Avoiding a Perfect Storm: Delving into the Consequences of a Complex case of Superimposed Cellulitis after a Herpes Zoster infection

Introduction: Cellulitis is an acute bacterial infection causing inflammation affecting the deep dermis layer as well as the surrounding subcutaneous tissue that does not contain an abscess. In this case study we aim to describe the clinical presentation of a middle aged Hispanic woman who developed a superimposed cellulitis infection following a flare-up of a zoster infection. Herpes Zoster is typically considered a typically benign infection but in immunocompromised individuals severe complications of the infection include bacterial superinfections, coagulopathies including disseminated intravascular coagulation, and central nervous system manifestations including encephalopathy with long term detrimental outcomes [1]. Management of Herpes Zoster Virus complications in immunocompromised patients has been a historically challenging task as there is limited reference data because of the unique presentation of each patient and their varying levels of immunocompetence adds an extra layer of variability to each patient’s presentation. Our patient’s past medical history of Polycystic Ovarian Syndrome, uncontrolled diabetes mellitus type 2, and hypertension created an immunocompromised state predisposing her to an acute cellulitis infection following her most recent flare-up of shingles rash. Social determinants that contributed to her disease progression were her lack of healthcare access including regular check-ups for glucose monitoring and suboptimal treatment for her chronic medical conditions [2]. This is a recurrent theme in patients in a similar situation located in the US-Mexico border where social determinants exponentially affect the healthcare outcomes of patients and often lead to severe outcomes that increase morbidity and mortality in this highly vulnerable population [3]. Case Description: Our patient is a 37-year-old Hispanic woman who presented to the clinic complaining of a rash in her left lower abdominal region, as well as systemic symptoms including a fever and an episode of chills. Her past medical history includes Polycystic Ovarian Syndrome (PCOS), Diabetes Mellitus type 2, hypertension, and hyperlipidemia. She has a history of a Zoster virus rash that flared-up 2 weeks ago that had not resolved and stated that it had progressively worsened and became more erythematous leading to increased pruritus. At the time of her flare-up she was treated with Acyclovir 800 mg Q5h which she said provided minimal resolution of her symptoms. Physical examination revealed a wound covered with a bullous pustular lesion with a warm erythematous portion in the right flank. Her vital signs revealed a low grade fever of 100.8 F and a tachycardic state with a pulse 112 bpm. Further evaluation included a point of care ultrasound (POCUS) to rule out a potential abscess, results were unremarkable . Her most recent laboratory values included a CBC significant for a WBC of 19 and a hemoglobin A1c of 13.6. Patient was treated with an antibiotic regimen including topical clindamycin and 1 dose of intramuscular injection of Ceftriaxone 750 mg. After the administration of the antibiotics available to us at the outpatient center, the patient was told to check in at the emergency room for closer monitoring and possible continuation of IV antibiotic treatment. The patient declined and decided she was going to monitor the symptoms herself because she stated she couldn’t cover the costs of a prolonged hospital stay. She was then advised to report to the emergency room if she noticed worsening symptoms including crackling or crepitation as well as worsening systemic symptoms such as high fevers, chills, or severe abdominal pain. She was seen at the clinic 1 week later to follow up on the progression of the rash and symptom resolution following the completion of her antibiotic regimen. Fig. 1 depicts the localization of the rash when the patient arrived at clinic Day 1. Following antibiotic treatment and appropriate symptomatic monitoring after 1 week, Fig. 2 reveals resolution and subsequent abdominal scarring. During the patient’s follow up, we discussed the importance of continuation of care for her chronic medical conditions to prevent further complications in the future including her predisposition to CAD and susceptibility to infections, her hyperglycemic monitoring, and compliance to treatment regimen. Discussion: This case highlights the unique clinical presentation of cellulitis post-shingles infection in a middle-aged Hispanic woman with multiple unmanaged chronic conditions. The summation of which led to a weakened immune response and superimposed cellulitis infection. This case highlights the potential for superimposed bacterial infections to occur on compromised skin. This case emphasizes the importance of prompt intervention and appropriate health care maintenance to prevent further complications. Limited access to healthcare services can hinder disease management and increase the risk of complications in underserved populations [2] . This case underscores the significance of addressing healthcare disparities and improving access to comprehensive healthcare resources, particularly for individuals with multiple unmanaged chronic conditions, in order to mitigate risk of disease progression and enhance overall patient outcomes. Conclusion: This case illustrates the impact of social determinants on disease progression in a middle-aged Hispanic woman with limited healthcare access and under-managed chronic conditions who developed superimposed cellulitis following HZV infection. The conclusion emphasizes the need for timely intervention, improved healthcare resources, and addressing healthcare disparities to mitigate complications which ultimately leads to improved patient outcomes, especially in underserved populations with limited resources

Penile Calciphylaxis in an End Stage Renal Disease patient.

