Cardiogenic shock with resultant multiple organ dysfunction syndrome.

The prognosis for a patient with multiple organ dysfunction syndrome (MODS)-also known as organ dysfunction or organ failure-is grave, and mortality can be high when three or more organ systems fail. This article reviews ongoing abnormalities of organ-specific parameters and a bedside clinical scoring assessment tool to identify the mortality of MODS, focusing on the management of MODS resulting from cardiogenic shock in ICU patients who require support of failing organs to survive.

A Multicenter Network Assessment of Three Inflammation Phenotypes in Pediatric Sepsis-Induced Multiple Organ Failure.

OBJECTIVES: Ongoing adult sepsis clinical trials are assessing therapies that target three inflammation phenotypes including 1) immunoparalysis associated, 2) thrombotic microangiopathy driven thrombocytopenia associated, and 3) sequential liver failure associated multiple organ failure. These three phenotypes have not been assessed in the pediatric multicenter setting. We tested the hypothesis that these phenotypes are associated with increased macrophage activation syndrome and mortality in pediatric sepsis. DESIGN: Prospective severe sepsis cohort study comparing children with multiple organ failure and any of these phenotypes to children with multiple organ failure without these phenotypes and children with single organ failure. SETTING: Nine PICUs in the Eunice Kennedy Shriver National Institutes of Child Health and Human Development Collaborative Pediatric Critical Care Research Network. PATIENTS: Children with severe sepsis and indwelling arterial or central venous catheters. INTERVENTIONS: Clinical data collection and twice weekly blood sampling until PICU day 28 or discharge. MEASUREMENTS AND MAIN RESULTS: Of 401 severe sepsis cases enrolled, 112 (28%) developed single organ failure (0% macrophage activation syndrome 0/112; < 1% mortality 1/112), whereas 289 (72%) developed multiple organ failure (9% macrophage activation syndrome 24/289; 15% mortality 43/289). Overall mortality was higher in children with multiple organ and the phenotypes (24/101 vs 20/300; relative risk, 3.56; 95% CI, 2.06-6.17). Compared to the 188 multiple organ failure patients without these inflammation phenotypes, the 101 multiple organ failure patients with these phenotypes had both increased macrophage activation syndrome (19% vs 3%; relative risk, 7.07; 95% CI, 2.72-18.38) and mortality (24% vs 10%; relative risk, 2.35; 95% CI, 1.35-4.08). CONCLUSIONS: These three inflammation phenotypes were associated with increased macrophage activation syndrome and mortality in pediatric sepsis-induced multiple organ failure. This study provides an impetus and essential baseline data for planning multicenter clinical trials targeting these inflammation phenotypes in children.

Klotho deficiency aggravates sepsis-related multiple organ dysfunction.

Sepsis-induced organ failure is characterized by a massive inflammatory response and oxidative stress. Acute kidney injury (AKI) occurs in approximately half of patients in septic shock, and the mortality associated with sepsis-induced AKI is unacceptably high. Klotho is a protein expressed by renal cells and has anti-senescence properties. Klotho has also been shown to protect the kidneys in ischemia-reperfusion injury and to have antioxidant properties. To analyze the role of Klotho in sepsis-related organ dysfunction and AKI, we used a cecal ligation and puncture (CLP) model of sepsis in heterozygous Klotho-haploinsufficient mice and their wild-type littermates (CLP- Kl/+ and CLP-WT mice, respectively). In comparison with the CLP-WT mice, CLP- Kl/+ mice showed lower survival, impaired renal function, impaired hepatic function, greater oxidative stress, upregulation of inflammatory pathways (at the systemic and kidney tissue levels), and increased NF-κB activation. It is noteworthy that CLP- Kl/+ mice also showed lower heart-rate variability, less sympathetic activity, impaired baroreflex sensitivity to sodium nitroprusside, and a blunted blood pressure response to phenylephrine. We also demonstrated that sepsis creates a state of acute Klotho deficiency. Given that low Klotho expression exacerbates sepsis and multiple organ dysfunction, Klotho might play a protective role in sepsis, especially in elderly individuals in whom Klotho expression is naturally reduced.

