and bilateral occipital infarcts ( Figs. 2B and 2C). A hyperintense area was noted in the right insular cortex with ipsilateral middle cerebral artery stenosis and slow intraluminal flow ( Fig. 2C). Routine chest radiograph reportedly confirmed " a right subclavian line in place" with the tip " at the expected junction of the right subclavian vein and superior vena cava" ( Fig. 3). The next day, a bedside ultrasound was used to locate the position of the CVC tip. The central line was described as extending into the right subclavian artery with the tip pointing toward the right common carotid artery ( Fig. 4). The line was removed the same day by the vascular surgery consultant. Results of repeat visual field testing 2 days later were normal with resolution of the left homonymous hemianopsia. No further focal neurologic symptoms or signs were detected, but splinter hemorrhages in fingers 2 through 5 of the right hand were noted on follow- up examination 2 days after removal of the CVC. DISCUSSION Central venous catheterization complications are described and include carotid puncture, air embolus, pneumothorax, malposition, Horner syndrome, dysrhythmias, uncontrolled bleeding, and death ( 4). Detailed instructions on avoiding, recognizing, and managing these complications are carefully given to interns and residents in their training programs. The location of CVC in a major vascular system adjacent to the heart and its great vessels has led to several studies assessing the relative safety of the procedure ( 5,6). A 1979 retrospective study at the University of Pennsylvania hospitals found a rate of inadvertent carotid ar- FIG. 3. Chest x- ray shows the central line " in place." tery puncture of 4.2% ( 43 of 1,021) with internal jugular vein cannulation ( 5). Surprisingly, in 5 of the 43 cases, they did not appreciate that an artery had been entered with a 20- gauge catheter until it was connected to a transducer in an attempt to confirm a venous waveform. One patient died of exsanguination into a right hemitho-rax. A prospective analysis of 66 patients at the Mayo Clinic in 1994 showed only a single case of Horner syndrome " probably associated with a large carotid sheath hematoma" ( 6). No cerebrovascular complications were found. They concluded that " the frequency of neurologic complications following internal jugular vein catheterization is low in critical illness." Nevertheless, an important and frightening report by Sloan et al. ( 7) in 1991 showed that vertebral basilar stroke caused by thrombosis and embolism can, and did, happen. Their patient's autopsy findings showed a vertebral artery thrombosis and secondary embolization. Their follow- up letter in 1992 confirmed the importance of the 1991 case and acknowledged several other reported cases of stroke syndrome associated with CVC ( 8). Analysis of the signs and symptoms in our patient indicates a pattern that included waxing and waning unilateral and bilateral homonymous hemianopsias, hallucinations, confusion, nausea, and vertigo. There was a demonstrable hemianopsia on one occasion, which resolved completely within 48 hours. The sudden appearance of these dramatic symptoms after transfer to our hospital and coincident with placement of the CVC FIG. 2. A right hemispheric cerebellar infarct ( A, white arrow) and bilateral occipital infarcts ( B, C, dark arrows) are noted. The right insular cortex is hyperintense compared with the contralateral side, and bright signal is identified within branches of the right middle cerebral artery, indicating slow flow ( C, white arrows). J Neuro- Ophthalmol, Vol. 20, No. 1, 2000 34 R. C. WANG ETAL. C:::' if-::;;: f r ' i . „ ! * - • . ' . • r - ' i , j C', t ' » . J, FIG. 4. Ultrasound imaging shows the catheter extending into the right subclavian artery. should have immediately alerted us to the role of the catheter in these transient ischemic attacks. Yet the impaired mental status of the patient ( attributed to drugs) and the false- negative chest x- ray localization led to considerations of UC- related ocular disease, multiple sclerosis, and hypercoagulation to explain the atypical complaints. This diagnostic confusion exists in the literature as well, with efforts of some reporters to suggest air embolism as a mechanism for cortical blindness in a patient with probable inadvertent arterial entry ( 9). In 1995, Lynch and Shehabi ( 10) reported a patient who suffered a major hemispheric stroke caused by misplacement of a CVC and intraarterial administration of TPN. They concluded that the "... probable cause of the CVA was cerebral vasospasm due to the high osmolar content of the TPN, resulting in microthrombosis in the distal microcirculation." Neurovascular thromboembolic complications in ulcerative colitis have been described ( 11) and are ". .. thought to be a hypercoaguable state characterized by thrombocytosis, short partial thromboplastin time, and elevated serum fibrinogen and factor VIII concen-trations"( 12). Although we considered a hematologic mechanism, the available history from the patient and from the ward personnel suggested a striking correlation between symptoms and CVC use. This led us to question the location of the catheter tip despite the confirmatory chest x- ray. Our experience joins a growing body of literature suggesting that more consideration be given to the possibility of arterial entry in patients with CVC, despite the absence of bright red blood on puncture and the absence of pulsations during placement and maintenance of the line ( 5,7,8,10). Because of the limitations of routine x-rays, catheter tip localization should be verified by transducer pulse waves, blood gases, or ultrasound when signs or symptoms suggest an atypical picture in such patients. REFERENCES 7 1. Meyers L. Intravenous catheterization. Am J Nurs 1945; 45: 930- 1. 2. Zimmermann B. Intravenous tubing for parenteral therapy. Science 1945; 101: 567- 8. 3. English IC, Frew RM, Pigott JF, Zaki M. Percutaneous catheteri-sation of the internal jugular vein. Anaesthesia 1969; 24: 521- 31. 4. McGoon MD, Benedetto PW, Greene BM. Complications of percutaneous central venous catheterization: a report of two cases and review of the literature. 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