193 resultados para anemia, blood transfusion, intensive care


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BACKGROUND AND OBJECTIVE: Arterial base excess and lactate levels are key parameters in the assessment of critically ill patients. The use of venous blood gas analysis may be of clinical interest when no arterial blood is available initially. METHODS: Twenty-four pigs underwent progressive normovolaemic haemodilution and subsequent progressive haemorrhage until the death of the animal. Base excess and lactate levels were determined from arterial and central venous blood after each step. In addition, base excess was calculated by the Van Slyke equation modified by Zander (BE(z)). Continuous variables were summarized as mean +/- SD and represent all measurements (n = 195). RESULTS: Base excess according to National Committee for Clinical Laboratory Standards for arterial blood was 2.27 +/- 4.12 versus 2.48 +/- 4.33 mmol(-l) for central venous blood (P = 0.099) with a strong correlation (r(2) = 0.960, P < 0.001). Standard deviation of the differences between these parameters (SD-DIFBE) did not increase (P = 0.355) during haemorrhage as compared with haemodilution. Arterial lactate was 2.66 +/- 3.23 versus 2.71 +/- 2.80 mmol(-l) in central venous blood (P = 0.330) with a strong correlation (r(2) = 0.983, P < 0.001). SD-DIFLAC increased (P < 0.001) during haemorrhage. BE(z) for central venous blood was 2.22 +/- 4.62 mmol(-l) (P = 0.006 versus arterial base excess according to National Committee for Clinical Laboratory Standards) with strong correlation (r(2) = 0.942, P < 0.001). SD-DIFBE(z)/base excess increased (P < 0.024) during haemorrhage. CONCLUSION: Central venous blood gas analysis is a good predictor for base excess and lactate in arterial blood in steady-state conditions. However, the variation between arterial and central venous lactate increases during haemorrhage. The modification of the Van Slyke equation by Zander did not improve the agreement between central venous and arterial base excess.

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Postoperative care of major neurosurgical procedures is aimed at the prevention, detection and treatment of secondary brain injury. This consists of a series of pathological events (i.e. brain edema and intracranial hypertension, cerebral hypoxia/ischemia, brain energy dysfunction, non-convulsive seizures) that occur early after the initial insult and surgical intervention and may add further burden to primary brain injury and thus impact functional recovery. Management of secondary brain injury requires specialized neuroscience intensive care units (ICU) and continuous advanced monitoring of brain physiology. Monitoring of intracranial pressure (ICP) is a mainstay of care and is recommended by international guidelines. However, ICP monitoring alone may be insufficient to detect all episodes of secondary brain insults. Additional invasive (i.e. brain tissue PO2, cerebral microdialysis, regional cerebral blood flow) and non-invasive (i.e. transcranial doppler, near-infrared spectroscopy, EEG) brain monitoring devices might complement ICP monitoring and help clinicians to target therapeutic interventions (e.g. management of cerebral perfusion pressure, blood transfusion, glucose control) to patient-specific pathophysiology. Several independent studies demonstrate such multimodal approach may optimize patient care after major neurosurgical procedures. The aim of this review is to evaluate some of the available monitoring systems and summarize recent important data showing the clinical utility of multimodal neuromonitoring for the management of main acute neurosurgical conditions, including traumatic brain injury, subarachnoid hemorrhage and stroke.

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PURPOSE: A misleading blood tacrolimus concentration (BTC) value caused by the contamination of a central venous catheter previously used for tacrolimus administration is described. SUMMARY: A 59-year-old woman with severe chronic obstructive pulmonary disease successfully underwent double lung transplantation. In the intensive care unit, she received a continuous i.v. infusion of tacrolimus from days 1 to 5 after transplantation through the distal lumen of a polyurethane triple-lumen central venous catheter. The catheter lumen was flushed twice a day with 0.9% sodium chloride injection. The proximal lumen was used for blood sampling after being flushed; the first 10 mL of blood was discarded. BTCs determined in whole blood one, four, and five days after transplantation were within the therapeutic range of 5-15 ng/mL. On day five the patient was transferred to the thoracic surgery ward and was switched to oral tacrolimus 1.5 mg twice daily. The BTC on day 6 was unexpectedly high at 134.5 ng/mL. The patient's clinical status was normal, and no signs of tacrolimus toxicity were observed. On day 7, blood samples were drawn from a peripheral vein and simultaneously through the central venous catheter. Although the central venous catheter had not been exposed to tacrolimus during the preceding two days, it yielded blood with a BTC eight times higher than the BTC in blood from the peripheral vein (41.4 ng/mL versus 5.1 ng/mL). CONCLUSION: The collection of blood from a central venous catheter lumen that had been used for tacrolimus administration resulted in a BTC about eight times higher than what was measured in peripheral blood.

