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1.
J Intensive Care Soc ; 19(4): 305-312, 2018 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-30515240

RESUMO

Objective: Patients undergoing tracheostomy represent a unique cohort, as often they have prolonged hospital stay, require multi-disciplinary, resource-intensive care, and may have poor outcomes. Currently, there is a lack of data around overall healthcare cost for these patients and their outcomes in terms of morbidity and mortality. The objective of the study was to estimate healthcare costs and outcomes associated in tracheostomy patients at a tertiary level hospital in South Australia. Design: Retrospective review of prospectively collected data in patients who underwent tracheostomy between July 2009 and May 2015. Methods: Overall healthcare-associated costs, length of mechanical ventilation, length of intensive care unit stay, and mortality rates were assessed. Results: A total of 454 patients with tracheostomies were examined. Majority of the tracheostomies (n = 386 (85%)) were performed in intensive care unit patients, predominantly using bedside percutaneous approach (85%). The median length of hospital stay was 44 (29-63) days and the in-hospital mortality rate was 20%. Overall total cost of managing a patient with tracheostomy was median $192,184 (inter-quartile range $122560-$295553); mean 225,200 (range $5942-$1046675) Australian dollars. There were no statistically significant differences in any of the measured outcomes, including costs, between patients who underwent percutaneous versus surgical tracheostomy and patients who underwent early versus late tracheostomy in their intensive care unit stay. Factors that predicted (adjusted R 2 = 0.53) the cost per patient were intensive care unit length of stay and hospital length of stay. Conclusion: Hospitalised patients undergoing tracheostomy experience high morbidity and mortality and typically experience highly resource-intensive and costly healthcare.

2.
Wound Repair Regen ; 26(5): 351-358, 2018 09.
Artigo em Inglês | MEDLINE | ID: mdl-29943888

RESUMO

Current therapies available to treat and heal ocular surface injuries and periocular burns are frequently inadequate, costly, and labor intensive. To address these limitations, we have employed a flexible, semitransparent ocular wound chamber (OWC) to provide protection as well as a watertight seal to allow for the constant delivery of therapeutics to the ocular surface and surrounding periocular tissue. This study demonstrates the safety and utilization of the OWC on uninjured eyes and in our exposure keratopathy model. For initial safety studies (N = 3 per group), the eyelids remained intact and the eye uninjured. A blepharotomy (N = 6 per group) was performed to remove the upper and lower eyelids surrounding the left (OS) eye to create our exposure keratopathy model. Right (OD) eyes served as uninjured controls in all studies. Following OWC placement, 0.5 mL HPMC gel or balanced saline solution (BSS) was injected into the chamber. Animals were monitored daily and fully assessed via white light, fluorescein, and OCT imaging at least through 72 hours post OWC placement. In studies that included a blepharotomy, skin samples were analyzed by multiplex cytokine analysis. Results of safety experiments revealed no significant differences between treatment groups in corneal thickness, fluorescein staining, OCT imaging, or histological eye or skin sections when compared to control eyes. In our exposure keratopathy model, OWC treated eyes showed significantly less fluorescein uptake and also were found to have significantly lower levels of cytokines IL-13 and IL-5 in skin samples. These results demonstrate for the first time that treatment using the OWC device is not only safe, but significantly protects against blepharotomy-induced exposure keratopathy. As a whole, this study advances our overall efforts to develop a feasible solution to treat ocular surface injuries, infections, and periocular burns.


Assuntos
Doenças da Córnea/prevenção & controle , Traumatismos Oculares/prevenção & controle , Pálpebras/cirurgia , Cicatrização/fisiologia , Animais , Modelos Animais de Doenças , Pálpebras/lesões , Feminino , Cobaias
3.
Clin Ophthalmol ; 12: 903-911, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-29785086

