Clinical Geriatrics

I was recently asked to consult on a 93-year-old man, Mr. M, who had fallen and broken his left femur and right humerus. He had underlying dementia and several chronic medical conditions. The patient’s initial liver function tests (LFTs) demonstrated a slightly increased total bilirubin of 2.1 mg/dL, but the rest were all within normal limits: aspartate aminotransferase (AST), 41 IU/L; alkaline phosphatase (ALP), 42 IU/L; and gamma glutamyl transpeptidase (GGT), 14 IU/L. He had a large hematoma in his thigh and upper arm, and a broken left 10th rib. Mr. M was treated acutely for his fractures, given pain medication, and appeared clinically to be stable.

The next day, however, upon review of his laboratory data, I noted that his total bilirubin had risen to 5 mg/dL, still with no other LFT abnormalities. There were no clinical findings referable, and his abdominal examination was completely normal. On his third hospital day, the patient’s total bilirubin was 6.8 mg/dL with a direct bilirubin of 4.1 mg/dL; his AST had now risen to 71 IU/L, his ALP was 54 IU/L, and his GGT was 28 IU/L. On the next day, his total bilirubin was 7.5 mg/dL; his AST had risen further to 98 IU/L and his GGT was now elevated at 73 IU/L. Mr. M’s ALP remained normal at 94 IU/L. On day 5, the patient’s total bilirubin was 8.0 mg/dL (4.8 mg/dL direct), AST was 85 IU/L, and ALP was 171 IU/L. The patient’s physical examination remained completely benign during this timeframe, though he had significant jaundice and scleral icterus.

While I had seen small increases in total bilirubin in persons who had traumatic injury before, this was the first time I noted it being so high. Mr. M’s family commented to me that the patient’s coloring was getting more “yellow” every day, something I had to agree with. They were concerned that there was something “seriously wrong.” An initial computed tomography (CT) scan of the abdomen was normal. Remembering all too well that elderly persons may not have abdominal changes noted on physical examination until late in a disease process, I pushed for a hepatic ultrasound, and, once again, no pathology was identified. The patient had no evidence of sepsis, hypotension, or hemolysis, and had not received multiple transfusions.

My internal medicine background wanted to believe that there was some biliary tree abnormality. I had thought that a repeat CT scan or hepatic ultrasound would identify the cause. My surgical colleagues, however, remained unimpressed by the lab values and told me that, based on clinical findings and imaging, the abnormal LFTs were due to “difficulties in absorption.” True, Mr. M had a hematoma, but so did many other patients I had encountered with similar injuries.

At this time, I performed a search of the literature about the relationship between a traumatic injury and jaundice. It appears that jaundice is not an uncommon finding after trauma, even in the absence of preexisting hepatobiliary disease. In fact, there have been 238 cases of jaundice following trauma reported in the literature in 63 separate articles. Eight were prospective or retrospective studies, 49 were single case reports, and six were case series. Of these reported 238 cases, 59 had bile duct injury or obstruction; the remaining individuals were found to have a variety of etiologies, including problems reabsorbing bilirubin from a hematoma or resulting from a transfusion(s), sepsis, multiple-organ failure, initial shock with hypotension, cirrhosis, viral hepatitis, or drug-induced hepatic injury. I was unable to determine how age related to the degree of hyperbilirubinemia and of course, even here, could not compare the degree of injury and bilirubin load presented to the liver. Age was not a particular concern or item of study in any of the papers.

A serum bilirubin greater than 2 mg/dL is classically used as the criteria for the presence of hepatic dysfunction.