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Colon perforation due to cholesterol embolism
CASE STUDIES
Nr\~ertll~lcas. ir remains uncertain whether AH E represents a oscular- neoplasm” of whether ii is a reactive inflammatorv condition. Kimur-a’s disease has been shown to be related r;, (2111tiin~1 sp infection.’ Some cases of AHE have been associated with tlerloch-Scholeiri purpura.’ Rosai et al” COIJImcntrd on l.his issue and concluded that perhaps the lesions lot atcd supc~rficiallc and within the mucosa could be reactive and possihl!, infectious. It is most important to correctly diagnose and distinguish be(ween the 5omctimes bizarre and pleomorphic cellular feamrcs of these conditions and angiosarcoma.’ In AHE, no anaplasia was pl.esent and the mitotic figures were noted with a frequency of 1 per 20 high-power fields.’ Anastomosis into re@ar cleft 5 was not observed. I,esions rich in lymphoid tissue could be mistahrn for lyniphonia or an atypical histiocytic granr~lon~a.“’ Ulcerated lrsions of the tongue rich in eosinophils must be disringuished from ulcerative eosinophilic granulonia of thca tongue; however. in the latter lesion, the prominrnt plump rndorhclial cells are not found.” Angic)l~nlphc)icl hyperplaxia with eosinophilia is a benign lehioil”,“; c~omplet~ es&ion is suggested as the treatment of (ho&‘-‘.” although other modes of treatment (corticotherapy. I-adiothrrap~. cvtotosic chemother-spy. and laser therapy) also tia1.e been us& a\ (,oacljuvant5 01. in recurrent cases.‘” In two cazes. spontaneous resolution of the lesions has been reported.’ Recut-rent-e?, arc not ~III(.oIJ~~~oI~“; they have been reported in up to 33% of patients, but are most fi-equent when blood rosinophilia is pI.Csent.” In Peters et al’s review of all cases recurrences were nor found in spite of without eosiriophilia.’ the fact rhat the srucl] included patients with multiple Iesionz. No metastasis w;is found.’ In our case, after the biopsy spec-inrcn was diagnosed as AHE, the patient was remitted to the onc~~lo~ service jot radiotherapy; however, he did n( PI receive
COLON
PERFORATION
DUE TO CHOLESTEROL
EMBOLISM
cardial infarction. Ful-thermore. simultaneous emboliLation to multiple organs may result in clinical symptlmls resembling polyarteritis nodosa.’ Atheroelnl~olizarion to the gastroilltrsrinal tract, initCdlly observed as incidental findings at autopsy, has received increasing recognition as a common compiication usually resulting in snlall necroses and multifocal ulcerations that may he asymptomaric hut which may result in gastrointestinal bleeding.’ In a few instances, extensive infar(:tions have also been observed.“-H as has the rare complication of intestinal perforation.“.’ ’ The purpose ot this study is to present the clinical and pathologic findings in a patient with atllert,c~lnbolization to the intestinal tract that resulted in extensive nec,rotizingcolitis and perforation complicated hy generalized peritonitis and death.
E~ilt)oli~.ation ot cholestrrol crj3Lals is a well-recognized complicntior~ of et-osive aortic and arterial atheromarosis that mav have major clinical sequelae. Complications of atheroemholism have been sunmlarized in several reviews,‘-” and ath~roembolizatic)n to various organs and viscera has been manifested by hvperlrlision. renal failure, blindness and visual disiur_barL~es. cerrbral infarction, acute pancrcatitis. and myo-
REPORT
OF A (:ASE
The 10th Ilospitat admission for this ti5-vear-old white for acute dyspnea due to bronchospasm ;tssociated with severe chronic obstructive pulrnonarv disease, occur-red 10 days antemortem. The patient’s medical history was significant in that he was hospitalized 5 months previouslv for acute nrcrosis of the left index finger, which was consider& tc) be cmbotic. Stenosis of the lefr hrachial artery W;ISdclllonstrated ;un~,rgr;~phic;~lly ~~xm,
839
HUMAN PATHOLOGY
Volume 22, No, 8 (August
1991)
/
using a femoral artery approach. This procedure was followed by acute renal failure attributed to atheroemholization and confirmed by renal biopsy. Continuous ambulatory dialysis was necessitated 2 months later for renal failure that had progressed to a chronic stage manifested by a SUN level in the range of 63 to 71 mg/dL, a creatinine level of 6.5 mg/dL, and creatinine clearances in the range of 6 to 11 ml./min. Other significant disorders included colonic diverticula, hybipertension, peripheral vascular disease . and asymptomatic lateral carotid bruits due to atherosclerosis.
