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Treatment of fibrositis with fluoxetine hydrochloride (Prozac®)
BRIEF CLINICAL
OBSERVATIONS
Figure scopic
tunately, survivors may be left with significant motor and sensory impairment re uiring long-term rehabilitation P161. Therapy generally requires early neurosurgical drainage with high-dose intravenous penicillin, metronidazole, or a similar regimen directed against the aforementioned microbiologic flora. Corticosteroids and anticonvulsants may be required to control cerebral edema and seizures [10,16]. We believe this case represents a complication of esophageal sclerotherapy that has not previously been documented. This case emphasizes the need for awareness of the possibility of remote (in this case intracranial) infectious complications in patients undergoing endoscopic injection sclerotherapy. THOMAS N. DEWAR, CLINTON E. THOMPSON, NATHAN M. BASS, M.D.,
M.D. M.D. Ph.D.
University
of California, San Francisco San Francisco, California
l.Schuman BM. Belkman JW. Tedesco FJ. et at Complications of endoscopic injection sclerolherapy. A review. Am J Gastroenterol 1987; 82: 823-830. 2. Ayres SJ, Gaff JS. Warren GH: Endoscopic sclerotherapy for bleeding esophageal varices; effects and complications. Ann Intern Med 1983: 98: 900-903. 3. Brayko CM, Kozarek RA, Sanowski RA. et ab Bacteremia during esophageal variceal sclerotherapy; its cause and prevention. Gastrointest Endosc 1985; 31: 10-12.
594
November
1989
The American
Journal
4. Snady H. Korsten MA. Waye JD: The relationship of bacteremia to the length of injection needle in endoscopic variceal sclerotherapy. Gastrointest Endosc 1985; 31: 243-246. 5. Camara DS. Gruber M, Barde CJ. et at Transient bacteremiafollowingendoscopicinjection sclerotherapy of esophageal varices. Arch Intern Med 1983: 143: 1350-1352. 6. Sauerbruch T. Holl J, Ruckdeschel G. efat Bacteraemia associated with endoscopic sclerotherapy of esophageal varices. Endoscopy 1985: 17: 170-172. 7. Low DE, Shoenut JP. Kennedy JK. et ah Infectious complications of endoscopic injection sclerotherapy. Arch Intern Med 1986: 146: 569-571. 8. Lange S. Laughlin 8. Hughes R. efat Septic complications of variceal hemorrhage and ethanolamine scferotherapy of varices (abstr). Gastrointest Endosc 1983; 29: 191. 9. Cohen FL, Koerner RS. Taub SJ: Solitary brain abscess following endoscopic injection sclerosis of esophageal varices. Gastrointest Endosc 1985; 31: 331-333. 10. Benson CA, Harris AA: Acute neurologic infections. Med Clin North Am 1986; 70: 987-1011. 11. Harris LF. Haws FP. Truplett JN. et al Subdural empyema and epidural abscess: recent experience in a community hospital. South Med J 1987; 80: 12541258. 12. Ariza J. Casanova P. Vladrich PF. efat Etiological agent and primary source of infection in 42 cases of focal intracranial suppuration. J Clin Microbial 1986:
24: 899-902. 13. Miller ES, Dias PS. Utley D: Management of subdural empyema: a series of 24 cases. J Neural Neurosurg Psychiatry 1987; 50: 1415-1418. 14. Farkas AG. Marks JC: Subdural empyema: an important diagnosis not to miss. Br Med J 1986; 293: 118-119. 15. Mauser HW, Van Houwelingen HC. Tufleken CAF: Factors affecting the outcome in subdural empyema. J Neural Neurosurg Psychiatry 1987; 50: 11361141. 16. Weisberg L: Subdural empyema. Arch Neurol 1986; 43: 497-500. SubmittedMay31.1989.andaccepted
