48 research outputs found

    Rituximab-induced Procalcitonin Elevation

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    Procalcitonin has been studied as a marker of bacterial lung infection. It frequently guides clinical practice and antibiotic management. However, procalcitonin is known to have false positive results in certain scenarios. This case describes an 86 year old African American woman with mantle cell lymphoma who presented with acute on chronic dyspnea. Diagnostic tests found a white blood cell count of 632 k/uL (95% lymphocytes) and procalcitonin of 1.29 ng/mL. Computed tomography of the chest demonstrated a right lung consolidation and hilar lymphadenopathy. She was treated empirically for pneumonia with ceftriaxone and azithromycin. Additionally, she received induction chemotherapy with rituximab and bendamustine. By hospital day three, she demonstrated clinical improvement despite a significant rise in her procalcitonin level to 42.83 ng/ml. This increase correlated with receiving rituximab. She continued to improve and was discharged to a rehab facility after finishing her induction chemotherapy. This case demonstrates a link between rituximab and false positive results of procalcitonin. Thus, clinicians should be aware of the limitations of procalcitonin as the exclusive marker in pneumonia diagnosis.https://scholarlycommons.henryford.com/merf2020caserpt/1025/thumbnail.jp

    Fundamentals of Arterial Blood Gas Interpretation

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    Acid-base disturbances in patients with cardiopulmonary or other disorders are common and are often misinterpreted or interpreted incompletely. Treating acid-base disorders in greater detail facilitates pathophysiologic understanding and improved therapeutic planning. Understanding the ratiometric relationship between the lungs, which excrete volatile acid as carbon dioxide, and the kidneys, which contribute to maintenance of plasma bicarbonate, allows precise identification of the dominant acid-base disturbance when more than a simple disorder is present and aids in executing a measured treatment response. Concordantly, mapping paired values of the partial pressure of carbon dioxide (PCO2) and the bicarbonate concentration ([HCO3–]) on a Cartesian coordinate system visually defines an acid-base disorder and validates the ratiometric methodology. We review and demonstrate the algebraic and logarithmic methods of arterial blood gas analysis through the example of a complex acid-base disorder, emphasizing examination of the PCO2-to-[HCO3–] ratio

    Sodium-Based Osmotherapy in Continuous Renal Replacement Therapy: a Mathematical Approach

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    Cerebral edema, in a variety of circumstances, may be accompanied by states of hyponatremia. The threat of brain injury from hypotonic stress-induced astrocyte demyelination is more common when vulnerable patients with hyponatremia who have end stage liver disease, traumatic brain injury, heart failure, or other conditions undergo overly rapid correction of hyponatremia. These scenarios, in the context of declining urinary output from CKD and/or AKI, may require controlled elevations of plasma tonicity vis-à-vis increases of the plasma sodium concentration. We offer a strategic solution to this problem via sodium-based osmotherapy applied through a conventional continuous RRT modality: predilution continuous venovenous hemofiltration

    Acute Tubular Necrosis

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    Epidemiology of Cardiorenal Syndrome

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    Cardiorenal syndrome is a spectrum of disorders that emphasizes the bidirectional nature of cardiac and kidney injury. Observational and retrospective studies have helped us to understand the prevalence and burden of each of the 5 types of cardiorenal syndromes. Cardiorenal syndrome type 1 is the most common. The nature of epidemiologic data limits clear delineation between cardiorenal syndrome types 2 and 4. Overall, the presence of cardiac or renal dysfunction strongly predicts a poor outcome of the contrary organ

    Acute Kidney Injury

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    A Case Of Amiodarone-Induced Sweet Syndrome

