BRIEF CLINICAL OBSERVATIONS
cal suspicion, and the diagnosis can be missed.Danner and Hartman [8] found that the correctdiagnosisof spinal epidural abscess was made initially in only 17.9% of cases.Fortunately, the history of a recent epidural catheter and the neurologicfindings in our patient suggestedthe possibility of an epidural process,and emergent diagnostic and therapeutic measureswere performed. The bacteriology of spinal epidural abscessesis somewhatvaried, with Staphylococcus aureus the most common pathogen isolated [9]. Although streptococci have been found, group G streptococci have not been reported. The most common sites of infection with group G streptococci are the skin and soft tissues [9]. During delivery, colonization of the skin and contamination by the vaginal flora with group G streptococci with introduction into the epidural spaceby the anesthesiacatheter is the probable sourceof infection in our patient. In general, spinal epidural abscessis a rare complication of spinal anesthesia [lo]. Of interest, there are also several reports of postpartum spinal epidural abscessnot related to epidural anesthesia [11,12]. Our case report describes a catheter-relatedgroup G streptococcalspinal epidural abscess,an associationnot previouslyreported in our review of the literature. More significantly, it underscores againthe importance of early diagnosisand treatment. Heusner [7] and others have shown that diagnosisand intervention in the earlier phasesof spinal epidural abscess lead to favorable outcomes,while those patients diagnosedin the later phasescan experience irreversible neurologic damageand evendeath. Furthermore, delays in diagnosis have preventedreduction in morbidity and mortality despite improvements in therapy over the de90
cades[7,8].The patient discussed here did well after presenting in phase 2 of Heusner’s classification becauseof prompt diagnosis and treatment. LINAS M. KLYGIS, M.D. BORIS E. REISBERG, M.D.
Northwestern Memorial Hospjtal Northwestern University M;fed;zE Chicago, Illinois 1. Lancefield RC, Hare R. The serological differentiation of pathogenic and nonpathogenic strains of hemolytic streptococci from parturient women. J Exp Med 1935; 61: 335-49. 2. Vartian C, Lerner PI. Shlaes DM, Gopalakrishna KV. Infections due to Lancefield group G streptococci. Medicine (Baltimore) 1985; 64: 75-88. 3. Duma RJ, Weinberg AN, Medrek TF, Kunz LJ. Streptococcal infections: a bacteriologicand clinical study of streptococcal bacteremia. Medicine (Baltimore) 1969; 48: 87-127. 4. Lam K, Bayer AS. Serious infections due to group G streptococci: report of 15 cases with in vitro-in viva correlations. Am J Med 1983; 75: 561-70. 5. Gossling J. Occurrence and pathogenicity of the Streptococcus millen’ group. Rev Infect Dis 1988; 10: 257-85. 6. Dandy WE. Abscesses and inflammatory tumors in the spinal epidural space (so-called pachymeningitis externa). Arch Surg 1926; 13: 477-94. 7. Heusner AP. Nontuberculous spinal epidural infections. N Engl J Med 1948; 239: 845-54. 8. Danner RL, Hartman BJ. Update of spinal epidural abscess: 35 cases and review of the literature. Rev Infect Dis 1987; 9: 265-74. S.Kaufman DM. Kaplan JG. Litman N. Infectious agents in spinal epidural abscesses. Neurology 1980; 30: 844-50. 10. North JB, Brophy BP. Epidural abscess: a hazard of spinal epidural anaesthesia. Aust NZ J Surg 1979: 49: 484-5. 11. Male CG, Martin R. Puerperal spinal epidural abscess. Lancet 1973; 1: 608-9. 12. Crawford JS. Pathology in the extradural space. Br J Anaesth 1975; 47: 412-5. Submitted
May 23, 1990, and accepted in revised form February 5, 1991
