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dures in that respect and should sys- tematically be performed.3

Jain and Rosner’ insist that IIH is a disease of “young obese women of childbearing age”-whereas it is true that, in patients presenting with iso- lated intracranial hypertension, the likelihood of finding CDST is much higher in non-obese than in obese pa- tients, it is nonetheless possible to be a young obese woman and to suffer CDST.4 Cerebral venous thrombosis should, therefore, be systematically ruled out, even in young obese women, and particularly so during pregnancy and oral contraceptive use which are listed as possible causes of IIH but are also well known causes of CDST?

Finally, if obesity is indeed a key feature of IIH, it is strange to list med- ications as possible causes since this can raise intracranial pressure in non-obese subjects.

In our opinion, W as described by Jain and Rosner is similar to the clas- sical benign intracranial hyperten- sion (BIH) and has indeed the same diagnostic criteria.5 In order to try and better define what this term cov- ers, we would like to suggest: (1) to add brain MRI and/ or cerebral an- giography3 (conventional, digitalised, or magnetic resonance angiography) to the diagnostic criteria of BIH;” (2) to keep the classical terms of BIH or pseudotumor cerebri for all cases of isolated intracranial hypertension without structural lesion (this would include drug induced raised intracra- nial pressure); (3) to restrict the term IIH to those cases of BIB without cause. This corresponds to the entity referred to by Jain and Rosner and mostly affects obese females.

Alain Djacoba Tehindraxanarivelo, MD,

Marie Germaine Bousser, MD Hdpital Saint-Antoine,

Paris, France

1. Jain N, Rosner F. Idiopathic intracranial hypertension: report of seven cases. Am J Med. 1992;93:391-395. 2. Symonds CP. Otitic hydrocephalus. Bram. 1931;54:55-71. 3. Bousser MG, Barn&t HJM. Cerebral venous thrombosis, in: Barnett HJM, Mohr JP, Stein BM,

Yatsu FM eds. Stroke: Pathophysiology, Diagnosis and Management. 2nd ed. Edinburgh: Churchill Livingstone;l992: 517-537. 4. Tehindrazanarivelo A, Evrad S, Schaison M, et al. Prospective study of cerebral sinus venous thrombosis in patients presenting with benign intracranial hypertension. Cebrovasc Dis. 1992; 2:22-29. 5. Ireland 6, Corbett JJ, Wallace RB. The search for causes of idiopathic intracranial hypertension. A preliminary case-control study. Arch Neurol. 1990;47:315-320.

Submitted January 14, 1993, and accepted March 8, 1993.

The Reply: We were pleased to review the

comments of Piette, Wechsler, and Vidailhet and offer the following re- sponse. The diagnosis of idiopathic intracranial hypertension (IIH) is one of exclusion-certain condi- tions thought to be causal such as steroid withdrawal, Addison’s dis- ease, vitamin A intoxication, oral contraceptives, and iron deficiency anemia should really be thought of as chance associations. It is true that certain cases of cerebral venous thrombosis (CVT)-those that pre- sent with isolated intracranial hy- pertension, headache, and pa- pilledema as reported by Ameri and Bousser,’ can be mistaken to be IIH; this may occur when complete neu- rodiagnostic studies are not or can- not be obtained.

Regarding our report,” magnetic resonance imaging (MRI) was not readily available at the Queens Hospital Center prior to 1990 and, thus, only one of the patients in our report had received this study. Cere- bral angiography was not performed, as it was not clinically indicated in these patients. Also, no clinical or laboratory data evidence suggested the possibility of collagen vascular disease in any of our patients.

Piette, Wechsler, and Vidailhet in- deed have a valid point that CVT should be considered prior to estab- lishing a diagnosis of IIH. It is advis- able that MRI, or in doubtful cases angiography, should be performed to fully rule out CVT.

In response to Tehindrazanarivelo and Bousser, we would like to men- tion that IIH was previously known

as benign intracranial hypertension until the 198Os, when the high inci- dence of visual loss was noted and the term “benign” was dropped.3 We do not feel that a distinction be- tween these terms is necessary.

Neelu Jain, MD, Fred Rosne?; MD,

Queens Hopital Jamaica, N. Y.

1. Ameri A, Bousser MG. Cerebral venous thrombosis. Neural C/in. 1992;10:87-111. 2. Jain N, Rosner F. Idiopathic intracranial hyper- tension: report of seven cases. Am J Med. 1992;93:391-395. 3. Wall M. Idiopathic intracranial hypertension. Neurol C/in. 1991;9:73-94.

Submitted March 4, 1993, and accepted March 8, 1993.

CELLULITIS AFTER AXILLARY LYMPH NODE DISSECTION To the Editor:

Regarding Dr. Simon and Dr. Cody’s review on cellulitis after ax- illary lymph node dissection for car- cinoma of the breast,’ we think that two additional aspects deserve very important consideration.

F’irst, streptococci have been re- ported as the most commonly in- volved bacteria in cellulitis. However, concerning group A streptococcus, there has been an emergence of se- vere group A streptococcus in the last 10 years, both in America and in Europe.2 The most frequently recog- nized portal of entry is cutaneous cel- h&is, although bacteremia, myositis, necrotizing fasciitis, and streptococ- ml toxic shock syndrome have been also described as invasive complica- tions. It seems that this newfound ag- gressiveness could be due in great part to a change in the virulence fac- tors of group A streptococcus. Strains of group A streptococcus isolated from patients with invasive disease have been predominantly M types 1 and 3, which produce pyrogenic exo- toxin A or B or both.

