Unilateral Pupil Sparing: Viral Oculomotor Neuritis With Concomitant Vestibular Neuritis.

Unilateral oculomotor nerve palsy is a common clinical condition with various etiologies, including aneurysm, diabetes mellitus, central nervous system (CNS) infections, pituitary tumors, and ischemic changes. Due to the plethora of possible causes, early and thorough investigation is essential for treatment. We report the case of a 45-year-old male who presented with left ptosis, vertigo, and blurry vision and was diagnosed with oculomotor neuritis. Past medical history (PMH) was significant for hyperlipidemia, diabetes, and chronic kidney disease. Patient imaging revealed chronic left cerebellar infarction but no acute changes. Significantly, he was experiencing intractable nausea, dizziness, and vomiting attributed to concomitant vestibular neuritis. Infectious etiologies of oculomotor neuritis are rarely reported. However, idiopathic vestibular and facial palsies are commonly attributed to viral infection. The patient was treated with a steroid taper for viral vestibular neuritis, with noticeable clinical improvement to his oculomotor neuritis manifestations. This postulates a common viral etiology uniquely causing both oculomotor and vestibular neuritis.

Cefazolin-induced hemolytic anemia: a case report and systematic review of literature.

BACKGROUND: Cefazolin is a first-generation cephalosporin commonly used for skin and soft tissue infections, abdominal and orthopedic surgery prophylaxis, and methicillin-sensitive staph aureus. Cephalosporins as a whole are known potential inducers of hemolytic anemia; however, mechanism of action is primarily autoimmune, and compared to other drugs, cefazolin is the least common. METHODS: A rare case report of cefazolin-induced hemolytic anemia "CIHA" and a systematic review of CIHA articles in English literature. Two authors performed review of publications and articles were selected based on inclusion and exclusion criteria. A systematic search of the literature yielded 768 entries with five case reports on cefazolin-induced hemolytic anemia. CASE PRESENTATION/RESULTS: An 80-year-old female with methicillin-sensitive Staphylococcus aureus "MSSA" endocarditis. The patient was started on intravenous "IV" cefazolin that that resulted in hemolytic anemia and eosinophilia. Switching to vancomycin improved hemoglobin level and resolved eosinophilia. Four cefazolin-induced hemolytic anemia case reports and one population-based article with a case reported were analyzed with respect to direct antiglobulin test "DAT" (also known as the direct Coombs test) results, prior penicillin sensitivity, and acute anemia causes exclusion. CONCLUSIONS: CIHA is a rare cause of clinically significant anemia. The diagnosis of drug-induced anemia is one of exclusion. It is important to consider DAT results and prior penicillin sensitivity when evaluating a patient for cefazolin-induced hemolytic anemia. However, the frequency of cefazolin use and resultant anemia necessitates early recognition of hemolytic anemia and prompt discontinuation of cefazolin, especially with long-term use.

A subgroup analysis of penetrating injuries to the pancreas: 777 patients from the National Trauma Data Bank, 2010-2014.

BACKGROUND: This study is the first to analyze penetrating injuries to the pancreas within subgroups of severe traumatic brain injury (TBI), early deaths, and potential survivors. Our objectives were to identify national patterns of injury, predictors of mortality, and to validate the American Association for Surgery of Trauma Organ Injury Scale (AAST-OIS) pancreas injury grades by mortality. Secondary outcomes included hospital and intensive care unit length of stay and days on mechanical ventilation. METHODS: Using the Abbreviated Injury Scale 2005 and ICD-9-CM E-codes, we identified 777 penetrating pancreatic trauma patients from the National Trauma Data Bank that occurred between 2010 and 2014. Severe TBI was identified by ICD-9-CM diagnosis codes and Glasgow Coma Score (GCS; n = 7), early deaths were those that occurred within 24 h of admission (n = 82), and potential survivors included patients without severe TBI who survived longer than 24 h following admission (n = 690). We estimated multivariable generalized linear mixed models to predict mortality to account for the nesting of potential survivors within trauma centers. RESULTS: Our results indicated that overall mortality decreased from 16.9% to 6.8% after excluding severe TBI and early deaths. Approximately, 11% of patients died within 24 h of admission, of whom 78% died in the first 6 h. Associated injuries to the stomach, liver, and major vasculature occurred in approximately 50% of patients; rates of associated injuries were highest in patients who died within 6 h of admission. In potential survivors, mortality increased by AAST-OIS grade: 3.5% I/II; 8.3% III; 9.6% IV; and 13.8% V. Predictors of mortality with significantly increased odds of death were patients with increasing age, lower admission GCS, higher admission pulse rate, and more severe injuries as indicated by Organ Injury Scale grade. CONCLUSIONS: From 777 patients, we identified national patterns of injury, predictors of outcome, and mortality by AAST-OIS grade within the subgroups of severe TBI, early deaths, and potential survivors. Because AAST-OIS is not a reported element in the National Trauma Data Bank, we correlated Abbreviated Injury Scale 2005 codes to injury grade and identified an increase in mortality. After controlling for covariance, we found that greater age, lower GCS in stab wounds, higher pulse, and presence of a grade V pancreatic injury independently predicted the likelihood of death in patients surviving beyond 24 h following penetrating injuries to the pancreas.