LOCALIZEDRHEUMATOID VASCULITISPRESENTINGAS ACUTE ALITHIASIC CHOLECYSTITIS Rheumatoid arthritis is occasionally complicatedby systemicnecrotizing vasculitis indistinguishable pathologically from the primary forms of polyarteritis nodosa (PAN) [l]. Although lo-
July 1991 The American Journal of Medicine
Volume 91
calizedforms are not uncommon, only one case of localized rheumatoid vasculitis of the gallbladder has been reported [2]. Our patient was a 69-year-old woman with a history of hypertension, atria1 fibrillation, and seropositive erosive rheumatoid arthritis with subcutaneousnodules since 11 years previously. She received nonsteroidal antiinflammatory drugs (NSAIDs), corticosteroids,and aurothiomalate, remaining in clinical and analytical remissionuntil 6 months ago,when shepresentedwith intense constitutional symptoms, anemia, and an increase in the erythrocyte sedimentation rate (ESR) with no arthritis. She was admitted to our hospital in a state of shock from a bleeding gastric ulcer, for which surgery was immediately performed. During the postoperativeperiod, she had supraventricular tachycardia, congestiveheart failure, and a high temperature.She was treated with antibiotics, but blood, urine, and intravenous catheter cultures performed previously were all negative.On the 10th postoperativeday, with the temperature still high, the patient developeddiffuse abdominal pain, and there wasa general overall worsening, hypotension, and oligoanuria.Echographyand abdominal computed tomography revealed a distended gallbladder with no calculi and two collections of liquid, one surrounding it and the other in the right ileac fossa.A culture on 15 mL of bile extracted from this latter site by needlepuncturewas negative. Cholecystectomy was carriedout, but the generalstate, anasarca, and fever persisted with no apparent septic focus. Laboratory studies showed the following values: leukocytosis 40 X log/L (granulocytes96.7%),hemoglobin 114g/L, platelets 525X log/L, reticulocytes 30 per 1,000, ESR 69 mm/hour, glucose 8.8
BRIEF CLINICAL
OBSERVATIONS
Figure 1. Gallbladder biopsy specimen showing focal fibrinoid necrosis and infiltration of all layers of the wall of the vessel by chronic inflammatory cells, predominantly lymphocytes (hematoxylin-eosin stain; original magnification X10, reduced by 5%).
mmol/L, urea 36.4 mmol/L, creatinine 106 pmol/L, sodium 147 mmol/L, potassium 3.4 mmol/L, chloride 106 mmol/L, lactate dehydrogenase776IU/L, and total bilirubin 22 hmol/L. Creatine phosphokinase, alkaline phosphatase, glutamic oxaloacetic transaminase, glutamic pyruvic transaminase,y-glutamyl transferase, cholesterol, triglycerides, calcium, phosphorus,coagulation study results, cryoglobuhns,haptoglobin, antinuclear antibody, and hepatitis B virus markers were all either within the normal range or negative. Other values were as follows: total protein 48 g/L, albumin 22.6 g/L, al-globulins 4.1 g/L, ag-globulins6.3 g/L, &globulins 3.8 g/L, yglobulins 11 g/L, IgG 7.1 g/L, IgA 1.6 g/L, IgM 1.9g/L, C3 0.41g/L, and C4 undetectable.Rheumatoid factor by latex testing was 1,210IU/mL and the result of a Coombs’ test waspositive. Urine and sediment were normal. Pathologic examination showeda gallbladder with no calculi and with a greenish, somewhatulcerated mucoussurface. Histologically, the normal mucosaalternatedwith ulcerated areas and the submucosahad a disperse lymphocytic infiltrate (Figure 1).There wasa widening
