Superior Vena Cava Syndrome

Letters, if clearly marked "For Publication," will be published as space permits and at the discretion of the editor. They should be typewritten triple-spaced, with five or fewer references, should not exceed two pages in length, and will be subject to editing. Letters are not acknowledged.

Temporal Arteritis To the Editor.\p=m-\Thepurpose of this communication is to highlight a serious disease that, although it often results in blindness and sometimes in death, is probably often overlooked. Yet its diagnosis need not be too difficult if the primary physician thinks of it and takes time to get a thorough history and determine the erythrocyte sedimentation rate (ESR). The

treatment quickly produces dramatic results. The disease is often misdiagnosed or diagnosed too late to prevent the catastrophe of irreversible sudden blindness in one or both

cases.

eyes.

This disease occurs in patients over 60 years of age, sometimes as a sudden loss of vision due to ischemic optic neuritis secondary to occlusion of the central retinal artery. It is commonly preceded by boring, intractable headache over a period of weeks or months. Tension headaches are less severe, more bizarre, of longer duration, and related to stress. It is thought to be part of a systemic dis¬ ease,

haps

scribed. Physical examination is of little help in its diagnosis, but, as al¬ ways, a good history and physical ex¬ amination should be done. In the differential diagnosis, we should think of early rheumatoid ar¬ thritis, fibromyositis, chronic hidden infection, neoplasms, and brain tu¬ mors, for example. If the ESR is highly elevated (50 to 90 mm/hr), it clues us in to the diagnosis. Temporal artery biopsy is not always necessary and arteriograms are contraindicated. A therapeutic test of prednisone, 10 mg four times a day, may help make the diagnosis in doubtful

polymyalgia rheumatica,

per¬

immune reaction disease. I believe that polymyalgia rheumatica without ocular symptoms occurs much more often than is realized. It is panarteritis (giant cell arteritis) fre¬ quently involving the branches of the carotid, most commonly the temporal, artery, which is often tender and pal¬ pable. Systemic symptoms consist of headache, myalgia, stiffness in the proximal arms and legs, fatigue, fe¬ an

weight loss, night sweats, ano¬ rexia, and depression. It is a self-lim¬ ited disease, lasting approximately

ver,

six months to two years, but it may months of incapacitation and suffering even when vision is not in¬ volved. I suspect that in the early stages, some of these patients are treated as "old crocks" with the usual aches and functional or neurotic com¬ plaints for which analgesics and the cause

ubiquitous tranquilizers Edited

by John

are

pre-

D. Archer, MD, Senior Editor.

This disease involving visual com¬ plaints is infrequent: the Wills Eye Hospital in Philadelphia (the largest eye hospital in the country) reported only 18 cases in 1970. Unfortunately, most of these

were

treated too late to

prevent serious visual loss. Transitory

visual loss (amaurosis fugax) occurs frequently and suggests occlusive ca¬ rotid artery disease. When there are visual symptoms such as blurred vi¬

sion, diplopia, or ocular palsy, a medi¬

cal emergency exists. I still vividly recall an elderly woman patient about 25 years ago who lost sight in both eyes within one week. Her condition was diagnosed "bilateral optic neuritis of unknown etiology" by the neurologist. More re¬ cently, I examined an elderly man who had boring headache, pain and tenderness over the temporal ar¬ teries, diplopia, and ptosis. He was admitted to the hospital the same day and given 60 mg of prednisone that evening by the neurologist. The head¬ ache was relieved by the next day, and the diplopia and ptosis disappeared after three days. He has remained

well. This

topic has been discussed in specialty journals, but the generalists have not been sufficiently alerted to it—and they are the first line of de¬

fense.

A. J. PODBOY, MD York, Pa

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To the Editor.\p=m-\Anexcellent review of the treatment of superior vena cava syndrome (SVCS) by Drs Lokich and Goodman (231:58, 1975) mentioned that chemotherapy is effective in treating SVCS resulting from acute lymphocytic leukemia (ALL) and non-Hodgkin lymphoma (NHL), but the authors did not refer to the drug combination best used. Therefore, we would like to report briefly two cases treated with a combination of chemotherapeutic agents\p=m-\prednisolone and vincristine\p=m-\that are known to cause rapid lysis of tumor cells, with the potential risk of uric acid nephropathy. Report of Cases.\p=m-\Case1.\p=m-\A13-year-old

