Cough as the Presenting Symptom of Pancreatic Adenocarcinoma

R. Todd Richwine, DO, MS; Nadeem Ahmed, MD; Marta Mortensen, MD

Disclosures

J Am Board Fam Med. 2004;17(1) 

In This Article

Introduction and Case Reports

Pancreatic cancer continues to be one of the most lethal of cancers. It is the 7th leading cause of cancer in the United States and the 4th leading cause of cancer-related death.[1] Although pulmonary metastases of pancreatic cancer is not uncommon, a nonproductive cough as the only complaint for greater than 6 months has not been previously reported.

A 49-year-old African American man presented to the family medicine clinic in July 2001 complaining of a persistent nonproductive cough not relieved by over-the-counter medications. He denied fever, chills, weight loss, pain, or other complaints. He continued to work at his job as a railroad engineer. The patient had a past medical history of hypertension, obesity, and hypercholesterolemia. He had never undergone surgery or been hospitalized. He had never smoked, nor had his wife, and he reported drinking less than 1 alcoholic beverage per month. There was no obvious history of exposure to infectious or occupational hazards. Family history was significant only for paternal cardiac disease. The patient's lungs were clear to auscultation, and results of the heart and abdominal examination were unremarkable. He did exhibit posterior pharyngeal nasal drip and clear rhinorrhea. Consequently, he was diagnosed with allergic rhinitis, treated with a nonsedating antihistamine, and told to return to clinic if he worsened.

In August 2001, his wife insisted that he return to the clinic. The patient's cough had not improved. A chart review indicated that the dosage of his angiotensin-converting enzyme (ACE) inhibitor was increased 1 month before his first visit for the cough. There were no changes in his physical examination, and his ACE inhibitor was discontinued. He continued without improvement and was evaluated by a second doctor in September 2001. This physician documented that the patient's lungs continued to be clear to auscultation and found no other abnormalities on physical examination. The patient's chest radiograph (Figure 1) was read as having "diffuse nodular infiltrates seen throughout both lungs. Etiology unknown. However, due to the nodular nature, the possibility of metastatic disease cannot be ruled out entirely."

Anteroposterior (a) and lateral (b) radiographs show diffuse nodular infiltrates throughout both lungs.

The chest radiograph was reviewed with the radiologist and a pulmonologist and a spiral computed tomograph (CT) was ordered (Figure 2). The spiral CT showed multiple bilateral nodules scattered throughout both lungs in all fields. No adenopathy was seen in either the hilar region or the rest of the mediastinum. No axillary or supraclavicular adenopathy was evident. Examination through the upper abdomen showed the visualized liver, spleen, suprarenal, and kidneys to be normal. The CT report stated "the differential diagnosis for scattered, diffuse bilateral pulmonary nodules includes sarcoidosis and fungal infections. [Tuberculosis] is a possibility but unlikely in proper settings. The appearance is not of metastasis or primary tumor."

CT of lung fields shows multiple pulmonary nodules scattered throughout both lungs. These measured from a few millimeters to 1.5 cm, No adenopathy is seen in either the hilar region or the rest of the mediastinum. No axillary or supraclavicular adenopathy is apparent.

Follow-up laboratory tests for ACE, HIV, and purified protein derivative were negative. Anti-nuclear antibody titers were negative, rapid plasma reagin was nonreactive, erythrocyte sedimentation rate was 60, and cytidine monophosphate and complete blood cell count (CBC) were normal. The patient continued to have a bothersome cough, not even improved with narcotics at this point, and agreed to undergo a bronchoscopy in early October 2001. The bronchoscopy showed no abnormalities on visualization. Biopsies showed normal tissue bilaterally. Cultures for bacteria, fungus, and tuberculosis were negative. The patient declined video-assisted thoracostomy (VAT). Therefore, serial CTs and close follow-up was recommended.

Over the next 2 months, medical (bronchodilators, inhaled steroids, and high-dose codeine) and behavioral treatments failed to improve his cough, his examination remained unchanged, and he continued his job without difficulty. A repeat spiral CT of his chest showed "no significant change" in December 2001. The patient did not return for evaluation until February 2002, when he called the clinic complaining of severe shortness of breath and dyspnea on exertion. He was immediately evaluated in the clinic, where he admitted to a significant worsening in his condition, and agreed to a VAT. His examination showed a 20-lb weight loss in the previous 2 months, and he appeared very fatigued. His cardiovascular examination was normal, his lung examination continued to be clear with no wheeze, rhonchi, or other abnormality. He had significant epigastric tenderness on palpation without rebound or guarding. Liver and spleen were of normal size.

He was admitted to our community hospital that day and labs were drawn. CBC and BMP continued to be normal except for an elevated CO2 of 30 mEq/L. Total bilirubin was elevated at 1.8 mg/dL, alanine aminotransferase was 772 IU/L, aspartate aminotransferase was 347 IU/L, amylase was 132 IU/L, lipase was 192 U/L, alkaline phosphatase was 826 IU/L, total protein was 7.8 g/dL, and albumin was 3.8 g/dL. Results of a hepatitis panel were negative, ESR continued to be 60 mm/hour, and rheumatoid factor was negative. Chest radiographs revealed increased densities of nodules in both lungs, with some associated inflammation or fluid. CT showed no significant change from the previous 2 CTs. Spiral CT with contrast of the abdomen and pelvis showed no abnormalities of the liver or spleen and no intrahepatic biliary ductal dilation. The pancreas and kidneys were read as normal. Because of the declining liver function, the VAT was canceled, and a gastroenterologist was consulted. A liver biopsy was performed and showed only mild acute hepatitis, with no evidence of tumor, metastases, or granulomatous inflammation. The patient continued to have a very slow increase in total bilirubin as the other liver enzymes slowly decreased, and he was released 3 days after admission pending the final liver biopsy results. The cultures of liver tissue were negative.

Two days after discharge, the patient, continuing to feel worse, was seen again. A repeat liver panel showed a doubling of the bilirubin and the patient was clearly jaundiced. His epigastric pain was now requiring high doses of oral narcotics. He was referred urgently to a GI specialist at a tertiary care center. He underwent an endoscopic retrograde cholangiopancreatography (ERCP), which showed a very tight stricture of the pancreatoduodenal duct and a small pancreatic head mass. A stent was placed with considerable difficulty to relieve the obstruction. CA 19-9 level was then ordered and was found to be 39,900 (normal <15). A repeat spiral CT showed a small pancreatic duct mass with minimal but significant posterior peritoneal involvement. A positron emission tomography scan showed characteristic and identical signatures in the pancreatic head and the lung. He was diagnosed with metastatic, nonoperable pancreatic carcinoma. A CT-guided biopsy of a lung nodule further confirmed metastatic pancreatic adenocarcinoma.

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