of the walls of the small- and medium-sizedvessels,with fibrinoid necrosisand abundant mixed inflammatory infiltrates with a predominance of perivascular lymphocytes.Administration of 500 mg of intravenous GM-prednisolone was added to the treatment regimen followed by 80 mg/day. The temperature returned to normal in 24 hoursand the metabolic disturbancesweregradually corrected.Three weekslater, she tolerated oral feeding and was in a generally good state, and the steroid dose was reduced. Her temperature once again roseand morethan lo5 coloniesof Enterococcus faecalis and Pseudomonas aeruginosa were isolated in the urine; this colonization was satisfactorily treated. The prednisone dosagewas gradually reduced over the next 3 weeks,but fever,productive cough,and dyspnea developed.Chest radiography showed bilateral bronchopneumonia. Despite treatment for septic shock and respiratory failure, the patient died 4 days later. Permission for autopsywas denied. Acute cholecystitis due to vasculitis has been reported previously as a manifestation of PAN [3], in systemic lupus erythemaJuly 1991
The American
tosus [4], and in giant cell arthritis [5], among other conditions, but only in onecaseasa localized form of rheumatoid vasculitis [2]. As well as having infarctions in the gallbladder, our patient had anemia, thrombocytosis, elevated ESR, hypocomplementemia, and increasedrheumatoid factor titer, supporting the diagnosisof rheumatoid vasculitis [1,6]. Severe hematemesis is a common manifestation of upper gastrointestinal tract vasculitis [l], but it is also responsible for the high morbidity and mortality that NSAIDs producein personsolder than 60 years of age [7]. Since both thesephenomenawere present in our patient and no histologic examination of the ulcus wascarried out, vasculitis cannot be ruled out as a causeof the hematemesis. Hypovolemic shock, previous surgery, and prolonged fast are etiopathogenicfactors in alithiasic cholecystitis [8], which, occurring in addition to a previously ischemicgallbladder due to vasculitis, could have been responsiblefor the exclusiveaffection of this organ in this case.In conclusion,our patient presented with rheumatoid vasculitis with localized affection of the gallbladder,aggravatedby complicaJournal
of Medicine
Volume
91
91
BRIEF CLINICAL
OBSERVATIONS
tions resulting from shock secondary to upper digestive tract hemorrhage.
A 23-year-old woman presented to the Bellevue Hospital Emergency Department with 3 ANTONIO FERNANDEZ-NEBRO,M.D. days of pleuritic right upper PEDROVALDIVIELSO;M.D. quadrant pain. The patient had JUANJ. SANCHEZ-CARRILLO.P~.D. no other symptoms. She had no Virgen de la Victoria Hospital School of Medicine history of previous illness, recent INESDOMENECH, M.D. immobilization, or oral contraENRIQVE DE RAMON, M.D. ceptive use. Physical examinaRegional Hospital of S.A.S. PEDROGONZALEZ-SANTOS,M.D. tion was notable for a healthy-apVirgen de la Victoria Hospital pearing young woman in moderSchool of Medicine Malaga, Spain ate pain. The blood pressure was 124/80 mm Hg, pulse 92/minute, 1. Conn DL. Hunder GG. Vasculitis and related disorrespirations 28/minute, and ders. In: Kelley WN, Harris ED Jr, Ruddy S, Sledge CB, editors. Textbook of rheumatology. 3rd ed. rectal temperature 37.9”C Philadelphia: WB Saunders, 1989: 1167-99. (100.3”F). The chest was clear 2. Fayemi AO, Ali M. Braun EV. Necrotizingvasculitis and the heart sounds were norof the gallbladder and the appendix. Similarity in the mal. There was mild right upper morphology of rheumatoid arteritis and polyarteritis nodosa. Am J Gastroenterol 1977; 67: 608-12. quadrant tenderness to deep pal3. Li Volsi VA, Perzin KH, Porter M. Polyarteritis nopation and mild right costovertedosa of the gallbladder, presenting as acute cholebra1 angle tenderness. Results of cystitis. Gastroenterology 1973; 65: 115. pelvic examination were unre4. Swanepoel C. Floyd A, Allison H. Learmonth GM, Cassidy MJD. Pascoe MD. Acute acalculous cholemarkable. An intrauterine device cystitis complicating systemic lupus erythematowas in place. The