Volume 25 Number 5, Part 2 November 1991
tumor might also be considered, the spread to noncontiguous locations on the side of the chest opposite the tumor and the absence of ectatic lymphatics in any of the biopsy specimens make this unlikely. Simple lymphatic obstruction also would fail to account for the epidermal neutrophilic infiltrate. No studies were performed to find mechanisms of paraneoplastic tumor action. We postulate a tumorrelated lymphokine that acts in a paracrine manner to stimulate keratinocytes and Langerhans cells to produce epidermal cell-derived thymocyte-activating factor (interleukin 1), which is a chemoattractant for neutrophils. 9 REFERENCES 1. Graham M. Non-Hodgkin's lymphomas. Pediatr Ann 1988;17:192-203. 2. Young JL, Ries LG, Silverberg E, et aJ. Cancer incidence, survival, and mortality for children younger than age 15 years. Cancer 1986;58s:598-602.
NHL presenting with inflammatory dermatosis 3. Murphy SB. Classification, staging and end results of treatment ofchildhood non-Hodgkin's lymphomas: dissimilarities from lymphomas in adults. Semin Oncol 1980; 7:332-9. 4. Hvizdala E, Schuster JJ, Falletta JM. The non-Hodgkin's lymphomas in adolescents. In: Tebbi CK, ed. Major topics in adolescent oncology. Mount Kisco, NY: Futura, 1987; 135-55. 5. Zaatari GS, Chan WC, Kim TH, et aJ. Malignant lymphoma in the skin of children. Cancer 1987;59:1040-5. 6. Murphy SB. Childhood non-Hodgkin's lymphoma. N Engl J Med 1978;299:1446-8. 7. DeVita VT, Hellman S, Rosenberg SA, eds. Cancer: principles and practice of oncology. 3rd ed. Philadelphia: JB Lippincott, 1989;1896-940. 8. Curth HO. Skin lesions and internal carcinoma. In: Andrade R, Gumport SL, Popkin GL, Rees TD, eds. Cancer of the skin. Philadelphia: WB Saunders, 1976:1308-41. 9. Sauder DN, Arsenault T, McKenzie RC, et al. Biology and molecular biology of epidermal cell-derived thymocyte activating factor. Ann N Y Acad Sci 1988;548:241-52.
Cutaneous reaction from a broken thermometer Purnima Sau, COL, Me, USA,a Gilberto SoHvan, MAJ, MC, USA,a and Frank B. Johnson, MDb Washington, D. C. A cutaneous and soft tissue reaction that resulted from a broken thermometer inside the mouth of a 10-year-old boy is described. Metallic mercury globules and glass pieces were identified in the excised tissue. On histologic examination, a zone of necrosis, polymorphonuclear leukocytes, macrophages, and multinucleated giant cells surrounded metallic mercury that appeared as dark opaque globules. Dense fibrosis and reactive lymphoid hyperplasia were also noted in the dermis and deeper tissues. The gold lysis test, scanning electron microscopy, and energy-dispersive x-ray analysis confirmed the presence of mercury in the tissue. A literature review on cutaneous mercury granuloma illustrates its unpredictable course. The cutaneous reaction may remain localized, but some cases are associated with an elevated mercury level in blood and urine, pulmonary embolism, mercury poisoning, and even with fatal outcome. Various manifestations of mercury poisoning and guidelines for the management of cutaneous mercury granuloma are discussed. (J AM ACAD DERMATOL 1991;25:915-9.)
From the Dermatology Service,· Walter Reed Army Medical Center, and the Department ofChemical Pathology,b Armed Forces Institute of Pa thology. The opinion or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the Department of the Army or the Department of the Defense. Reprint requests; Col. Purnima Sau, Dermatology Service, Walter Reed Medical eLr., Washington, DC 20307.
16/4/29971
Soft tissue injury from metallic mercury is probably more common than the paucity of reports indicates. Johnson and Koumides 1 found only 27 cases of injury or poisoning by metallic mercury and added one of their cases. Of 28 patients, 4 died of mercury poisoning. Subsequent to this review, several case reports2-8 and a small series of cases9 of injury from metallic mercury have been published. 915
916 Sau et al.
Journal of the American Academy of Dermatology
Fig. 1. Swelling under the chin with a bright red papule and a linear scar anterior to the papule.
