Risk factors for respiratory failure among hospitalized patients with Guillain-Barré syndrome.

BACKGROUND: Guillain-Barré syndrome (GBS) is an acute inflammatory polyneuropathy that can lead to respiratory failure. In this study, we evaluate early clinical risk factors for respiratory failure at the time of hospital admission. METHODS: We studied a retrospective cohort of patients with GBS admitted to a tertiary care center. The potential risk factors studied were sociodemographic characteristics, GBS symptoms, overall and cervical muscle weakness (Medical Research Council [MRC] scores), electromyography findings, and cerebrospinal fluid analysis findings. Unadjusted odds ratios (OR) were calculated and exact logistic regression analysis (adjusted OR) performed to assess the association between baseline risk factors and respiratory failure. RESULTS: Overall, 13 of 113 (12%) patients included in the study developed respiratory failure. Unadjusted analyses showed that involvement of any cranial nerve (OR: 14.7; 95% CI, 1.8-117.1), facial palsy (OR: 17.3; 95% CI, 2.2-138.0), and bulbar weakness (OR: 10.7; 95% CI, 2.3-50.0) were associated with increased risk of respiratory failure. Lower MRC sum scores (for scores <30, OR: 14.0; 95% CI, 1.54-127.2) and neck MRC scores (for scores ≤3, OR: 21.0; 95% CI, 3.5-125.2) were associated with higher likelihood of respiratory failure. Adjusted analyses showed that presence of bulbar weakness (OR: 7.6; 95% CI, 1.3-43.0) and low neck MRC scores (scores ≤3, OR: 9.2; 95% CI, 3.5-125.2, vs scores >3) were independently associated with respiratory failure. CONCLUSIONS: Bulbar and neck muscle weakness at admission are clinical predictors of increased risk of respiratory failure in patients with GBS. These findings could guide the adequate management of high-risk patients.

Risk factors for respiratory failure among hospitalized patients with Guillain-Barré syndrome.

BACKGROUND: Guillain-Barré syndrome (GBS) is an acute inflammatory polyneuropathy that can lead to respiratory failure. In this study, we evaluate early clinical risk factors for respiratory failure at the time of hospital admission. METHODS: We studied a retrospective cohort of patients with GBS admitted to a tertiary care center. The potential risk factors studied were sociodemographic characteristics, GBS symptoms, overall and cervical muscle weakness (Medical Research Council [MRC] scores), electromyography findings, and cerebrospinal fluid analysis findings. Unadjusted odds ratios (OR) were calculated and exact logistic regression analysis (adjusted OR) performed to assess the association between baseline risk factors and respiratory failure. RESULTS: Overall, 13 of 113 (12%) patients included in the study developed respiratory failure. Unadjusted analyses showed that involvement of any cranial nerve (OR: 14.7; 95% CI, 1.8-117.1), facial palsy (OR: 17.3; 95% CI, 2.2-138.0), and bulbar weakness (OR: 10.7; 95% CI, 2.3-50.0) were associated with increased risk of respiratory failure. Lower MRC sum scores (for scores <30, OR: 14.0; 95% CI, 1.54-127.2) and neck MRC scores (for scores ≤3, OR: 21.0; 95% CI, 3.5-125.2) were associated with higher likelihood of respiratory failure. Adjusted analyses showed that presence of bulbar weakness (OR: 7.6; 95% CI, 1.3-43.0) and low neck MRC scores (scores ≤3, OR: 9.2; 95% CI, 3.5-125.2, vs scores >3) were independently associated with respiratory failure. CONCLUSIONS: Bulbar and neck muscle weakness at admission are clinical predictors of increased risk of respiratory failure in patients with GBS. These findings could guide the adequate management of high-risk patients.

Mortality in patients with respiratory distress syndrome. / Mortalidad en pacientes con síndrome de distress respiratorio.

INTRODUCTION: Mortality in Acute Respiratory Distress Syndrome (ARDS) is decreasing, although its prognosis after hospital discharge and the prognostic accuracy of Berlin's new ARDS stratification are uncertain. METHODS: We did a restrospective analysis of hospital and 6 month mortality of patients with ARDS admitted to the Intensive Care Unit of a Univeristy Hospital in Buenos Aires, between January 2008 and June 2011. ARDS was defined by PaO2/FiO2 lower than 200 mmHg under ventilation with at least 10 cm H2O of PEEP and a FiO2 higher or equal than 0.5. and the presence of bilateral infiltrates in chest radiography, in the absence of cardiogenic acute pulmonary edema, during the first 72 hs of mechanical ventilation. Mortality associated risk factors, the use of rescue therapies and Berlin's stratification for moderate and severe ARDS patients were considered. RESULTS: Ninety eight patients were included; mean age was 59±19 years old, 42,9% had mayor co-morbidities; APACHE II at admission was 22±7; SOFA at day 1 was 8±3. Prone position ventilation was applied in 20,4% and rescue measures in 12,2% (12 patients with nitric oxide and 1 with extracorporeal membrane oxygenation). Hospital and 6 months mortality were 37.7 and 43.8% respectively. After logistic regression analysis, only age, the presence of septic shock at admission, Ppl >30 cmH2O, and major co-morbidities were independently associated with hospital outcome. There was no difference between moderate and severe groups (41,2 and 36,8% respectively; p=0,25). CONCLUSION: In this cohort, including patients with severe hypoxemia and high percentage of mayor co-morbidities, ARDS associated mortality was lower than some previous studies. There was no increase in mortality after hospital discharge. There was no difference in mortality between moderate and severe groups according to Berlin's definition.