FIGURE 2. A medium-sized submucosal artery is occluded by acicular clefts (arrows) typical of cholesterol emboli associated with necrosis of overlying mucosa. (Hematoxylin-eosin stain; magnification X 225.)
840
FIGURE I. A segment of descending colon shows two perforations surrounded by an area of necrotizing colitis.
Episodic bronchospasms continued during hospitalization despite treatment with bronchodilators. steroids, and inhaled beta agonists. During peritoneal dialysis 1 week antemortem, the patient developed severe abdominal pain. Although peritoneal fluid examination revealed 3,020 leukocytes with 97% neutrophils, this was attributed to a chemical peritonitis since free air could not be demonstrated radiographically. The patient sustained a cardiac arrest on the fifth hospital day; he responded to resuscitation, although his condition remained On the eighth hospital day. electrocardiocritical thereafter.
CORRESPONDENCE
graphic chamges indicated acute ischemic myocardial injury, and the patient again experienced severe abdominal pain, which was associated with a pneumoperitoneum. Peritoneal fluid cultures were positive for group D enterococcus, Butftwidf5 sp, and C’loslridi~m prlfringenc. The patient was riot considered a candidate for surgery: he died 2 days lateif’um refractory hypotension and peritonitis with sepsis.
1’0st111~mei~~examination revealed approximately 2 L of p~~rulcnt al~dominal fluid. generalized peritonitis. and two perforation.< at the tip of a diverticulum of the descending colon (Fig 11. AIXextensive necrotizing colitis was also present that W;IS limited 10 the c-olonic segment that contained the pc’rforated diver-ticulum. Microscopic examination of multiple src.tions of colon bordering perforations demonstrared extensite cholesteroL cmholization of submucosal vessels ranging up to 600 pm ill diameter (Fig 2). These emboli were both acure and chronic. and the latter were associated with intimal fibrosis and infrequent giant cell reaction. The source of embolization was undoubtedly thr aorta, which was the site of a marked, gerlrrali~ed erosive atheromatosis involving the thoracic and abdominal portions. Cholesterol emboli of vari011s sta es VGVIVa1so identified in the spleen, pancreas, and kidnrvs!
Tile clinic.opatl~r~lo~c features in this patient al-e exemplay of multisystemic cholesterol embolization. which is first manifested b\ (IIronic renal failure and terminally by the rare colnplication of intestinal perforation. <:holest~rol emholization 10 the gastrointestinal tract was init ially obsel-\ed as XII incidental finding at autopsy. However, bec‘ause subsequent I-eports describe ulcerations hf the stomx11 and intestinal tract as a cause of intestinal bleeding,“~“~“’ rhcrc is incrcGng recognition that this may result in significant ,~a”tl-ointestill~ll lesions. Not all lesions are symptomatic; instances of g..l\tri(..’ ’ duodenal,‘” and jejunal”’ ulcerations attributrd to .ltheromatous emboli have been clinically silent. FurThermore. clinical and experimental observaGons indicate that cholesterol rnlbolization to the intestinal tract may be rxrensivr ant1 rnq re$tllt in significant bleedillg, yet the induced Icsioils arc frequently quite small, re-epithelialize rapidly, cannot be detec.trd radiographically. and are easily overlooked a1 ;1uc0ps)-.’
Other illrestinal tract complications attributed to atheromatous emlboli have been described. Mulliken and Bartlett” rel)or’ ow pa’iellt with small-bowel obstruction attributed to c.ontraction and scarring response to necrosis induced by cholesterol emboli~ation. In ;I recent study, Rank et :II’~ describe angiotl~spln?.i.~ 01’ the stomach resulting in hemorrhage and
CORRESPONDENCE Postmortem Examination of the Brain in Acquired lmmunodeficiency Syndrome I,ettel-s IO the Editor- will be published at the disc’rcticjn OILthe editor as space permits and are subject IO editing and abridgement. They should be typewritten. double-spaced, and submitted in triplicate. They should he limited to 500 words or less and to no more than five pertinent references.