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PURPOSE: To report the sudden onset of reversible Charles Bonnet syndrome precipitated byacute severe anemia. METHODS: The charts of three patients (Usher syndrome, bilateral macular degeneration, and bilateral retinal vein occlusion) with acute Charles Bonnet syndrome in the setting of severe anemia were reviewed. RESULTS: Anemia resulted from bladder surgery, recto-colitis, and severe urinary tract infection. Hemoglobin ranged from 78 to 86 g/L. Decreased visual acuity and formed visual hallucinations (giants, flowers, animals) were present in all three patients. Rapid reversal of Charles Bonnet syndrome and visual acuity improvement followed blood transfusion. CONCLUSIONS: Acute severe anemia can precipitate Charles Bonnet syndrome, which may be reversible by blood transfusion.

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The authors evaluated ten years of surgical reanimation in the University Centre of Lausanne (CHUV). Irreversible coagulopathy (IC) is the predominant cause of death for the polytraumatized patient. Acidosis, hypothermy, and coagulation troubles are crucial elements of this coagulopathy. The authors looked for a criterion allowing the identification of dying of IC. In a retrospective study, laboratory results of pH, TP, PTT, thrombocyte count and the need for blood transfusion units were checked for each major step of the primary evaluation and treatment of the polytraumatized patients. These results were considered as critical according to criteria of the literature (30). The authors conclude that the apparation of a third critical value may be useful to identify the polytraumatized patient at risk of dying of IC status. This criterion may also guide the trauma team in selecting a damage control surgical approach (DCS). This criterion was then introduced into an algorithm involving the Emergency Department, the operating room and the Intensive Care Unit. This criterion is a new tool to address the patient at the crucial moment to the appropriate hospital structure.

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Background. Anastomotic leak remains a common and potentially deleterious complication after esophagectomy. Preoperative embolization of the left gastric artery and splenic artery (PAE) has been suggested to lower anastomotic leak rates. We present the results of our 5-year experience with this technique.Methods. All patients undergoing PAE before esophagectomy since introduction of this technique in 2004 were compared in a 1: 2 matched-pair analysis with patients without PAE. Matching criteria were type of anastomosis, neoadjuvant treatment, comorbidity, and age. Data were derived from a retrospective chart review from 2000 to 2006 that was perpetuated as a prospective database up to date. Outcome measures were anastomotic leak, overall complications, and hospital stay.Results. Between 2000 and 2009, 102 patients underwent esophagectomy for cancer in our institution with an overall leak rate of 19% and a mortality of 8%. All 19 patients having PAE since 2004 were successfully matched 1: 2 to 38 control patients without PAE; both groups were similar regarding demographics and operation characteristics. Two PAE (11%) and 8 control patients (21%) had an anastomotic leak, but the difference was statistically not significant (p = 0.469). Overall and major complication rates for PAE and control group were 89% versus 79% (p = 0.469) and 37% versus 34% (p = 1.000), respectively. Median intensive care unit and hospital stay were 3 versus 3 days (p = 1.000) and 22 versus 17 days (p = 0.321), respectively.Conclusions. In our experience, PAE has no significant impact on complications and anastomotic leak in particular after esophagectomy. (Ann Thorac Surg 2011;91:1556-61) (C) 2011 by The Society of Thoracic Surgeons

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It has been suggested that determination of the neutrophil elastase alpha1-proteinase inhibitor complex (E-alpha1PI) improves the diagnosis of bacterial infection in newborns. We evaluated the use of E-alpha1PI measurements in 143 newborns, consecutively admitted to a tertiary intensive care unit, employing a new random access assay and a sampling procedure that minimises post-collection artefacts. The 95% range for noninfected newborns was 20-110 microg/l up to the 5th day of life and 20-85 microg/l thereafter. The sensitivity as to the diagnosis of culture-proven bloodstream infection was 80% for E-alpha1PI, 86% for the immature to total neutrophil ratio, 64% for C-reactive protein and 37% for the total white blood cell count. The corresponding specificity amounted to 97%, 85%, 85% and 86%, respectively. E-alpha1PI increases preceded elevations of C-reactive protein by 18 h. Like C-reactive protein, E-alpha1PI levels did not distinguish between bloodstream infection and non-bacterial inflammatory responses. Results of E-alpha1PI became available within 1 h of collection and usually 2-3 h before manual leucocyte counts. CONCLUSION: Determination of neutrophil elastase alpha1-proteinase inhibitor levels yields diagnostic advantages comparable to those of manual differential counts but provide faster turnaround times.