RESUMO

Purpose: Currently available ocular moisture chambers are not adequate to manage the treatment of periocular burns, corneal injuries, and infection. The purpose of these studies was to demonstrate that a flexible, semi-transparent ocular wound chamber device adapted from technology currently used on dermal wounds is safe for use on corneal epithelial injuries. Materials and methods: A depilatory cream (Nair™, 30 seconds) was utilized to remove the excess hair surrounding the left eyes of anesthetized Institute Armand Frappier (IAF) hairless, female guinea pigs (Crl:HA-Hrhr). A 4 mm corneal epithelium defect was created using a corneal rust ring remover (Algerbrush®II). Epithelial defects were either left untreated or the eyes were fitted with an ocular wound chamber and 0.5 mL of hydroxypropyl methylcellulose (HPMC) gel (GenTeal®) or HPMC liquid (GenTeal®) was injected into each chamber (N=5 per group). At 0, 24, 48, and 72 hours fluorescein and optical coherence tomography imaging was collected and the intraocular pressure (IOP) was measured. H&E staining was performed on corneal and eyelid skin samples and evaluated by a veterinary pathologist. Results: Corneal epithelial wounds demonstrated 100% closure rates when left untreated or treated with an ocular wound chamber containing HPMC gel at 72 hours while wounds treated with an ocular wound chamber containing HPMC liquid were 98% healed. No significant differences were found in corneal thickness and wound healing, IOP, or eyelid skin pathology in any treatment group when compared to controls. Conclusions: This study indicates that adapted wound chamber technology can be safely used on sterile, corneal epithelial wounds without adverse effects on periocular or ocular tissue when filled with a liquid or gel.

4.
Cytometry A ; 91(3): 270-280, 2017 03.
Artigo em Inglês | MEDLINE | ID: mdl-27984679

RESUMO

Application of fluid shear stress to adherent cells dramatically influences their cytoskeletal makeup and differentially regulates their migratory phenotype. Because cytoskeletal rearrangements are necessary for cell motility and migration, preserving these adaptations under in vitro conditions and in the presence of fluid flow are physiologically essential. With this in mind, parallel plate flow chambers and microchannels are often used to conduct in vitro perfusion experiments. However, both of these systems currently lack capacity to accurately study cell migration in the same location where cells were perfused. The most common perfusion/migration assays involve cell perfusion followed by trypsinization which can compromise adaptive cytoskeletal geometry and lead to misleading phenotypic conclusions. The purpose of this study was to quantitatively highlight some limitations commonly found with currently used cell migration approaches and to introduce two new advances which use additive manufacturing (3D printing) or laser capture microdissection (LCM) technology. The residue-free 3D printed insert allows accurate cell seeding within defined areas, increases cell yield for downstream analyses, and more closely resembles the reported levels of fluid shear stress calculated with computational fluid dynamics as compared to other residue-free cell seeding techniques. The LCM approach uses an ultraviolet laser for "touchless technology" to rapidly and accurately introduce a custom-sized wound area in otherwise inaccessible perfusion microchannels. The wound area introduced by LCM elicits comparable migration characteristics compared to traditional pipette tip-induced injuries. When used in perfusion experiments, both of these newly characterized tools were effective in yielding similar results yet without the limitations of the traditional modalities. These innovative methods provide valuable tools for exploring mechanisms of clinically important aspects of cell migration fundamental to the pathogenesis of many flow-mediated disorders and are applicable to other perfusion-based models where migration is of central importance. © 2016 International Society for Advancement of Cytometry.


Assuntos
Técnicas de Cultura de Células/métodos , Movimento Celular/efeitos dos fármacos , Estresse Mecânico , Citoesqueleto/ultraestrutura , Humanos , Perfusão , Tripsina/farmacologia
5.
Cell Signal ; 28(9): 1364-79, 2016 09.
Artigo em Inglês | MEDLINE | ID: mdl-27302407