To (hr f+fit,,r:-‘l‘he ideal method to examine the postmortem brain is to remove the entire brain in the standal-d autopsy fashion, In acquired iinmuiiod~ficietic~ syndrome (AIDS) patients, sclme pathologists, for a variety of reasons. prefer not to remove the brain in the usual fashion. I do not wish to engage in a discussion of the pros and cons of this
/_ 841
Nr\~ertll~lcas. ir remains uncertain whether AH E represents a oscular- neoplasm” of whether ii is a reactive inflammatorv condition. Kimur-a’s disease has been shown to be related r;, (2111tiin~1 sp infection.’ Some cases of AHE have been associated with tlerloch-Scholeiri purpura.’ Rosai et al” COIJImcntrd on l.his issue and concluded that perhaps the lesions lot atcd supc~rficiallc and within the mucosa could be reactive and possihl!, infectious. It is most important to correctly diagnose and distinguish be(ween the 5omctimes bizarre and pleomorphic cellular feamrcs of these conditions and angiosarcoma.’ In AHE, no anaplasia was pl.esent and the mitotic figures were noted with a frequency of 1 per 20 high-power fields.’ Anastomosis into re@ar cleft 5 was not observed. I,esions rich in lymphoid tissue could be mistahrn for lyniphonia or an atypical histiocytic granr~lon~a.“’ Ulcerated lrsions of the tongue rich in eosinophils must be disringuished from ulcerative eosinophilic granulonia of thca tongue; however. in the latter lesion, the prominrnt plump rndorhclial cells are not found.” Angic)l~nlphc)icl hyperplaxia with eosinophilia is a benign lehioil”,“; c~omplet~ es&ion is suggested as the treatment of (ho&‘-‘.” although other modes of treatment (corticotherapy. I-adiothrrap~. cvtotosic chemother-spy. and laser therapy) also tia1.e been us& a\ (,oacljuvant5 01. in recurrent cases.‘” In two cazes. spontaneous resolution of the lesions has been reported.’ Recut-rent-e?, arc not ~III(.oIJ~~~oI~“; they have been reported in up to 33% of patients, but are most fi-equent when blood rosinophilia is pI.Csent.” In Peters et al’s review of all cases recurrences were nor found in spite of without eosiriophilia.’ the fact rhat the srucl] included patients with multiple Iesionz. No metastasis w;is found.’ In our case, after the biopsy spec-inrcn was diagnosed as AHE, the patient was remitted to the onc~~lo~ service jot radiotherapy; however, he did n( PI receive
COLON
PERFORATION
DUE TO CHOLESTEROL
EMBOLISM
cardial infarction. Ful-thermore. simultaneous emboliLation to multiple organs may result in clinical symptlmls resembling polyarteritis nodosa.’ Atheroelnl~olizarion to the gastroilltrsrinal tract, initCdlly observed as incidental findings at autopsy, has received increasing recognition as a common compiication usually resulting in snlall necroses and multifocal ulcerations that may he asymptomaric hut which may result in gastrointestinal bleeding.’ In a few instances, extensive infar(:tions have also been observed.“-H as has the rare complication of intestinal perforation.“.’ ’ The purpose ot this study is to present the clinical and pathologic findings in a patient with atllert,c~lnbolization to the intestinal tract that resulted in extensive nec,rotizingcolitis and perforation complicated hy generalized peritonitis and death.
E~ilt)oli~.ation ot cholestrrol crj3Lals is a well-recognized complicntior~ of et-osive aortic and arterial atheromarosis that mav have major clinical sequelae. Complications of atheroemholism have been sunmlarized in several reviews,‘-” and ath~roembolizatic)n to various organs and viscera has been manifested by hvperlrlision. renal failure, blindness and visual disiur_barL~es. cerrbral infarction, acute pancrcatitis. and myo-
REPORT
OF A (:ASE
The 10th Ilospitat admission for this ti5-vear-old white for acute dyspnea due to bronchospasm ;tssociated with severe chronic obstructive pulrnonarv disease, occur-red 10 days antemortem. The patient’s medical history was significant in that he was hospitalized 5 months previouslv for acute nrcrosis of the left index finger, which was consider& tc) be cmbotic. Stenosis of the lefr hrachial artery W;ISdclllonstrated ;un~,rgr;~phic;~lly ~~xm,
839
HUMAN PATHOLOGY
Volume 22, No, 8 (August
1991)
/
using a femoral artery approach. This procedure was followed by acute renal failure attributed to atheroemholization and confirmed by renal biopsy. Continuous ambulatory dialysis was necessitated 2 months later for renal failure that had progressed to a chronic stage manifested by a SUN level in the range of 63 to 71 mg/dL, a creatinine level of 6.5 mg/dL, and creatinine clearances in the range of 6 to 11 ml./min. Other significant disorders included colonic diverticula, hybipertension, peripheral vascular disease . and asymptomatic lateral carotid bruits due to atherosclerosis.