Fig. 2. Lateral x-ray view of the neck demonstrates metallic densities at the floor of the mouth.
We report a case of soft tissue injury caused by mercury and glass from a broken thermometer. CASE REPORT
A ID-year-old boy was seen in February 1989 because of a slowly growing mass in his submental region present for about 2 months. He had been seen on several occasions since August 1987 by his local physician for submental and submandibular swelling, sore throat, and constitutional symptoms. Tonsillectomy and adenoidectomy were performed in November 1987. In December 1987 he underwent exploratory surgery that revealed shiny metallic globules and surrounding inflammatory reaction and fibrosis in the submental region. Subsequent history revealed that 6 months earlier the patient had accidentally broken a mercury thermometer in his mouth. The post-
operative blood level of mercury was reported to be normal. After surgery the wound healed promptly, but swelling in the submental area persisted and increased slowly in size to the present. Two months ago, the mother noticed a reddish protrusion at the center of the submental mass. The patient had been healthy and without symptoms. Physical examination revealed a mobile, firm, nontender 3.5 cm by 2.0 cm mass in the submental region. A bright red papule that protruded from the center of the mass was noted (Fig. 1). The remainder of the physical examination was unremarkable. Routine laboratory examinations revealed no abnormalities. Results of a chest x-ray study were normal with no evidence of metallic densities in the lung fields. The x-ray studies ofthehead and neckdemonstrated high-density metallic collections in the floor of the mouth (Fig. 2).
Volume 25 Number 5, Part 2 November 1991
Cutaneous reactionfrom a broken thermometer 917
Fig. 3. Photomicrograph shows epidermal hyperplasia and infiltration ofPMNs and macrophages containing phagocytized PMNs. Metallic mercury appears as a dark black globule with a peripheral ring of birefringence. A thick eosinophilic homogeneous band (arrow) surrounds this mercury globule. (Hematoxylin-eosin stain, polarized; X75.)
The patient was admitted to the hospital for further surgery. All granulomatous tissue in the submental area and lymph nodes was removed. No further mercury deposits were found by fluoroscopic examination. The postoperative mercury level of urine was 25 J.LgjL (normal, 0 to 20 J.LgjL). The patient recovered without complications. During the I year follow-up period, he has been healthy and has had no recurrence. He shows no systemic signs or symptoms of mercury toxicity. Pathologic findings. The cut surfaces of the excised specimen revealed shiny metallic globules, flecks ofsilvery material, and fragments of glass embedded in the yellowtan tissue. Sections from the tissue revealed epidermal hyperplasia and an area of epidermal necrosis and ulceration. Opaque globules were noted in the dermis and subcutaneous tissue surrounded by numerous polymorphonuclear leukocytes (PMNs) and macrophages that contained phagocytic debris and nuclei of PMNs in the cytoplasm. These were surrounded by a fibroblastic and vascular proliferation and by a mixed cellular infiltrate of lymphocytes, plasma cells, and a few multinucleated giant cells (Fig. 3). A thick, homogeneous, eosinophilic, capsule-like material was observed around some opaque globules. Dense fibrosis was observed in the surrounding soft tissue. The opaque globules were dark at the center but had a peripheral ring of birefringence by polariscopy. The lymph nodes showed features ofreactive hyperplasia. Paraffin was removed from sections of the tissue taken from the paraffin block. These sections were covered with a coverslip coated with 50% reflecting gold. The coated surface was placed facing the tissue. The positive result was demonstrated as a dark zone around the spherical
Fig. 4. Findings of scanning electron microscopy show spherical globules of metallic mercury (arrow). droplets of metallic mercury in the section because of lysis of the gold that coated the coverslip. Scanning electron microscopy revealed ovoid or spherical globules characteristic of metallic mercury (Fig. 4). Energy-dispersive