of Medicine
Volume
July25.1989
87
1. Subdural sclerotherapy.
empyema
after
endo-
TREATMENT OF FIBROSITIS WITH FLUOXETINE HYDROCHLORIDE (PROZAC=) Fibrositis is a common clinical syndrome that has been difficult to treat in the past. Standard treatment has been amitriptyline (Elavii@) and cyclobenzaprine (Flexeril@), but they have been only moderately successful. We report on a patient who did not respond to amitriptyline or cyclobenzaprine but who was completely cured by fluoxetine hydrochloride (Prozac@). A 29-year-old white female patient was first seen in September 1988when she complained of neck stiffness, difficulty in sleeping, and muscle tenderness. Physical examination revealed multiple tender points but results were otherwise unremarkable. Findings on laboratory studies were entirely normal, including a complete blood count, SMA-19, erythrocyte sedimentation rate, thyroid function tests, antinuclear antibody, rheumatoid factor, and lumbar sacral spine radiographs. Two independent rheumatology consultations produced a diagnosis of fibrositis. Treatment was initiated with amitriptyline, cyclobenzaprine, TENS unit, and multiple nonsteroidal anti-inflam-
BRIEF CLINICAL
matory drugs, but there was no relief of the muscle tenderness or other symptoms. She was then treated with fluoxetine hydrochloride at a dose of 20 mglday, which was later increased to 40 mglday, and she experienced complete relief over a period of about one month. Six months of follow-up have shown no recurrence of the symptoms of fibrositis. This is the first documented report of successful treatment of fibrositis with fluoxetine hydrochloride. There have been suggestions that the sleep disturbances in fibrositis may be related to serotonin metabolism [l]. Another study also suggested that abnormal serotoninergic mechanisms were responsible for the pain of fibrositis [2]. Fluoxetine hydrochloride is known to block reuptake of serotonin in the brain. Therefore, it is not surprising that fluoxetine hydrochloride was beneficial in treating fibrositis in this case. STEVENA.GELLER,M.D. Howard County General Hospital Cotumbia, Marytand 21044 1. Moldofsky H: Sleep and musculoskeletal pain. Am J Med 1986; 81 (suppl3A): 85-89. 2. Moldofsky H. Warsh JJ: Plasma byptophan and musculoskeletal pain in non-articular rheumatism (“fibrositis syndrome”). Pain 1978: 5: 65-71. Submitted
June
22. 1989,
and accepted
July 31. 1989
ECTHYMA GANGRENOSUM IN THE ABSENCE OF PSEUDOMONAS BACTEREMIA IN A BONE MARROW TRANSPLANT RECIPIENT The association between systemic Pseudomonas aeruginosa infections and the characteristic necrotic skin lesions of ecthyma gangrenosum is well known. This bacterium, commonly isolated from hospital environments, seems to have a predilection to cause infection in patients with leukemia, severe burns, neutropenia, or organ transplant, or in those receiving immunosuppressive therapy. Lesions that appear during the course of P. aeruginosa-associated septicemia often portend a potentially life-threatening infection. However, in recent years, a number of reports have described patients with ecthyma gangrenosum who have no evidence of bacteremia and therefore have a better prognosis
[l-5]. In this article we describe such a patient with an unusual presentation of localized cutaneous pseudomonas infection, and offer several possibilities as to its origin. Case Report. A 29-year-old man who had undergone allogeneic bone marrow transplantation in 1986 for myelodysplastic syndrome was hospitalized on October 19, 1988, with chills, rigors, and a temperature of 39.4”C. He had returned from a brief Caribbean vacation two days before admission, when he noted crusting scabs on his forehead and the development of slightly painful and pruritic weeping lesions in the groin, which failed to improve after treatment with hydrogen peroxide and topical steroids. He had no history of trauma, insect or animal bites, or any hot tub exposure during his trip; however, he did recall the presence of mites in his hotel room. No one else on the trip became ill. The patient denied any other associated symptoms. Medications included cyclosporin A and penicillin VK for pneumococcal prophylaxis. Physical examination revealed a well-developed white man with an oral temperature of 38.6”C, who appeared comfortable and otherwise had normal vital signs. Several crusted, excoriated areas were noted at the hairline over both temples. The suprapubic region demonstrated multiple tender, weeping