Background: Penile Calciphylaxis occurs in about 1–4% of hemodialysis patients worldwide. Associated mortality rates are very high, and hyperparathyroidism is the second most frequently associated disorder. Addressing the resulting metabolic imbalance, and surgical intervention guided by findings of radiological studies may improve quality of life. The pathogenesis is thought to be mediated by vascular smooth muscle cells which differentiate into osteoblast-like cells. Decrease in vascular calcification inhibitory proteins fetuin-A and matrix Gla is found in patients on dialysis causing systemic medial calcification of arterioles, leading to epidermal ischemia, tissue infarction, and ulceration. Case presentation: 47-year-old male with history of coronary arterial disease, type 2 diabetes mellitus, and end stage renal disease on dialysis presented with penile pain. Onset was 1.5 months earlier. Patient was evaluated multiple times, resulting in several antibiotic cycles without much perceived improvement. On presentation patient’s vital signs were unremarkable. Genitourinary exam showed a penis with a necrotic center around the urethral meatus opening and white ischemic patches on the glans. Additionally, darkened penis shaft and ulcerative foreskin lesions were visible. Parathyroid hormone and phosphorus were elevated, 480 pg/mL and 5.1 mg/dL respectively. CT scan of the abdomen showed calcification along the shaft of the penis and glans. The patient started antibiotic therapy, pain management, cinacalcet and a trial of sodium thiosulfate. Total penectomy and suprapubic catheter placement were done successfully. Pathology report confirmed the diagnosis. Conclusion: Because penile calciphylaxis is a metabolically mediated progressive disease, systemic treatment is vital in attempting to slow its progression. These do little to address the pain and urinary retention from necrosis, so the need of a wider and proximal resection, which also helps foster better wound healing. This case illustrates the importance of a prompt and accurate diagnosis of penile calciphylaxis, and management of its systemic manifestation

Euglycemic Diabetic Ketoacidosis in a patient using Sodium-Glucose Cotransporter-2 inhibitor (SGLT 2 inhibitor)

Background: Diabetic Ketoacidosis (DKA) is a life-threatening complication of Diabetes Mellitus type-1 and occasionally type-2 diabetes, associated with high blood glucose levels\u3e250 mg/dl. Normal glucose levels in all diabetic patients may delay diagnosis and management of DKA and result in increased morbidity and mortality. Case Presentation: A 68-year-old male having a medical history of Diabetes Mellitus type-2, atrial fibrillation, aortic stenosis status post total valve replacement, coronary artery disease, gastric bypass surgery, and previous stroke presented with two episodes of hematemesis a few hours prior to admission. The patient denied using drugs or ingestion of methanol, ethylene glycol, and salicylate. His home medications include apixaban (Eliquis), Empagliflozin (Jardiance) SGLT-2 inhibitor, and metformin. Physical exam was unremarkable except for dry mucous membrane. While in the emergency department, the patient suffered shortness of breath with increased respiratory rate 24/min (12-16/min) and use of accessory muscles. IV fluid was administered, and initial laboratory data indicated negative ethanol and salicylate levels, with normal parameters including electrolytes and glucose level of 192mg/dl (\u3c250mg/dl). To eliminate the rare probability of Euglycemic Diabetic Ketoacidosis (EDKA), an extensive lab work showed PH 7.07 (7.35-7.45), bicarbonate 3.5mmol (23-30mmol/L), anion gap 24mmol/L (3-10mmol/L), serum ketone 8mmol/L (0.6-1.5mmol/L), serum osmolality 323mmol/kg (285-295mmol/kg) and osmolar gap 28mmol/kg (\u3c10mml/kg). Euglycemic DKA was diagnosed, and treatment started with insulin drip, IV fluid, discontinuation of Jardiance and Eliquis. Endoscopy showed stomach inflammation with no ulcer. Pathology confirmed mild active gastritis, but no intestinal metaplasia, dysplasia, or malignancy was identified. The patient’s condition improved drastically and was discharged on the third day. Conclusion: Diagnosis of DKA is challenging especially with normal glucose levels. SGLT-2 inhibitor was believed to be the culprit. Ketones should be checked in all admitted diabetic patients with high anion gap metabolic acidosis, regardless of blood glucose level

Metagenomic Sequencing of Monkeypox Virus, Northern Mexico

Monkeypox virus (MPXV) has gained interest because of a multicountry outbreak of mpox (formerly monkeypox) cases with no epidemiologic link to MPXV-endemic regions. We sequenced the complete genome of MPXV isolated from a patient in northern Mexico. Phylogenetic analysis grouped the virus with isolates from Germany