A one-year-old boy presented to the emergency department with a sudden onset of fulminant edema of the right eyelid, making it impossible to open his right eye (Figure 1 ). The ophthalmologic examination showed painful eyelid edema with conjunctival chemosis. Due to the extensive eyelid swelling, it wasn’t possible to examine pupillary light reflexes or ocular motility nor to perform a fundus examination. The boy had a temperature up to 39.1°C. Physical examination showed an alert patient, without neurological or meningeal signs, but with cutaneous varicella lesions spread over his entire body.\nLaboratory work up showed normal leukocytes (9.23 x 103/µl), thrombocytopenia (platelets 67 x 103/µl) and elevated CRP (52 mg/l). The boy hadn’t received his vaccination for varicella yet, which usually takes place between the age of 12 to 15 months. Clinical examination couldn’t exclude orbital cellulitis and revealed multiple enlarged lymph nodes in the neck region. There was a clinical suspicion of a secondary bacterial infection of the cutaneous varicella lesions around the eyelid. CT of the orbit revealed pronounced superficial soft tissue inflammation of the right periorbit without evidence of an intraorbital inflammation or abscess formation, cavernous sinus thrombosis or intracranial extension of the inflammation (Figure 2 ).\nThe boy was hospitalized for a trial of intravenously antiviral (acyclovir) and antibiotic therapy (amikacin, flucloxacillin, and ceftriaxone). The antibiotic therapy was changed to clindamycin after 2 days due to poor clinical response with also increasing swelling of his left eyelid (Figure 1 ). In immunocompetent children, VZV usually causes a benign infection without the need for systemic antiviral treatment, in this case the pediatrician decided to treat the varicella infection with intravenously acyclovir for 5 days (30 mg/kg/day in 3 divided doses). The laboratory markers of inflammation raised with a maximal leucocytosis of 23.8 x 103/µl and a CRP level of 190 mg/l. There weren’t any clinical signs of sepsis. The peripheral blood count and culture of vesicular fluid obtained at the emergency department were negative. On the second day of admission, the right upper eyelid ruptured spontaneously (Figure 1 ). We removed the overlying crusts and debris and took a swab of the underlying ulcer. Culture grew the anaerobic organism Veillonella parvula, without identifying any other bacterial or fungal organisms. Clindamycin was continued to cover anaerobe bacteria. The antibiogram showed resistance to penicillin, amoxicillin clavulanic acid and even metronidazole, but sensitivity to clindamycin and meropenem. The source of infection was most likely a superinfection of the varicella skin lesion. Clindamycin was given intravenously for 3 weeks with a good clinical response showing a slow but progressive decline of the eyelid edema. When the boy was discharged from the hospital, clindamycin was continued orally for another 4 weeks, resulting in a total antibiotic treatment duration of 7 weeks. The eyelid swelling with a hardened eyelid persisted for 4 months. Because of this, the boy was unable to fully open his eye in the first 4 months, obscuring the child’s visual axis and putting him at great risk for developing occlusion amblyopia (Figure 3 ). The patient gained a full recovery with a complete resolution of the eyelid edema and a clear visual axis without need for surgical intervention. He is still in follow-up with a pediatric ophthalmologist for regular amblyopia screening and early treatment if necessary.
A 31-year-old male with a history of heavy alcohol use presented to our hospital with a 3-day history of lower extremity edema, abdominal swelling, and periumbilical pain. He reported use of 6 cans of beer daily, with the most recent use 3 days prior to admission. On presentation, the patient was alert and oriented only to person and self. His vital signs were a temperature of 38.5°C, heart rate 129 beats/minute, and blood pressure 132/74 mmHg. Physical exam was significant for scleral icterus, asterixis, systolic murmur, abdominal distention with caput medusae, palmar erythema, and spider angiomas on his chest.\nLaboratory tests revealed a white blood cell (WBC) count of 11.7 K/mm3 (with 78% neutrophils, absolute lymphocyte count 1.3 K/mm3, and absolute monocyte count 1.0 K/mm3), platelets 88 K/mm3, lactate 2.1 mmol/L, alkaline phosphatase (ALP) 503 U/L, aspartate aminotransferase (AST) 172 U/L, and alanine aminotransferase (ALT) 19 U/L. Maddrey's Discriminant Function score was 35.3 (Prothrombin time 19.2 seconds and total bilirubin 6.8 mg/dL). Ascitic fluid analysis after paracentesis was negative for spontaneous bacterial peritonitis, with a nucleated cell count of 79/cumm and 23% segmented neutrophils. Further hepatitis workup yielded antinuclear antibodies positive for nuclear, speckled pattern with 1 : 1280 titer, actin antibodies IgG 57 units, and negative viral hepatitis panel for hepatitis A, B, and C. Abdominal ultrasound showed cirrhosis with hepatosplenomegaly and trace abdominal ascites.\nTwo sets of blood cultures obtained on hospital day 0 were negative. Intravenous ceftriaxone was started after collection of the initial blood cultures. Two additional anaerobic blood culture bottles obtained on day 2 of hospital stay were positive for Veillonella atypica, identified using MALDI-TOF (). Repeat blood cultures after 2 days of intravenous ceftriaxone were negative. The infectious disease team recommended discontinuing IV ceftriaxone as repeat cultures were negative and the patient had completed a 7-day course of ceftriaxone. Transthoracic echocardiogram was negative for valvular lesions. Liver biopsy obtained on hospital day 8 demonstrated bridging fibrosis and was consistent with alcoholic hepatitis with cholestasis (Figures and ).\nHospital course was complicated by hemodynamic instability and acute encephalopathy on day 3 and 4, where patient was tachycardic to 120 beats per minute, tachypneic to 30 shallow breaths per second, and febrile to 38.3°C. The patient's mental status was waxing and waning; there was a concern for sepsis, grade II hepatic encephalopathy, and alcohol withdrawal. Hemodynamic instability and mental status improved with IV lorazepam and lactulose, and the patient was subsequently discharged on hospital day 9. After confirmation of alcoholic hepatitis on liver biopsy, the patient started prednisolone 40 mg oral daily on day 7 after hospital discharge due to difficulty obtaining the prescription.\nPatient was evaluated in outpatient hepatology clinic 7 days after prednisolone therapy (14 days after hospital discharge). Pertinent labs showed a white blood cell count of 23.9 K/mm3, sodium of 123 mmol/L, and potassium of 2.9 mmol/L. Prothrombin time and total bilirubin had increased to 23.4 sec and 20.2 mg/dL, respectively. Calculated Lille score on day 7 of treatment was 0.577 and suggestive of treatment failure of alcoholic hepatitis. The patient was sent to the emergency room after the clinic visit for tachycardia and concern for sepsis. He was then readmitted to the hospital for further management. Repeat blood cultures and ascitic fluid culture on admission were negative. The patient was deemed a poor transplant candidate due to continued alcohol use and non-United States citizen status. After appropriate counseling, he left the hospital against medical advice to be home with family.\nDuring a phone follow-up 3 months after discharge, the medical team was informed that the patient was deceased.