Etiology of hyperglycemia in critically ill children and the impact of organ dysfunction. / Etiologia da hiperglicemia em crianças críticas e o impacto da disfunção de órgãos.

OBJECTIVE: This study aimed to study the incidence of stress hyperglycemia in critically ill children and to investigate the etiological basis of the hyperglycemia based on homeostasis model assessment. METHODS: This was a prospective cohort study in one of the pediatric intensive care units of Cairo University, including 60 critically ill children and 21 healthy controls. Serum blood glucose, insulin, and C-peptide levels were measured within 24 hours of admission. Homeostasis model assessment was used to assess ß-cell function and insulin sensitivity. RESULTS: Hyperglycemia was estimated in 70% of patients. Blood glucose values ≥ 180mg/dL were associated with a poor outcome. Blood glucose levels were positively correlated with Pediatric Risk for Mortality (PRISM III) score and number of organ dysfunctions (p = 0.019 and p = 0.022, respectively), while insulin levels were negatively correlated with number of organ dysfunctions (r = -0.33, p = 0.01). Homeostasis model assessment revealed that 26 (43.3%) of the critically ill patients had low ß-cell function, and 18 (30%) had low insulin sensitivity. Combined pathology was detected in 2 (3.3%) patients only. Low ß-cell function was significantly associated with the presence of multi-organ dysfunction; respiratory, cardiovascular, and hematological dysfunctions; and the presence of sepsis. CONCLUSIONS: ß-Cell dysfunction appeared to be prevalent in our cohort and was associated with multi-organ dysfunction.

OBJETIVO: Verificar a incidência da hiperglicemia de estresse em crianças em condição grave e investigar a etiologia da hiperglicemia com base em um modelo de avaliação da homeostasia. MÉTODOS: Estudo prospectivo de coorte, conduzido em uma unidade de terapia intensiva pediátrica da Cairo University, que incluiu 60 crianças com doença grave e 21 controles saudáveis. Utilizaram-se os níveis séricos de glicose, insulina e peptídeo C, avaliados em até 24 horas após a admissão. O modelo de avaliação da homeostasia foi utilizado para analisar a função das células beta e a sensibilidade à insulina. RESULTADOS: A hiperglicemia foi estimada em 70% dos pacientes. Valores de glicemia ≥ 180mg/dL se associaram com desfechos piores. Os níveis de glicemia se correlacionaram de forma positiva com o Pediatric Risk for Mortality (PRISM III) e o número de órgãos com disfunção (p = 0,019 e p = 0,022, respectivamente), enquanto os níveis de insulina se correlacionaram de forma negativa com o número de órgãos com disfunção (r = -0,33; p = 0,01). O modelo de avaliação da homeostasia revelou que 26 (43,3%) das crianças em condições graves tinham baixa função de células beta e 18 (30%) baixa sensibilidade à insulina. Detectou-se patologia combinada em apenas dois (3,3%) pacientes. Baixa função de células beta se associou de forma significante com a presença de disfunção de múltiplos órgãos, disfunção respiratória, cardiovascular e hematológica, e presença de sepse. CONCLUSÕES: A disfunção de células beta pareceu ser prevalente em nossa coorte e se associou com disfunção de múltiplos órgãos.

Etiologia da hiperglicemia em crianças críticas e o impacto da disfunção de órgãos / Etiology of hyperglycemia in critically ill children and the impact of organ dysfunction