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    Learning Objective #1: Recognize and differentiate Sweet syndrome (acute febrile neutrophilic dermatosis) from an infectious process. Learning Objective #2: Recognize amiodarone as a potential cause of drug-induced Sweet syndrome. CASE: Our patient was a 41-year-old Caucasian male, with a past medical history of atrial fibrillation (Afib), non-ischemic cardiomyopathy (Ejection Fraction 9 %), and diabetes mellitus presented to the hospital with signs and symptoms of decompensated heart failure and skin lesions. He was febrile and had innumerable tender, pruritic, violaceous, annular plaques with central ulceration which had a contiguous centripetal spread from extremities extending to abdomen and chest over a period of 2 weeks. Careful medication review suggested recent re-initiation of amio-darone for Afib. Additional history revealed similar rashes in the past which were temporally related to amiodarone use. Interestingly each subsequent exposure resulted in increased severity and rapidity of skin lesions. Thought to be infectious in origin the patient had been treated with antibiotics each time, however, the patient identified improvement after stopping the offending drug. Differential diagnosis included amiodarone-induced adverse drug reaction, leukocytoclastic vasculitis, Sweet syndrome, IgA dermatosis, atypical infection or septic thrombi. Autoimmune serology was unyielding and empiric antibiotics failed to improve skin lesions. Confirmatory punch biopsy of the lesions revealed perivascular neutrophilic dermal infiltrate consistent with Sweet syndrome. Due to the severity of the disease and systemic involvement intravenous methylprednisolone was initiated, resulting in rapid clinical remission of symptoms, cutaneous lesions, and leukocytosis. IMPACT/DISCUSSION: Sweet syndrome is characterized by a constellation of fever, neutrophilia, tender erythematous skin lesions with diffuse perivascular neutrophilic dermal infiltrate. It has been correlated with inflammatory bowel disease, antecedent respiratory/gastrointestinal infection, active malignancy, autoimmune disease, vaccines, and medications. Pathophysiologically hypersensitivity reaction is thought to play a role, given recurrence of the dermatosis with re-exposure of the offending agent and prompt response to corticosteroid therapy, as demonstrated in our patient. Amiodarone has been associated with various dermatological reactions, including photosensitivity, blue/grey hyperpigmentation and rarely vasculitis. The temporal association with amiodarone in our patient highlights amioda-rone as a potential cause of drug-induced Sweet syndrome, which to the best of our knowledge has not been previously described in the literature. Conclusion: Sweet syndrome can resemble an infectious process, usually, patients receive antibiotic treatments before glucocorticoid therapy, delaying definitive treatment. Hence clinicians should maintain a high suspicion of drug-induced Sweet syndrome in such patients, in order to improve patient-related outcomes

    Diffuse alveolar hemorrhage associated with rsv infection and supratherapeutic warfarin therapy.

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    Learning Objectives: Oral anticoagulants such as warfarin are used for the prevention of thrombo-embolic complications in various hypercoagulable conditions such as atrial fibrillation. A significant adverse effect of anticoagulation therapy is hemorrhage. However, diffuse alveolar hemorrhage (DAH) is rarely reported as a complication of warfarin therapy. Diffuse alveolar hemorrhage (DAH) is rare but is more commonly associated with pulmonary infections, granulomatosis with polyangiitis, Behcets syndrome, anti-GBM disease, and Systemic Lupus Erythematosis. We report a case of Respiratory Syctial virus (RSV) pneumonitis complicated by DAH in the setting of supratherapeutic warfarin therapy. Methods: A 75-year-old man presented with persistent cough for 1 month and new onset respiratory failure and hemoptysis. CT scan revealed diffuse ground glass opacities bilaterally. The patient was intubated due to worsening hemoptysis and hypoxia. The diagnosis of DAH was confirmed by bronchoscopy after intubation. Vasculitis and autoimmune causes of DAH was ruled out with serologic testing but work up was positive for RSV infection confirmed by PCR. The patient was noted to have a supratherapeutic INR of 4.63 on warfarin for atrial fibrillation. Results: Diffuse alveolar hemorrhage (DAH) is a rare yet fatal medical emergency that requires immediate intervention. Diagnosis of DAH is difficult as chest radiographs often reveal findings that are indistinguishable from pulmonary edema or diffuse infectious process. DAH precipitated by a supratherapeutic INR is a rare complication of RSV respiratory infection. It is vital to recognize DAH and proceed with reversing the warfarin-induced coagulopathy and provide the patient with adequate respiratory support
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