RESUMO

Coronary artery disease (CAD) accounts for over half of all cardiovascular disease-related deaths. Uncontrolled arterial smooth muscle (ASM) cell migration is a major component of CAD pathogenesis and efforts aimed at attenuating its progression are clinically essential. Cyclic nucleotide signaling has long been studied for its growth-mitigating properties in the setting of CAD and other vascular disorders. Heme-containing soluble guanylyl cyclase (sGC) synthesizes cyclic guanosine monophosphate (cGMP) and maintains vascular homeostasis predominantly through cGMP-dependent protein kinase (PKG) signaling. Considering that reactive oxygen species (ROS) can interfere with appropriate sGC signaling by oxidizing the cyclase heme moiety and so are associated with several CVD pathologies, the current study was designed to test the hypothesis that heme-independent sGC activation by BAY 60-2770 (BAY60) maintains cGMP levels despite heme oxidation and inhibits ASM cell migration through phosphorylation of the PKG target and actin-binding vasodilator-stimulated phosphoprotein (VASP). First, using the heme oxidant ODQ, cGMP content was potentiated in the presence of BAY60. Using a rat model of arterial growth, BAY60 significantly reduced neointima formation and luminal narrowing compared to vehicle (VEH)-treated controls. In rat ASM cells BAY60 significantly attenuated cell migration, reduced G:F actin, and increased PKG activity and VASP Ser239 phosphorylation (pVASP·S239) compared to VEH controls. Site-directed mutagenesis was then used to generate overexpressing full-length wild type VASP (FL-VASP/WT), VASP Ser239 phosphorylation-mimetic (FL-VASP/239D) and VASP Ser239 phosphorylation-resistant (FL-VASP/239A) ASM cell mutants. Surprisingly, FL-VASP/239D negated the inhibitory effects of FL-VASP/WT and FL-VASP/239A cells on migration. Furthermore, when FL-VASP mutants were treated with BAY60, only the FL-VASP/239D group showed reduced migration compared to its VEH controls. Intriguingly, FL-VASP/239D abrogated the stimulatory effects of FL-VASP/WT and FL-VASP/239A cells on PKG activity. In turn, pharmacologic blockade of PKG in the presence of BAY60 reversed the inhibitory effect of BAY60 on naïve ASM cell migration. Taken together, we demonstrate for the first time that BAY60 inhibits ASM cell migration through cGMP/PKG/VASP signaling yet through mechanisms independent of pVASP·S239 and that FL-VASP overexpression regulates PKG activity in rat ASM cells. These findings implicate BAY60 as a potential pharmacotherapeutic agent against aberrant ASM growth disorders such as CAD and also establish a unique mechanism through which VASP controls PKG activity.


Assuntos
Artérias/citologia , Moléculas de Adesão Celular/metabolismo , Movimento Celular , Proteínas Quinases Dependentes de GMP Cíclico/metabolismo , Proteínas dos Microfilamentos/metabolismo , Miócitos de Músculo Liso/citologia , Fosfoproteínas/metabolismo , Guanilil Ciclase Solúvel/metabolismo , Actinas/metabolismo , Animais , Benzoatos/farmacologia , Compostos de Bifenilo/farmacologia , Movimento Celular/efeitos dos fármacos , Ativação Enzimática/efeitos dos fármacos , Hidrocarbonetos Fluorados/farmacologia , Masculino , Mutagênese Sítio-Dirigida , Proteínas Mutantes/metabolismo , Miócitos de Músculo Liso/efeitos dos fármacos , Miócitos de Músculo Liso/enzimologia , Oxirredução , Fosforilação/efeitos dos fármacos , Fosfosserina , Ratos Sprague-Dawley , Reprodutibilidade dos Testes , Remodelação Vascular/efeitos dos fármacos
6.
J Crit Care ; 33: 200-6, 2016 06.
Artigo em Inglês | MEDLINE | ID: mdl-26948252

RESUMO

BACKGROUND: Fluid and sodium overload are a common problem in critically ill patients. Frusemide may result in diuresis in excess of natriuresis. The addition of indapamide may achieve a greater natriuresis, and also circumvent some of the problems associated with frusemide. The objective of this study was to examine the effect of adding indapamide to frusemide on diuresis, natriuresis, creatinine clearance and serum electrolytes. METHODS: Fluid overloaded ICU patients were randomised to either intravenous frusemide (Group F) or intravenous frusemide and enteral indapamide (Group F + I). Comprehensive exclusion criteria were applied to address confounders. 24 hour urine was analysed for electrolytes and creatinine. Serum electrolytes were measured before and 24 hours after administration of diuretics. RESULTS: Forty patients (20 in each group) were included in the study. The groups were similar in their baseline characteristics. Over the 24 h study period, patients in Group F + I, had a larger natriuresis (P = 0.01), chloride loss (P = 0.01) and kaliuresis (P = 0.047). Patients in Group F + I also had a greater 24 hour urinary creatinine clearance (P = 0.01). The 24 hour urine volume and fluid balance was similar between the groups. Patients in Group F had an increase in serum sodium (P = 0.04), while patients in Group F + I had a decrease in both serum chloride (P = 0.01) and peripheral oedema (P < 0.001) during the study duration. CONCLUSION: In fluid overloaded ICU patients, addition of indapamide to frusemide led to a greater natriuresis and creatinine clearance. Such a strategy might be utilised in optimising sodium balance in ICU patients.