RESUMO Objetivo: Verificar a incidência da hiperglicemia de estresse em crianças em condição grave e investigar a etiologia da hiperglicemia com base em um modelo de avaliação da homeostasia. Métodos: Estudo prospectivo de coorte, conduzido em uma unidade de terapia intensiva pediátrica da Cairo University, que incluiu 60 crianças com doença grave e 21 controles saudáveis. Utilizaram-se os níveis séricos de glicose, insulina e peptídeo C, avaliados em até 24 horas após a admissão. O modelo de avaliação da homeostasia foi utilizado para analisar a função das células beta e a sensibilidade à insulina. Resultados: A hiperglicemia foi estimada em 70% dos pacientes. Valores de glicemia ≥ 180mg/dL se associaram com desfechos piores. Os níveis de glicemia se correlacionaram de forma positiva com o Pediatric Risk for Mortality (PRISM III) e o número de órgãos com disfunção (p = 0,019 e p = 0,022, respectivamente), enquanto os níveis de insulina se correlacionaram de forma negativa com o número de órgãos com disfunção (r = -0,33; p = 0,01). O modelo de avaliação da homeostasia revelou que 26 (43,3%) das crianças em condições graves tinham baixa função de células beta e 18 (30%) baixa sensibilidade à insulina. Detectou-se patologia combinada em apenas dois (3,3%) pacientes. Baixa função de células beta se associou de forma significante com a presença de disfunção de múltiplos órgãos, disfunção respiratória, cardiovascular e hematológica, e presença de sepse. Conclusões: A disfunção de células beta pareceu ser prevalente em nossa coorte e se associou com disfunção de múltiplos órgãos.

ABSTRACT Objective: This study aimed to study the incidence of stress hyperglycemia in critically ill children and to investigate the etiological basis of the hyperglycemia based on homeostasis model assessment. Methods: This was a prospective cohort study in one of the pediatric intensive care units of Cairo University, including 60 critically ill children and 21 healthy controls. Serum blood glucose, insulin, and C-peptide levels were measured within 24 hours of admission. Homeostasis model assessment was used to assess β-cell function and insulin sensitivity. Results: Hyperglycemia was estimated in 70% of patients. Blood glucose values ≥ 180mg/dL were associated with a poor outcome. Blood glucose levels were positively correlated with Pediatric Risk for Mortality (PRISM III) score and number of organ dysfunctions (p = 0.019 and p = 0.022, respectively), while insulin levels were negatively correlated with number of organ dysfunctions (r = −0.33, p = 0.01). Homeostasis model assessment revealed that 26 (43.3%) of the critically ill patients had low β-cell function, and 18 (30%) had low insulin sensitivity. Combined pathology was detected in 2 (3.3%) patients only. Low β-cell function was significantly associated with the presence of multi-organ dysfunction; respiratory, cardiovascular, and hematological dysfunctions; and the presence of sepsis. Conclusions: β-Cell dysfunction appeared to be prevalent in our cohort and was associated with multi-organ dysfunction.

Evaluation of Repeated Quick Sepsis-Related Organ Failure Assessment Measurements Among Patients With Suspected Infection.

OBJECTIVES: Among patients with suspected infection, a single measurement of the quick Sepsis-related Organ Failure Assessment has good predictive validity for sepsis, yet the increase in validity from repeated measurements is unknown. We sought to determine the incremental predictive validity for sepsis of repeated quick Sepsis-related Organ Failure Assessment measurements over 48 hours compared with the initial measurement. DESIGN: Retrospective cohort study. SETTING: Twelve hospitals in southwestern Pennsylvania in 2012. PATIENTS: All adult medical and surgical encounters in the emergency department, hospital ward, postanesthesia care unit, and ICU. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Among 1.3 million adult encounters, we identified those with a first episode of suspected infection. Using the maximum quick Sepsis-related Organ Failure Assessment score in each 6-hour epoch from onset of suspected infection until 48 hours later, we characterized repeated quick Sepsis-related Organ Failure Assessment with: 1) summary measures (e.g., mean over 48 hr), 2) crude trajectory groups, and 3) group-based trajectory modeling. We measured the predictive validity of repeated quick Sepsis-related Organ Failure Assessment using incremental changes in the area under the receiver operating characteristic curve for in-hospital mortality beyond that of baseline risk (age, sex, race/ethnicity, and comorbidity). Of 37,591 encounters with suspected infection, 1,769 (4.7%) died before discharge. Both the mean quick Sepsis-related Organ Failure Assessment at 48 hours (area under the receiver operating characteristic, 0.86 [95% CI, 0.85-0.86]) and crude trajectory groups (area under the receiver operating characteristic, 0.83 [95% CI, 0.83-0.83]) improved predictive validity compared with initial quick Sepsis-related Organ Failure Assessment (area under the receiver operating characteristic, 0.79 [95% CI, 0.78-0.80]) (p < 0.001 for both). Group-based trajectory modeling found five trajectories (quick Sepsis-related Organ Failure Assessment always low, increasing, decreasing, moderate, and always high) with greater predictive validity than the initial measurement (area under the receiver operating characteristic, 0.85 [95% CI, 0.84-0.85]; p < 0.001). CONCLUSIONS: Repeated measurements of quick Sepsis-related Organ Failure Assessment improve predictive validity for sepsis using in-hospital mortality compared with a single measurement of quick Sepsis-related Organ Failure Assessment at the time a clinician suspects infection.

