Incidentalitis: When an Abdominal CT Reveals More than its Indication
A 57-year-old female with no significant past medical history consulted the emergency room (ER) for a 3-day history of headache, nausea, and bilious vomiting. The headache was partially relieved by nonsteroidal anti-inflammatory drugs (NSAIDs) and rest and had no associated neurological symptoms. She later started to experience intermittent chest tightness at rest which prompted her to go to the ER. Upon arrival, she denied any pleuritic or positional characteristics to her chest pain. She also denied any dyspnea or infectious symptoms. She had no regular medication and her vaccination status is up to date.
On arrival, she was found to be in sinus tachycardia (heart rate of 107 beats per minute), febrile (temperature 100.4°F) with a transient episode of hypotension, which improved with intravenous fluids.
On physical examination, cardiopulmonary exam was unremarkable (no pericardial friction rub). Jugular venous pressure (JVP) was initially low. A mild right upper quadrant and epigastric tenderness were noted on deep palpation. The electrocardiogram (ECG) was unremarkable except for the sinus tachycardia (Figure 1).
Initial laboratory work-up revealed a mild anemia 105 g/L with a normal white blood cell and platelets count, an abnormal liver profile consisting of a bilirubin of 24.4 μmol/L (normal <18 μmol/L), alanine aminotransferase (ALT) 170 U/L (normal <45 U/L) and alkaline phosphatase (ALK) 255 U/L (normal <98 U/L). The INR was mildly elevated at 1.31 (normal value <1.1) and the albumin was low (32 g/L). Inflammatory markers were elevated with a C-reactive protein (CRP) 182,9 mg/L (normal <5 mg/L) and an erythrocyte sedimentation rate (ESR) of 47 mm/h (normal <10 mm/h). High sensitivity troponins were normal. Creatinine and lactates were both within the normal limits.
Serologic panel for hepatitis, mononucleosis and toxicologic screening came back negative after a few days, except for the hepatitis B positive immunity due to prior vaccination.
In order to further investigate the abnormal liver tests and epigastric discomfort, an
abdominal computed tomography (CT) (with contrast administration) was performed and raised concern about hepatitis or liver congestion related to cardiac disease. In addition, a mild enhancement of the nondilated common biliary duct (CBD) was described, which was worrisome for possible early-stage cholangitis. Interestingly, the late contrast images acquisition revealed a small pericardial effusion with thickened pericardium and pericardial enhancement suggestive of pericarditis (Figure 2-A).
In addition, a magnetic resonance cholangiopancreatography (MRCP) was performed for better definition of the liver and biliary tree anatomy. This exam showed hepatic edema with abnormal enhancement and prominent inferior vena cava (IVC), suggesting congestive hepatopathy, in addition to bilateral pleural effusions and generalized anasarca. Of note, there was a small volume rim-enhancing pericardial effusion again suggestive of acute pericarditis.
To investigate the concern for congestive hepatopathy, a transthoracic echocardiogram was performed and demonstrated minimal pericardial effusion (Figure 2-B). The interventricular septum was dyssynergic without any sign of ventricular interdependence. The IVC was plethoric with very little respiration variation (Figure 2-C).
The patient was initially started on broad-spectrum antibiotics, for the suspicion of cholangitis and sepsis, which were quickly changed to colchicine and NSAIDs in light of these investigations. Diuretics were also started to treat the anasarca. Upon discharge, the patient had a CRP of 1,9 mg/L (normal <5 mg/L) with minimal residual symptoms and a cardiac magnetic resonance imaging (MRI) was ordered as an outpatient.
The cardiac MRI subsequently showed a pericardial thickening up to 3 millimeters with enhancement compatible with sequelae of pericarditis (Figure 3D-E). Equivocal findings of constriction (septal dyssynergy and mildly dilated IVC) were noted, but not diagnostic for constrictive pericarditis, and there was no evidence of pericardial tethering of the myocardium.
Given the initial presentation, what would be the mechanism for the patient's liver enzymes perturbation?