Journal of the American Academy of Dermatology
918 Sau et al.
x-ray analysis of the globules yielded energies of x-rays characteristic for mercury. DISCUSSION
A review of the published literature on cutaneous mercury granuloma revealed that the tissue injury was caused either by a broken thermometer,3, 5, 9-11 as in our case, by an anaerobic blood sampling procedure in which mercury was used as a sealant in the syringes,12, 13 or by deliberate injection of metallic mercury. 1, 2, 4, 6, 7, 9, 14 In all cases there was a local tissue reaction characterized by acute and chronic inflammation, necrosis, foreign body granuloma, and abscess formation. The cutaneous tissue reaction to metallic mercury may remain localized as it did in the case described here. Cases described by Rachman, 5 Theodorou et a1.,ll Lanthem et aLp and cases land 3 described by Lupton et aL9 were in this category. Systemic absorption from cutaneous sites has resulted in elevated blood and urine levels of mercury but no evidence ofmercury poisoning as reported by Hill2 and Krohn et a1. 6 However, systemic absorption of metallic mercury from cutaneous sites can have serious consequences. Pulmonary embolism after the introduction of metallic mercury into the skin and subcutaneous tissue has been reported. 1, 7, 8,10,13,14 In a few cases they were associated with a fatal outcome. 1, 10 Metallic mercury embolism, however, was not always associated with serious consequences. Mercury may remain in the body tissue for long periods in some instances. 1 In several cases, serial x-ray films showed the gradual disappearance of the mercury. Recently Hargreaves et aL 15 reported persistent mercury in nerve cells 16 years after metallic mercury poisoning. The diagnosis of a cutaneous mercury granuloma from metallic mercury can be made easily if a history of injury with a mercury-containing object or of self-injection of mercury is obtained. In its absence, the diagnosis will depend on the examination of the tissue removed by surgery. Often metallic mercury can be seen in the cut section of the excised tissue. The gold lysis test, scanning electron microscopy findings, and emission spikes on energy-dispersive x-ray analysis are specific for the presence of mercury. The following guidelines for the management of cutaneous injury by metallic mercury are rec-
ommended.2, 6, 7, 9,16 Measurement of the mercury level of blood and urine should be made in all cases to determine systemiC absorption. 16 All readily accessible cutaneous and subcutaneous tissue suspected of containing mercury should be promptly excised. This is accomplished best under fluoroscopic guidance. Surgical excision of mercury granulomas will lower serum and urinary mercury concentrations. 2,6 Patients should have appropriate monitoring of central nervous system and renal function for evidence of mercurial toxicity. No specific therapy other than frequent follow-up examination is indicated for systemic emboli. 7 It is believed that the emboli are very slowly converted to metallic oxides and organic compounds of mercury and are then excreted by the kidneys. Chelation therapy is recommended if there is evidence of systemic toxicity. Dimercaprol is used for high levels of exposure or acute poisoning and N-acetyl-DL-penicillamine for the treatment of subacute or chronic mercury poisoning. Psychiatric consultation is recommended in cases of self-injection. REFERENCES 1. Johnson HRM, Koumides O. Unusual case of mercury poisoning. Br Med J 1967;1:340-1. 2. Hill DM. Self-administration of mercury by subcutaneous injection. Br Med J 1967;1:342-3. 3. Arcadio F, Thivolet J, Perrot H. Acrodynia following the accidental subcutaneous infiltration of mercury from a broken thermometer. Bull Soc Fr Dermatol Syphiligr 1968;75:509-10. 4. Kern FB, Condo F, Michel SL. Mercury granuloma with systemic absorption. JAMA 1972;222:88-9. 5. Rachman R. Soft-tissue injury by mercury from a broken thermometer: a case report and review of the literature. Am J Clin PathoI1974;61:296-300. 6. Krohn IT, Solof A, Mobini J, Wagner DK. Subcutaneous injection of metallic mercury. JAMA 1980;243:548-9. 7. Grenga TE, Peitrocola DM. Subcutaneous injection of mercury mimicking nodular melanoma. NY State J Moo 1982;82:1231-3. 8. Spizarny DL, Renzi P. Metallic mercury pulmonary emboli. J Can Radiol Assoc 1987;38:60-1. 9. Lupton GP, Kao GF, Johnson FB, Graham JH, Helwig EB. Cutaneous mercury granuloma: a clinicopathologic study and review of the literature. J AM ACAD DERMATOL 1985;12:296-303. 10. Popper L. Tod nach thermometerrverletzung. Wien Med Wochenschr 1960;116:779-80. 11. TheodorouSD, VlachosP, Vamvasakis E.Kneejointinjury by mercury from a broken thermometer. Clin Orthop 1981;160:159-62. 12. Lathem W, Lesser GT, Messinger WJ, Gladston M. Peripheral embolism by metallic mercury during arterial blood sampling. Arch Intern Med 1954;93:550-5. 13. Buxton JT Jr., Hewitt C, Gadsden RH, Bradham GB.