FIGURE 2. A medium-sized submucosal artery is occluded by acicular clefts (arrows) typical of cholesterol emboli associated with necrosis of overlying mucosa. (Hematoxylin-eosin stain; magnification X 225.)
840
FIGURE I. A segment of descending colon shows two perforations surrounded by an area of necrotizing colitis.
Episodic bronchospasms continued during hospitalization despite treatment with bronchodilators. steroids, and inhaled beta agonists. During peritoneal dialysis 1 week antemortem, the patient developed severe abdominal pain. Although peritoneal fluid examination revealed 3,020 leukocytes with 97% neutrophils, this was attributed to a chemical peritonitis since free air could not be demonstrated radiographically. The patient sustained a cardiac arrest on the fifth hospital day; he responded to resuscitation, although his condition remained On the eighth hospital day. electrocardiocritical thereafter.
CORRESPONDENCE
graphic chamges indicated acute ischemic myocardial injury, and the patient again experienced severe abdominal pain, which was associated with a pneumoperitoneum. Peritoneal fluid cultures were positive for group D enterococcus, Butftwidf5 sp, and C’loslridi~m prlfringenc. The patient was riot considered a candidate for surgery: he died 2 days lateif’um refractory hypotension and peritonitis with sepsis.
1’0st111~mei~~examination revealed approximately 2 L of p~~rulcnt al~dominal fluid. generalized peritonitis. and two perforation.< at the tip of a diverticulum of the descending colon (Fig 11. AIXextensive necrotizing colitis was also present that W;IS limited 10 the c-olonic segment that contained the pc’rforated diver-ticulum. Microscopic examination of multiple src.tions of colon bordering perforations demonstrared extensite cholesteroL cmholization of submucosal vessels ranging up to 600 pm ill diameter (Fig 2). These emboli were both acure and chronic. and the latter were associated with intimal fibrosis and infrequent giant cell reaction. The source of embolization was undoubtedly thr aorta, which was the site of a marked, gerlrrali~ed erosive atheromatosis involving the thoracic and abdominal portions. Cholesterol emboli of vari011s sta es VGVIVa1so identified in the spleen, pancreas, and kidnrvs!
Tile clinic.opatl~r~lo~c features in this patient al-e exemplay of multisystemic cholesterol embolization. which is first manifested b\ (IIronic renal failure and terminally by the rare colnplication of intestinal perforation. <:holest~rol emholization 10 the gastrointestinal tract was init ially obsel-\ed as XII incidental finding at autopsy. However, bec‘ause subsequent I-eports describe ulcerations hf the stomx11 and intestinal tract as a cause of intestinal bleeding,“~“~“’ rhcrc is incrcGng recognition that this may result in significant ,~a”tl-ointestill~ll lesions. Not all lesions are symptomatic; instances of g..l\tri(..’ ’ duodenal,‘” and jejunal”’ ulcerations attributrd to .ltheromatous emboli have been clinically silent. FurThermore. clinical and experimental observaGons indicate that cholesterol rnlbolization to the intestinal tract may be rxrensivr ant1 rnq re$tllt in significant bleedillg, yet the induced Icsioils arc frequently quite small, re-epithelialize rapidly, cannot be detec.trd radiographically. and are easily overlooked a1 ;1uc0ps)-.’
Other illrestinal tract complications attributed to atheromatous emlboli have been described. Mulliken and Bartlett” rel)or’ ow pa’iellt with small-bowel obstruction attributed to c.ontraction and scarring response to necrosis induced by cholesterol emboli~ation. In ;I recent study, Rank et :II’~ describe angiotl~spln?.i.~ 01’ the stomach resulting in hemorrhage and
CORRESPONDENCE Postmortem Examination of the Brain in Acquired lmmunodeficiency Syndrome I,ettel-s IO the Editor- will be published at the disc’rcticjn OILthe editor as space permits and are subject IO editing and abridgement. They should be typewritten. double-spaced, and submitted in triplicate. They should he limited to 500 words or less and to no more than five pertinent references.
To (hr f+fit,,r:-‘l‘he ideal method to examine the postmortem brain is to remove the entire brain in the standal-d autopsy fashion, In acquired iinmuiiod~ficietic~ syndrome (AIDS) patients, sclme pathologists, for a variety of reasons. prefer not to remove the brain in the usual fashion. I do not wish to engage in a discussion of the pros and cons of this
/_ 841