reports indicate that it is comparable to surgery in terms of therapeutic outcome . as the survival rate after chemoradiotherapy increases , management of the late adverse effects of radiation becomes increasingly important .
since patients with esophageal cancer receive a wide range of irradiation to the mediastinum and heart , they may develop postirradiation complications such as cardiac and pulmonary toxicities that have been reported in hodgkin 's disease .
severe late toxicity , especially cardiac toxicity , is sometimes difficult to treat and associated with mortality .
however there is little published information with regard to patients with delayed pericardial effusion following chemoradiotherapy in esophageal cancer and its management . here , we report a patient with advanced synchronous esophagus and gastric cardia cancers who presented with severe pericardial effusion as late toxicity . he was successfully treated with corticosteroid therapy following pericardial drainage .
hematological tests revealed the levels of all tumor markers , namely squamous cell carcinoma antigen , carcinoembryonic antigen , and carbohydrate 19 - 9 , to be in the normal range .
the patient was diagnosed to have synchronous esophageal ulcerative tumor in the middle thoracic esophagus ( fig .
1a ) directly invading the thoracic aorta , accompanied by a gastric ulcerative tumor in the cardia ( fig .
an endoscopic forceps biopsy specimen revealed moderately differentiated squamous cell carcinoma in the esophagus and well - differentiated adenocarcinoma in the stomach under microscopic examination .
the patient was subsequently diagnosed with stage iii ( t4n1m0 ) esophageal carcinoma and stage iii ( t3n1m0 ) gastric carcinoma according to the tnm classification of the international union against cancer .
he was treated with definitive chemoradiotherapy using a daily low dose of nedaplatin ( cdgp ) ( 10 mg / day ) and a continuous infusion of 5-fu ( 500 mg / day ) for 20 days .
fractionated radiotherapy was performed since initiating chemotherapy and a total dose of 66 gy was delivered at the rate of 2 gy per fraction .
initially , both tumors could be encompassed in a single radiation field that included the celiac nodes ( fig .
the field was changed to avoid spinal cord irradiation following a dose of 40 gy , and only thoracic macroscopic lesions were irradiated with a margin of at least 1 cm .
an additional two cycles of maintenance chemotherapy were performed for 5 days following chemoradiotherapy with cdgp ( 20 mg / day ) and 5-fu ( 750 mg / day ) .
however , 14 months after the chemoradiotherapy , the patient was readmitted to our hospital presenting with dyspnea and chest pain .
his blood pressure fell to 92/68 mm hg accompanied by a pulse rate of 116 bpm . a paradoxical pulse was observed .
echocardiography indicated an enlarged pericardium and collapsed ventricles with a left ventricular ejection fraction of 63% . according to these findings pericardial and pleural effusions with cardiac tamponade were diagnosed .
pericardial fluid analysis showed a specific gravity of 1.033 , protein 4.8 g / dl , and ldh 336 iu / l .
cultures and cytologic examinations of fluid specimens were repeatedly negative for bacteria and cancer cells .
pericardial drainage was performed for 5 days . however , the pericardial and left pleural effusions increased again .
pleural fluid composition was similar to that of pericardial fluid and its cytology was negative for cancer cells .
therapy with 40 mg prednisolone daily was started 30 days after pericardiocentesis . immediately after adding steroid , the patient 's condition improved dramatically and a chest radiograph showed a decrease in cardiomegaly as well as pleural effusion ( fig .
3b ) . steroid was gradually reduced every 2 weeks since then . as local recurrence of both the esophageal and the gastric tumors
was revealed by endoscopy 7 months after the treatment for pericardial and pleural effusion , chemotherapy using s-1 was performed . during a follow - up period of 2 years
the patient survived until may 2008 , after which he died from esophagorespiratory fistula and tumor bleeding .
we present a case of cardiac tamponade with pericardial effusion following chemoradiotherapy for advanced synchronous middle esophageal and cardial cancers , and successful treatment with corticosteroid therapy combined with pericardiocentesis .
when pleural and pericardial effusions occur following chemoradiotherapy for esophageal or cardial cancer , the possibility of treatment - related complications must be considered by the physicians .
few clinical reports discussing late cardiac toxicity management following chemoradiotherapy in esophageal cancer therapy exist till date .
the present case suggests the feasibility of steroid therapy as an alternative treatment for refractory pericardial effusion following chemoradiotherapy .