Volume 25 Number 5, Part 2 November 1991 Metallic mercury embolism: report of cases. JAMA 1965;193:103-5. 14. Conrad ME, Sanford JP, Preston JA. Metallic mercury embolism-clinical and experimental. Arch Intern Med 1957;100:59-65. 15. Hargreaves RJ, Evans JG, Janota I, et aI. Persistent mer-
Cutaneous reaction from a broken thermometer cury in nerve cells 16 years after metallic mercury poisoning. Neuropathol Appl NeurobioI1988;14:443-52. 16. Gilman AG, Goodman 1S. Heavy metals and heavy-metal antagonists. In: Gilman AG, Goodman LS, Rail TW, Murad F, eds. The pharmacological basis oftherapeutics. New York: Macmillan 1985:1611-4.
Cutaneous lesions of hemophagocytic syndrome in a patient with T-cell lymphoma and active Epstein-Barr infection Kathleen 1. Smith, LTC, MC, USA,a Henry G. Skelton III, CDR, MC, USN,b Walter L. Giblin, MAJ, MC, USA,c and William D. James, COL, MC, USAd Washington, D.C. The hemophagocytic syndrome (BPS) was first described in immune-compromised patients with secondary viral infections. Immunodeficiency has not always been diagnosed before the onset of HPS, but most patients who develop HPS have known immune deficits. HPS has also been reported in association with lymphoreticular malignancies. In HPS the most prominent histologic change is phagocytosis of red blood cells and other bone marrow-derived elements by cytologically benign histiocytes. Considerable confusion exists about the similarities and differences between HPS and other conditions in which hemophagocytosis may occur, for example, histiocytic medullary reticulosis, T-')' lymphoma, malignant histiocytic lymphoma, and cytophagic histiocytic panniculitis. We report a patient with HPS and cutaneous lesions of cytophagic histiocytic panniculitis who also had an active Epstein-Barr virus infection, and a CDS+ T-cell lymphoma. (J AM ACAD DERMATOL 1991;25:919-24.) The hemophagocytic syndrome (HPS) is a systemic disease characterized by fever, anemia, thrombocytopenia, leukopenia, hepatosplenomegaly, lymphadenopathy, and in most cases, a coagulopathy.l Histologically there is histiocytic proliferation throughout the reticuloendothelial system that involves most prominently the bone marrow, splenic
From the Walter Reed Army Institute of Research,' Department of Dermatopathology. Armed Forces Institute ofPathology,b the Dermatology Service, Fort Dix, New Jersey,C and the Department of Dermatology, Walter Reed Army Medical Center. d The opinions or assertions contained herein are the private views of the authors and not to be considered as official or as reflecting the views of the Departments of the Army or Navy or of the Department of Defense. Reprint requests: CDR Henry G. Skelton III, MC, USN, Department of Dermatopathology, Armed Forces Institute of Pathology, Washington, DC 20306.