papulovesicular lesions. He had no significant adenopathy. The lungs were clear, and a grade 216 systolic murmur was appreciated at the apex. The abdomen was benign, and findings on rectal examination were nontender with heme-negative stool. The hemoglobin level was 11.9 g/ dL, the white blood cell count was 6,800/mm3 with 53% segmented neutrophils, 27% lymphocytes, 19% monocytes, and 1% eosinophils, and the platelet count was 103,000/ mm3. The erythrocyte sedimentation rate was 11 nun/hour. Liver function tests, known to demonstrate abnormal findings secondary to chronic graft-versus-host disease, revealed an alkaline phosphatase level of 773 IU/mL, lactate dehydrogenase level of 682 IU/mL, and serum glutamic oxaloacetic transaminase level of 83 IU/mL. The serum creatinine level was 1.4 mg/dL, and a chest roentgenograrn was normal. The patient was seen in consulNovember
1989
OBSERVATIONS
tation by a dermatologist, who believed the lesions to be most consistent with bullous impetigo. However, while the results of cultures of blood, urine, and skin lesions were pending, antibiotic therapy with nafcillin, cefotaxime, and acyclovir was initiated. Results of blood and urine cultures remained negative, but Staphylococcus aureus (sensitive to nafcillin) was isolated from the skin lesions. Antibiotic therapy was changed to vancomycin alone because of a question of a 8-lactaminduced cutaneous drug eruption manifested by a diffuse erythematous papular rash and peripheral eosinophilia. Viral cultures of the skin lesion failed to reveal herpes infection, and acyclovir was discontinued. Within a couple of days the rash and original skin lesions resolved, but on the seventh hospital day, the patient became febrile to 405°C and complained of new painful bullous lesions over both upper medial thighs and pubic area, with each lesion measuring approximately 1 cm in diameter. These bullae soon became hemorrhagic and developed central black eschars with surrounding erythema (Figures 1 and 2), consistent with ecthyma gangrenosum. He also noted some perirectal tenderness, although no lesions were evident. Blood cultures remained negative, but a culture of biopsy material from the new lesions grew P. aeruginosa. Antibiotics were changed to aztreonam and tobramycin, and clindamycin was added because there was concern about a perirectal process. The patient had rapid defervescence, and the lesions began to slowly resolve. An abdominal computed tomographic scan failed to reveal any perirectal collection, but Clostridium difficjle toxin was isolated from the stool, and the patient was treated with oral vancomycin. After 14 days of in-hospital therapy for his ecthyma gangrenosum, the patient was discharged to receive another two weeks of axtreonam and tobramycin via home intravenous theraPYComments. Ecthyma gangrenosum represents a vasculitis caused by direct bacterial invasion of tissue. Although the most common etiologic agent is P. aeruginosa, similar lesions have been described in infections caused by Aeromonas hydrophila, S. aureus, Serratia marcescens, Escherichia coli, and,
The American
Journal
of Medlclne
Volume
97
595
OBSERVATIONS
Figure scopic
tunately, survivors may be left with significant motor and sensory impairment re uiring long-term rehabilitation P161. Therapy generally requires early neurosurgical drainage with high-dose intravenous penicillin, metronidazole, or a similar regimen directed against the aforementioned microbiologic flora. Corticosteroids and anticonvulsants may be required to control cerebral edema and seizures [10,16]. We believe this case represents a complication of esophageal sclerotherapy that has not previously been documented. This case emphasizes the need for awareness of the possibility of remote (in this case intracranial) infectious complications in patients undergoing endoscopic injection sclerotherapy. THOMAS N. DEWAR, CLINTON E. THOMPSON, NATHAN M. BASS, M.D.,
M.D. M.D. Ph.D.
University
of California, San Francisco San Francisco, California
l.Schuman BM. Belkman JW. Tedesco FJ. et at Complications of endoscopic injection sclerolherapy. A review. Am J Gastroenterol 1987; 82: 823-830. 2. Ayres SJ, Gaff JS. Warren GH: Endoscopic sclerotherapy for bleeding esophageal varices; effects and complications. Ann Intern Med 1983: 98: 900-903. 3. Brayko CM, Kozarek RA, Sanowski RA. et ab Bacteremia during esophageal variceal sclerotherapy; its cause and prevention. Gastrointest Endosc 1985; 31: 10-12.