girl

was seen at Oklahoma Children's Memorial Hospital with a three-week history of progressive pain in the right shoulder, shortness of breath, cervical adenopathy, and facial edema. Substantial enlargement of the mediastinum was noted on the chest x-ray film. Non-Hodgkin lymphoma was diagnosed by a mediastinal biopsy. Preventive measures were initiated against hyperuricemia. Substantial reduction in the extent of facial edema and dyspnea was noted within 24 hours after initiating treatment with intravenously given vin¬ cristine, 2 mg/sq m, and prednisolone, 1,000 mg/sq m. Over the next two days, all signs and symptoms of SVCS abated. Case 2.-A 3-year-old girl had a twoweek history of progressive distress (dysp¬ nea, orthopnea, and cyanosis) in the res¬ piratory tract. She was transferred to OCMH when a chest x-ray film showed an enlarged mediastinum, with pleural and pericardial effusion. A pericardiocentesis (120 ml) resulted in a notable decrease of the orthopnea and cyanosis. On the second hospital day, a left thoracotomy was per¬ formed to obtain a biopsy specimen of the mediastinal mass and to create a peri¬ cardial window. Vincristine and predni¬ solone therapy and preventive measures for uric acid nephropathy were initiated postoperatively for the treatment of a pre¬ sumed lymphoma. On the third hospital day, there was much improvement in the dyspnea, with no signs or symptoms of SVCS on the fourth day. The mediastinal biopsy disclosed NHL.

To our knowledge, there is no infor¬ mation available regarding the effec¬ tiveness of radiation therapy in com¬ parison with that of chemotherapy in children with SVCS resulting from ALL or NHL. Even though there is no comparative study, radiation therapy is almost universally effective and is, therefore, the treatment of choice as emphasized in Lokich and Goodman's review. However, in selected cases, chemotherapy can be an effective al-

ternative to radiation therapy. Our cases demonstrate well that chemo¬ therapy is fast and effective. Prednisolone together with vincristine, therefore, may be considered as effec¬ tive therapy for ALL and NHL, espe¬ cially when transportation of pa¬ tients from an intensive care unit to the radiation therapy section might compromise that patient's well-being. Ruprecht Nitchke, MD Stephen Acker, MD David Campbell, MD Edward DePersio, MD Ronald Elkins, MD G. Bennett Humphrey, MD Webb Thompson, MD Morris Wizenberg, MD The University of Oklahoma Health Sciences Center Oklahoma

City

Antibiotic-Associated Colitis To the Editor.\p=m-\Itshould be noted in

and Milligan the apparent successful use of the anion-exchange resin, cholestyramine, in two cases of colitis associated with lincomycin and clindamycin, that one of the patients was constipated for four days postoperatively and that both were given constipating agents when diarrhea began. One received paregoric, codeine, and an atropine sulfate-diphenoxylate hydrochloride mixture (Lomotil), the other Lomotil alone. In our early experience with colitis fol-

the report

by Burbige

(231:1157, 1975)

on

lowing lincomycin administration,1 we noted that those patients with the most severe mucosal injury, as well as those with prolonged symptoms and sigmoidoscopic findings, gave histories of chronic constipation or had been given Lomotil at the onset of diarrhea. The bacteriologic and light and electron microscopic studies of mucosal biopsy specimens did not suggest bacterial overgrowth or invaThese clinical observations, coupled with the knowledge that lincomycin is very poorly absorbed and sion.

is excreted in the bile in an active form, suggested the hypothesis that the colitis resulted from the presence of some toxic substance in the colonie lumen that accumulated as a result of constipation. We postulated the toxic substance might be the antibiotic it¬ self, a metabolite secreted in the bile

formed as a result of intraluminal chemical alterations, or a product pro¬ duced by antibiotic-resistant bacteria that were permitted to overgrow. We considered an abnormality of bile salt metabolism unlikely because (1) there was little evidence of small-bowel dysfunction in these patients2; (2) co-

or

litis has not been described in pa¬ tients with severe diarrhea associated with ileal resection and bile salt malabsorption; and (3) the bacteria usu¬ ally associated with bile salt abnor¬ malities in stagnant bowel problems are sensitive to lincomycin and clin-

damycin. Our suggestion that preexisting constipation or the use of constipat¬ ing agents such as Lomotil may play a role in the pathogenesis of this type of colitis has been challenged by Tedesco et al.:i Although these authors state that they have seen no compli¬ cation of Lomotil therapy in patients with diarrhea following clindamycin administration, they report in their article4 that in patients so treated, diarrhea persisted for up to 26 days

