Varicella Zoster when described has the typical presentation of a dermatomal distribution of a rash and can further lead to CNS complications. This can be treated accordingly with the proper protocol, but if the presentation is atypical and the protocol is challenged or changed per specific patient outcomes, new developments can occur. Here we present a case of a 29-year-old Caucasian female that presented to the emergency department with headache, photophobia, and chills for 5 days. She was previously healthy and immunocompetent; CSF PCR analysis revealed a VZV infection causing acute aseptic meningitis with no shingles rash eruption on physical examination. The patient was not willing to stay hospitalized for the duration of the treatment. This gave us an opportunity to treat her with an oral, rather than IV, antiviral. The patient was successfully treated with oral valacyclovir 2 g Q6H after only receiving two days of IV acyclovir. To the best of our knowledge, this is the first reported case of a patient with VZV-associated meningitis successfully treated with oral valacyclovir.
Sump syndrome is a rare, long-term complication with a prevalence ranging from 0% to 9.6% in patients with a history of side-to-side choledochoduodenostomy. Choledochoduodenostomy was originally performed to achieve drainage of the common bile duct in high-risk patients with low morbidity, which was commonly done in the pre-endoscopic retrograde cholangiopancreatography era. “Sump” comes from the segment of the common bile duct between the anastomosis and the ampulla of Vater, which acts as a stagnant reservoir for debris, stones, and static bile. This predisposes patients to changes in the biliary tree with signs and symptoms in relation to that area. If left untreated, cholangitis, pancreatitis, hepatic abscesses, and secondary biliary cirrhosis can develop. Here, we have a case of a 77-year-old male with a history significant for choledochoduodenostomy, who presented with the clinical signs and symptoms of pancreatitis, choledocholithiasis, and urinary tract infection. Computed tomography (CT) scan findings revealed choledocholithiasis and an enlarged common bile duct with smaller adjacent calculi along with pneumobilia consistent with sump syndrome. The patient’s clinical status improved without invasive measures being taken, i.e. endoscopic retrograde cholangiopancreatography. He was subsequently discharged home after improving clinically and no invasive measures were pursued.
Tumefactive multiple sclerosis (TMS) is a rare entity which can be difficult to diagnose unless definitive diagnostic measures are taken. TMS is characterized by solitary or multiple lesions that are sized > 2 cm, with/without mass effect, edema, and ring enhancement on magnetic resonance imaging (MRI). The demyelinating lesion can mimic infections, vascular lesions, and inflammatory lesions. The clinical presentation is highly dependent on the area of the brain which is affected, and this can lead to a variety of signs and symptoms. Herein, we present the case of a 40-year-old immunocompetent female with a history of right-sided numbness of her face, arm, and leg associated with muscle weakness for about a week. Workup included an MRI showing ring-enhancing lesions in the white matter of the brain, zero oligoclonal bands in the CSF, a normal immunoglobulin G (IgG) index, and an elevated myelin basic protein (MBP) in the CSF. A biopsy was obtained that showed predominant macrophage infiltrate with loss of myelin but the preservation of axons. Suspecting a demyelinating pathology, the patient was informed that she would be started on intravenous dexamethasone for an eight-day course. With subsequent completion of this course in the hospital, the patient was discharged on oral prednisone daily for a month and a referral leading to a definitive diagnosis of TMS. The patient was started on interferon beta-1a and subsequently relapsed due to noncompliance. However, further workup showed a reduction in the mass-like lesions and a response to therapy. If suspicion for TMS is high despite workup, steroids can be used with immunomodulators in the interim to combat symptoms and potentially reduce lesions and potentially subvert the need for biopsy.
The etiology of lactic acidosis can potentially be misleading, especially in a critically ill patient with malignancy. Type B lactic acidosis represents a rare and often lethal complication of malignancy. When differentiating the types of lactic acidosis, Type A is due to marked tissue hypoperfusion and Type B is due to causes in the setting of a normal perfused state.We report the case of a 56-year-old male with newly diagnosed poorly differentiated neuroendocrine metastatic carcinoma and renal cell carcinoma who presented with a decreased level of consciousness and appetite. The patient was started on a sepsis protocol from an initial intensive care unit (ICU) admission. Broad spectrum antibiotics were initiated, and despite management, his mentation and respiratory status worsened, leading to intubation and mechanical ventilation. The patient continued to have elevated lactic acid and white count levels throughout the hospital course. After extensive workup and an ICU stay of 16 days, a decision was made to pursue comfort care measures and the patient passed away shortly thereafter.The patient's persistently elevated lactic acidosis may have resulted from the inherent malignancy. The literature mentions glycolysis with enhanced metabolism as a proposed mechanism. One theory states that these changes enable cancer cells to acquire and metabolize nutrients in a way that favors proliferation over efficient adenosine triphosphate (ATP) production, resulting in elevations of lactate production. Patients presenting to the ICU with elevated lactic acid levels need to be thoroughly worked up for all potential causes. In our case, the underlying malignancies likely caused the persistently elevated lactic acidosis, despite subtherapeutic treatment and resuscitative measures.
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