The by-products of black licorice metabolism are toxic in high concentrations. Patients who consume large quantities of black licorice are at risk of developing an acquired syndrome of apparent mineralocorticoid excess. This presents clinically as hypertension, hypernatremia, and hypokalemia. Here, we present the unique case of a 74-year-old woman with a past medical history of neurogenic orthostatic hypotension, on fludrocortisone, who presented to the emergency department with asymptomatic hypokalemia (2.4 mmol/L) as detected in outpatient laboratory studies. During her hospital stay, it was discovered that the patient was consuming excessive amounts of black licorice. With this information, the synergistic interaction of fludrocortisone and black licorice was recognized as the cause of the patient's severe hypokalemia. The patient's fludrocortisone was stopped and she was treated with multiple courses of potassium repletion. Upon discharge, her fludrocortisone was discontinued, and she was prescribed midodrine to treat her neurogenic orthostatic hypertension. While small amounts of black licorice are safe, excessive licorice consumption can cause severe disease. Our case presents an opportunity to appreciate the plethora of etiologies for severe hypokalemia and the importance of taking a thorough patient history to avoid potentially fatal clinical outcomes.

Thrombotic thrombocytopenic purpura (TTP) is typically characterized by the symptomatic pentad of fever, thrombocytopenia, microangiopathic hemolytic anemia, neurologic abnormalities, and renal failure. Atypical TTP is the diagnosis used to describe the subset of patients with TTP who present with symptoms that deviate from the classic pentad. We report a case an 86-year-old woman who presented to the emergency department complaining of chest pain for one day. She was reportedly on antibiotics for sinus infection. Physical examination revealed multiple bilateral superficial hematomas, predominantly on her extremities. On admission, her lab values were as follows: platelet count of 6,000/cubic millimeter, hemoglobin of 10.4 grams/deciliter, leukocyte count of 5100 cells/cubic millimeter, total bilirubin of 2.3 milligrams/deciliter, and troponin-I of 5.190 nanograms/milliliter. Peripheral blood smear was normal and did not reveal any schistocytes. The patient was admitted to the intensive care unit with a diagnosis of a non-ST-elevation myocardial infarction and a presumed diagnosis of immune thrombocytopenic purpura from antibiotic use. She was treated with intravenous solumedrol and a high-intensity statin. On the third day of her admission, the patient's mental functioning deteriorated and was intubated to protect her airway. A second peripheral smear revealed schistocytes, and subsequent laboratory studies supported the diagnosis of TTP. Plasma exchange therapy was planned. However, the patient succumbed to cardiac arrest before it could be initiated. The diagnosis was later confirmed with an ADAMTS13 (a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13) assay. This case serves as an example of one of the many ways in which TTP can present, and emphasizes the importance of considering TTP as a differential diagnosis.

The management of sepsis in patients with pulmonary hypertension (PH) is challenging due to significant conflicting goals of management and complex hemodynamics. As PH progresses, the ability of right heart to perfuse lungs at a normal central venous pressure (CVP) is impaired. Elevated pulmonary vascular pressure, due to pulmonary vasoconstriction and vascular remodeling, opposes blood flow through lungs thus limiting the ability of right ventricle (RV) to increase cardiac output (CO) and maintain adequate oxygen delivery to tissue. In sepsis without PH, avoidance of volume depletion with intravascular volume replacement, followed by vasopressor therapy if hypoperfusion persists, remains the cornerstone of therapy. Intravenous fluid (IVF) resuscitation based on individualized hemodynamic assessment can help improve the prognosis of critically ill patients. This is accomplished by optimizing CO by maintaining adequate preload, afterload and contractility. Particular challenges in patients with PH include RV failure as a result of pressure and volume overload, gas exchange abnormalities, and managing IVF and diuretic use. Suggested approaches to remedy these difficulties include early recognition of symptoms associated with pressure and volume overload, intravascular volume management strategies and serial lab monitoring to assess electrolytes and renal function.

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Pyoderma gangrenosum is a rare neutrophilic dermatosis characterized by painful, rapidly progressing necrotic ulcers. Although PG has been reported in association with various autoimmune diseases, its coexistence with rheumatoid arthritis (RA) mimicking vasculitis is uncommon. We present a case report of a 75-year-old female with a longstanding history of RA who developed ulcerative skin lesions that initially presented as vasculitis. She presented with new-onset painful, ulcerative skin lesion on the lower extremity, accompanied by malaise. Physical examination revealed asymmetric, deep necrotic ulcers with undermined borders. Laboratory investigations showed elevated acute phase reactants and negative rheumatoid factor. Skin biopsy demonstrated neutrophilic infiltration, confirming the diagnosis of PG. Further investigations, including imaging studies and vasculitis-specific laboratory tests, were negative, ruling out vasculitis. The patient was managed with systemic corticosteroids and immunosuppressive therapy, resulting in significant improvement of skin lesions. This case highlights the importance of considering PG as a potential differential diagnosis in patients with RA presenting with ulcerative skin lesions resembling vasculitis.