QTc prolongation after brain surgery.

OBJECTIVE: Abnormalities observed in the electrocardiogram (ECG) after acute central nervous system (CNS) events have been reported. Our objective was to assess the incidence of heart rate-corrected QT interval (QTc) prolongation in patients admitted to the intensive care unit (ICU) after brain surgery. METHODS: Admission standard 12-lead ECGs were analyzed blinded to patient data. The QT interval was measured and Bazzett's formula was used to obtain QTc. Prolonged QTc was defined as ≧450 ms. RESULTS: We included 114 patients in the study. The mean age was 49±17 years. Brain neoplasm was the surgical indication in 90% of the patients. The mean QTc was 470±42 ms. Prolonged QTc was found in 71% patients. The heart rate-corrected QT interval was between 450 ms and 500 ms in 52% and >500 ms in 19% of the patients. The heart rate and concentration of serum glucose were higher in the prolonged QTc group. Only 7·5% of all patients had hypokalemia (≤3 mEq/l). In the prolonged QTc group 9·2% had hypokalemia compared to 3·2% in normal QTc patients (P = 0·406). There were no significant associations between categories of QTc and the serum levels of creatinine, magnesium, calcium, sodium, or pH. Phenytoin and metoclopramide were not frequently used in patients with prolonged QTc. DISCUSSION: This study supports our hypothesis that prolonged QTc is frequently observed after a brain surgery. Hypokalemia, hypocalcaemia, and drugs such as metoclopramide or phenytoin could not explain the high incidence of prolonged QTc. Brain injury during a surgical procedure may be one of the primary causes of QTc prolongation after neurosurgery.

Obesidad y excreción urinaria de sodio en niños y adolescentes / Obesity and urinary sodium excretion in children and adolescents

Background: Qbesity is a disease characterized by an abnormal accumulation body fat that results in neuroen-docrine changes that alter the homeostasis of sodium, producing an increased risk of hypertension in adulthood. objective: To evaluate the effect of obesity on urinary sodium excretion in children and adolescents. subjects and Methods: 266 male and female children in the age group of 5-15 years were studied: 154 obese (OB) with > 95th percentile of BMI, and 112 normal-weight patients (C) with percentile 5-85 of BMI, from the outpatient service of the Children Hospital, Posadas, Misiones, Argentina during the years 2008 -2009. The determinations of serum sodium (Na s) and 24-hour urine (Na ur) were performed using Ion Selective Electrode. The fractional excretion of sodium (FENa percent) was calculated. results: Na ur values (mEq/kg/day) and FENa percent reported significantly lower differences in the obese group compared to controls: OB Na ur 2.23 vs C Na ur 3.40 (p < 0.0001); OB FENa percent 0.59 vs C FENa percent 0.71 (p = 0.001). Conclusion: Results obtained in the present study showed that obese children have a significantly decreased urinary sodium excretion compared to normal weight children. This difference could be caused by renal retention of this ion.

Introducción: La obesidad es una enfermedad caracterizada por el aumento de grasa corporal, que genera modificaciones neuroendocrinas involucrando alteraciones en la homeostasis del sodio, que podrían generar hipertensión arterial en la adultez. Objetivo: Evaluar el efecto de la obesidad sobre la excreción urinaria de sodio en niños y adolescentes. Pacientes y Método: Se estudiaron 266 niños de ambos sexos, entre 5 y 15 años: 154 obesos (OB) definidos como IMC percentil > 95, y 112 normopeso (C), IMC percentil 5-85, provenientes del Servicio de Consultorio Externo del Hospital de Pediatría-Posadas, Misiones, Argentina, durante los años 2008-2009. Las determinaciones de sodio en suero (Na s) y orina de 24 h (Na ur) se realizaron con electrodo ion selectivo. Se calculó la excreción fraccional de sodio (EFNa por ciento). Resultados: Los valores de Naur (mEq/ kg/día) y la EFNa por ciento significativamente menores en el grupo de obesos con respecto a los controles: Na ur QB 2,23 vs Na ur C 3,40 (p < 0,0001); EFNa por ciento OB 0,59 vs EFNa por ciento C 0,71 (p = 0,001). Conclusión: En el presente estudio los resultados mostraron que los niños y adolescentes obesos presentan una disminución significativa de la excreción urinaria de sodio respecto de los niños normopeso. Dicha diferencia podría estar generada por la retención renal de dicho ion.

