Sara Fernández

ADAMTS-13 in Critically Ill Patients With Septic Syndromes and Noninfectious Systemic Inflammatory Response Syndrome.

ABSTRACT Purpose: Decreased ADAMTS-13 (A Disintegrin and Metalloprotease with a ThromboSpondin type 1 motif, member 13) seems to be associated with a poor prognosis in sepsis. However, its role in different septic syndromes and other causes of systemic inflammatory response syndrome (SIRS) remains unclear. The aims of this study were to assess ADAMTS-13 levels in patients with septic syndromes or noninfectious SIRS and to determine their association with morbidity and mortality. Methods: The study population consisted of 178 patients admitted to the medical intensive care unit presenting either septic syndromes or noninfectious SIRS. ADAMTS-13 levels were analyzed. Results: Patients with septic syndromes showed significantly lower levels of ADAMTS-13 compared with those with noninfectious SIRS (P = 0.014). Patients with severe sepsis or septic shock presented lower levels than those of patients with sepsis (P = 0.086). A significant negative correlation was found between ADAMTS-13 levels and delta Sequential Organ Failure Assessment and Acute Physiology and Chronic Health Evaluation II scores at admission in the septic patients. Patients who died had significantly lower levels of ADAMTS-13 compared with survivors, both in the whole population and among the septic patients (P = 0.002 and P = 0.009, respectively). Logistic regression analysis showed that decreased ADAMTS-13 levels were associated with an increased risk of in–intensive care unit mortality (odds ratio, 0.985; 95% confidence interval, 0.973–0.998; P = 0.023). Conclusions: Septic patients have lower levels of ADAMTS-13 than do patients with noninfectious SIRS. Levels of ADAMTS-13 are correlated with illness severity in patients with septic syndromes. ADAMTS-13 levels were associated with an increased risk of mortality in critically ill patients with SIRS especially those with septic syndromes.

Pulmonary tumor thrombotic microangiopathy: report of 3 cases and review of the literature.

AbstractPulmonary tumor thrombotic microangiopathy (PTTM) is a rare clinical entity where tumor cell embolisms in pulmonary circulation induce thrombotic microangiopathy (TMA), respiratory failure, and subacute cor pulmonale.We describe 3 cases of PTTM that presented as the initial manifestation of metastatic gastric adenocarcinoma with TMA and pulmonary infiltrates.All 3 cases had similar clinical and laboratory features, which included moderate thrombocytopenia without renal failure, hemolysis with extremely high serum lactate dehydrogenase levels, leukoerythroblastosis in peripheral blood smear, altered coagulation tests, lymphadenopathies, and interstitial pulmonary infiltrates. All patients died within 2 weeks of diagnosis. Two cases were initially misdiagnosed as idiopathic thrombotic thrombocytopenic purpura and treated with plasma exchange with no response. One patient had bone marrow infiltration by malignant cells. Autopsies revealed PTTM associated with gastric disseminated adenocarcinoma (signet-ring cell type in 2 patients and poorly differentiated type in 1).PTTM should be considered in the differential diagnosis of patients with fulminant microangiopathic hemolytic anemia, such as atypical thrombotic thrombocytopenic purpura, mainly those with pulmonary infiltrates, disseminated intravascular coagulation, or Trousseau syndrome.

Evaluation of a Mixing versus a Cycling Strategy of Antibiotic Use in Critically-Ill Medical Patients: Impact on Acquisition of Resistant Microorganisms and Clinical Outcomes

Objective To compare the effect of two strategies of antibiotic use (mixing vs. cycling) on the acquisition of resistant microorganisms, infections and other clinical outcomes. Methods Prospective cohort study in an 8-bed intensive care unit during 35- months in which a mixing-cycling policy of antipseudomonal beta-lactams (meropenem, ceftazidime/piperacillin-tazobactam) and fluoroquinolones was operative. Nasopharyngeal and rectal swabs and respiratory secretions were obtained within 48h of admission and thrice weekly thereafter. Target microorganisms included methicillin-resistant S. aureus, vancomycin-resistant enterococci, third-generation cephalosporin-resistant Enterobacteriaceae and non-fermenters. Results A total of 409 (42%) patients were included in mixing and 560 (58%) in cycling. Exposure to ceftazidime/piperacillin-tazobactam and fluoroquinolones was significantly higher in mixing while exposure to meropenem was higher in cycling, although overall use of antipseudomonals was not significantly different (37.5/100 patient-days vs. 38.1/100 patient-days). There was a barely higher acquisition rate of microorganisms during mixing, but this difference lost its significance when the cases due to an exogenous Burkholderia cepacia outbreak were excluded (19.3% vs. 15.4%, OR 0.8, CI 0.5–1.1). Acquisition of Pseudomonas aeruginosa resistant to the intervention antibiotics or with multiple-drug resistance was similar. There were no significant differences between mixing and cycling in the proportion of patients acquiring any infection (16.6% vs. 14.5%, OR 0.9, CI 0.6–1.2), any infection due to target microorganisms (5.9% vs. 5.2%, OR 0.9, CI 0.5–1.5), length of stay (median 5 d for both groups) or mortality (13.9 vs. 14.3%, OR 1.03, CI 0.7–1.3). Conclusions A cycling strategy of antibiotic use with a 6-week cycle duration is similar to mixing in terms of acquisition of resistant microorganisms, infections, length of stay and mortality.