delayed complications following mediastinal radiotherapy or chemoradiotherapy include pericarditis , myocardial fibrosis , coronary artery disease , valvular abnormalities , conduction disturbances , and pulmonary fibrosis [ 8 , 9 ] .
benign pericardial effusion following radiation therapy for esophageal or cardial cancer is considered a relatively rare event and accurate incidence data were not obtained until recently . a recent retrospective study revealed pericardial effusion to be the commonest cardiac toxicity in esophageal cancer patients with a crude incidence of 27.7% ( 28 of 101 patients ) and median time at onset was 5.3 months ( range 1.016.7 months ) following chemoradiotherapy . in this
study the actual incidence at 18 months was 48% ( 95% confidence interval 3463 ) .
treatment of pericardial effusion is not necessary in asymptomatic patients , whereas ishikura et al .
reported severe pericarditis ( grade =3 ) in 10% ( 8 of 78 patients ) and a few patients died as a result of heart failure despite pericardiocentesis or pericardial window placement .
it may be necessary to determine whether the effusion is associated with cancer relapses on observing such an effusion for the first time . in our case ,
external irradiation with a total dose of 66 gy , delivered at the rate of 2 gy per fraction , was performed in this case .
it is known that a total dose greater than 3540 gy , daily fractionation in excess of 2 gy , and volume of heart irradiated have been associated with an increased incidence of effusion . as both lower esophageal cancer and cardial cancer were irradiated in our case ,
daily low dose of cdgp and continuous infusion of 5-fu were given with radiation therapy in our case .
5-fu also has a cardiotoxic effect   and is commonly used to treat esophageal cancer . however , it is not known whether it interacts with radiation to potentiate cardiotoxicity . in our recent clinical study , daily low dose of cdgp and 5-fu together with radiation for esophageal cancer did not seem to increase late cardiac toxicity . to date , no other clinical factors have been found to influence the risk of pericardial effusion significantly following chemoradiotherapy for esophageal cancer , and high - dose radiation to the pericardium is the only significant risk associated with pericardial effusion [ 10 , 14 ] .
once delayed radiation cardiopulmonary toxicity occurs , there is no specific treatment other than steroids , diuretics , vasodilators , pericardiocentesis , pleurocentesis , pericardial window placement , and so on .
there are only two clinical case reports in which radiation - induced pericardial effusions were successfully treated by steroid therapy : one was a case of breast cancer   and the other a case of hodgkin 's disease .
the pathology of radiation - induced heart disease is well characterized in an experimental rabbit model .
myocardial and pericardial fibroses , which appear to result from microcirculatory insufficiency and subsequent ischemia , dominate the late stage of radiation - induced heart disease [ 17 , 18 ] . in this experimental model , early administration of methylprednisolone or ibuprofen decreases the incidence of pericardial effusion , reduces myocardial fibrosis , and improves survival .
another clinical report indicated that rapid withdrawal of high - dose corticosteroids may activate subclinical radiation injury in the lungs and heart in hodgkin 's disease .
therefore , steroid treatment is a candidate for promising means of improving radiation - induced pericardial effusion .
pericardial effusion following chemoradiotherapy may sometimes be self - limited and asymptomatic , but is also sometimes difficult to treat and associated with mortality .
further clinical experience is necessary to establish the initiation of steroid therapy in treating pericardial effusion following chemoradiotherapy in the clinical setting .
it is also important to determine the optimal dose of radiation , because the higher radiation dose did not increase survival or local / regional control and the dose of 50.4 gy was recommended for patients treated with concurrent 5-fu and cisplatin chemotherapy according to the int 0123 trial [ 21 , 22 ] .
possible future treatments also include the use of new chemotherapeutic agents with both systemic and radiosensitizing activity so as to reduce toxicity .
 severe late toxicity following chemoradiotherapy in esophageal cancer , especially cardiac toxicity , is sometimes difficult to treat and is associated with mortality . 
 however there is little published information with regard to patients with delayed pericardial effusion following chemoradiotherapy and its management . 
 we herein report the case of a 63-year - old man with advanced synchronous esophageal and gastric cancers . 
 this patient presented with pericardial effusion with cardiac tamponade after definitive chemoradiotherapy and was successfully treated with corticosteroid after pericardiocentesis . 
 no instances of pericardial and pleural effusions were observed during the 2-year follow - up period until his death from cancer relapses . 
Introduction
Case Report
Discussion