Assuntos
Diuréticos/uso terapêutico , Furosemida/uso terapêutico , Hipernatremia/tratamento farmacológico , Indapamida/uso terapêutico , Idoso , Idoso de 80 Anos ou mais , Creatinina/sangue , Cuidados Críticos , Diurese/efeitos dos fármacos , Diuréticos/administração & dosagem , Diuréticos/farmacologia , Quimioterapia Combinada , Feminino , Furosemida/administração & dosagem , Furosemida/farmacologia , Humanos , Hipernatremia/sangue , Hipernatremia/urina , Indapamida/administração & dosagem , Indapamida/farmacologia , Unidades de Terapia Intensiva , Masculino , Pessoa de Meia-Idade , Natriurese/efeitos dos fármacos , Estudos Prospectivos , Sódio/farmacologia , Resultado do Tratamento
7.
Am J Physiol Heart Circ Physiol ; 309(8): H1251-9, 2015 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-26276823

RESUMO

Dysfunctional vascular growth is a major contributor to cardiovascular disease, the leading cause of morbidity and mortality worldwide. Growth factor-induced activation of vascular smooth muscle cells (VSMCs) results in a phenotypic switch from a quiescent, contractile state to a proliferative state foundational to vessel pathology. Transforming growth factor-ß (TGF-ß) is a multifunctional signaling protein capable of growth stimulation via Smad signaling. Although Smad signaling is well characterized in many tissues, its role in VSM growth disorders remains controversial. Recent data from our lab and others implicate the metabolic regulator AMP-activated protein kinase (AMPK) in VSM growth inhibition. We hypothesized that AMPK inhibits VSMC proliferation by reducing TGF-ß-mediated growth in a Smad-dependent fashion. Treatment of rat VSMCs with the AMPK agonist AICAR significantly decreased TGF-ß-mediated activation of synthetic Smad2 and Smad3 and increased inhibitory Smad7. Flow cytometry and automated cell counting revealed that AICAR reversed TGF-ß-mediated cell cycle progression at 24 h and elevated cell numbers at 48 h. TGF-ß/Smad signaling increased the G0/G1 inducers cyclin D1/cyclin-dependent kinase (CDK) 4 and cyclin E/CDK2; however, AICAR reversed these events while increasing cytostatic p21. The specific role of Smad3 in AMPK-mediated reversal of TGF-ß-induced growth was then explored using adenovirus-mediated Smad3 overexpression (Ad-Smad3). Ad-Smad3 cells increased cell cycle progression and cell numbers compared with Ad-GFP control cells, and these were restored to basal levels with concomitant AICAR treatment. These findings support a novel AMPK target in TGF-ß/Smad3 for VSMC growth control and support continued investigation of AMPK as a possible therapeutic target for reducing vascular growth disorders.


Assuntos
Proteínas Quinases Ativadas por AMP/metabolismo , Proliferação de Células/efeitos dos fármacos , Músculo Liso Vascular/efeitos dos fármacos , Miócitos de Músculo Liso/efeitos dos fármacos , Proteína Smad3/metabolismo , Fator de Crescimento Transformador beta1/farmacologia , Animais , Aorta Torácica/efeitos dos fármacos , Aorta Torácica/enzimologia , Aorta Torácica/patologia , Ciclo Celular/efeitos dos fármacos , Proteínas de Ciclo Celular/metabolismo , Células Cultivadas , Relação Dose-Resposta a Droga , Ativação Enzimática , Ativadores de Enzimas/farmacologia , Masculino , Músculo Liso Vascular/enzimologia , Músculo Liso Vascular/patologia , Miócitos de Músculo Liso/enzimologia , Miócitos de Músculo Liso/patologia , Fosforilação , Ratos Sprague-Dawley , Transdução de Sinais/efeitos dos fármacos , Proteína Smad3/genética , Fatores de Tempo , Transfecção
8.
ISRN Minim Invasive Surg ; 20132013 Mar 31.
Artigo em Inglês | MEDLINE | ID: mdl-23762781

RESUMO

In cardiovascular research, translation of benchtop findings to the whole body environment is often critical in order to gain a more thorough and comprehensive clinical evaluation of the data with direct extrapolation to the human condition. In particular, developmental and/or pathophysiologic vascular growth studies often employ in vitro approaches such as cultured cells or tissue explant models in order to analyze specific cellular, molecular, genetic and/or biochemical signaling factors under pristine controlled conditions. However, validation of in vitro data in a whole body setting complete with neural, endocrine and other systemic contributions provides essential proof-of-concept from a clinical perspective. Several well-characterized experimental in vivo models exist that provide excellent proof-of-concept tools with which to examine vascular growth and remodeling in the whole body. This article will examine the rat carotid artery balloon injury model, the mouse carotid artery wire denudation injury model, and rat and mouse carotid artery ligation models with particular emphasis on minimally invasive surgical access to the site of intervention. Discussion will include key scientific and technical details as well as caveats, limitations, and considerations for practical use for each of these valuable experimental models.