extremities sus: case report and review. BMJ 1983; 286: 251-2. were normal. An electrocardio5. Papaioannou CC, Hunder GG. Lie JT. Vasculitis of gram, urinalysis results, complete the gallbladder in a 70 year old man with giant cell arteritis. J Rheumatol 1979; 6: 1. blood count, and electrolyte lev6. Scott DGI. Bacon PA, Tribe CR. Systemic rheuels were unremarkable. A serum matoid vasculitis: a clinical and laboratory study of pregnancy test was negative. A 50 cases. Medicine (Baltimore) 1981; 60: 28&97. room-air arterial blood gas study 7. Barrier CH, Hirschowitz BI. Controversies in the detection and management of nonsteroidal antiinshowed a pH of 7.41, a partial carflammatory drug-induced side effects of the upper bon dioxide pressure of 36 mm gastrointestinal tract. Arthritis Rheum 1989; 32: Hg, and a partial oxygen pressure 926-32. 6. Way LW. Sleisenger MH. Cholelithiasis; chronic of 109 mm Hg. The initial chest and acute cholecystitis. In: Sleisenger MH, Fordtran radiograph was normal. Further JS. editors. Gastrointestinal diseases. 4th ed. Philaquestioning revealed that the padelphia: WB Saunders, 1989: 1691-714. tient had recently used crack coSubmitted October 29, 1990, and accepted in recaine. There was no history of invised form February 15. 1991 travenous drug use. A urine toxicology screen was positive for a cocaine metabolite. A pulmonary ventilation-perfusion scan was ordered because of the clinical impression of diaphragmatic irriPULMONARYINFARCTION tation. The perfusion scan (FigASSOCIATEDWITH CRACK ure 1) demonstrated two unCOCAINEUSE IN A matched subsegmental defects in PREVIOUSLYHEALTHY the right lower lung, and intrave23-YEAR-OLDWOMAN nous heparin therapy was begun. A pulmonary angiogram (Figure Cocaine-associated ischemic in- 2) showed a large vascular objury has been documented in struction in the area that was premany organ systems [l-7]. We viously implicated by the ventiladescribe the first reported case of tion-perfusion scan. Hemoptysis pulmonary infarction associated occurred on the second day. Heparin was discontinued and a with “crack” cocaine use. 92
July
1991 The American
Journal
of Medicine
Volume
91
Greenfield filter was inserted. Subsequent pelvic ultrasonography, echocardiography, and Doppler plethysmography failed to reveal any source of emboli. Fever developed on the third day. A computed tomographic scan of the chest revealed a loculated pleural effusion with partial collapse of the right lower lobe. Thoracentesis yielded brown fluid with a pH of 6.9, lactate dehydrogenase of 481 IU, protein of 4 g/dL, glucose of 11 mg/dL, and a white blood cell count of 25/mm3. Results of repeated bacteriologic studies remained negative. Thoracotomy revealed a fibrinous peel entrapping all three lobes, and infarction of 20% of the right lower lobe. After decortication, the patient recovered without further complications. The mechanisms of cocaine-related ischemic injury are multifactorial. Phentolamine-reversible arterial spasm has been demonstrated during cardiac catheterization following administration of therapeutic doses of cocaine [8]. Recurrent episodes of silent myocardial ischemia attributed to dopamine-mediated vasospasm were documented by Holter monitoring in 38% of chronic cocaine users during a 2week withdrawal period [9]. Late angiography in patients with cocaine-related acute myocardial infarction frequently reveals normal vessels, suggesting vasospasm as an associated event [lO,ll]. Cocaine-induced vasospasm also occurs independent of a-receptor stimulation and can be blocked by calcium channel antagonists [ 121. Placental vasospasm has been shown to precipitate fetal distress following maternal administration of cocaine
P31.