16/4/30246
red pulp, hepatic sinusoids, and lymph node sinuses, and, in some patients also the skin. 1 The histiocytes are cytologically benign. They have abundant cytoplasm and may contain few to numerous phagocy~ tosed red blood cells and less frequently lymphocytes, neutrophils, platelets, and nuclear fragments. Cutaneous lesions in patients with HPS principally involve the subcutaneous fat and contain the same benign phagocytosinghistiocytes. Patients withthese lesions are given the diagnosis of cytophagic histiocytic panniculitis. 2-10 Although HPS was originally described in immune-suppressed patients with a primary or reactivated viral infection, patients with vast bacterial, fungal, and parasitic infections have also developed HPS.l, 11 Immune deficits that predispose patients to BPS may be congenital or iatrogenically induced such as in organ transplant recipients. In addition, patients with lymphoid neoplasms may
919
tumor might also be considered, the spread to noncontiguous locations on the side of the chest opposite the tumor and the absence of ectatic lymphatics in any of the biopsy specimens make this unlikely. Simple lymphatic obstruction also would fail to account for the epidermal neutrophilic infiltrate. No studies were performed to find mechanisms of paraneoplastic tumor action. We postulate a tumorrelated lymphokine that acts in a paracrine manner to stimulate keratinocytes and Langerhans cells to produce epidermal cell-derived thymocyte-activating factor (interleukin 1), which is a chemoattractant for neutrophils. 9 REFERENCES 1. Graham M. Non-Hodgkin's lymphomas. Pediatr Ann 1988;17:192-203. 2. Young JL, Ries LG, Silverberg E, et aJ. Cancer incidence, survival, and mortality for children younger than age 15 years. Cancer 1986;58s:598-602.
NHL presenting with inflammatory dermatosis 3. Murphy SB. Classification, staging and end results of treatment ofchildhood non-Hodgkin's lymphomas: dissimilarities from lymphomas in adults. Semin Oncol 1980; 7:332-9. 4. Hvizdala E, Schuster JJ, Falletta JM. The non-Hodgkin's lymphomas in adolescents. In: Tebbi CK, ed. Major topics in adolescent oncology. Mount Kisco, NY: Futura, 1987; 135-55. 5. Zaatari GS, Chan WC, Kim TH, et aJ. Malignant lymphoma in the skin of children. Cancer 1987;59:1040-5. 6. Murphy SB. Childhood non-Hodgkin's lymphoma. N Engl J Med 1978;299:1446-8. 7. DeVita VT, Hellman S, Rosenberg SA, eds. Cancer: principles and practice of oncology. 3rd ed. Philadelphia: JB Lippincott, 1989;1896-940. 8. Curth HO. Skin lesions and internal carcinoma. In: Andrade R, Gumport SL, Popkin GL, Rees TD, eds. Cancer of the skin. Philadelphia: WB Saunders, 1976:1308-41. 9. Sauder DN, Arsenault T, McKenzie RC, et al. Biology and molecular biology of epidermal cell-derived thymocyte activating factor. Ann N Y Acad Sci 1988;548:241-52.
Cutaneous reaction from a broken thermometer Purnima Sau, COL, Me, USA,a Gilberto SoHvan, MAJ, MC, USA,a and Frank B. Johnson, MDb Washington, D. C. A cutaneous and soft tissue reaction that resulted from a broken thermometer inside the mouth of a 10-year-old boy is described. Metallic mercury globules and glass pieces were identified in the excised tissue. On histologic examination, a zone of necrosis, polymorphonuclear leukocytes, macrophages, and multinucleated giant cells surrounded metallic mercury that appeared as dark opaque globules. Dense fibrosis and reactive lymphoid hyperplasia were also noted in the dermis and deeper tissues. The gold lysis test, scanning electron microscopy, and energy-dispersive x-ray analysis confirmed the presence of mercury in the tissue. A literature review on cutaneous mercury granuloma illustrates its unpredictable course. The cutaneous reaction may remain localized, but some cases are associated with an elevated mercury level in blood and urine, pulmonary embolism, mercury poisoning, and even with fatal outcome. Various manifestations of mercury poisoning and guidelines for the management of cutaneous mercury granuloma are discussed. (J AM ACAD DERMATOL 1991;25:915-9.)
From the Dermatology Service,· Walter Reed Army Medical Center, and the Department ofChemical Pathology,b Armed Forces Institute of Pa thology. The opinion or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the Department of the Army or the Department of the Defense. Reprint requests; Col. Purnima Sau, Dermatology Service, Walter Reed Medical eLr., Washington, DC 20307.
16/4/29971
Soft tissue injury from metallic mercury is probably more common than the paucity of reports indicates. Johnson and Koumides 1 found only 27 cases of injury or poisoning by metallic mercury and added one of their cases. Of 28 patients, 4 died of mercury poisoning. Subsequent to this review, several case reports2-8 and a small series of cases9 of injury from metallic mercury have been published. 915
916 Sau et al.
Journal of the American Academy of Dermatology
Fig. 1. Swelling under the chin with a bright red papule and a linear scar anterior to the papule.