and proctoscopy remained abnormal for up to six weeks. An association between Lomotil usage and the devel¬ opment of severe antibiotic colitis has been made by others.'6 There is also one published case report7 of toxic megacolon developing in a patient with antibiotic-associated colitis who

received Lomotil. Most of our patients with anti¬ biotic-associated colitis were referred because of overt colitis (bloody diarrhea). In each instance, Lomotil or other constipating therapy was discontinued. If the patient was still taking the antibiotic, it was stopped. All patients were given lactobacilli (Lactinex) orally, and those with sig¬ nificant mucosal pathology were treated with hydrocortisone retention enemas (Cortenema) twice daily for five days. Patients with tenesmus and anal and perianal irritation also re¬ ceived suppositories (containing bis¬ muth resorcin compound, bismuth subgallate, Peruvian balsam, zinc oxide, and boric acid [Anusol-HC]) and hot sitz baths twice daily for two to three days. Sigmoidoscopic find¬ ings improved markedly or returned to normal at the conclusion of steroid

therapy. Recently, we chose to use corticotropin followed by a short course of systemic prednisone in an 83-year-old woman who received both systemic lincomycin and oral clindamycin for treatment of a chronic leg ulcer and in whom a life-threatening colitis de¬ veloped with a confluent pseudomem¬ brane

seen

on

sigmoidoscopy.

This

patient's condition deteriorated rap¬ idly after Lomotil was given to con¬ trol diarrhea, which began during the last three days of therapy. She was referred to our hospital for colectomy.

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Although the course was stormy, with pneumonia, the diarrhea im¬ proved after three to four days of medical treatment. Sigmoidoscopy performed just prior to discharge, 19

severe

days following admission,

was nor¬

mal. There have been no controlled stud¬ ies of topical or systemic steroid ther¬ apy in nonstaphylococcal antibioticassociated colitis. Our uncontrolled experience suggests to us that the therapy works. We have withheld steroid therapy for several days in a few patients with moderately severe colitis in an effort to determine if hospitalization alone would result in im¬ provement. In these patients, no im¬ provement was noted until steroid enemas were begun. However, pa¬ tients with mild mucosal abnormal¬ ities on sigmoidoscopy have improved following no therapy other than dis¬ continuation of the antibiotic or Lomotil or both. Should cholestyramine be found ineffective in doubleblind evaluation, a similar study of topical steroid therapy in antibioticassociated colitis may be in order. Fred E. Pittman, MD, PhD Joan C. Pittman, MA Charles D. Humphrey, PhD Medical University of South Carolina Charleston 1. Pittman

lowing

134:368,

oral 1974.

FE, Pittman JC, Humphrey CD: Colitis follincomycin therapy. Arch Intern Med

2. Spanknebel GL, Patterson JF, Levitan R: On the mechanism of lincomycin-induced diarrhea: Studies in ileostomy patients. Gastroenterology 52:1121, 1967. 3. Tedesco FJ, Barton RW, Alpers DH: Clindamycin and colitis. Ann Intern Med 82:280, 1975. 4. Tedesco FJ, Barton RW, Alpers DH: Clindamycin\x=req-\ associated colitis: A prospective study. Ann Intern Med

81:429, 1974.

5. Stroehlin

JR, Sedlack RE, Hoffman RE II: Clincolitis. Mayo Clin Proc 49:240, 1974.

damycin-associated

6. Ramirez-Ronda CH: Incidence of

clindamycin-asso-

ciated colitis. Ann Intern Med 81:860, 1974.

7. Brown CH, Ferrante WA, Davis WD Jr: Toxic dilatation of the colon complicating pseudomembranous enterocolitis. Am J Dig Dis 13:813, 1968.

Aerosol Sprays To the Editor.\p=m-\A recent Questions and Answers section (231:1289, 1975) had a nicely balanced and very fair answer to the question of hazard from aerosol hair sprays and anti-

perspirants. However, though very fair and evenly balanced, I would

think that it would leave your questioner almost exactly where he started. Dr. Jerome states "the present state of knowledge gives aerosol products, in normal use, a clean bill of health." At the same time, Mr. Wheater states "it must be concluded that all aerosol consumer products are potentially dangerous to humans." Both answers are correct and not as

Letter: Superior vena cava syndrome.

Superior Vena Cava Syndrome Letters, if clearly marked "For Publication," will be published as space permits and at the discretion of the editor. The...
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