Thromboses are frequently demonstrated by early angiographic and autopsy studies of acute myocardial infarction in cocaine users [7,10,14]. Endothe-
cal suspicion, and the diagnosis can be missed.Danner and Hartman [8] found that the correctdiagnosisof spinal epidural abscess was made initially in only 17.9% of cases.Fortunately, the history of a recent epidural catheter and the neurologicfindings in our patient suggestedthe possibility of an epidural process,and emergent diagnostic and therapeutic measureswere performed. The bacteriology of spinal epidural abscessesis somewhatvaried, with Staphylococcus aureus the most common pathogen isolated [9]. Although streptococci have been found, group G streptococci have not been reported. The most common sites of infection with group G streptococci are the skin and soft tissues [9]. During delivery, colonization of the skin and contamination by the vaginal flora with group G streptococci with introduction into the epidural spaceby the anesthesiacatheter is the probable sourceof infection in our patient. In general, spinal epidural abscessis a rare complication of spinal anesthesia [lo]. Of interest, there are also several reports of postpartum spinal epidural abscessnot related to epidural anesthesia [11,12]. Our case report describes a catheter-relatedgroup G streptococcalspinal epidural abscess,an associationnot previouslyreported in our review of the literature. More significantly, it underscores againthe importance of early diagnosisand treatment. Heusner [7] and others have shown that diagnosisand intervention in the earlier phasesof spinal epidural abscess lead to favorable outcomes,while those patients diagnosedin the later phasescan experience irreversible neurologic damageand evendeath. Furthermore, delays in diagnosis have preventedreduction in morbidity and mortality despite improvements in therapy over the de90
cades[7,8].The patient discussed here did well after presenting in phase 2 of Heusner’s classification becauseof prompt diagnosis and treatment. LINAS M. KLYGIS, M.D. BORIS E. REISBERG, M.D.
Northwestern Memorial Hospjtal Northwestern University M;fed;zE Chicago, Illinois 1. Lancefield RC, Hare R. The serological differentiation of pathogenic and nonpathogenic strains of hemolytic streptococci from parturient women. J Exp Med 1935; 61: 335-49. 2. Vartian C, Lerner PI. Shlaes DM, Gopalakrishna KV. Infections due to Lancefield group G streptococci. Medicine (Baltimore) 1985; 64: 75-88. 3. Duma RJ, Weinberg AN, Medrek TF, Kunz LJ. Streptococcal infections: a bacteriologicand clinical study of streptococcal bacteremia. Medicine (Baltimore) 1969; 48: 87-127. 4. Lam K, Bayer AS. Serious infections due to group G streptococci: report of 15 cases with in vitro-in viva correlations. Am J Med 1983; 75: 561-70. 5. Gossling J. Occurrence and pathogenicity of the Streptococcus millen’ group. Rev Infect Dis 1988; 10: 257-85. 6. Dandy WE. Abscesses and inflammatory tumors in the spinal epidural space (so-called pachymeningitis externa). Arch Surg 1926; 13: 477-94. 7. Heusner AP. Nontuberculous spinal epidural infections. N Engl J Med 1948; 239: 845-54. 8. Danner RL, Hartman BJ. Update of spinal epidural abscess: 35 cases and review of the literature. Rev Infect Dis 1987; 9: 265-74. S.Kaufman DM. Kaplan JG. Litman N. Infectious agents in spinal epidural abscesses. Neurology 1980; 30: 844-50. 10. North JB, Brophy BP. Epidural abscess: a hazard of spinal epidural anaesthesia. Aust NZ J Surg 1979: 49: 484-5. 11. Male CG, Martin R. Puerperal spinal epidural abscess. Lancet 1973; 1: 608-9. 12. Crawford JS. Pathology in the extradural space. Br J Anaesth 1975; 47: 412-5. Submitted
May 23, 1990, and accepted in revised form February 5, 1991
