Spinal cord infarction resulting from cardiac catheterization

BRIEF CLINICAL

nal damage in the sensory and motor fibers of the median, radial, common peroneal, and sural nerves, and severe denervation of the deltoid, biceps, abductor pollicis brevis, and tibialis anterior muscles. Laboratory investigations revealed the following: moderate normochromic, normocytic anemia (hemoglobin, 10.7 g/dL; mean corpuscular volume, 90 fL) with basophilic stippling of some erythrocytes, increased reticulocytes (180,000/ mm3), indirect hyperbilirubinemia, negative direct and indirect Coombs’ test results, and erythroblastic hyperplasia on bone marrow examinations; altered porphyrin metabolism and abnormal lead levels in urine and blood, with or without chelating agents (Table I); normal cerebrospinal fluid levels of proteins, glucose, immunoglobulins, and cellularity. Sural nerve biopsy showed axonal degeneration with segmental demyelination secondary to axonal damage. The patient underwent a chelating course with slight improvement in the laboratory data. Nevertheless, the clinical picture worsened and was complicated by respiratory failure. Despite respiratory assistance, the patient died 14 days later. To identify the source of lead poisoning, we evaluated blood lead levels in four close family members. All these persons had abnormally high concentrations except the six-year-old grandson. Neurologic examination of the deceased’s wife showed subclinical signs of neuropathy. The blood lead content of persons living in the same building was within the normal range and no water pollution was detected. These results suggested a poisoning source within the household environment, to which the child was not exposed. Tests revealed lead contamination of the home-produced wine. The source of pollution was finally identified as the container used for storing the wine, which was lined with lead-glaze ceramic tiles. Only one case of contaminated wine as a source of lead poisoning has been reported recently in Italy [3]; lead poisoning in ancient Rome has, however, been expertly discussed [4]. We think it important to stress wine handling and storage

TABLE I Levels of Lead and Porphyrin

in a Woodcutter

OBSERVATIONS

with Wine Lead Poisoning* Ofl Admission

After One Week of Therapy

In blood Lead &VW (<40 rg/W Zinc protoporphyrin (rg/dL) (<40 rg/dL) Total porphyrins &g/24 hours) (<220 pg/24

hours)

In urine Lead (a/U (40 rg/W Coproporphyrins(pg/24 hours) (<160pg/24hours) Uroporphyrins (rg/24 hours) (<60 rg/24 hours) Porphobilinogen (mg/dL) (<0.2 mg/dL) Urinary aminolevulinic acid (mg/dL) (0.6 mg/dL)

in parentheses are expressed

125 ~ 4,700

5::

1,011

:;

0.40

0.04

10

In wine? Lead in red wine Lead in white wine l Values + Values

-

130 335 1,554

0.7

!:, are normal values. in parts per million.