Fig. 2. Lateral x-ray view of the neck demonstrates metallic densities at the floor of the mouth.
We report a case of soft tissue injury caused by mercury and glass from a broken thermometer. CASE REPORT
A ID-year-old boy was seen in February 1989 because of a slowly growing mass in his submental region present for about 2 months. He had been seen on several occasions since August 1987 by his local physician for submental and submandibular swelling, sore throat, and constitutional symptoms. Tonsillectomy and adenoidectomy were performed in November 1987. In December 1987 he underwent exploratory surgery that revealed shiny metallic globules and surrounding inflammatory reaction and fibrosis in the submental region. Subsequent history revealed that 6 months earlier the patient had accidentally broken a mercury thermometer in his mouth. The post-
operative blood level of mercury was reported to be normal. After surgery the wound healed promptly, but swelling in the submental area persisted and increased slowly in size to the present. Two months ago, the mother noticed a reddish protrusion at the center of the submental mass. The patient had been healthy and without symptoms. Physical examination revealed a mobile, firm, nontender 3.5 cm by 2.0 cm mass in the submental region. A bright red papule that protruded from the center of the mass was noted (Fig. 1). The remainder of the physical examination was unremarkable. Routine laboratory examinations revealed no abnormalities. Results of a chest x-ray study were normal with no evidence of metallic densities in the lung fields. The x-ray studies ofthehead and neckdemonstrated high-density metallic collections in the floor of the mouth (Fig. 2).
Volume 25 Number 5, Part 2 November 1991
Cutaneous reactionfrom a broken thermometer 917
Fig. 3. Photomicrograph shows epidermal hyperplasia and infiltration ofPMNs and macrophages containing phagocytized PMNs. Metallic mercury appears as a dark black globule with a peripheral ring of birefringence. A thick eosinophilic homogeneous band (arrow) surrounds this mercury globule. (Hematoxylin-eosin stain, polarized; X75.)
The patient was admitted to the hospital for further surgery. All granulomatous tissue in the submental area and lymph nodes was removed. No further mercury deposits were found by fluoroscopic examination. The postoperative mercury level of urine was 25 J.LgjL (normal, 0 to 20 J.LgjL). The patient recovered without complications. During the I year follow-up period, he has been healthy and has had no recurrence. He shows no systemic signs or symptoms of mercury toxicity. Pathologic findings. The cut surfaces of the excised specimen revealed shiny metallic globules, flecks ofsilvery material, and fragments of glass embedded in the yellowtan tissue. Sections from the tissue revealed epidermal hyperplasia and an area of epidermal necrosis and ulceration. Opaque globules were noted in the dermis and subcutaneous tissue surrounded by numerous polymorphonuclear leukocytes (PMNs) and macrophages that contained phagocytic debris and nuclei of PMNs in the cytoplasm. These were surrounded by a fibroblastic and vascular proliferation and by a mixed cellular infiltrate of lymphocytes, plasma cells, and a few multinucleated giant cells (Fig. 3). A thick, homogeneous, eosinophilic, capsule-like material was observed around some opaque globules. Dense fibrosis was observed in the surrounding soft tissue. The opaque globules were dark at the center but had a peripheral ring of birefringence by polariscopy. The lymph nodes showed features ofreactive hyperplasia. Paraffin was removed from sections of the tissue taken from the paraffin block. These sections were covered with a coverslip coated with 50% reflecting gold. The coated surface was placed facing the tissue. The positive result was demonstrated as a dark zone around the spherical
Fig. 4. Findings of scanning electron microscopy show spherical globules of metallic mercury (arrow). droplets of metallic mercury in the section because of lysis of the gold that coated the coverslip. Scanning electron microscopy revealed ovoid or spherical globules characteristic of metallic mercury (Fig. 4). Energy-dispersive
