Bolus Of Albumin Research Articles

Rapid 500 mL albumin bolus versus rapid 200 mL bolus followed by slower continuous infusion in post-cardiac surgery patients: a pilot before-and-after study

Objective: To evaluate the haemodynamic effects of rapid fluid bolus therapy (FBT) (500 mL of 4% albumin over several minutes) versus combined FBT (rapid 200 mL FBT followed by a 300 mL infusion over 30 minutes).Design: Single centre, prospective, before-and-after trial.Setting: A tertiary intensive care unit in Australia.Participants: Fifty mechanically ventilated post-cardiac surgery patients.Interventions: Rapid 4% albumin FBT versus combined FBT.Main outcome measures: We recorded haemodynamic parameters from before FBT to 30 minutes after FBT. A mean arterial pressure (MAP) response was defined by a MAP increase > 10%, and a cardiac index (CI) response was defined by a CI increase > 15%.Results: Immediately after rapid FBT versus combined FBT, there was a CI response in 13 patients (52%) compared with five patients (20%) respectively (P = 0.038), and a MAP response in 11 patients (44%) in each group. However, from FBT administration to 30 minutes, there was a time and group interaction such that MAP was higher in the rapid FBT group (P = 0.003), as was the case for central venous pressure (P = 0.002) and mean pulmonary artery pressure (P < 0.001). Body temperature fell immediately and was lower with rapid FBT but became warmer than with combined FBT later (P < 0.001). At 30 minutes, a MAP response was seen in ten patients (40%) compared with nine patients (36%) (P < 0.99) and a CI response was present in eight patients (32%) compared with 11 patients (44%) (P = 0.56) in the rapid versus combined FBT groups respectively.Conclusion: Rapid FBT was superior to combined FBT in terms of mean MAP levels and immediate CI response. However, the number of MAP responders or CI responders was similar at 30 minutes.

Effects of saline or albumin fluid bolus in resuscitation: evidence from re-analysis of the FEAST trial

SummaryBackgroundFluid resuscitation is the recommended management of shock, but increased mortality in febrile African children in the FEAST trial. We hypothesised that fluid bolus-induced deaths in FEAST would be associated with detectable changes in cardiovascular, neurological, or respiratory function, oxygen carrying capacity, and blood biochemistry.MethodsWe developed composite scores for respiratory, cardiovascular, and neurological function using vital sign data from the FEAST trial, and used them to compare participants from FEAST with those from four other cohorts and to identify differences between the bolus (n=2097) and no bolus (n=1044) groups of FEAST. We calculated the odds of adverse outcome for each ten-unit increase in baseline score using logistic regression for each cohort. Within FEAST participants, we also compared haemoglobin and plasma biochemistry between bolus and non-bolus patients, assessed the effects of these factors along with the vital sign scores on the contribution of bolus to mortality using Cox proportional hazard models, and used Bayesian clustering to identify subgroups that differed in response to bolus. The FEAST trial is registered with ISRCTN, number ISRCTN69856593.FindingsIncreasing respiratory (odds ratio 1·09, 95% CI 1·07–1·11), neurological (1·26, 1·21–1·31), and cardiovascular scores (1·09, 1·05–1·14) were associated with death in FEAST (all p<0·0001), and with adverse outcomes for specific scores in the four other cohorts. In FEAST, fluid bolus increased respiratory and neurological scores and decreased cardiovascular score at 1 h after commencement of the infusion. Fluid bolus recipients had mean 0·33 g/dL (95% CI 0·20–0·46) reduction in haemoglobin concentration after 8 h (p<0·0001), and at 24 h had a decrease of 1·41 mEq/L (95% CI 0·76–2·06; p=0·0002) in mean base excess and increase of 1·65 mmol/L (0·47–2·8; p=0·0070) in mean chloride, and a decrease of 0·96 mmol/L (0·45 to 1·47; p=0·0003) in bicarbonate. There were similar effects of fluid bolus in three patient subgroups, identified on the basis of their baseline characteristics. Hyperchloraemic acidosis and respiratory and neurological dysfunction induced by saline or albumin bolus explained the excess mortality due to bolus in Cox survival models.InterpretationIn the resuscitation of febrile children, albumin and saline boluses can cause respiratory and neurological dysfunction, hyperchloraemic acidosis, and reduction in haemoglobin concentration. The findings support the notion that fluid resuscitation with unbuffered electrolyte solutions may cause harm and their use should be cautioned. The effects of lower volumes of buffered solutions should be evaluated further.FundingMedical Research Council, Department for International Development, National Institute for Health Research, Imperial College Biomedical Research Centre.