Pattern of soluble CD5 and CD6 lymphocyte receptors in critically ill patients with septic syndromes

PURPOSE Soluble forms of CD5 and CD6 lymphocyte surface receptors (sCD5 and sCD6) are molecules that seem to prevent experimental sepsis when exogenously administered. The aim of this study was to assess sCD5 and sCD6 levels in patients with septic syndromes. MATERIALS AND METHODS The study population consisted of 218 patients admitted to the medical intensive care unit (ICU) presenting either septic syndromes or noninfectious systemic inflammatory response syndrome at admission or within the first 48 hours. The sCD5 and sCD6 levels were analyzed by sandwich enzyme-linked immunosorbent assay. RESULTS Almost 50% of the patients had undetectable levels of sCD5 or sCD6, with no differences in clinical or biological variables with detectable patients. There was a correlation between the delta Sequential Organ Failure Assessment score and both sCD6 and sCD5 levels in all groups. Patients with sCD5 or sCD6 levels greater than 1500 ng/mL presented a higher in-ICU mortality (P < .05). Logistic regression analysis showed that increased sCD6 levels were associated with an increased risk of in-ICU mortality. CONCLUSIONS Levels of sCD5 and sCD6 in critically ill patients with systemic inflammatory response syndrome present a high variation and an elevated proportion of undetectability. Levels of sCD6 are associated with an increased risk of mortality in these patients.

A case of Mycoplasma hominis disseminated infection in a human immunodeficiency virus-1-infected pregnant woman with hypogammaglobulinemia

We describe the case of a disseminated infection due to Mycoplasma hominis in a 25-weeks pregnant woman with vertically transmitted human immunodeficiency virus 1 (HIV-1) infection on combined antiretroviral therapy. Her CD4þ T-cell count was 600 cells/mm and the plasma HIV-1 RNA viral load was undetectable. She had been diagnosed with Burkitt’s lymphoma, and was successfully treated with chemotherapy. One year later, hypogammaglobulinemia attributed to rituximab treatment was detected, and she started treatment with human immunogobulins (Igs). Her last IgA, IgM, and IgG serum levels were <0.30 g/L, <0.21 g/L, and 3.4 g/L, respectively. The patient was admitted to our hospital with 48 hours of fever, cough, and mucopurulent sputum. C-reactive protein was 94.5 mg/L and white cell count 12.90 10/ L. Chest X-ray showed alveolar infiltrates in the lingula and right pulmonary base (Fig. 1A). Empiric broadspectrum antibiotics with meropenem and vancomycin were started (she had been treated for a communityacquired pneumonia 1 month previously). However, high fever persisted. A computed tomography scan showed right supraclavicular and bilateral paratracheal adenopathies and consolidations in both pulmonary bases. A bronchoalveolar lavage was performed and all microbiologic results were negative, including polymerase chain reaction for Mycobacterium tuberculosis. The patient developed respiratory failure and was transferred to the intensive care unit. A mediastinoscopy was done with biopsies of the adenopathies. Afterwards, a massive right pleural effusion appeared (Fig. 1B). Fetal maturation and HIV prophylaxis with zidovudine were then started and a cesarean section was performed. The baby was transferred to the incubator. A pleural drainage was performed

Massive erythrophagocytosis by peripheral monocytes and neutrophils in parvovirus-B19 autoimmune hemolytic anemia

