Eur J Cardiothorac Surg 2000;18:120-122
© 2000 Elsevier Science NL
Massive haemoptysis due to chronic pancreatitis: control with inferior phrenic artery embolization
Iwao Takanami
Department of Surgery, Teikyo School of Medicine, 2-11 Kaga 2-Chome, Itabashi-Ku, Tokyo 173, Japan
Received 11 January 2000;
received in revised form 21 March 2000;
accepted 26 April 2000.
Tel.: +81-3-3964-1211; fax: +81-3-3962-2128
e-mail: takanami{at}med.teikyo-u.ac.jp
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Abstract
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Massive haemoptysis is a rare complication of chronic pancreatitis. We describe a patient with massive haemoptysis due to chronic pancreatitis who was treated successfully by means of selective inferior phrenic artery embolization.
Key Words: Massive haemoptysis • Chronic pancreatitis • Pancreaticopleural fistula • Inferior phrenic artery • Embolization
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1. Introduction
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Although massive pleural effusion is rarely associated with chronic pancreatitis, it is being reported with increasing frequency [1,2]. Haemoptysis due to chronic pancreatitis is less common, and the management of haemoptysis due to chronic pancreatitis has not previously been described. Our patient, who had a history of chronic pancreatitis had, massive haemoptysis, which was found to be due to a pancreaticopleural fistula. The patient was spared surgery by the use of inferior phrenic artery embolization to control the massive haemoptysis.
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2. Case report
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A 40-year-old man was admitted to our hospital in September 1999 with massive haemoptysis. He had been drinking four 300 ml glasses of beer daily for 20 years, and smoked cigarettes occasionally. He first presented with acute pancreatitis at the age of 35 years in April 1994. Over the next 3 years, he was treated for recurrent pancreatitis. In November 1998, he was admitted to our hospital with left pleuritic chest pain and massive pleural effusion on the left side. Thoracentesis yielded 2500 ml of bloody fluid with a high amylase content (155 000 IU/l). No pathogens were detected in pleural and sputum cultures.
Abdominal CT scan revealed stones in the tail of his pancreas and pancreatic pseudocyst. Endoscopic retrograde cholangiopancreaticography (ERCP) disclosed an internal fistulous tract, with contrast medium extravasated upwards from the tail to the esophageal hiatus. A diagnosis of chronic pleural effusion due to pancreaticopleural fistula was made from these findings. The patient underwent conservative therapy, and so he was kept nil orally and peripheral hyperalimentation was instituted for two weeks.
Physical examination on admission to our hospital in September 1999 showed a temperature of 37.0°C, pulse of 86/min, blood pressure of 100/64 mmHg, and respiratory rate of 25/min. Laboratory values were as follows: haemoglobin 7.6 g/dl, haematocrit 26.4%, platelet count 343 000/mm3, serum amylase 817 IU/l. Coagulation values were normal. The left lung was dull to percussion and had diminished breath sounds. The abdomen was soft and not tender. The patient underwent fiberoptic bronchoscopy on the first hospital day, and active bleeding was found from the left lower lobe bronchus. A chest roentgenogram on the same day demonstrated probable atelectasis by bloody aspiration in the left (Fig. 1) . The haemoptysis continued, and an incomplete 24-h sputum collection per day yielded 200 ml of frank light red blood mixed with a small amount of sputum for four days. A clinical diagnosis of pulmonary inflammation due to pancreaticopleural fistula was given as the most likely cause of this patient's haemoptysis in association with chronic pancreatitis. Angiograms were performed on the fifth hospital day. Selective bronchial arteriogram showed normal, but selective inferior phrenic arteriogram showed multiple serpentine arteries in the left diaphragm and left lower lobe region and anastmoses between the inferior phrenic artery and the pulmonary artery (Fig. 2)
, and subsequent metallic coils and gelatin sponge embolization in the inferior phrenic artery were urgently performed. Frank light red haemoptysis stopped immediately, although the patient did continue to produce blood-streaked sputum for the next several days. No pathogens were detected in sputum culture. Bronchofiberscopy after embolization showed normalcy. Chest roentgenogram and chest CT after embolization showed slight left-sided pleural adhesion with the diaphragm and chest wall. Peripheral hyperalimentation was instituted for 3 weeks, and as the serum amylase level returned to a normal level, the patient was discharged. Three months after embolization, his condition remained stable with slight left-sided pleural adhesion on chest X-ray, without further haemoptysis or chest pain. Though ERCP was not repeatedly performed, abdominal CT scan showed no substantial changes have occurred in pancreatic stones and pseudocyst.