Journal of the American Academy of Dermatology
918 Sau et al.
x-ray analysis of the globules yielded energies of x-rays characteristic for mercury. DISCUSSION
A review of the published literature on cutaneous mercury granuloma revealed that the tissue injury was caused either by a broken thermometer,3, 5, 9-11 as in our case, by an anaerobic blood sampling procedure in which mercury was used as a sealant in the syringes,12, 13 or by deliberate injection of metallic mercury. 1, 2, 4, 6, 7, 9, 14 In all cases there was a local tissue reaction characterized by acute and chronic inflammation, necrosis, foreign body granuloma, and abscess formation. The cutaneous tissue reaction to metallic mercury may remain localized as it did in the case described here. Cases described by Rachman, 5 Theodorou et a1.,ll Lanthem et aLp and cases land 3 described by Lupton et aL9 were in this category. Systemic absorption from cutaneous sites has resulted in elevated blood and urine levels of mercury but no evidence ofmercury poisoning as reported by Hill2 and Krohn et a1. 6 However, systemic absorption of metallic mercury from cutaneous sites can have serious consequences. Pulmonary embolism after the introduction of metallic mercury into the skin and subcutaneous tissue has been reported. 1, 7, 8,10,13,14 In a few cases they were associated with a fatal outcome. 1, 10 Metallic mercury embolism, however, was not always associated with serious consequences. Mercury may remain in the body tissue for long periods in some instances. 1 In several cases, serial x-ray films showed the gradual disappearance of the mercury. Recently Hargreaves et aL 15 reported persistent mercury in nerve cells 16 years after metallic mercury poisoning. The diagnosis of a cutaneous mercury granuloma from metallic mercury can be made easily if a history of injury with a mercury-containing object or of self-injection of mercury is obtained. In its absence, the diagnosis will depend on the examination of the tissue removed by surgery. Often metallic mercury can be seen in the cut section of the excised tissue. The gold lysis test, scanning electron microscopy findings, and emission spikes on energy-dispersive x-ray analysis are specific for the presence of mercury. The following guidelines for the management of cutaneous injury by metallic mercury are rec-
ommended.2, 6, 7, 9,16 Measurement of the mercury level of blood and urine should be made in all cases to determine systemiC absorption. 16 All readily accessible cutaneous and subcutaneous tissue suspected of containing mercury should be promptly excised. This is accomplished best under fluoroscopic guidance. Surgical excision of mercury granulomas will lower serum and urinary mercury concentrations. 2,6 Patients should have appropriate monitoring of central nervous system and renal function for evidence of mercurial toxicity. No specific therapy other than frequent follow-up examination is indicated for systemic emboli. 7 It is believed that the emboli are very slowly converted to metallic oxides and organic compounds of mercury and are then excreted by the kidneys. Chelation therapy is recommended if there is evidence of systemic toxicity. Dimercaprol is used for high levels of exposure or acute poisoning and N-acetyl-DL-penicillamine for the treatment of subacute or chronic mercury poisoning. Psychiatric consultation is recommended in cases of self-injection. REFERENCES 1. Johnson HRM, Koumides O. Unusual case of mercury poisoning. Br Med J 1967;1:340-1. 2. Hill DM. Self-administration of mercury by subcutaneous injection. Br Med J 1967;1:342-3. 3. Arcadio F, Thivolet J, Perrot H. Acrodynia following the accidental subcutaneous infiltration of mercury from a broken thermometer. Bull Soc Fr Dermatol Syphiligr 1968;75:509-10. 4. Kern FB, Condo F, Michel SL. Mercury granuloma with systemic absorption. JAMA 1972;222:88-9. 5. Rachman R. Soft-tissue injury by mercury from a broken thermometer: a case report and review of the literature. Am J Clin PathoI1974;61:296-300. 6. Krohn IT, Solof A, Mobini J, Wagner DK. Subcutaneous injection of metallic mercury. JAMA 1980;243:548-9. 7. Grenga TE, Peitrocola DM. Subcutaneous injection of mercury mimicking nodular melanoma. NY State J Moo 1982;82:1231-3. 8. Spizarny DL, Renzi P. Metallic mercury pulmonary emboli. J Can Radiol Assoc 1987;38:60-1. 9. Lupton GP, Kao GF, Johnson FB, Graham JH, Helwig EB. Cutaneous mercury granuloma: a clinicopathologic study and review of the literature. J AM ACAD DERMATOL 1985;12:296-303. 10. Popper L. Tod nach thermometerrverletzung. Wien Med Wochenschr 1960;116:779-80. 11. TheodorouSD, VlachosP, Vamvasakis E.Kneejointinjury by mercury from a broken thermometer. Clin Orthop 1981;160:159-62. 12. Lathem W, Lesser GT, Messinger WJ, Gladston M. Peripheral embolism by metallic mercury during arterial blood sampling. Arch Intern Med 1954;93:550-5. 13. Buxton JT Jr., Hewitt C, Gadsden RH, Bradham GB.