Response to Fluid Boluses in the Fluid and Catheter Treatment Trial

Recent emphasis has been placed on methods to predict fluid responsiveness, but the usefulness of using fluid boluses to increase cardiac index in critically ill patients with ineffective circulation or oliguria remains unclear. This retrospective analysis investigated hemodynamic responses of critically ill patients in the ARDS Network Fluid and Catheter Treatment Trial (FACTT) who were given protocol-based fluid boluses. Fluid responsiveness was defined as ≥ 15% increase in cardiac index after a 15 mL/kg fluid bolus. A convenience sample of 127 critically ill patients enrolled in FACTT was analyzed for physiologic responses to 569 protocolized crystalloid or albumin boluses given for shock, low urine output (UOP), or low pulmonary artery occlusion pressure (PAOP). There were significant increases in mean central venous pressure (9.9 ± 4.5 to 11.1 ± 4.8 mm Hg, P < .0001) and mean PAOP (11.6 ± 3.6 to 13.3 ± 4.3 mm Hg, P < .0001) following fluid boluses. However, there were no significant changes in UOP, and there were clinically small changes in heart rate, mean arterial pressure, and cardiac index. Only 23% of fluid boluses led to a ≥ 15% change in cardiac index. There was no significant difference in the frequency of fluid responsiveness between boluses given for shock or oliguria vs boluses given only for low PAOP (24.0% vs 21.8%, P = .59). There were no significant differences in 90-day survival, need for hemodialysis, or return to unassisted breathing between patients defined as fluid responders and fluid nonresponders. In this cohort of critically ill patients with ARDS who were previously resuscitated, the rate of fluid responsiveness was low, and fluid boluses only led to small hemodynamic changes.

PO-0230 Management Of Severe Malaria In Children, An Audit Of Clinical Practise In A Rural Hospital In Zambia

Introduction The malarial mortality rate remains highest in African infants and children. The purpose of this audit was to review our clinical practice and to assess our compliance with the WHO guideline for the management of severe malaria. Method A retrospective chart review of malaria cases over 14 weeks was undertaken. 43 cases of malaria in paediatric inpatients were identified. Data extraction included duration and nature of presenting symptoms, clinical signs recorded, time to diagnosis, time to anti-malarial treatment and fluid management. Results There were 43 cases of malaria, 20 males, 23 females, median age 3 years (3 mths - 12 years), median length of stay 4.3 days (1–11 days). 35/40 (80%) of these cases were classified severe malaria by WHO criteria. The overall mortality rate was 16.3%. 29/40 (73%) were diagnosed prior to admission: only 22(55%) received a first dose of anti malarial drug within 4 h of presentation. 12% experienced significant diagnostic delays. No child received either normal saline or albumin bolus. 12% received a bolus of dextrose. 10 patients (25%) received blood transfusions. 30 patients (75%) received intravenous quinine, as artesunate, the WHO recommended first line for the treatment of severe malaria, is not currently available in our hospital. Discussion Children hospitalised with malaria in rural Zambia continue to have unacceptably high mortality. This audit highlights the importance of urgent medical review, need for earlier diagnosis and prompt initiation of better antimalarial agents. Late diagnosis and lack of availability of artesunate were identified as potential significant contributors to the high mortality rates in this audit.