LOCALIZEDRHEUMATOID VASCULITISPRESENTINGAS ACUTE ALITHIASIC CHOLECYSTITIS Rheumatoid arthritis is occasionally complicatedby systemicnecrotizing vasculitis indistinguishable pathologically from the primary forms of polyarteritis nodosa (PAN) [l]. Although lo-
July 1991 The American Journal of Medicine
Volume 91
calizedforms are not uncommon, only one case of localized rheumatoid vasculitis of the gallbladder has been reported [2]. Our patient was a 69-year-old woman with a history of hypertension, atria1 fibrillation, and seropositive erosive rheumatoid arthritis with subcutaneousnodules since 11 years previously. She received nonsteroidal antiinflammatory drugs (NSAIDs), corticosteroids,and aurothiomalate, remaining in clinical and analytical remissionuntil 6 months ago,when shepresentedwith intense constitutional symptoms, anemia, and an increase in the erythrocyte sedimentation rate (ESR) with no arthritis. She was admitted to our hospital in a state of shock from a bleeding gastric ulcer, for which surgery was immediately performed. During the postoperativeperiod, she had supraventricular tachycardia, congestiveheart failure, and a high temperature.She was treated with antibiotics, but blood, urine, and intravenous catheter cultures performed previously were all negative.On the 10th postoperativeday, with the temperature still high, the patient developeddiffuse abdominal pain, and there wasa general overall worsening, hypotension, and oligoanuria.Echographyand abdominal computed tomography revealed a distended gallbladder with no calculi and two collections of liquid, one surrounding it and the other in the right ileac fossa.A culture on 15 mL of bile extracted from this latter site by needlepuncturewas negative. Cholecystectomy was carriedout, but the generalstate, anasarca, and fever persisted with no apparent septic focus. Laboratory studies showed the following values: leukocytosis 40 X log/L (granulocytes96.7%),hemoglobin 114g/L, platelets 525X log/L, reticulocytes 30 per 1,000, ESR 69 mm/hour, glucose 8.8
BRIEF CLINICAL
OBSERVATIONS
Figure 1. Gallbladder biopsy specimen showing focal fibrinoid necrosis and infiltration of all layers of the wall of the vessel by chronic inflammatory cells, predominantly lymphocytes (hematoxylin-eosin stain; original magnification X10, reduced by 5%).
mmol/L, urea 36.4 mmol/L, creatinine 106 pmol/L, sodium 147 mmol/L, potassium 3.4 mmol/L, chloride 106 mmol/L, lactate dehydrogenase776IU/L, and total bilirubin 22 hmol/L. Creatine phosphokinase, alkaline phosphatase, glutamic oxaloacetic transaminase, glutamic pyruvic transaminase,y-glutamyl transferase, cholesterol, triglycerides, calcium, phosphorus,coagulation study results, cryoglobuhns,haptoglobin, antinuclear antibody, and hepatitis B virus markers were all either within the normal range or negative. Other values were as follows: total protein 48 g/L, albumin 22.6 g/L, al-globulins 4.1 g/L, ag-globulins6.3 g/L, &globulins 3.8 g/L, yglobulins 11 g/L, IgG 7.1 g/L, IgA 1.6 g/L, IgM 1.9g/L, C3 0.41g/L, and C4 undetectable.Rheumatoid factor by latex testing was 1,210IU/mL and the result of a Coombs’ test waspositive. Urine and sediment were normal. Pathologic examination showeda gallbladder with no calculi and with a greenish, somewhatulcerated mucoussurface. Histologically, the normal mucosaalternatedwith ulcerated areas and the submucosahad a disperse lymphocytic infiltrate (Figure 1).There wasa widening