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Fig. 2. Inferior phrenic arteriogram prior to embolization shows multiple serpentine arteries at pleural surface with retrograde filling of segmental left lower lobe pulmonary arteries.
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3. Discussion
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Pleuropulmonary complications of chronic pancreatitis are non-specific – a raised hemidiaphragm, basal atelectasis or pleural reaction. Pleural effusion or haemorrhagic pleural effusion associated with chronic pancreatitis is not very common. The cause of pleural effusion in chronic pancreatitis is usually the direct extension of a pseudocyst across the diaphragm or from the formation of a fisulous tract between the pancreas and pleural space.
Most patients with pancreatic pleural effusion are treated initially by conservative therapy such as thoracentesis, fasting, intravenous hyperalimentation, and drugs which reduce pancreatic endocrine secretion [3]. Medical management for pleural effusion should usually be attempted for 2–3 weeks and results in resolution in up to 40% of cases [3]. Ten months after the drainage of pleural effusion, our patient had heamoptysis. A possible mechanism postulated in producing haemoptysis. Haemoptysis due to chronic pancreatitis rarely has been reported and has always required pancreatic surgical intervention [4]. A possible mechanism postulated in producing haemoptysis is chronic pancreatitis and direct contact of pancreatic enzymes with the diaphragm and pleura, and consequent pleural inflammation. In the present case, direct contact of pancreatic enzymes from the formation of a fistulous tract between the pancreas and pleural space is thought to have brought about pleural and pulmonary inflammation and produced massive haemoptysis. In addition to the difficulties in diagnosis, this case was further complicated by the urgency of life-threatening haemoptysis. Massive heamoptysis can be managed successfully utilizing not only rigid instrument but also the fiberoptic bronchofiberscope [5], so the patient underwent fiberoptic bronchoscopy but active bleeding was not managed by fiberoptic bronchoscopy. In patient with chronic pulmonary infection, large anastomoses can develop between systemic and pulmonary arteries. Most commonly, systemic-pulmonary artery anastomoses occur between bronchial artery and small pulmonary artery branches. And bronchial artery embolization has been successful in controlling haemoptysis of various etiologies of the lung. In our case, however, bronchial arteriograms were normal, and inferior phrenic arteriogram with subsequent embolization was effective for haemoptysis. Transpleural systemic-pulmonary artery anastomoses can develop in the presence of pleural adhesions [6]. In the inferior phrenic artery invests the parietal pleura over much of diaphragma and is the most common abdominal branch responsible for systemic-pulmonary anastomoses [6]. In this case, in the inferior phrenic artery had a connection to the lower lobe segment of pulmonary artery branches, but marked inflammatory pleural adhesion may not exist between parietal pleura and visceral pleura of the upper lobe segment, so there was not subsequent retrograde filling the upper lobe segment of pulmonary artery branches. Communication between the inferior phrenic artery and the pulmonary artery in our case was not congenital. Because the inferior phrenic artery divided into numerous small anastomonic twigs at the pleural surface, and these small branches were not feature of sequestration. In the majority of patients with sequestration, abdominal arteries penetrate the lung via pulmonary ligament, and supply of sequestration from normal abdominal branches is rare. The entrance of high pressure systemic artery blood into the low pressure pulmonary artery may reflect the pathologic conditions which have a tendency to rupture the pulmonary capillary. Furthermore, when these conditions are present with inflammation, haemoptysis may result. Rockey and Cello [7] reported a 41% success rate for non-surgical therapy for pleural effusion due to pancreaticopleural fistula. In the case of massive haemoptysis due to pancreaticopleural fistula, we believe that primary non-operative therapy is justified and artery embolization should be performed as long as necessary. Whenever conservative treatment is unsuccessful, surgical resection of the pancreas or lung has to be performed.
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References
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Abstract
1. Introduction 