Oedema in kwashiorkor is caused by hypoalbuminaemia

It has been argued that the oedema of kwashiorkor is not caused by hypoalbuminaemia because the oedema disappears with dietary treatment before the plasma albumin concentration rises. Reanalysis of this evidence and a review of the literature demonstrates that this was a mistaken conclusion and that the oedema is linked to hypoalbuminaemia. This misconception has influenced the recommendations for treating children with severe acute malnutrition. There are close pathophysiological parallels between kwashiorkor and Finnish congenital nephrotic syndrome (CNS) pre-nephrectomy; both develop protein-energy malnutrition and hypoalbuminaemia, which predisposes them to intravascular hypovolaemia with consequent sodium and water retention, and makes them highly vulnerable to develop hypovolaemic shock with diarrhoea. In CNS this is successfully treated with intravenous albumin boluses. By contrast, the WHO advise the cautious administration of hypotonic intravenous fluids in kwashiorkor with shock, which has about a 50% mortality. It is time to trial intravenous bolus albumin for the treatment of children with kwashiorkor and shock.

Anesthesia Literature Review

Anesthesia Literature Review

Fluid Boluses Possibly Harmful in Some Settings

Source: Maitland K, Kiguli S, Poka RO, et al. Mortality after fluid bolus in African children with severe infection. N Engl J Med. Epub 2011 May 26; doi: 10.1056/NEJMoa1101549The Fluid Expansion as Supportive Therapy (FEAST) group of investigators from Africa and the United Kingdom evaluated the effects of rapid infusion normal saline or albumin compared with intravenous maintenance fluids in children with a severe febrile illness and impaired consciousness and/or respiratory distress accompanied by impaired perfusion. This clinical trial in Uganda, Kenya, and Tanzania enrolled more than 3,000 children aged 60 days to 12 years from January 2009 to January 2011. Stratum A included children without severe hypotension who had one or more of: capillary refill at least three seconds; lower extremity temperature gradient; weak radial pulse; or severe tachycardia. Stratum B included children with impaired perfusions and severe hypotension. Children with severe malnutrition, gastroenteritis, or noninfectious causes of shock were excluded. Stratum A children were randomized to receive 20 ml/kg normal saline, 20 ml/kg albumin, or no boluses (controls). Stratum B children were randomized to receive either normal saline or albumin bolus. Children received intravenous maintenance fluids, antibiotics, antimalarials, anticonvulsants, treatment for hypoglycemia, and transfusions for hemoglobin less than 5 g/dL. The primary end point was mortality at 48 hours. Secondary end points included hypotensive shock within 48 hours, neurologic sequelae at 4 or 24 weeks, and mortality at 4 weeks.Stratum A randomized 3,141 and Stratum B randomized 29 children. Baseline characteristics for all groups were similar: median age 24 months; 62% with prostration; 15% comatose; 83% in respiratory distress; 51% with moderate to severe acidosis; malaria in 57%; and 4% positive for HIV. Children in the two treatment arms received four times more fluid than did control children (40 ml/kg vs 10 ml/kg). Stratum A mortality within the first 48 hours was 10.5% receiving saline bolus, 10.6% receiving albumin, and 7.3% receiving maintenance fluids, with a relative risk of death of 1.45 for any bolus as compared to controls (95% CI, 1.13–1.86; P=.003). Mortality at four weeks was 12.0%, 12.2%, and 8.7% in the three groups, respectively (P=.004 for bolus vs control). Stratum B mortality was 56% in the saline group and 69% in the albumin group (P=.17). Prior to achieving the enrollment goal of 3,600, the study was stopped due to higher mortality among children receiving bolus fluids.The investigators conclude that fluid boluses significantly increased 48-hour mortality in critically ill children with impaired perfusion in these resource-limited settings.Drs Berg and Bratton have disclosed no financial relationship relevant to this commentary. This commentary does not contain a discussion of an unapproved/investigative use of a commercial product/device.This study calls into question the rapid administration of a fluid bolus as an important determinant of positive resuscitation outcome. 1 In resource-limited areas where intensive care facilities are lacking, WHO guidelines reserve fluid resuscitation for advanced shock. Hence, most children in sub-Saharan Africa receive no more than maintenance fluids along with blood transfusions for severe anemia.2There are unique factors in the study population and setting that deserve consideration before application to a wider population, including limited equipment, monitoring capability, and treatments as compared to a modern critical care unit. The value of the intensive care unit environment should not be underestimated.3 It allows the careful titration of fluid, vasopressors to optimize hemodynamics, and mechanical ventilation for pulmonary edema and respiratory failure. Fluid bolus administration in this study was done over one hour, much slower than recommended for sepsis in the critical care literature (up to 60 ml/kg in 15 minutes). Only 7% to 9% of subjects were dehydrated, an unusual finding in pediatric shock patients in resource-rich areas.One important potential confounder can be found in the Supplement Appendix Table 3a accompanying this article (nejmoa1101549_appendix.pdf). In the first hour, 20% of the no-bolus group received a blood transfusion, versus 4% in the saline and 2% in the albumin group. This may have skewed the results to show the beneficial effect of a blood transfusion in the control group, rather than a negative effect of bolus fluids in the intervention groups. The harmful effect of a saline bolus versus no-bolus was statistically significant in patients with a hemoglobin less than 5 gm/dL but not in those with a higher hemoglobin. Could this be because the severely anemic patients needed blood, not a fluid bolus? The conclusions, while perhaps applicable to patients in sub-Saharan Africa, should not be applied to wider populations or locations without further investigation. The results of a single study performed in a unique environment do not disprove the beneficial effects of bolus fluid resuscitation on mortality4 and hospital length of stay when advanced critical care resources are available.5,6

