A Case of Post-operative Jaundice After Cardiac Surgery.

Hyperbilirubinemia is a common gastrointestinal complication seen post-cardiac surgery. Here, we describe a case of a 72-year-old male with a past medical history of chronic obstructive pulmonary disease, chronic kidney disease (CKD), pulmonary hypertension, and valvular heart disease with severe aortic stenosis, severe mitral and tricuspid regurgitations who underwent elective aortic valve replacement (AVR), mitral valve replacement (MVR), and tricuspid valve (TV) repair; in addition, he required left thoracotomy for the repair of pulmonary artery perforation from a Swan-Ganz catheter that resulted in a large left pleural bleed. Post-operatively, he developed severe jaundice, which was predominantly conjugated that peaked at 24 mg/dL. He also required multiple blood products' transfusion in the perioperative period and was supported temporarily with hemodialysis for acute kidney injury superimposed on his CKD. He underwent extensive evaluation for jaundice, which included ultrasound of the liver, hepatobiliary iminodiacetic (HIDA) scan, and magnetic resonance cholangiopancreatography (MRCP), which were all normal. The patient eventually got better and was discharged from the hospital. The hyperbilirubinemia slowly got better without any specific therapy and on his follow-up visit to the office following discharge, his bilirubin level was found completely normalized. Although most cases of post-cardiac surgery hyperbilirubinemia resolve without any specific therapy, the occurrence is not completely benign since it can increase morbidity and mortality. It is paramount that intensivists and cardiothoracic surgeons caring for these patients are aware of this occurrence to prevent unnecessary diagnostic evaluation. Most early cases of hyperbilirubinemia are transient and do not usually increase morbidity and mortality. In the late cases, infectious etiology resulting in sepsis needs to be entertained early and treated aggressively.

A 50-Year-Old Man With a History of Recurrent Exudative Right-Sided Pleural Effusion.

In this case report, we describe a 50-year-old man who presented to our facility for a second opinion after a year-long history of recurrent and now persistent right-sided exudative pleural effusion. On review of previous records, negative findings were seen in microbiological studies, including acid-fast bacilli, cytology, flow cytometry, and pleural biopsy using video-assisted thoracoscopy. On transthoracic echocardiography performed during our evaluation, the expected respiratory variations across the mitral and tricuspid valves were not appreciated. This necessitated subsequent cardiac workup via magnetic resonance imaging, which showed a small pericardial fluid, thickened pericardium, and a septal bounce. The patient was surgically treated using a phrenic-to-phrenic pericardiectomy, following which his symptoms resolved completely. Pleural effusions occur in approximately 40-60% of patients with constrictive pericarditis, and despite the known association of pleural effusions with constrictive pericarditis, the diagnosis of constrictive pericarditis is not readily entertained in patients with undiagnosed pleural effusions.

A 68-year-old woman with a diagnosis of asthma and multiple fleeting pulmonary nodules- a case report.

Diffuse idiopathic pulmonary neuroendocrine cell (DIPNECH syndrome) remains unfamiliar to most clinicians even though it was first described almost 30 years ago. Diagnosis is usually confirmed histopathologically after lung biopsy, but often, a diagnosis or suspected diagnosis can be made radiographically. In this paper, we present a case report of a 68-year-old female with shortness of breath and fleeting pulmonary nodules observed on chest CT scan. She was initially misdiagnosed with asthma based on an abnormal pulmonary function test which revealed an obstructive ventilatory defect. The classic radiographic findings of DIPNECH syndrome and the typical patient demographics that should arouse suspicion of a DIPNECH diagnosis were also illustrated. DIPNECH syndrome is a clinicopathological syndrome whereas focal NECH is a pathological diagnosis that is often made incidentally on histological examination and is encountered in a variety of settings, including in resected carcinoid tumors, in the context of reactive changes concomitant with infection, in metastatic cancer, radiation pneumonitis, intra-lobar sequestration, smokers, interstitial lung disease, and lung adenocarcinoma. There are no proven treatments for DIPNECH syndrome. In patients with obstructive ventilatory symptoms, bronchodilators with inhaled steroids are usually prescribed. Some severe cases may require parenteral steroids. Somatostatin analogs (SSA) have also been used in some cases with mixed results. Rapamycin has been used in several cases based on the purported activation of the mammalian target of rapamycin (mTOR) in DIPNECH. Some patients with large carcinoid tumors may benefit from resection.

Multiple electrolyte imbalances and mixed acid-base disorder posing a diagnostic dilemma: a case report.

BACKGROUND: In clinical practice, both the history and laboratory testing are paramount to making an accurate diagnosis. Situations in which laboratory findings and patient history are not congruent pose a diagnostic dilemma. We report a case of a young woman presenting with a myriad of electrolyte and acid-base disorders. Difficulty in reaching a unifying diagnosis persisted due to discordant patient history. We believe this case shows that lab findings will clearly portray the problems a patient has and should be given more credence in a case where the history is discordant with lab findings. CASE PRESENTATION: A 28-year-old Hispanic American woman presented to the emergency room of our institution with a complaint of painless and sudden onset of stiffness in her upper and lower limbs. Associated weakness worse in the distal limbs was also reported. She experienced shortness of breath with minimal exertion, diaphoresis, and anxiety. Her vital signs revealed tachycardia without corresponding fever. She was conscious, oriented, and alert. Her physical exam revealed dry mucous membranes and warm extremities. She denied recent consumption of a large carbohydrate meal, diarrhea, vomiting, use of laxatives, and use of alcohol or recreational drugs. She vaguely described two previous similar episodes in the last 7 months that spontaneously resolved. Her medical history was significant only for hypothyroidism treated with daily levothyroxine tablets. Laboratory analysis revealed the following abnormalities: an elevated anion gap with significant lactate, hypokalemia, hypomagnesemia, elevated mean corpuscular volume, elevated mean cell hemoglobin, and elevated liver enzymes with aspartate aminotransferase/alanine aminotransferase ratio > 2. She was hydrated with balanced crystalloids, and her electrolyte deficiencies corrected. The etiology of her multiple electrolyte abnormalities was unclear because alcohol use was vehemently denied. Extensive evaluation for causes of electrolyte disorder was undertaken, which was unrevealing. On further interrogation, she admitted to recent alcohol intoxication and several episodes of vomiting before presentation. She was advised to refrain from alcohol use and discharged afterward. CONCLUSION: Both patient history and laboratory analysis have a role in identifying and confirming a diagnosis. In cases in which laboratory tests are incongruous with reported history, making a unifying diagnosis can be challenging or delayed. The importance of taking a comprehensive history cannot be overemphasized, but history provided by patients may be prone to intentional or unintentional distortion, whereas laboratory findings are more objective. The case presented underscores why the lab findings should be given credence in cases in which there is discordance between lab results and the provided patient history.