Second, another important aspect is that bacterial cultures from the cellulitic skin are often helpless to isolate putative pathogens. The skin is provided with a unique set of lym-

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phoid and reticular cells with the ca- pacity to secrete lymphokines and cytokines. These substances rapidly reduce the number of viable bacte- ria from infection by enhancing the infiltration of skin by circulating macrophages and neutrophils. The inflammatory signs associated with cellulitis are most likely produced by a small number of residual bacteria and by fragmented remnants, and amplified by the lymphokines that are secreted in response to antigenic challenge.3 Therefore, the use of anti-inflammatory agents, together with antistreptococcal antibiotics, may play a significant role in en- hancing the resolution of infection by reducing the production of solu- ble mediators by the lymphoid and the reticular intraepithelial cells.

We believe that the consideration of these two aspects in potentially predisposed patients (such as those with axillary lymph node dissection for carcinoma of the breast) could help to treat those patients more quickly and accurately and to pre- vent in them the development of in- vasive complications.

Esteban Ma&hex, MD Hospital de la Santa Creu i Sant Pau

Angeles Marcos, MD Hospital Clinic

Pere Domingo, MD Hospital de la Santa Creu i Sant Pau

Barcelona, Spain.

1. Simon MS, Cody RL. Cellulitis after axillary lymph node dissection for carcinoma of the breast. Am J Med. 1992;93:543-548. 2. Stevens DL. Invasive group A streptococcal infections. Clin Infect Dis. 1992;14:2-13. 3. Sachs MK. Cutaneous cellulitis. Arch Dermatol. 1991;127:493-496.

Submitted December 29, 1992, accepted April 15, 1993.

PREVENTING CELLULITIS AFTER AXILLARY LYMPH NODE DISSECTION To the Editor:

We read with great interest the re- view by Simon and Cody’ on celluli- tis of the upper extremity following axillary lymph node dissection for breast cancer. As the authors point out, cellulitis is frequently underap-

TABLE How to Prevent Infections

After Axillary Lymph Node Dissection-10 Simple Rules for the

Care of the Arm and Hand lpsilateral to the Intervention

1. Wash and disinfect the smallest break in the skin.

2. Wear canvas gloves when gardening, and rubber gloves when washing dishes or cleaning utensils with steel wool.

3. Wear a thimble when sewing. 4. Apply a lanolin hand cream several

times daily. 5. Do not hold a cigarette in this hand. 6. Do not cut or pick at cuticles or

hangnails on this hand. 7. Do not allow injections or

vaccinations in this arm; whenever possible, do not allow blood to be drawn from this arm.

8. Use an electric razor for shaving; avoid nicks and scrapes.

9. Do not get sunburned. 10. Contact the physician if the arm

appears swollen, hot, or red.

preciated by the patient and the pri- mary care physician. However, if the purpose was to emphasize +e need for a recognition of the important role of this infection and its interrelation- ship with lymphedema, the article, in our opinion, should have better de- tailed the mainstay of a correct clini- cal approach to the problem-pre- vention. Proper patient education is essential to reduce the risk of lym- phedema. Simple rules for the pro- phylaxis of infections of the arm ip- silateral to the original breast surgery, which can be found in manuals of cancer rehabilitation or nursing care, should be taught before hospital dis- charge: a list of typical rules is pre- sented in the Table. Traumas, ex- cessive heat, constrictive clothing, and exaggerated exercise should also be avoided; weight gain should be dis- couraged, not only because obese pa- tients seem more prone to the devel- opment of lymphedema, but also because it is a significant prognostic factor of unresponsiveness to lym- phedema treatment.3

Another point of the article de- serves comment, the fact that from the case series presented one can er- roneously think that cellulitis should be suspected only in lymphedema-

tous patients. Although the objective criteria used by the authors (eg, cen- timetric or volumetric measure- ments) and the threshold for defini- tion of lymphedema are not de- scribed, all the patients of the report are, in fact, said to have preceding or concurrent lymphedema at the moment of diagnosis of cell&is. We consider it important to remark that all patients who undergo axillary lymph node dissection are at life- long risk of cellulitis; those who have an already clinically evident swelling of the limb have just an increased risk. In a similar case series of 21 mastectomized patients with clinical signs of cellulitis referred to our de- partment during 1992, 7 (33.3%) had no lymphedema (as defined by com- parison of circumferential measure- ments of both upper limbs, detailed in reference 3). In all patients a 7- to lo-day domiciliary course of treat- ment with the antibiotic teicoplanin (400 mg IM on day 1 and 200 mg IM on the following days, in single daily administrations) successfully eradi- cated all signs of infection, without unwanted side effects. The differ- ence in limb measurements de- creased, on average, 38.5% among the 14 patients with lymphedema, 3 of whom (21.4%) had no more de- tectable swelling at the end of treat- ment. This confirms the importance of prompt empiric antibiotic ther- apy, which can be easily managed by the primary care physician without the need for blood and tissue cul- tures, in most cases, as noted in Simon and Cody’s results.’

In conclusion, we think it reason- able to consider a subclinical lymph drainage impairment as universal af- ter axillary surgery and/or radiother- apy, although an evident lymphedema does not develop in the majority of pa- tients. When it does, even many years after surgery,4 it is often possible to identify a triggering event, like infec- tion or trauma, producing a worsen- ing of the drainage. Thus, it is impor- tant for the clinician who cares for breast cancer patients to remind them of the importance of life-long obser-

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