Mortality after Fluid Bolus in African Children with Severe Infection

The role of fluid resuscitation in the treatment of children with shock and life-threatening infections who live in resource-limited settings is not established. We randomly assigned children with severe febrile illness and impaired perfusion to receive boluses of 20 to 40 ml of 5% albumin solution (albumin-bolus group) or 0.9% saline solution (saline-bolus group) per kilogram of body weight or no bolus (control group) at the time of admission to a hospital in Uganda, Kenya, or Tanzania (stratum A); children with severe hypotension were randomly assigned to one of the bolus groups only (stratum B). All children received appropriate antimicrobial treatment, intravenous maintenance fluids, and supportive care, according to guidelines. Children with malnutrition or gastroenteritis were excluded. The primary end point was 48-hour mortality; secondary end points included pulmonary edema, increased intracranial pressure, and mortality or neurologic sequelae at 4 weeks. The data and safety monitoring committee recommended halting recruitment after 3141 of the projected 3600 children in stratum A were enrolled. Malaria status (57% overall) and clinical severity were similar across groups. The 48-hour mortality was 10.6% (111 of 1050 children), 10.5% (110 of 1047 children), and 7.3% (76 of 1044 children) in the albumin-bolus, saline-bolus, and control groups, respectively (relative risk for saline bolus vs. control, 1.44; 95% confidence interval [CI], 1.09 to 1.90; P=0.01; relative risk for albumin bolus vs. saline bolus, 1.01; 95% CI, 0.78 to 1.29; P=0.96; and relative risk for any bolus vs. control, 1.45; 95% CI, 1.13 to 1.86; P=0.003). The 4-week mortality was 12.2%, 12.0%, and 8.7% in the three groups, respectively (P=0.004 for the comparison of bolus with control). Neurologic sequelae occurred in 2.2%, 1.9%, and 2.0% of the children in the respective groups (P=0.92), and pulmonary edema or increased intracranial pressure occurred in 2.6%, 2.2%, and 1.7% (P=0.17), respectively. In stratum B, 69% of the children (9 of 13) in the albumin-bolus group and 56% (9 of 16) in the saline-bolus group died (P=0.45). The results were consistent across centers and across subgroups according to the severity of shock and status with respect to malaria, coma, sepsis, acidosis, and severe anemia. Fluid boluses significantly increased 48-hour mortality in critically ill children with impaired perfusion in these resource-limited settings in Africa. (Funded by the Medical Research Council, United Kingdom; FEAST Current Controlled Trials number, ISRCTN69856593.).