of the walls of the small- and medium-sizedvessels,with fibrinoid necrosisand abundant mixed inflammatory infiltrates with a predominance of perivascular lymphocytes.Administration of 500 mg of intravenous GM-prednisolone was added to the treatment regimen followed by 80 mg/day. The temperature returned to normal in 24 hoursand the metabolic disturbancesweregradually corrected.Three weekslater, she tolerated oral feeding and was in a generally good state, and the steroid dose was reduced. Her temperature once again roseand morethan lo5 coloniesof Enterococcus faecalis and Pseudomonas aeruginosa were isolated in the urine; this colonization was satisfactorily treated. The prednisone dosagewas gradually reduced over the next 3 weeks,but fever,productive cough,and dyspnea developed.Chest radiography showed bilateral bronchopneumonia. Despite treatment for septic shock and respiratory failure, the patient died 4 days later. Permission for autopsywas denied. Acute cholecystitis due to vasculitis has been reported previously as a manifestation of PAN [3], in systemic lupus erythemaJuly 1991
The American
tosus [4], and in giant cell arthritis [5], among other conditions, but only in onecaseasa localized form of rheumatoid vasculitis [2]. As well as having infarctions in the gallbladder, our patient had anemia, thrombocytosis, elevated ESR, hypocomplementemia, and increasedrheumatoid factor titer, supporting the diagnosisof rheumatoid vasculitis [1,6]. Severe hematemesis is a common manifestation of upper gastrointestinal tract vasculitis [l], but it is also responsible for the high morbidity and mortality that NSAIDs producein personsolder than 60 years of age [7]. Since both thesephenomenawere present in our patient and no histologic examination of the ulcus wascarried out, vasculitis cannot be ruled out as a causeof the hematemesis. Hypovolemic shock, previous surgery, and prolonged fast are etiopathogenicfactors in alithiasic cholecystitis [8], which, occurring in addition to a previously ischemicgallbladder due to vasculitis, could have been responsiblefor the exclusiveaffection of this organ in this case.In conclusion,our patient presented with rheumatoid vasculitis with localized affection of the gallbladder,aggravatedby complicaJournal
of Medicine
Volume
91
91
BRIEF CLINICAL
OBSERVATIONS
tions resulting from shock secondary to upper digestive tract hemorrhage.
A 23-year-old woman presented to the Bellevue Hospital Emergency Department with 3 ANTONIO FERNANDEZ-NEBRO,M.D. days of pleuritic right upper PEDROVALDIVIELSO;M.D. quadrant pain. The patient had JUANJ. SANCHEZ-CARRILLO.P~.D. no other symptoms. She had no Virgen de la Victoria Hospital School of Medicine history of previous illness, recent INESDOMENECH, M.D. immobilization, or oral contraENRIQVE DE RAMON, M.D. ceptive use. Physical examinaRegional Hospital of S.A.S. PEDROGONZALEZ-SANTOS,M.D. tion was notable for a healthy-apVirgen de la Victoria Hospital pearing young woman in moderSchool of Medicine Malaga, Spain ate pain. The blood pressure was 124/80 mm Hg, pulse 92/minute, 1. Conn DL. Hunder GG. Vasculitis and related disorrespirations 28/minute, and ders. In: Kelley WN, Harris ED Jr, Ruddy S, Sledge CB, editors. Textbook of rheumatology. 3rd ed. rectal temperature 37.9”C Philadelphia: WB Saunders, 1989: 1167-99. (100.3”F). The chest was clear 2. Fayemi AO, Ali M. Braun EV. Necrotizingvasculitis and the heart sounds were norof the gallbladder and the appendix. Similarity in the mal. There was mild right upper morphology of rheumatoid arteritis and polyarteritis nodosa. Am J Gastroenterol 1977; 67: 608-12. quadrant tenderness to deep pal3. Li Volsi VA, Perzin KH, Porter M. Polyarteritis nopation and mild right costovertedosa of the gallbladder, presenting as acute cholebra1 angle tenderness. Results of cystitis. Gastroenterology 1973; 65: 115. pelvic examination were unre4. Swanepoel C. Floyd A, Allison H. Learmonth GM, Cassidy MJD. Pascoe MD. Acute acalculous cholemarkable. An intrauterine device cystitis complicating systemic lupus erythematowas in place. The extremities sus: case report and review. BMJ 1983; 286: 251-2. were normal. An