594
November
1989
The American
Journal
4. Snady H. Korsten MA. Waye JD: The relationship of bacteremia to the length of injection needle in endoscopic variceal sclerotherapy. Gastrointest Endosc 1985; 31: 243-246. 5. Camara DS. Gruber M, Barde CJ. et at Transient bacteremiafollowingendoscopicinjection sclerotherapy of esophageal varices. Arch Intern Med 1983: 143: 1350-1352. 6. Sauerbruch T. Holl J, Ruckdeschel G. efat Bacteraemia associated with endoscopic sclerotherapy of esophageal varices. Endoscopy 1985: 17: 170-172. 7. Low DE, Shoenut JP. Kennedy JK. et ah Infectious complications of endoscopic injection sclerotherapy. Arch Intern Med 1986: 146: 569-571. 8. Lange S. Laughlin 8. Hughes R. efat Septic complications of variceal hemorrhage and ethanolamine scferotherapy of varices (abstr). Gastrointest Endosc 1983; 29: 191. 9. Cohen FL, Koerner RS. Taub SJ: Solitary brain abscess following endoscopic injection sclerosis of esophageal varices. Gastrointest Endosc 1985; 31: 331-333. 10. Benson CA, Harris AA: Acute neurologic infections. Med Clin North Am 1986; 70: 987-1011. 11. Harris LF. Haws FP. Truplett JN. et al Subdural empyema and epidural abscess: recent experience in a community hospital. South Med J 1987; 80: 12541258. 12. Ariza J. Casanova P. Vladrich PF. efat Etiological agent and primary source of infection in 42 cases of focal intracranial suppuration. J Clin Microbial 1986:
24: 899-902. 13. Miller ES, Dias PS. Utley D: Management of subdural empyema: a series of 24 cases. J Neural Neurosurg Psychiatry 1987; 50: 1415-1418. 14. Farkas AG. Marks JC: Subdural empyema: an important diagnosis not to miss. Br Med J 1986; 293: 118-119. 15. Mauser HW, Van Houwelingen HC. Tufleken CAF: Factors affecting the outcome in subdural empyema. J Neural Neurosurg Psychiatry 1987; 50: 11361141. 16. Weisberg L: Subdural empyema. Arch Neurol 1986; 43: 497-500. SubmittedMay31.1989.andaccepted
of Medicine
Volume
July25.1989
87
1. Subdural sclerotherapy.
empyema
after
endo-
TREATMENT OF FIBROSITIS WITH FLUOXETINE HYDROCHLORIDE (PROZAC=) Fibrositis is a common clinical syndrome that has been difficult to treat in the past. Standard treatment has been amitriptyline (Elavii@) and cyclobenzaprine (Flexeril@), but they have been only moderately successful. We report on a patient who did not respond to amitriptyline or cyclobenzaprine but who was completely cured by fluoxetine hydrochloride (Prozac@). A 29-year-old white female patient was first seen in September 1988when she complained of neck stiffness, difficulty in sleeping, and muscle tenderness. Physical examination revealed multiple tender points but results were otherwise unremarkable. Findings on laboratory studies were entirely normal, including a complete blood count, SMA-19, erythrocyte sedimentation rate, thyroid function tests, antinuclear antibody, rheumatoid factor, and lumbar sacral spine radiographs. Two independent rheumatology consultations produced a diagnosis of fibrositis. Treatment was initiated with amitriptyline, cyclobenzaprine, TENS unit, and multiple nonsteroidal anti-inflam-
BRIEF CLINICAL
matory drugs, but there was no relief of the muscle tenderness or other symptoms. She was then treated with fluoxetine hydrochloride at a dose of 20 mglday, which was later increased to 40 mglday, and she experienced complete relief over a period of about one month. Six months of follow-up have shown no recurrence of the symptoms of fibrositis. This is the first documented report of successful treatment of fibrositis with fluoxetine hydrochloride. There have been suggestions that the sleep disturbances in fibrositis may be related to serotonin metabolism [l]. Another study also suggested that abnormal serotoninergic mechanisms were responsible for the pain of fibrositis [2]. Fluoxetine hydrochloride is known to block reuptake of serotonin in the brain. Therefore, it is not surprising that fluoxetine hydrochloride was beneficial in treating fibrositis in this case. STEVENA.GELLER,M.D. Howard County General Hospital Cotumbia, Marytand 21044 1. Moldofsky H: Sleep and musculoskeletal pain. Am J Med 1986; 81 (suppl3A): 85-89. 2. Moldofsky H. Warsh JJ: Plasma byptophan and musculoskeletal pain in non-articular rheumatism (“fibrositis syndrome”). Pain 1978: 5: 65-71. Submitted
June
22. 1989,
and accepted
July 31. 1989
ECTHYMA GANGRENOSUM IN THE ABSENCE OF PSEUDOMONAS BACTEREMIA IN A BONE MARROW TRANSPLANT RECIPIENT The association between systemic Pseudomonas aeruginosa infections and the characteristic necrotic skin lesions of ecthyma gangrenosum is well known. This bacterium, commonly isolated from hospital environments, seems to have a predilection to cause infection in patients with leukemia, severe burns, neutropenia, or organ transplant, or in those receiving immunosuppressive therapy. Lesions that appear during the course of P. aeruginosa-associated septicemia often portend a potentially life-threatening infection. However, in recent years, a number of reports have described patients with ecthyma gangrenosum who have no evidence of bacteremia and therefore have a better prognosis