as a possiblecauseof sporadic cases Spinal cord infarction or cholesterof lead poisoning. ol embolization have not been reGIOVANNI ANTONINI, M.D. ported after cardiac catheterizaSTEFANO FERRACUTI, M.D. tion. We report two casesof spinal ELENA PENNISI, M.D. cord infarction after cardiac catheBRUNO MONARCA, M.D. terization, one with documented University of Rome “La Sapienza” cholesterol embolization as the Rome, Italy cause. Patient 1. A 74-year-old white 1. Araki S, Honma T: Relationship between lead absorption and peripheral nerve conduction velocities in man presenting with acute anterior lead workers. Stand J Work Environ Health 1976; 4: myocardial infarction was treated 225-231. with tissue plasminogen activator. 2. Murata K. Araki S. Aono H: Effects of lead, zinc and Routine cardiac catheterization copper absorption on peripheral nerve conduction in metal workers. Int Arch Occup Environ Health 1987; three days later was performed 59: 11-20. without difficulty, using Judkin’s 3. Loi F. Battista G. Malentacchi GM, et al: Familial technique with eight French cathelead poisoning from contaminated wine. ltal J Neurol ters advanced over flexible j-tipped Sci 1981; 3: 283-290. 4. Nriagu JO: Saturntne gout among Roman aristoguidewires under fluoroscopic obcrats N Engl J Med 1983; 308: 660463. servation. No complications were apparent at the time of the proceSubmitted April 20. 1989, and accepted May 18, 1989 dure. Thirty minutes after all catheters were removed, the patient developed sudden severe low back pain and lossof sensation and motion in his legs.Results of emergency myelography and aortography SPINAL CORD INFARCTION were normal, and a clinical diagnoRESULTING FROM CARDIAC sis of spinal cord infarction was CATHETERIZATION made. His neurologic status did not Ischemic myelopathy occurs when improve, and he died of bradythe blood supply to the spinal cord asystolic arrest on the 57th hospiis compromised by emboli. Emboli tal day. Autopsy showed severe atherosclerotic aortic disease but arise from cardiac thrombus or tumor, atherosclerotic aortic plaques, no dissection or trauma. Extensive or fibrocartilaginous material in spinal cord infarction was present. the intervertebral discs [1,2]. Spi- Cholesterol emboli were present in nal cord embolization may occur the spleen, kidney, and spinal cord. spontaneously or be provoked by Patient 2. An 80-year-old white myocardial infarction, aortic cross- man presented with three hours of chest pain. Myocardial infarction clamping during surgery, intraaortic ballon pump insertion, or was ruled out. Cardiac catheterizacatheterization of the great vessels. tion was performed without appar-

August

1989

The American

Journal

of Medicine

Volume

87

239

BRIEF CLINICAL

OBSERVATIONS

ent complication using Judkin’s technique with six French diagnostic catheters passed over flexible jtipped guidewires under fluoroscopic guidance. Within 24 hours, the patient developed bilateral leg weakness and decreased vibratory sense. Complete spine radiographs and spinal cord magnetic resonance imaging showed no significant abnormalities. A clinical diagnosis of spinal cord infarction was made. The patient subsequently had coronary bypass surgery. The postoperative course was complicated by congestive heart failure, renal insufficiency, and catheter sepsis, leading to death on the 32nd postoperative day. During that time, his spinal cord syndrome did not improve. Permission for autopsy ‘was refused. In both patients, symptoms diagnostic of spinal cord damage arose within hours of apparently uncomplicated cardiac catheterization. Extrinsic compression and aortic dissection were ruled out, and spinal cord infarction was diagnosed clinically. In both cases, the neurologic deficit persisted until death. Infarction and cholesterol emboli in the spinal cord were found in the one patient in whom autopsy was performed. The other patient was seen by three neurologists who concurred with the diagnosis of spinal cord infarction, with cholesterol embolization the most likely cause. We could find no cases of spinal cord infarction documented after cardiac catheterization. Only three cases have been reported after catheterization of the great vessels in the past 20 years. Two of these followed aortography [3,4]; one followed vertebral arteriography [l]. In both cases for which clinical information is available, catheterization was technically complicated and could not be successfully completed; symptoms began during the procedure. In contrast, both of our patients had no symptoms during the procedure, and catheterization itself was performed successfully without complications apparent at the time. It is not clear why catheterization led to cholesterol embolization in our patients. All catheters were passed over flexible j-tipped guidewires under fluoroscopic visualization. Some factors previously reported to predispose to cholesterol embolization were not present; in neither case was there any 240