SRIS y SDOM constructos asociados a sepsis / SRIS and SDOM constructs associated with sepsis

La sepsis es un síndrome de respuesta inflamatoria sistémica (SRIS) que se activa por infección. Por su parte, el síndrome de disfunción orgánica múltiple (SDOM) es el fallo de la función de órganos y sistemas críticos en pacientes que han desarrollado una SRIS. Debido a que SRIS y SDOM son consecuencias de una excesiva activación inflamatoria. El objetivo de este artículo es ofrecer una revisión sobre algunos aspectos fisiopatológicos del constructo SRIS / SDOM de origen infeccioso, utilizando a la colangitis aguda como un ejemplo de esta cadena de eventos.

Sepsis is a systemic inflammatory response syndrome (SIRS) that is triggered by infection. On the other hand, multiple organ dysfunction syndrome (MODS) is the failure of critical organ function in patients suffering from SIRS.Because SIRS and SDOM are consequences of excessive inflammatory activation. The aim of this article is to provide a review of some pathophysiological aspects of the SRIS / SDOM construct of infectious origin, using the acute cholangitis as an example of this chain of events.

Acute paraquat exposure determines dose-dependent oxidative injury of multiple organs and metabolic dysfunction in rats: impact on exercise tolerance.

This study investigated the pathological morphofunctional adaptations related to the imbalance of exercise tolerance triggered by paraquat (PQ) exposure in rats. The rats were randomized into four groups with eight animals each: (a) SAL (control): 0.5 ml of 0.9% NaCl solution; (b) PQ10: PQ 10 mg/kg; (c) PQ20: PQ 20 mg/kg; and (d) PQ30: PQ 30 mg/kg. Each group received a single injection of PQ. After 72 hours, the animals were subjected to an incremental aerobic running test until fatigue in order to determine exercise tolerance, blood glucose and lactate levels. After the next 24 h, lung, liver and skeletal muscle were collected for biometric, biochemical and morphological analyses. The animals exposed to PQ exhibited a significant anticipation of anaerobic metabolism during the incremental aerobic running test, a reduction in exercise tolerance and blood glucose levels as well as increased blood lactate levels during exercise compared to control animals. PQ exposure increased serum transaminase levels and reduced the glycogen contents in liver tissue and skeletal muscles. In the lung, the liver and the skeletal muscle, PQ exposure also increased the contents of malondialdehyde, protein carbonyl, 8-hydroxy-2'-deoxyguanosine, superoxide dismutase and catalase, as well as a structural remodelling compared to the control group. All these changes were dose-dependent. Reduced exercise tolerance after PQ exposure was potentially influenced by pathological remodelling of multiple organs, in which glycogen depletion in the liver and skeletal muscle and the imbalance of glucose metabolism coexist with the induction of lipid, protein and DNA oxidation, a destructive process not counteracted by the upregulation of endogenous antioxidant enzymes.

Crises in Sickle Cell Disease.

