Propofol Infusion and Acute Pancreatitis: A Review.

BACKGROUND: Propofol is a short-acting anesthetic used to induce sedation in various ambulatory and inpatient surgical procedures. It is a US Food and Drug Administration approved lipid-based intravenous hypnotic agent, which has been used clinically for the induction and maintenance of anesthesia for over 3 decades. In addition to general anesthesia, it is used to sedate patients undergoing mechanical ventilation or short procedures such as endoscopy, transesophageal echocardiogram, and abscess drainage. An infrequent but serious complication of propofol is acute pancreatitis (AP), with potentially significant morbidity and possible mortality. In this review, we will discuss the proposed mechanisms of AP secondary to propofol, a number of reported cases, studies conducted, and treatment strategies. AREAS OF UNCERTAINTY: There are several case reports in the literature that have shown an association between propofol and pancreatitis. The exact mechanism behind propofol-induced pancreatitis is not fully understood, but proposed mechanisms include hypertriglyceridemia (HTG), hypersensitivity, or direct pancreatic toxicity of the drug. Although the association of propofol and pancreatitis has not been proven conclusively, clinicians should be aware of this possible rare complication to prevent the devastating consequences of AP. DATA SOURCES: We gathered articles on previously documented case reports and up-to-date studies on propofol-induced pancreatitis by searching databases such as PubMed and Google Scholar. RESULTS: Based on previous studies and case reports, we suggest that propofol should be added to a list of drugs having a direct association with AP. CONCLUSIONS: Although, the mechanism of propofol-induced pancreatitis is not fully understood, and the causal relationship of propofol-induced hypertriglyceridemia or idiosyncratic drug reaction has remained unproven. Clinicians should be aware of the association between propofol and pancreatitis, and any patient presenting with abdominal pain after propofol infusion should be evaluated for AP and treated promptly to avoid complications.

Sputum Smear and Culture-negative Tuberculosis with Associated Pleural Effusion: A Diagnostic Challenge.

Tuberculosis (TB) is an important cause of morbidity and mortality in the United States. Due to the unpredictable or nonspecific nature of its clinical presentations, TB can be a diagnostic challenge for physicians. In 2013, 23% of reported TB cases were culture-negative in the United States; in New York City, this was approximately 27%. The increasing number of sputum smear- and culture-negative TB patients is a serious concern because misdiagnosis and delayed treatment can lead to increased morbidity and mortality and increased infectious transmission. We report a case of a 26-year-old-female recent immigrant, who was initially managed for community-acquired pneumonia but was later found to have TB with complicated pleural effusion, despite having multiple smear- and culture-negative sputum specimens, Xpert Mycobacterium tuberculosis (MTB)/resistance to rifampin (RIF) assay (real-time polymerase chain reaction (PCR)) and pleural fluid analysis. She improved clinically on anti-tuberculosis therapy and, later, the diagnosis was confirmed by pleural biopsy.

Type II Renal Tubular Acidosis Secondary to Topiramate: A Review.

Topiramate (TMP) is a broad-spectrum anticonvulsant drug used to treat a wide variety of seizure disorders, for migraine prophylaxis, and for many other indications. An important side effect of TMP is metabolic acidosis, which is mediated by renal tubular defects. TMP inhibits carbonic anhydrase, an enzyme that is necessary for acid handling in the proximal renal tubule. Patients can present with asymptomatic serum electrolyte derangements, acute change in mental status, hyperventilation, cardiac arrhythmias, or other sequelae of metabolic acidosis and associated respiratory compensation. If taken chronically, TMP can cause renal stone formation, bone mineralization defects, and several other effects secondary to changes in serum and urine pH and electrolytes. There is no well-studied way to prevent metabolic acidosis in patients taking TMP, but physicians should be vigilant when prescribing this drug to patients with the history of renal diseases and other comorbidities, and aware of this potential etiology of metabolic acidosis. We present a literature review of the underlying mechanisms involved in the development of renal tubular acidosis secondary to TMP and its clinical consequences.