Volume 25 Number 5, Part 2 November 1991 Metallic mercury embolism: report of cases. JAMA 1965;193:103-5. 14. Conrad ME, Sanford JP, Preston JA. Metallic mercury embolism-clinical and experimental. Arch Intern Med 1957;100:59-65. 15. Hargreaves RJ, Evans JG, Janota I, et aI. Persistent mer-
Cutaneous reaction from a broken thermometer cury in nerve cells 16 years after metallic mercury poisoning. Neuropathol Appl NeurobioI1988;14:443-52. 16. Gilman AG, Goodman 1S. Heavy metals and heavy-metal antagonists. In: Gilman AG, Goodman LS, Rail TW, Murad F, eds. The pharmacological basis oftherapeutics. New York: Macmillan 1985:1611-4.
Cutaneous lesions of hemophagocytic syndrome in a patient with T-cell lymphoma and active Epstein-Barr infection Kathleen 1. Smith, LTC, MC, USA,a Henry G. Skelton III, CDR, MC, USN,b Walter L. Giblin, MAJ, MC, USA,c and William D. James, COL, MC, USAd Washington, D.C. The hemophagocytic syndrome (BPS) was first described in immune-compromised patients with secondary viral infections. Immunodeficiency has not always been diagnosed before the onset of HPS, but most patients who develop HPS have known immune deficits. HPS has also been reported in association with lymphoreticular malignancies. In HPS the most prominent histologic change is phagocytosis of red blood cells and other bone marrow-derived elements by cytologically benign histiocytes. Considerable confusion exists about the similarities and differences between HPS and other conditions in which hemophagocytosis may occur, for example, histiocytic medullary reticulosis, T-')' lymphoma, malignant histiocytic lymphoma, and cytophagic histiocytic panniculitis. We report a patient with HPS and cutaneous lesions of cytophagic histiocytic panniculitis who also had an active Epstein-Barr virus infection, and a CDS+ T-cell lymphoma. (J AM ACAD DERMATOL 1991;25:919-24.) The hemophagocytic syndrome (HPS) is a systemic disease characterized by fever, anemia, thrombocytopenia, leukopenia, hepatosplenomegaly, lymphadenopathy, and in most cases, a coagulopathy.l Histologically there is histiocytic proliferation throughout the reticuloendothelial system that involves most prominently the bone marrow, splenic
From the Walter Reed Army Institute of Research,' Department of Dermatopathology. Armed Forces Institute ofPathology,b the Dermatology Service, Fort Dix, New Jersey,C and the Department of Dermatology, Walter Reed Army Medical Center. d The opinions or assertions contained herein are the private views of the authors and not to be considered as official or as reflecting the views of the Departments of the Army or Navy or of the Department of Defense. Reprint requests: CDR Henry G. Skelton III, MC, USN, Department of Dermatopathology, Armed Forces Institute of Pathology, Washington, DC 20306.
16/4/30246
red pulp, hepatic sinusoids, and lymph node sinuses, and, in some patients also the skin. 1 The histiocytes are cytologically benign. They have abundant cytoplasm and may contain few to numerous phagocy~ tosed red blood cells and less frequently lymphocytes, neutrophils, platelets, and nuclear fragments. Cutaneous lesions in patients with HPS principally involve the subcutaneous fat and contain the same benign phagocytosinghistiocytes. Patients withthese lesions are given the diagnosis of cytophagic histiocytic panniculitis. 2-10 Although HPS was originally described in immune-suppressed patients with a primary or reactivated viral infection, patients with vast bacterial, fungal, and parasitic infections have also developed HPS.l, 11 Immune deficits that predispose patients to BPS may be congenital or iatrogenically induced such as in organ transplant recipients. In addition, patients with lymphoid neoplasms may
919