August

1989

The American

Journal

question of intimal dissection by catheter or guidewire, or injection of contrast into the intima. Neither patient had received warfarin or streptokinase, which have been associated with multiple cholesterol embolizations to other organs [5,6]. Neither patient had procedural hypotension, which may predispose to spinal cord infarction. However, both patients had two conditions commonly associated with cholesterol embolization. Both had aortic disease, manifested by severe atherosclerosis in Patient 1 and a very tortuous aorta in Patient 2. In addition, both patients had unstable coronary syndromes: recent large anterior myocardial infarction with residual high-grade coronary artery stenosis in Patient 1; resting angina with severe three-vessel coronary disease in Patient 2. Although spinal cord emboli may arise from cardiac tumors or fibrocartilaginous material from intervertebral discs [1,2], the most likely source in the setting of aortic instrumentation is atheromatous, cholesterol-laden emboli from the aortic intima. Cholesterol embolization to other organs after catheterization has been well documented. Inspection of atheromatous aortas at autopsy confirms that mural thrombi on atherosclerotic plaques are “soft, mushy, and easily brushed off” [7]. Catheters and guidewires, even if soft and flexible, may be able to dislodge plaque material from the aortic intima, showering cholesterol-laden emboli downstream. Cardiac catheterization carries a major complication rate of about 1 percent. The most devastating complications are death, myocardial infarction, and cerebrovascular stroke. Although it may be exceedingly rare, spinal cord infarction must be added to thislist. Physicians performing or referring patients for cardiac catheterization must be aware of the potential for fatal complications and be sure the benefits outweigh these risks. JAMES C. BLANKENSHIP, M.D., F.A.C.C. Geisinger Medical Center Danville, Pennsylvania 17822 SUSANMICKEL, M.D. Marshfield Clinic Marshfield, Wisconsin 1. El-Toraei I, Juler G: lschemic myelopathy. Angiolow 1979: 30: 781-794. z Hirose G. Kosoegawa H. Takado M. Shimazaki K, Murakami E: Spinal cord ischemia and left atrial myxoma. Arch Neural 1979; 36: 439. 3. Harrington D. Amplatz K: Cholesterol embolization of Medicine

Volume

87

and spinal infarction following aortic catheterization. Am J Roent RadTher Nucl Med 1972; 115: 171-174. 4. Gaines PA, Cumberland DC, Kennedy A, Welsh CL, Moorhead P. Rutley MS: Cholesterol embolisation: a lethal complication of vascular catheterization. Lancet 1988; I: 16&170. 5. Moldveen-Geronimus M, Merriam JC Jr: Cholesterol embolization. From pathological curiosity to clinical entity. Circulation 1967; 35: 946-953. 6. Schwartz MW. McDonald GE: Cholesterol embolization syndrome. Occurrence after intravenous streptokinase therapy for myocardial infarction. JAMA 1987: 258: 1934-1935. 7. Castleman B. McNeely BU: Case records of Massachusetts General Hospital. N Engl J Med 1967: 276: 1368-1377. Submitted

February

23, 1989. and accepted in revised form May la, 1989

SARCOID MYOSITIS WITH PSEUDOHYPERTROPHY Muscle involvement is thought to occur in 50% to 80% of patients with sarcoidosis [l]. It is usually asymptomatic but can be associated with chronic weakness,palpable nodules, muscular pseudohypertrophy, and evidence of other major organ involvement. Only nine cases of acute myositis have been reported thus far [2]. We recently examined a 36-yearold man with pulmonary sarcoidosis who had experienced six episodes(five unilateral, one bilateral) of acute myalgias with swelling of the calf musculature over a fiveyear period. The onset of each episode was acute and resolved completely over a three-week period without treatment. The first episode occurred prior to the diagnosisof sarcoid, at which time the patient had no evidence of other organ involvement. The second episode was associated with respiratory symptoms. At that time, deep venous thrombosis was excluded by venography and ventilation-perfusion scanning. Granulomatous diseasetypical of sarcoidosis was documented by pulmonary biopsy, and a one-year course of corticosteroids was begun. A third event occurred while the patient was taking 10 mg of prednisonea day; its coursewas of similar intensity and length as the previous two episodes. At the time of the fifth episode, all medications had been terminated for two years. The attack was associated with severe pain and swelling that increased over a nineday period and resolved completely within two weeks. As with previous episodes,it was not preceded by evidence of infection, trauma, or