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OBJECTIVE: Critical care is a working environment with frequent exposure to stressful events. High levels of psychological stress have been associated with increased prevalence of burnout. Psychological distress acts as a potent trigger of cortisol secretions. We attempted to objectify endocrine stress reactivity. DESIGN: Observational cohort study during two 12-day periods in successive years. SETTING: A tertiary multidisciplinary neonatal and pediatric intensive care unit (33 beds). SUBJECTS: One hundred and twelve nurses and 27 physicians (94% accrual rate). INTERVENTIONS AND MEASUREMENTS: Cortisol determined from salivary samples collected every 2 hrs and after stressful events. Participants recorded the subjective perception of stress with every sample. Endocrine reactions were defined as transient surges in cortisol of &gt;50% and 2.5 nmol/L over the baseline. MAIN RESULTS: During 7,145 working hours, we observed 474 (12.5%) endocrine reactions from 3,781 samples. The mean cortisol increase amounted to 10.6 nmol/L (219%). The mean occurrence rate of endocrine reactions per subject and sample was 0.159 (range, 0-0.43). Although the mean raw cortisol levels were lower in experienced team members (&gt;3 yrs of intensive care vs. &lt;3 yrs, 4.1 vs. 4.95 nmol/L, p &lt; .001), professional experience failed to attenuate the frequency and magnitude of endocrine reactions, except for the subgroup of nurses and physicians with &gt;8 yrs of intensive care experience. A high proportion (71.3%) of endocrine reactions occurred without conscious perception of stress. Unawareness of stress was higher in intensive care nurses (75.1%) than in intermediate care nurses (51.8%, p &lt; .01). CONCLUSIONS: Stress-related cortisol surges occur frequently in neonatal and pediatric critical care staff. Cortisol increases are independent of subjective stress perception. Professional experience does not abate the endocrine stress reactivity.

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Wound care made great progress during last years related to several factors. The first is an awakening of the importance of wounds. The progress made in the comprehension of the physiopathology of wounds led to innovations in all stages of this complex process which is the wound healing. Autologus platelet concentrate producing growth factors are in use to stimulate the first phase of the healing. The second phase which is the phase of proliferation and secretion is currently better managed with new categories of bandages which are true local treatments. The nutrition became one of the pillars of wound treatments especially among old patients. The reconstructive surgery took great steps since the physiology and the vascular anatomy of the skin and soft tissues are better known. Finally the bio-engineering has entered the treatment of the wound there is more than 20 years ago and methods have improved and become more reliable

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PURPOSE OF REVIEW: This special commentary addresses recent clinical reviews regarding appropriate nutrition and metabolic support in the critical care setting. RECENT FINDINGS: There are divergent approaches between North America and Europe for the use of early nutrition support and combined enteral nutrition and parenteral nutrition support possibly due to the commercial availability of specific parenteral nutrients. The advent of intensive insulin therapy has changed the landscape of metabolic support in the intensive care unit, and previous notions about infective risk of parenteral nutrition will need to be re-addressed. Patients with brain failure may benefit from an intensive insulin therapy with a blood glucose target that is higher than that used in patients without brain failure. Patients with heart failure may benefit from the addition of nutritional pharmacology that targets proximate oxidative pathophysiological pathways. Intradialytic parenteral nutrition may be viewed as another form of supplemental parenteral nutrition when enteral nutrition is insufficient in patients on hemodialysis in the intensive care unit. SUMMARY: It is proposed that intensive metabolic support be routinely implemented in the intensive care unit based on the following steps: intensive insulin therapy with an appropriate blood glucose target, nutrition risk assessment, early and if needed combined enteral nutrition and parenteral nutrition to target 20-25 kcal/kg/day and 1.2-1.5 g protein/kg/day, and nutritional and metabolic monitoring.

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Maintenance of adequate oxygenation is a mainstay of intensive care, however, recommendations on the safety, accuracy, and the potential clinical utility of invasive and non-invasive tools to monitor brain and systemic oxygenation in neurocritical care are lacking. A literature search was conducted for English language articles describing bedside brain and systemic oxygen monitoring in neurocritical care patients from 1980 to August 2013. Imaging techniques e.g., PET are not considered. A total of 281 studies were included, the majority described patients with traumatic brain injury (TBI). All tools for oxygen monitoring are safe. Parenchymal brain oxygen (PbtO2) monitoring is accurate to detect brain hypoxia, and it is recommended to titrate individual targets of cerebral perfusion pressure (CPP), ventilator parameters (PaCO2, PaO2), and transfusion, and to manage intracranial hypertension, in combination with ICP monitoring. SjvO2 is less accurate than PbtO2. Given limited data, NIRS is not recommended at present for adult patients who require neurocritical care. Systemic monitoring of oxygen (PaO2, SaO2, SpO2) and CO2 (PaCO2, end-tidal CO2) is recommended in patients who require neurocritical care.