9.
Crit Care Resusc ; 14(1): 33-7, 2012 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-22404059

RESUMO

BACKGROUND: Recommended daily intake of sodium is 1- 2mmol/kg. Sodium administration is rarely separated from fluid administration in critically ill patients. OBJECTIVE: To estimate the amount of sodium administered to patients who were invasively ventilated, and to investigate whether sodium administration affected oxygenation, length of stay in ICU and serum sodium level. DESIGN, PARTICIPANTS AND SETTING: Retrospective audit of adult patients who received invasive mechanical ventilation for ≥ 5 days in a tertiary-level intensive care unit. MAIN OUTCOME MEASURES: Total sodium administered from resuscitation and maintenance fluids, infusions, flushes, medicines, transfusions, enteral feeds and total parenteral nutrition; oxygenation, length of ICU stay and serum sodium level. RESULTS: 13 men and 7 women were included. Their median age was 71.9 years (range, 19.8-89.2 years). Median duration of mechanical ventilation was 9 days (range, 6-20 days) and median ICU stay 11.6 days (range, 6-21 days). Median APACHE II score was 29 (range, 18-41). Daily sodium administration was 225.5mmol (151-355mmol). The median daily net fluid balance was 351mL (range, - 759 to +1125mL) and median daily fluid intake was 2352mL (range, 1437- 3798mL). Daily sodium administered correlated with net fluid balance (P<0.001; r=0.35). Of total sodium administered, infusions contributed 22.2% (1.2%-39.9%); drugs 21.6% (0.0-35.5%); flushes 17.4% (9.3%-24.5%); enteral feeds 17% (0.0-39.5%); resuscitation 16.0% (2.5%-36.9%); maintenance fluids 5.8% (0.0-24.0%); transfusions 3.9% (0.0-9.5%) and parenteral nutrition 0.1% (0.0-2.6%). CONCLUSION: Sodium administration to this cohort of critically ill patients requiring prolonged mechanical ventilation was high. Further studies should examine ways of limiting the amount of sodium administered to such patients and to examine if this influences patient outcomes.


Assuntos
Estado Terminal/mortalidade , Erros de Medicação/estatística & dados numéricos , Compostos de Sódio/administração & dosagem , Compostos de Sódio/envenenamento , Adulto , Idoso , Idoso de 80 Anos ou mais , Feminino , Mortalidade Hospitalar , Humanos , Unidades de Terapia Intensiva/estatística & dados numéricos , Masculino , Pessoa de Meia-Idade , Respiração Artificial/mortalidade , Estudos Retrospectivos , Compostos de Sódio/sangue , Austrália do Sul/epidemiologia , Adulto Jovem
10.
Brain Res ; 1222: 118-28, 2008 Jul 30.
Artigo em Inglês | MEDLINE | ID: mdl-18586226

RESUMO

The brain is a steroidogenic organ and is thus dependent on estrogen for many aspects of its development and maintenance in both males and females. The purpose of this study was to develop a model to investigate the effect of estrogen on zebrafish sensory-motor (S-M) maturation through mechanisms found in the central nervous (CNS) and peripheral nervous (PNS) systems. In these experiments the aromatase inhibitor (AI), 4-hydroxy androstenedione (4-OH-A), which blocks estrogen synthesis, was used to diminish estrogen's effects on zebrafish CNS and PNS development. During these various treatments the zebrafish were analyzed for neurological deficits, including tactile response, swimming movements, vestibular behavior, pectoral fin and eye movements. Over a three to five day time period (48-168 h post fertilization), in response to AI treatment, none of these S-M behaviors were developmentally expressed creating a "listless" or non-responding condition. Furthermore, when the AI was removed from the treatment medium the S-M behaviors were fully expressed over a two to three day time period. Most importantly, when estrogen was added at the same time as the AI in a co-treatment paradigm, normal developmental appearance of S-M behaviors was rescued in all neurological parameters measured. Furthermore, the addition of estrogen alone after AI washout accelerated the recovery of the tactile response during the first 24 h of treatment. Treatment of developing zebrafish with the selective estrogen receptor blocker ICI 182,780 mimicked the deficit in S-M behaviors caused by AI treatment. This deficit was overcome by low concentrations of estrogen in a co-treatment paradigm with high ICI levels indicating the possibility of a non-genomic mechanism for estrogen's actions on the developmental expression of these S-M behaviors. Eventually, AI exposed fish died of cardiac arrest 4 to 5 days after the start of treatment; however, AI/estrogen co-treatment allowed for 90-100% survival and the maintenance of normal heart rates during this time period. In conclusion, these studies have demonstrated that the presence of estrogen in the early developing zebrafish embryo is necessary for the proper developmental expression of critical nervous system S-M behaviors necessary for survival, as well as the health of the cardiovascular system. These studies also establish a unique "listless" model for further analysis of estrogen's role in the development of brain, brainstem, and spinal cord circuitry related to the maturation of these behavioral and cardiovascular phenomena.