In spite of significant strides in the treatment of sickle cell disease (SCD), SCD crises are still responsible for high morbidity and early mortality. While most patients initially seek care in the acute setting for a seemingly uncomplicated pain episode (pain crisis or vaso-occlusive crisis), this initial event is the primary risk factor for potentially life-threatening complications. The pathophysiological basis of these illnesses is end-organ ischemia and infarction combined with the downstream effects of hemolysis that results from red blood cell sickling. These pathological changes can occur acutely and lead to a dramatic clinical presentation, but are frequently superimposed over a milieu of chronic vasculopathy, immune dysregulation, and decreased functional reserve. In the lungs, acute chest syndrome is a particularly ominous lung injury syndrome with a complex pathogenesis and potentially devastating sequelae, but all organ systems can be affected. It is, therefore, critical to understand the SCD patients' susceptibility to acute complications and their risk factors so that they can be recognized promptly and managed effectively. Blood transfusions remain the mainstay of therapy for all severe acute crises. Recommendations and indications for the safest and most efficient implementation of transfusion strategies in the critical care setting are therefore presented and discussed, together with their pitfalls and potential future therapeutic alternatives. In particular, the importance of extended phenotypic red blood cell matching cannot be overemphasized, due to the high prevalence of severe complications from red cell alloimmunization in SCD.

Toma de medición intraabdominal a personas en estado crítico, por el profesional de enfermería / Taking measurement intraabdominal people in critical condition, by the nursing professional", "_e": "n

El aumento de la presión dentro de la cavidad abdominal se asocia a múltiples alteraciones fisiopatológicas, con una importante repercusión en aparatos y sistemas originando disfunción orgánica múltiple, lo que conlleva a un incremento en la morbimortalidad en pacientes en estado crítico, la medición de presión intraabdominal es un procedimiento que se está realizando con mayor frecuencia en las Unidades de Cuidados Intensivos, en donde los profesionales de enfermería tienen un papel muy importante en la toma e identificación de posibles complicaciones que ponen en riesgo la vida del paciente. La siguiente revisión tiene la finalidad de difundir el conocimiento y dar a conocer la importancia e intervenciones de enfermería en la medición de la presión intraabdominal.

The increase in the pressure inside the abdominal cavity is associated with multiple pathophysiological changes, with a significant impact in systems causing multiple organic dysfunction, leading to increased the morbidity and mortality in critically ill patients, the measurement of intra-abdominal pressure is a procedure that is being performed more frequently in the intensive care units, where nurses have an important role in taking and identifying possible complications that endanger the patient’s life. The following review has the purpose of disseminate knowledge and explain the importance and the nursing interventions in measuring intra-abdominal pressure.

Intercomunicación pulmón-riñón en el paciente crítico / Pulmonary-renal crosstalk in the critically ill patient

A pesar de los avances en el desarrollo de las terapias de reemplazo renal, la mortalidad de la falla renal aguda permanece elevada, especialmente, cuando se manifiesta simultáneamente con fallas orgánicas distantes, como es en el caso del síndrome de distrés respiratorio agudo. Se revisa la relación bidireccional deletérea entre pulmón y riñón, en el escenario de disfunción orgánica, la cual presenta aspectos clínicos relevantes de conocer. Se discuten los efectos renales del síndrome de distrés respiratorio agudo y del uso de la ventilación mecánica a presión positiva, siendo el daño inducido por este (ventilator induced lung injury) uno de los modelos utilizado frecuentemente para el estudio de la interacción pulmón-riñón. Se enfatiza el rol de la falla renal inducida por la ventilación mecánica (ventilator-induced kidney injury) en la patogenia de la falla renal aguda. Asimismo se analizan las repercusiones pulmonares de la falla renal aguda, reconociéndose que esta condición patológica induce un incremento en la permeabilidad vascular pulmonar, inflamación y alteración de los canales de sodio y agua del epitelio alveolar, entre otros efectos. Este modelo conceptual puede ser la base para el desarrollo de nuevas estrategias terapéuticas a utilizar en el paciente con síndrome de disfunción orgánica múltiple.