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PURPOSE: Unlike in the outpatient setting, delivery of aerosols to critically ill patients may be considered complex, particularly in ventilated patients, and benefits remain to be proven. Many factors influence aerosol delivery and recommendations exist, but little is known about knowledge translation into clinical practice. METHODS: Two-week cross-sectional study to assess the prevalence of aerosol therapy in 81 intensive and intermediate care units in 22 countries. All aerosols delivered to patients breathing spontaneously, ventilated invasively or noninvasively (NIV) were recorded, and drugs, devices, ventilator settings, circuit set-up, humidification and side effects were noted. RESULTS: A total of 9714 aerosols were administered to 678 of the 2808 admitted patients (24 %, CI95 22-26 %), whereas only 271 patients (10 %) were taking inhaled medication before admission. There were large variations among centers, from 0 to 57 %. Among intubated patients 22 % (n = 262) received aerosols, and 50 % (n = 149) of patients undergoing NIV, predominantly (75 %) inbetween NIV sessions. Bronchodilators (n = 7960) and corticosteroids (n = 1233) were the most frequently delivered drugs (88 % overall), predominantly but not exclusively (49 %) administered to patients with chronic airway disease. An anti-infectious drug was aerosolized 509 times (5 % of all aerosols) for nosocomial infections. Jet-nebulizers were the most frequently used device (56 %), followed by metered dose inhalers (23 %). Only 106 (<1 %) mild side effects were observed, despite frequent suboptimal set-ups such as an external gas supply of jet nebulizers for intubated patients. CONCLUSIONS: Aerosol therapy concerns every fourth critically ill patient and one-fifth of ventilated patients.

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Pyroglutamic acidemia is an uncommon metabolic disorder, which is usually diagnosed at early ages. The mechanism of action is thought to be glutathione depletion, and its clinical manifestations consist of hemolytic anemia, mental retardation, ataxia, and chronic metabolic acidosis. However, an acquired form has been described in adult patients, who usually present with confusion, respiratory distress, and high anion gap metabolic acidosis (HAGMA). It is also associated with many conditions, including chronic acetaminophen consumption. A 68-year-old white male, with chronic acetaminophen use presented to our service on multiple occasions with severe HAGMA. The patient was admitted to the intensive care unit and required mechanical ventilation and aggressive supportive measures. After ruling out the most frequent etiologies for his acid-base disorder and considering the long history of Tylenol ingestion, his 5-oxiproline (pyroglutamic acid) levels were sent to diagnose pyroglutamic acidemia. Clinicians need to be aware of this cause for metabolic acidosis since it might be a more common metabolic disturbance in compromised patients than would be expected. Subjects with HAGMA that cannot be explained by common causes should be tested for the presence of 5-oxoproline. Discontinuation of the offending drug is therapeutic.

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BACKGROUND: Autologous blood transfusion (ABT) efficiently increases sport performance and is the most challenging doping method to detect. Current methods for detecting this practice center on the plasticizer di(2-ethlyhexyl) phthalate (DEHP), which enters the stored blood from blood bags. Quantification of this plasticizer and its metabolites in urine can detect the transfusion of autologous blood stored in these bags. However, DEHP-free blood bags are available on the market, including n-butyryl-tri-(n-hexyl)-citrate (BTHC) blood bags. Athletes may shift to using such bags to avoid the detection of urinary DEHP metabolites. STUDY DESIGN AND METHODS: A clinical randomized double-blinded two-phase study was conducted of healthy male volunteers who underwent ABT using DEHP-containing or BTHC blood bags. All subjects received a saline injection for the control phase and a blood donation followed by ABT 36 days later. Kinetic excretion of five urinary DEHP metabolites was quantified with liquid chromatography coupled with tandem mass spectrometry. RESULTS: Surprisingly, considerable levels of urinary DEHP metabolites were observed up to 1 day after blood transfusion with BTHC blood bags. The long-term metabolites mono-(2-ethyl-5-carboxypentyl) phthalate and mono-(2-carboxymethylhexyl) phthalate were the most sensitive biomarkers to detect ABT with BTHC blood bags. Levels of DEHP were high in BTHC bags (6.6%), the tubing in the transfusion kit (25.2%), and the white blood cell filter (22.3%). CONCLUSIONS: The BTHC bag contained DEHP, despite being labeled DEHP-free. Urinary DEHP metabolite measurement is a cost-effective way to detect ABT in the antidoping field even when BTHC bags are used for blood storage.