electrocardio5. Papaioannou CC, Hunder GG. Lie JT. Vasculitis of gram, urinalysis results, complete the gallbladder in a 70 year old man with giant cell arteritis. J Rheumatol 1979; 6: 1. blood count, and electrolyte lev6. Scott DGI. Bacon PA, Tribe CR. Systemic rheuels were unremarkable. A serum matoid vasculitis: a clinical and laboratory study of pregnancy test was negative. A 50 cases. Medicine (Baltimore) 1981; 60: 28&97. room-air arterial blood gas study 7. Barrier CH, Hirschowitz BI. Controversies in the detection and management of nonsteroidal antiinshowed a pH of 7.41, a partial carflammatory drug-induced side effects of the upper bon dioxide pressure of 36 mm gastrointestinal tract. Arthritis Rheum 1989; 32: Hg, and a partial oxygen pressure 926-32. 6. Way LW. Sleisenger MH. Cholelithiasis; chronic of 109 mm Hg. The initial chest and acute cholecystitis. In: Sleisenger MH, Fordtran radiograph was normal. Further JS. editors. Gastrointestinal diseases. 4th ed. Philaquestioning revealed that the padelphia: WB Saunders, 1989: 1691-714. tient had recently used crack coSubmitted October 29, 1990, and accepted in recaine. There was no history of invised form February 15. 1991 travenous drug use. A urine toxicology screen was positive for a cocaine metabolite. A pulmonary ventilation-perfusion scan was ordered because of the clinical impression of diaphragmatic irriPULMONARYINFARCTION tation. The perfusion scan (FigASSOCIATEDWITH CRACK ure 1) demonstrated two unCOCAINEUSE IN A matched subsegmental defects in PREVIOUSLYHEALTHY the right lower lung, and intrave23-YEAR-OLDWOMAN nous heparin therapy was begun. A pulmonary angiogram (Figure Cocaine-associated ischemic in- 2) showed a large vascular objury has been documented in struction in the area that was premany organ systems [l-7]. We viously implicated by the ventiladescribe the first reported case of tion-perfusion scan. Hemoptysis pulmonary infarction associated occurred on the second day. Heparin was discontinued and a with “crack” cocaine use. 92
July
1991 The American
Journal
of Medicine
Volume
91
Greenfield filter was inserted. Subsequent pelvic ultrasonography, echocardiography, and Doppler plethysmography failed to reveal any source of emboli. Fever developed on the third day. A computed tomographic scan of the chest revealed a loculated pleural effusion with partial collapse of the right lower lobe. Thoracentesis yielded brown fluid with a pH of 6.9, lactate dehydrogenase of 481 IU, protein of 4 g/dL, glucose of 11 mg/dL, and a white blood cell count of 25/mm3. Results of repeated bacteriologic studies remained negative. Thoracotomy revealed a fibrinous peel entrapping all three lobes, and infarction of 20% of the right lower lobe. After decortication, the patient recovered without further complications. The mechanisms of cocaine-related ischemic injury are multifactorial. Phentolamine-reversible arterial spasm has been demonstrated during cardiac catheterization following administration of therapeutic doses of cocaine [8]. Recurrent episodes of silent myocardial ischemia attributed to dopamine-mediated vasospasm were documented by Holter monitoring in 38% of chronic cocaine users during a 2week withdrawal period [9]. Late angiography in patients with cocaine-related acute myocardial infarction frequently reveals normal vessels, suggesting vasospasm as an associated event [lO,ll]. Cocaine-induced vasospasm also occurs independent of a-receptor stimulation and can be blocked by calcium channel antagonists [ 121. Placental vasospasm has been shown to precipitate fetal distress following maternal administration of cocaine
P31.
Thromboses are frequently demonstrated by early angiographic and autopsy studies of acute myocardial infarction in cocaine users [7,10,14]. Endothe-