[l-5]. In this article we describe such a patient with an unusual presentation of localized cutaneous pseudomonas infection, and offer several possibilities as to its origin. Case Report. A 29-year-old man who had undergone allogeneic bone marrow transplantation in 1986 for myelodysplastic syndrome was hospitalized on October 19, 1988, with chills, rigors, and a temperature of 39.4”C. He had returned from a brief Caribbean vacation two days before admission, when he noted crusting scabs on his forehead and the development of slightly painful and pruritic weeping lesions in the groin, which failed to improve after treatment with hydrogen peroxide and topical steroids. He had no history of trauma, insect or animal bites, or any hot tub exposure during his trip; however, he did recall the presence of mites in his hotel room. No one else on the trip became ill. The patient denied any other associated symptoms. Medications included cyclosporin A and penicillin VK for pneumococcal prophylaxis. Physical examination revealed a well-developed white man with an oral temperature of 38.6”C, who appeared comfortable and otherwise had normal vital signs. Several crusted, excoriated areas were noted at the hairline over both temples. The suprapubic region demonstrated multiple tender, weeping papulovesicular lesions. He had no significant adenopathy. The lungs were clear, and a grade 216 systolic murmur was appreciated at the apex. The abdomen was benign, and findings on rectal examination were nontender with heme-negative stool. The hemoglobin level was 11.9 g/ dL, the white blood cell count was 6,800/mm3 with 53% segmented neutrophils, 27% lymphocytes, 19% monocytes, and 1% eosinophils, and the platelet count was 103,000/ mm3. The erythrocyte sedimentation rate was 11 nun/hour. Liver function tests, known to demonstrate abnormal findings secondary to chronic graft-versus-host disease, revealed an alkaline phosphatase level of 773 IU/mL, lactate dehydrogenase level of 682 IU/mL, and serum glutamic oxaloacetic transaminase level of 83 IU/mL. The serum creatinine level was 1.4 mg/dL, and a chest roentgenograrn was normal. The patient was seen in consulNovember
1989
OBSERVATIONS
tation by a dermatologist, who believed the lesions to be most consistent with bullous impetigo. However, while the results of cultures of blood, urine, and skin lesions were pending, antibiotic therapy with nafcillin, cefotaxime, and acyclovir was initiated. Results of blood and urine cultures remained negative, but Staphylococcus aureus (sensitive to nafcillin) was isolated from the skin lesions. Antibiotic therapy was changed to vancomycin alone because of a question of a 8-lactaminduced cutaneous drug eruption manifested by a diffuse erythematous papular rash and peripheral eosinophilia. Viral cultures of the skin lesion failed to reveal herpes infection, and acyclovir was discontinued. Within a couple of days the rash and original skin lesions resolved, but on the seventh hospital day, the patient became febrile to 405°C and complained of new painful bullous lesions over both upper medial thighs and pubic area, with each lesion measuring approximately 1 cm in diameter. These bullae soon became hemorrhagic and developed central black eschars with surrounding erythema (Figures 1 and 2), consistent with ecthyma gangrenosum. He also noted some perirectal tenderness, although no lesions were evident. Blood cultures remained negative, but a culture of biopsy material from the new lesions grew P. aeruginosa. Antibiotics were changed to aztreonam and tobramycin, and clindamycin was added because there was concern about a perirectal process. The patient had rapid defervescence, and the lesions began to slowly resolve. An abdominal computed tomographic scan failed to reveal any perirectal collection, but Clostridium difficjle toxin was isolated from the stool, and the patient was treated with oral vancomycin. After 14 days of in-hospital therapy for his ecthyma gangrenosum, the patient was discharged to receive another two weeks of axtreonam and tobramycin via home intravenous theraPYComments. Ecthyma gangrenosum represents a vasculitis caused by direct bacterial invasion of tissue. Although the most common etiologic agent is P. aeruginosa, similar lesions have been described in infections caused by Aeromonas hydrophila, S. aureus, Serratia marcescens, Escherichia coli, and,
The American
Journal
of Medlclne
Volume
97
595