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OBJECTIVE: To provide an update to the original Surviving Sepsis Campaign clinical management guidelines, "Surviving Sepsis Campaign Guidelines for Management of Severe Sepsis and Septic Shock," published in 2004. DESIGN: Modified Delphi method with a consensus conference of 55 international experts, several subsequent meetings of subgroups and key individuals, teleconferences, and electronic-based discussion among subgroups and among the entire committee. This process was conducted independently of any industry funding. METHODS: We used the Grades of Recommendation, Assessment, Development and Evaluation (GRADE) system to guide assessment of quality of evidence from high (A) to very low (D) and to determine the strength of recommendations. A strong recommendation (1) indicates that an intervention's desirable effects clearly outweigh its undesirable effects (risk, burden, cost) or clearly do not. Weak recommendations (2) indicate that the tradeoff between desirable and undesirable effects is less clear. The grade of strong or weak is considered of greater clinical importance than a difference in letter level of quality of evidence. In areas without complete agreement, a formal process of resolution was developed and applied. Recommendations are grouped into those directly targeting severe sepsis, recommendations targeting general care of the critically ill patient that are considered high priority in severe sepsis, and pediatric considerations. RESULTS: Key recommendations, listed by category, include early goal-directed resuscitation of the septic patient during the first 6 hrs after recognition (1C); blood cultures before antibiotic therapy (1C); imaging studies performed promptly to confirm potential source of infection (1C); administration of broad-spectrum antibiotic therapy within 1 hr of diagnosis of septic shock (1B) and severe sepsis without septic shock (1D); reassessment of antibiotic therapy with microbiology and clinical data to narrow coverage, when appropriate (1C); a usual 7-10 days of antibiotic therapy guided by clinical response (1D); source control with attention to the balance of risks and benefits of the chosen method (1C); administration of either crystalloid or colloid fluid resuscitation (1B); fluid challenge to restore mean circulating filling pressure (1C); reduction in rate of fluid administration with rising filing pressures and no improvement in tissue perfusion (1D); vasopressor preference for norepinephrine or dopamine to maintain an initial target of mean arterial pressure > or = 65 mm Hg (1C); dobutamine inotropic therapy when cardiac output remains low despite fluid resuscitation and combined inotropic/vasopressor therapy (1C); stress-dose steroid therapy given only in septic shock after blood pressure is identified to be poorly responsive to fluid and vasopressor therapy (2C); recombinant activated protein C in patients with severe sepsis and clinical assessment of high risk for death (2B except 2C for postoperative patients). In the absence of tissue hypoperfusion, coronary artery disease, or acute hemorrhage, target a hemoglobin of 7-9 g/dL (1B); a low tidal volume (1B) and limitation of inspiratory plateau pressure strategy (1C) for acute lung injury (ALI)/acute respiratory distress syndrome (ARDS); application of at least a minimal amount of positive end-expiratory pressure in acute lung injury (1C); head of bed elevation in mechanically ventilated patients unless contraindicated (1B); avoiding routine use of pulmonary artery catheters in ALI/ARDS (1A); to decrease days of mechanical ventilation and ICU length of stay, a conservative fluid strategy for patients with established ALI/ARDS who are not in shock (1C); protocols for weaning and sedation/analgesia (1B); using either intermittent bolus sedation or continuous infusion sedation with daily interruptions or lightening (1B); avoidance of neuromuscular blockers, if at all possible (1B); institution of glycemic control (1B), targeting a blood glucose < 150 mg/dL after initial stabilization (2C); equivalency of continuous veno-veno hemofiltration or intermittent hemodialysis (2B); prophylaxis for deep vein thrombosis (1A); use of stress ulcer prophylaxis to prevent upper gastrointestinal bleeding using H2 blockers (1A) or proton pump inhibitors (1B); and consideration of limitation of support where appropriate (1D). Recommendations specific to pediatric severe sepsis include greater use of physical examination therapeutic end points (2C); dopamine as the first drug of choice for hypotension (2C); steroids only in children with suspected or proven adrenal insufficiency (2C); and a recommendation against the use of recombinant activated protein C in children (1B). CONCLUSIONS: There was strong agreement among a large cohort of international experts regarding many level 1 recommendations for the best current care of patients with severe sepsis. Evidenced-based recommendations regarding the acute management of sepsis and septic shock are the first step toward improved outcomes for this important group of critically ill patients.