Despite advances in the development of renal replacement therapy, mortality of acute renal failure remains high, especially when occurring simultaneously with distant organic failure as it is in the case of the acute respiratory distress syndrome. In this update, birideccional deleterious relationship between lung and kidney on the setting of organ dysfunction is reviewed, which presents important clinical aspects of knowing. Specifically, the renal effects of acute respiratory distress syndrome and the use of positive-pressure mechanical ventilation are discussed, being ventilator induced lung injury one of the most common models for studying the lung-kidney crosstalk. The role of renal failure induced by mechanical ventilation (ventilator-induced kidney injury) in the pathogenesis of acute renal failure is emphasized. We also analyze the impact of the acute renal failure in the lung, recognizing an increase in pulmonary vascular permeability, inflammation, and alteration of sodium and water channels in the alveolar epithelial. This conceptual model can be the basis for the development of new therapeutic strategies to use in patients with multiple organ dysfunction syndrome.

[Pulmonary-renal crosstalk in the critically ill patient]. / Intercomunicación pulmón-riñón en el paciente crítico.

Despite advances in the development of renal replacement therapy, mortality of acute renal failure remains high, especially when occurring simultaneously with distant organic failure as it is in the case of the acute respiratory distress syndrome. In this update, birideccional deleterious relationship between lung and kidney on the setting of organ dysfunction is reviewed, which presents important clinical aspects of knowing. Specifically, the renal effects of acute respiratory distress syndrome and the use of positive-pressure mechanical ventilation are discussed, being ventilator induced lung injury one of the most common models for studying the lung-kidney crosstalk. The role of renal failure induced by mechanical ventilation (ventilator-induced kidney injury) in the pathogenesis of acute renal failure is emphasized. We also analyze the impact of the acute renal failure in the lung, recognizing an increase in pulmonary vascular permeability, inflammation, and alteration of sodium and water channels in the alveolar epithelial. This conceptual model can be the basis for the development of new therapeutic strategies to use in patients with multiple organ dysfunction syndrome.

Continuous renal replacement therapy in children with multiple organ dysfunction syndrome: A case series

There is a lack of definitive information regarding the precise indications, implementation, and outcomes of continuous renal replacement therapy (CRRT) for the treatment of critically ill children. Six children (three boys, three girls) aged from 3 days to 8 years, all of whom had multiple organ failure, were submitted to bedside CRRT using M60 filter membranes. Modified Port carbonate formula was used and clotting time was maintained between 20 and 30 minutes. Activated partial thromboplastin time was 1.5- to 2-fold normal. One patient discontinued treatment due to family decision. Marked improvements were seen in the remaining five patients, including normalization of blood urea nitrogen and creatinine levels, stabilization of electrolytes, and improvements in markers of organ function. Of note, one patient (a six-year-old male) underwent the treatment for 241 hours. All five patients were subsequently discharged and recovered uneventfully. CRRT is effective for the management of children who are critically ill due to multiple organ failure.

Doença de Haff complicada por falência de múltiplos órgãos após ingestão de lagostim: estudo de caso / Haff disease complicated by multiple organ failure after crayfish consumption: a case study

A doença de Haff é uma síndrome que consiste de rabdomiólise não explicada. Pacientes que apresentam a doença de Haff relatam ter ingerido pescado nas últimas 24 horas antes do início da doença. A maioria dos pacientes sobrevive apresentando breve recuperação. O presente artigo é o primeiro relato de doença de Haff complicada por falência de múltiplos órgãos após ingestão de lagostim. Um homem chinês de 66 anos de idade ingeriu lagostim cozido na noite de 23 de junho de 2013. Chegou ao hospital 2 dias mais tarde, sendo admitido à unidade de terapia intensiva. Após a admissão, o paciente recebeu o diagnóstico de doença de Haff complicada por falência de múltiplos órgãos. Apesar dos tratamentos de suporte e sintomático, a condição do paciente deteriorou, vindo o mesmo a falecer em consequência da doença. A doença de Haff é uma rara síndrome clínica que é, às vezes, mal diagnosticada. O diagnóstico precoce e o tratamento adequado são essenciais para prevenir a progressão para falência de múltiplos órgãos.