Dear Editor, In response to the interesting case of diffuse large B cell lymphoma (DLBCL) and hemophagocytosis in peripheral blood (PB) reported in [1] associated to a fatal outcome, we would like to point out the relevance to detect this rare phenomenon and the clinical utility for this morphologic finding. A 37-year-oldmale, with clinical history of severe combined immunodeficiency (SCID), Evans syndrome, splenectomy, and autoimmune hemolytic anemia, was admitted to the hospital because of rapidly progressive fatigue, jaundice, and dark urine. The SCID was diagnosed after repeated respiratory infections during infancy; it was associated to hypogammaglobulinemia and he received replacement therapy with intravenous immunoglobulin (IvIg). The first determination of Ig in our center in 1996 (18 years old) showed IgA<0.25 g/l, IgM<0.54 g/l, and IgG 5.9 g/l values. On physical examination, he showed pallor and no lymphadenopathy was palpable. His full blood count showed hemoglobin (Hb) concentration 63 g/l, leucocytes (WBC) 67 × 10/l, monocytes 4.7 × 10/l, neutrophils 39.5 × 10/l, platelets 440 × 10/l, and absolute reticulocyte count 100 × 10/l. During several years, he showed a markedly elevatedWBC and it was interpreted as a leukemoid reaction in a splenectomized patient in the context of acute infections. Differential count in the current episode was neutrophils 60%, lymphocytes 33%, and monocytes 7%. Inversion on the CD4/ CD8 ratio was foundwithout any signs of clonality (IGHVFR1 polyclonal, TCR polyclonal). Biochemical tests showed increased LDH 1562 IU/l (normal <450), total bilirubin 15.6 mg/dl (normal <1.2), being indirect bilirubin 13.5 mg/dl (normal <0.6), and haptoglobin value was below the detection limit. Direct Coombs test was positive for IgG and negative for C3b/C3d. A specific real-time polymerase chain reaction for Parvovirus B19 was performed obtaining a viral load of 10,310 copies/ml. Automated PB examination using the CellaVision DM96 (Lund, Sweden) revealed massive erythrophagocytosis by monocytes and neutrophils. Images acquired on an Olympus BX43 microscope at ×1000 magnification are shown in Fig. 1. A bone marrow aspirate showed normal cellularity with isolate islands of giant erythroblasts and numerous figures of erythrophagocytosis. On day 2, he presented despite high dose steroids and RBC transfusion a rapidly worsening of his cardiorespiratory condition (dyspnea and chest pain) associated to increased values of myocardial enzymes. Hb values dropped to 28 g/l and serum lactate increased. In this situation, the patient was transferred to the intensive care unit (ICU) for sedation, orotracheal intubation, and mechanical ventilation. High dose IvIg (1 g/ kg/d for 3 days), rituximab (375 mg/m, the second dose was given at day 11), and a bolus of intravenous cyclophosphamide (750 mg/m) were administered. Over the following days, Hb and reticulocyte values increased. Serum lactate levels turned to normal allowing extubation after 4 days. Erythrophagocytosis was no longer seen in PB after the first dose of IvIg and on day 18, he was discharged. The analytical signs of hemolysis improved under * Anna Merino amerino@clinic.cat

Acute iron intoxication: change in urine color during chelation therapy with deferoxamine

A 21-year-old woman presented to the emergency department 8 h after the ingestion of 5,100 mg of ferrous sulfate (110 mg/kg) in a suicide attempt. At admission she was hemodynamically stable without pathologic findings at examination. Laboratory tests showed a mild decrease in prothrombin time and a compensated metabolic acidosis with normal renal function and liver enzymes. An abdominal x-ray showed normal findings without visible radiopaque pills. Initial serum iron levels were 300 lg/dL. The patient was transferred to the intensive care unit for monitoring. Chelation therapy with deferoxamine was then started at 15 mg/kg/24 h and the patient’s urine turned a red– orange color after starting this treatment (Fig. 1). After 24 h of treatment serum iron levels decreased to 87 lg/dL and chelation therapy was withdrawn. The patient remained clinically stable with no medical complications. She was discharged from hospital 5 days after admission. Deferoxamine is a specific iron chelator that binds ferric iron forming a water-soluble compound that is rapidly excreted by the kidney, causing a vin rosé discoloration to the urine. It is considered the drug of choice for the treatment of significant iron intoxication. Change in urine color may confirm the effectiveness of this antidote.