Accuracy of weight and height estimation in an intensive care unit.

We report the findings from a prospective study determining the magnitude of errors in the visual estimation of weight and height of critically ill patients. Forty-two consecutive patients were weighed by a physician with a calibrated stretcher scale and length measured with a steel measuring tape. The predicted body weight was calculated using the ARDSnet formulae. Attending physicians and nurses were asked to estimate patient's actual weight, predicted weight and height. The average percent errors in estimation of actual and predicted weight were 11.4 and 14.6%, respectively. Errors greater than 20% in patient's actual and predicted weight were observed in 15 and 24% of cases, respectively. The majority of height estimations (86%) had an error < 10%. There were non-significant differences between the estimations made by intensive care unit physicians and nurses. Our study shows that estimations of patient's weight made by intensive care unit staff are often inaccurate. In contrast, estimations of height made by intensive care unit staff are usually adequate. Estimated body weight of critically ill patients has implications for drug and respiratory therapy and should be used with caution.

Duropleural fistula revealed by neurological manifestations: an unusual cause of pleural effusion.

Symptomatic pleural collection of cerebrospinal fluid is a rare but accepted complication in hydrocephalic paediatric patients treated with ventriculopleural shunts. Few cases have been described in adults, usually as complication of trauma, tumours or spinal surgery, particularly post-laminectomy. It should be considered in the differential diagnosis of pleural effusion after neurosurgical procedures involving the spine. We describe two patients with large cerebrospinal fluid collections in the pleural cavity caused by postoperative duropleural fistula, who presented with neurological symptoms, cerebrospinal fluid pressure headache and meningitis.

Involvement of the cytoskeleton in Junin virus multiplication.

The role of the cellular cytoskeleton in Junin virus (JV) infection was explored in two ways. Firstly, the action of inhibitors that affect individual cytoskeletal systems (microtubules or microfilaments) selectively was analysed. It was found that perturbations of microtubule or microfilament networks caused by colchicine, nocodazole, nifedipine, EGTA or DMSO strongly affected virion production and viral protein expression at non-cytotoxic concentrations. Secondly, the extent of association of viral proteins and infectious virus particles with the cytoskeletal fraction of monkey Vero cells was determined by using three non-ionic detergents, Triton X-100 (TX-100), NP-40 and octyl glucoside (OG). The cytoskeleton retained nearly 70% of the external JV envelope glycoprotein GP38 and about 40% of the JV nucleoprotein NP, according to TX-100 and OG insolubility results. Furthermore, 1% of the total cell-bound infectivity was detected in the detergent-insoluble fraction, suggesting that cytoskeletal components are involved in the initiation of the assembly and budding processes of JV particles at the plasma membrane.

Inhibition of arenavirus multiplication in vitro by phenotiazines.

Trifluoperazine (TFP) and chlorpromazine (CPZ), two pharmacologically active phenotiazine derivatives, were evaluated for their inhibitory activity on the replication of the arenaviruses Junin (JV), the etiological agent of Argentine hemorrhagic fever, Tacaribe virus and Pichinde virus. Both compounds achieved a concentration-dependent inhibition of viral multiplication at concentrations not affecting cell viability. The 50% inhibitory concentration (IC50) values determined by a virus yield inhibition assay for several strains of JV, including a human pathogenic strain, were in the range of 7.7-23.0 microM and the 90% inhibitory concentration (IC90) fluctuated between 16.6 and 35.2 microM. From time of addition and removal experiments, it can be concluded that CPZ inhibited an early stage in the replicative cycle of JV, probably viral entry. TFP also affected JV penetration when present soon after virus adsorption, and also interfered with a later step of viral maturation when added after 7 h of infection. The expression of viral antigens in the cytoplasm of infected cells was highly reduced in the presence of the compounds, as revealed by immunofluorescence staining, whereas no JV proteins were detected at the cell membrane. The distribution pattern of viral proteins was altered in the few cells exhibiting positive fluorescence after treatment with the phenotiazines. The TFP-induced inhibitory effect on JV multiplication was significantly reversed in the presence of 5 microM calmodulin. These data indicate that TFP and CPZ inhibit JV replication in vitro. Our findings suggest that the integrity of the actin microfilaments may be required for optimal arenavirus multiplication.