Haff disease is a syndrome consisting of unexplained rhabdomyolysis. Patients suffering from Haff disease report having eaten fish within 24 hours before the onset of illness. Most patients survive and recover quickly. The present study is the first report of Haff disease complicated by multiple organ failure after crayfish consumption. A 66-year-old Chinese man ate cooked crayfish on the night of June 23, 2013. He arrived at our hospital 2 days later and was admitted to the intensive care unit. After admission, the patient was diagnosed with Haff disease complicated by multiple organ failure. Despite supportive and symptomatic treatments, the condition of the patient deteriorated, and he died due to his illness. Haff disease is a rare clinical syndrome that is sometimes misdiagnosed. Early diagnosis and proper treatment are essential to prevent progression to multiple organ failure.

[Tuberculosis in perinatal stage. A challenge to the binomial care mother-son. Report of two cases]. / Tuberculosis en la etapa perinatal. Un reto en la atención de la madre y su hijo. Reporte de dos casos clínicos.

Case report of 18-year old female patient with clinical signs of pulmonary tuberculosis during pregnancy at beginning of fourth month into term, with airway impairment, as evidenced by dry cough, fever and night sweats, as well as a 6 kg. weightloss. Twenty-two days after giving birth, the patient was hospitalized with high fever and deteriorated health conditions, requiring treatment in the intensive care unit due to complications such as severe malnutrition, septic shock, pulmonary abscess, pachypleuritis, empyema and bronchopleural fistula. The tuberculosis diagnosis was established through ABF identification with Ziehl-Neelsen stain of the pleural fluid. The patient was hospitalized for 42 days, including eleven days on a mechanical ventilator, before being discharged. Her newborn daughter was admitted to the Pediatric Intensive Care Unit on the 19th day of life due to coughing, fever, difficulty in breathing, liquid stool and rejecting food. The newborn was hospitalized in the newborn intensive care unit for twenty-two days, developing major sepsis and multiple organ failure, which complications led to her death. An autopsy was conducted, revealing granulomatous lesions consistent with tuberculosis in lungs, liver, small intestine, large intestine and peritoneum; additionally the PCR of bronchial aspirate was positive to Mycobacterium tuberculosis DNA.

Multiple organ dysfunction syndrome in humans and animals.

Multiple organ dysfunction syndrome (MODS), defined as the presence of altered organ function in an acutely ill patient such that homeostasis cannot be maintained without intervention, is a cause of high morbidity and mortality in humans and animals. Many advances have been made in understanding the pathophysiology and treatment of this syndrome in human medicine, but much still is unknown. This comparative review will provide information regarding the history and pathophysiology of MODS in humans and discuss how MODS affects each major organ system in animals.

Effect of flow rate and temperature on transmembrane blood pressure drop in an extracorporeal artificial lung.

INTRODUCTION: Transmembrane pressure drop reflects the resistance of an artificial lung system to blood transit. Decreased resistance (low transmembrane pressure drop) enhances blood flow through the oxygenator, thereby, enhancing gas exchange efficiency. This study is part of a previous one where we observed the behaviour and the modulation of blood pressure drop during the passage of blood through artificial lung membranes. METHODS: Before and after the induction of multi-organ dysfunction, the animals were instrumented and analysed for venous-venous extracorporeal membrane oxygenation, using a pre-defined sequence of blood flows. RESULTS: Blood flow and revolutions per minute (RPM) of the centrifugal pump varied in a linear fashion. At a blood flow of 5.5 L/min, pre- and post-pump blood pressures reached -120 and 450 mmHg, respectively. Transmembrane pressures showed a significant spread, particularly at blood flows above 2 L/min; over the entire range of blood flow rates, there was a positive association of pressure drop with blood flow (0.005 mmHg/mL/minute of blood flow) and a negative association of pressure drop with temperature (-4.828 mmHg/(°Celsius). These associations were similar when blood flows of below and above 2000 mL/minute were examined. CONCLUSIONS: During its passage through the extracorporeal system, blood is exposed to pressure variations from -120 to 450 mmHg. At high blood flows (above 2 L/min), the drop in transmembrane pressure becomes unpredictable and highly variable. Over the entire range of blood flows investigated (0-5500 mL/min), the drop in transmembrane pressure was positively associated with blood flow and negatively associated with body temperature.