Report of a patient with severe transfusion-related acute lung injury after multiple transfusions, resuscitated with albumin

Objective: To report a patient with a large gastrointestinal stromal tumor (GIST) who received multiple blood transfusions intraoperatively and developed a transfusion-related acute lung injury (TRALI). Design: Case report. Setting: Intensive care unit of a tertiary care hospital. Patient and history: A 58-year-old man with GIST metastatic to the right lobe of the liver, treated with tyrosine kinase inhibitors, underwent a right hepatectomy requiring multiple transfusions. Prior to abdominal closure, he developed copious pulmonary secretions, hypoxemia, and hypotension. Chest radiograph revealed diffuse bilateral infiltrates. Intervention: Volume resuscitation, vasopressors, high PEEP mechanical ventilation, paralysis, nitric oxide, steroids, rapid albumin infusion. Measurements and main results: Extensive noncardiogenic pulmonary edema. After unsuccessful fluid resuscitation with crystalloid fluid, the patient's condition improved rapidly with human albumin boluses. No neurological deficit was detected despite prolonged hypoxemia. Acute renal failure required dialysis but with subsequent recovery. Patient was discharged home on postoperative day 19. Conclusion: Rapid infusion of albumin might be a rescue option in cases of severe TRALI with extensive pulmonary capillary leak during the acute phase.

Response:

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Changes in serum albumin concentration and volume expanding effects following a bolus of albumin 20% in septic patients

Patients with systemic sepsis develop a capillary leak syndrome, and serum -albumin concentration decreases. Hyperoncotic albumin infusion can be used for volume expansion in these patients, but the degree and duration of effect are not well described. We assessed volume expansion by albumin 20% infusion and compared the retention of infused albumin in septic patients and healthy controls. We gave albumin 20%, 200 ml as a rapid infusion to 70 patients with septic shock and 26 controls. Blood samples were taken before and 1, 5, 15, 30, 60, 120 and 240 min after the infusion for measurement of serum albumin concentration and haematocrit. Haemodilution and the percentage of administered albumin remaining intravascularly at each time were calculated. The mean proportion of the increase in albumin remaining at 4 h was 68.5 (sd 10)% in septic patients and 79 (5)% in controls (P<0.001). The albumin 20%, 200 ml caused a secondary fluid resorption and volume expansion maximal at 30 min, equivalent to a 430 ml infusion in septic patients and 500 ml in controls. After giving albumin, serum albumin concentrations decrease significantly faster in septic patients than in healthy controls.

Effect of protein on glomerular filtration rate and prostanoid synthesis in normal and uremic rats.

Normal and uremic conscious rats that had been maintained on a low-protein diet were given oral protein or carbohydrate loads, and clearance studies were performed. Both the normal and uremic animals demonstrated a approximately 30% increase in glomerular filtration rate (GFR) in response to the protein bolus, but no significant increase in GFR was seen following the carbohydrate bolus. Similar studies were performed in uremic rats on a standard protein diet. The changes in GFR that were seen after an albumin bolus were similar but not as pronounced as those noted in the animals on the low-protein diet. Pretreatment with either aspirin or meclofenamate, cyclooxygenase inhibitors, completely blocked the protein-induced rise in GFR. The rats of glomerular production of prostaglandin (PG) E2 and 6-keto-PGF1 alpha (a stable metabolite of prostacyclin, PGI2) were determined by radioimmunoassay in a similar group of normal rats. The synthetic rates of PGE2 and 6-keto-PGF1 alpha following the protein bolus were 40 and 52% greater, respectively, than those observed following the carbohydrate load (P less than 0.005). Aspirin decreased glomerular prostanoid production in protein-treated animals by greater than 60%. Thus it appears that in the setting of protein restriction, the percent increase in GFR following a protein load is similar in both the normal and uremic rats, the increase in GFR in uremic rats is attenuated when animals were allowed to ingest a normal protein diet prior to study, and the increase in GFR seen in response to a protein load may be related to an increase in the synthesis of one or more vasodilatory glomerular prostanoids.

Quantitative gated radionuclide cine cardiography. I Technical basis and methods (author's transl)

Scintigraphic evaluation of the heart function is performed by means of sequential camera scintigraphy following i.v. injection of a 99mTc albumin bolus. The first tracer passage is registered during 30 seconds. About 10 minutes later--after equilibration of the tracer in the blood pool--volume curves of the left ventricle are recorded from a series of about 500 heart cycles. The principles of a computer program which has been developed for this method are described and discussed in detail.