Assuntos
Comportamento Animal/fisiologia , Desenvolvimento Embrionário/fisiologia , Estrogênios/fisiologia , Atividade Motora/fisiologia , Fatores Etários , Androstenodiona/análogos & derivados , Androstenodiona/farmacologia , Animais , Inibidores da Aromatase/farmacologia , Comportamento Animal/efeitos dos fármacos , Relação Dose-Resposta a Droga , Embrião não Mamífero , Desenvolvimento Embrionário/efeitos dos fármacos , Estradiol/análogos & derivados , Estradiol/farmacologia , Antagonistas de Estrogênios/farmacologia , Estrogênios/farmacologia , Fulvestranto , Frequência Cardíaca/efeitos dos fármacos , Locomoção/efeitos dos fármacos , Locomoção/fisiologia , Atividade Motora/efeitos dos fármacos , Sistema Nervoso/efeitos dos fármacos , Sistema Nervoso/crescimento & desenvolvimento , Estimulação Física/métodos , Natação/fisiologia , Vestíbulo do Labirinto/efeitos dos fármacos , Vestíbulo do Labirinto/fisiologia , Peixe-Zebra
13.
Intensive Care Med ; 28(11): 1649-55, 2002 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-12415456

RESUMO

OBJECTIVE: To determine the relationship between conventional and thromboelastograph (TEG) coagulation parameters and continuous renal replacement therapy (CRRT) circuit longevity. DESIGN: Conventional coagulation and TEG parameters were measured at the commencement of and during CRRT. Time to circuit cessation was measured and only circuits reaching a predetermined rise from baseline in the pressure gradient across the haemofilter were diagnosed as failing due to clotting. All other circuits were excluded from analysis. SETTING: A general critical care unit of a metropolitan tertiary hospital. PATIENTS AND PARTICIPANTS: Fourteen consecutive patients requiring CRRT were studied. The CRRT technique used was continuous veno-venous haemodialysis. INTERVENTIONS: Thromboelastograph measurements were made prior to the commencement of CRRT and daily thereafter for each circuit. The international normalised ratio (INR), activated partial thromboplastin time (APTT) and platelet numbers were measured at commencement and 8 hourly thereafter. Heparin was used for anticoagulation unless considered contraindicated. MEASUREMENTS AND RESULTS: Forty-seven circuits with a mean (SD) circuit life of 33.0 (30.2) h were entered. Twenty-five circuits fulfilled circuit clotting criteria; the mean circuit life was 30.8 (22.1) h. Heparin anticoagulation was found to prolong circuit life significantly despite adequate mean circuit life, 33.2 (35.7) h, in heparin-free circuits. The starting APTT and the TEG variables reaction time (R) and coagulation time (RK) were significantly correlated. The starting APTT, starting RK and mean time taken for the amplitude to increase from 2 to 20 mm (K) were predictive of circuit life. None of these variables predicted which patients would need heparin. CONCLUSION: While TEG variables more closely predicted circuit longevity than conventional coagulation variables, the clinical benefit of TEG monitoring of anticoagulation for CRRT would appear to be minimal.


Assuntos
Lesão Renal Aguda/terapia , Cuidados Críticos/métodos , Terapia de Substituição Renal/métodos , Tromboelastografia , Anticoagulantes/administração & dosagem , Falha de Equipamento , Heparina/administração & dosagem , Humanos , Coeficiente Internacional Normatizado , Tempo de Tromboplastina Parcial , Contagem de Plaquetas , Análise de Regressão
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