Although the clinical presentation was suggestive also for CAPS, the biochemical and pathological findings do not confirm this diagnosis. Table 5 Possible differential diagnoses of fulminant MODS. thead th align=”left” rowspan=”1″ colspan=”1″ Diagnosis /th th align=”center” rowspan=”1″ colspan=”1″ Pro /th th align=”center” rowspan=”1″ colspan=”1″ Against /th th align=”center” rowspan=”1″ colspan=”1″ Likelihood /th /thead Septic shock(1) Immusuppression(1) Fulminant time course of MODSH(2) Drospirenone Blood culture positive for em E. receptors uncovered on the surface of the neoplastic cells or able to boost the immune capabilities against them, such as the Chimeric Antigen Receptor Altered T-cell (CAR-T) [1, 2]; consequently, an increasing number of these patients are now admitted to the Intensive Care Unit (ICU) both for the underlying disease and/or for its complications, including sepsis and septic shock (SS) [3, 4]. According to the 3rd International Consensus Definitions, this latter is considered a condition characterized by a multiple organ dysfunction (MODS) severe enough to increase the risk of death [5]; notably, this definition does not consider the following items: first of all the time course, the fulminant forms rapidly leading to MODS and death are lumped Rabbit Polyclonal to RPL3 together with lesser aggressive ones than the different timeframes of SS, which can be characterized by an initial hyper-inflammatory condition switching later on to a reduced immune response, consisting of low-grade inflammatory state, hypercatabolism and the occurrence of secondary infections caused by multiple drug resistant germs and/or the reactivation of latent computer virus, such as EpsteinCBarr computer virus, Cytomegalovirus (CMV) and Herpes virus [6, 7]. The classical symptoms of SS include fever or hypothermia, tachycardia, arterial hypotension, and other indicators related to the MODS making the diagnosis relatively straightforward. Nevertheless, in patients with hematologic cancers causes other that SS can account for this clinical phenotype, including a life-threatening hyper-inflammation associated either to the underlying disease and/or to its treatment. The recognition and treatment of these conditions appear particularly challenging for the intensivist since (a) they are relatively uncommon; (b) they can occur in the very same circumstances of SS and the related symptoms could overlap; (c) the time course can be so fast that this clinical presentation could be represented by an overt MODS just from the onset; and, perhaps most important, (d) the mainstay of the treatment is based on an aggressive Drospirenone immunosuppression, which is usually Drospirenone contraindicated in SS. Hereby we describe and review a case of a patient treated for a hematologic cancer in whom the admission in ICU with the diagnosis of SS appear to have been too simplistic, because other noninfectious factors may have contributed to the MODS and to the outcome. 2. Case Description A 53-year-old man was admitted to the Emergency Department due to 6-hour-lasting acute abdominal pain; the first CT scan demonstrated an edematous pancreatitis and a small amount of ascites; a second CT confirmed the results at 6?h from the first one. A couple of hours after hospitalization, he was transferred to our Intensive Care Unit (ICU) because he became confused, hypotensive, and anuric. The history revealed an advanced stage non-Hodgkin lymphoma (DLCBL, stage III) discovered two months before the current admission and treated with 5 cycles of Rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP), the last completed the day before the admission in ICU. On a scheduled outpatient visit occurred two weeks before this hospitalization, the patient was prescribed a 10-day course of oral valganciclovir due a reactivation of CMV, but it was suspended after 7?days due to a rise of hepatic liver enzymes and the disappearance of the viral DNA. In the ICU, the patient was intubated and mechanically ventilated; lab investigations demonstrated a deep metabolic acidosis, hyperlactatemia in association with severe leukopenia, and reduced platelet count; these abnormalities worsened in the following hours (Table 1). With the clinical suspicion of SS, IV vancomycin, meropemen, and valganciclovir were initiated, along with the administration of IgM- and IgA-enriched intravenous immunoglobulins (Pentaglobin?, Biotest, Dreieich, Germany); at the same time, a renal replacement treatment was started Drospirenone in association with the extracorporeal removal of sepsis mediators (Cytosorb?, Aferetica, Mirandola, Italy). The arterial hypotension was unresponsive to the administration of incremental doses of fluids, norepinephrine.