Human African Trypanosomiasis in a Spanish traveler returning from Tanzania

Human African Trypanosomiasis (HAT) is a parasitic disease usually confined to endemic areas in sub-Saharan Africa, but it occasionally may occur among travelers, migrants, or expatriates. Although it is an uncommon diagnosis in returning travelers attending travel and tropical medicine clinics [1], the number of HAT diagnoses in travelers has been rising in recent years [2], most likely in connection with an increase of tourists visiting endemic areas and improved reporting systems. Trypanosoma brucei is the etiological agent of HAT, and is transmitted by tsetse flies of the genus Glossina. Two species can cause the disease: T. brucei gambiense in West and Central Africa (g-HAT) and T. brucei rhodesiense (r-HAT) in Eastern and Southern Africa. The disease usually presents in two stages: a first or hemolymphatic stage, where the parasite is located in the lymphatic system and blood; and a second or meningo-encephalitic stage, which occurs when trypanosomes penetrate the central nervous system. Although a vast majority of sleeping sickness cases are caused by infection with T. brucei gambiense [3], most cases of HAT reported in nonendemic countries are caused by T. brucei rhodesiense [4]. These cases occur mainly in tourists, who are usually diagnosed in the first stage, shortly after returning from their visit. Tourists commonly contract the disease after visiting game parks in sub-Saharan Africa [5], including those in Tanzania, where outbreaks in travelers have been described [6]. In contrast, g-HAT cases in nonendemic countries mainly occur in expatriates or refugees, who are usually diagnosed in the second stage and after a protracted diagnostic process [4]. Since it is rare in nonendemic countries, physicians may not suspect or find it difficult to diagnose this disease, especially if fever and/or unspecific complaints are the only presenting symptoms. Neuropsychiatric disorders are rarely present in travelers with r-HAT [7]. An accurate anamnesis, including travel history and incubation and prodromal periods, together with a thorough physical examination, is helpful to guide the diagnostic workup. r-HAT is usually easy to diagnose by blood smear examination, as parasitaemia in these patients tends to be high [8]. Examination of chancre or lymph node fluid should also be performed, if possible. Despite its uncommon occurrence in travel clinics in nonendemic settings, clinicians should be aware of the potential presentation of patients with this disease. Here, we report a

Brote de saturnismo asociado a un tratamiento basado en la medicina ayurvédica

BACKGROUND AND OBJECTIVE Lead poisoning is normally caused by repeated occupational inhalation of lead. However, lead may also be absorbed through the digestive route. Some alternative medical treatments, such as Ayurvedic medicine, can also contain lead and may result in poisoning. PATIENTS AND METHOD We collected cases of lead poisoning related to Ayurvedic treatments attended at the Hospital Clinic of Barcelona. RESULTS Two female patients, aged 45 and 57 years, respectively, who initiated Ayurvedic treatments which involved the ingestion of various medicaments, were included. The first patient presented with anemia and abdominal pain. The lead level was 74μg/dL and free erythrocyte protoporphyrin was 163μg/dL. She was treated with intravenous calcium disodium ethylenediaminetetraacetic acid (CaNa2EDTA) and later with oral dimercaptosuccinic acid (DMSA) with a good evolution. The second patient presented with abdominal pain and a Burtons line. The lead level was 52μg/dL and free erythrocyte protoporphyrin was 262μg/dL. She was treated with oral DMSA and evolved favorably. Lead concentrations in some of the tablets supplied to the patients reached 2,003 and 19,650μg/g of tablet. CONCLUSIONS Lead poisoning may result from treatments based on Ayurvedic medicine and may reach epidemic proportions. Health control of alternative medicines is necessary.

Imagen de la semanaOrina verde secundaria a propofolGreen urine due to propofol

Varón de 51 años con antecedentes de alcoholismo crónico. Ingresó en la Unidad de Cuidados Intensivos por una intoxicación aguda grave por quetiapina, con disminución del nivel de consciencia y neumonı́a aspirativa, requiriendo intubación orotraqueal y ventilación mecánica. Para facilitar el acoplamiento a la ventilación mecánica se inició una perfusión intravenosa continua de propofol (4,3 mg/kg/h), presentando horas más tarde una coloración verdosa de la orina (fig. 1). Tras disminuir la dosis de propofol, se normalizó el color de la orina. El tratamiento con propofol se puede asociar a esta coloración urinaria, por acúmulo de metabolitos glucuronoconjugados. Otras causas de orina verde, como la infección por Pseudomonas aeruginosa o la administración de azul de metileno u otros fármacos, no estaban presentes en este paciente. Figura 1. ww w.els evier .es /med i c in ac l in i c a