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Biomedical subjects

A D Bersten

Publications and source records attributed to A D Bersten.

At least 19 recordsLinked to original sources
PubMed2002

Effect of CPAP on intrinsic PEEP, inspiratory effort, and lung volume in severe stable COPD.

BACKGROUND: Intrinsic positive end expiratory pressure (PEEPi) constitutes an inspiratory threshold load on the respiratory muscles, increasing work of breathing. The role of continuous positive airway pressure (CPAP) in alleviating PEEPi in patients with severe stable chronic obstructive pulmonary disease is uncertain. This study examined the effect of CPAP on the inspiratory threshold load, muscle effort, and lung volume in this patient group. METHODS: Nine patients were studied at baseline and with CPAP increasing in increments of 1 cm H(2)O to a maximum of 10 cm H(2)O. Breathing pattern and minute ventilation (I), dynamic PEEPi, expiratory muscle activity, diaphragmatic (PTPdi/min) and oesophageal (PTPoes/min) pressure-time product per minute, integrated diaphragmatic (EMGdi) and intercostal EMG (EMGic) and end expiratory lung volume (EELV) were measured. RESULTS: Expiratory muscle activity was present at baseline in one subject. In the remaining eight, PEEPi was reduced from a mean (SE) of 2.9 (0.6) cm H(2)O to 0.9 (0.1) cm H(2)O (p<0.05). In two subjects expiratory muscle activity contributed to PEEPi at higher pressures. There were no changes in respiratory pattern but I increased from 9.2 (0.6) l/min to 10.7 (1.1) l/min (p<0.05). EMGdi remained stable while EMGic increased significantly. PTPoes/min decreased, although this did not reach statistical significance. PTPdi/min decreased significantly from 242.1 (32.1) cm H(2)O.s/min to 112.9 (21.7) cm H(2)O.s/min). EELV increased by 1.1 (0.3) l (p<0.01). CONCLUSION: High levels of CPAP reduce PEEPi and indices of muscle effort in patients with severe stable COPD, but only at the expense of substantial increases in lung volume.

Aged↗
PubMed2002

Serum levels of CC16, SP-A and SP-B reflect tobacco-smoke exposure in asymptomatic subjects.

Since the 16-kDa bronchiolar Clara cell protein (CC16) and the alveolar surfactant-associated proteins (SP)-A and -B leak into the circulation when parenchymal health is disturbed, the aim of this study was to determine whether their serum levels could serve as early peripheral markers of tobacco smoke-induced epithelial injury. Sixty-nine (51 yrs (32-54) median (25-75th percentile)) nonsmokers and 54 (42 yrs (31-53)) asymptomatic smokers were enrolled in the study. Serum levels of SP-A did not differ between subjects (270 (208-389) versus 259 (168-392) microg x L(-1)), however, CC16 levels decreased (10.6 (8.7-14.6) versus 7.6 (6.0-11.2) microg x L(-1)) and SP-B levels increased (2,529 (2,091-2,943) versus 3,053 (2,613-4,188) microg x L(-1)) in the smokers. When tobacco smoke exposure, serum creatinine (renal index), age and sex were used as independent variables, CC16 was negatively influenced by cumulative smoking and positively influenced by age. SP-A and -B were negatively influenced by creatinine and positively influenced by cumulative smoking. Serum SP-B was inversely correlated with forced expiratory volume in one second/vital capacity, suggesting an association between obstructive disease and parenchymal lung health. The authors suggest that serum surfactant-associated proteins-A and -B reflect increased alveolocapillary leakage whereas Clara cell secretory protein 16 reflects tobacco smoke-induced Clara cell toxicity. Their evaluation may allow the effects of tobacco smoke on different levels of the respiratory tract, cellular toxicity and epithelial leakage to be distinguished.

Adolescent↗
PubMed2001

Elevated plasma surfactant protein-B predicts development of acute respiratory distress syndrome in patients with acute respiratory failure.

Surfactant protein-B is a lung specific protein secreted into the air spaces by pulmonary epithelial type II cells that leaks into the bloodstream in increased amounts in patients with ARDS. To test whether elevated plasma levels of surfactant protein-B would predict the development of ARDS in patients with acute hypoxemic respiratory failure, plasma and lung injury scores were collected at study entry and daily thereafter for 3 d from 54 patients admitted to our intensive care unit. ARDS was defined as a new bilateral infiltrate on chest radiograph and a lung injury score > or = 2.5. Twenty patients developed ARDS, of whom seven died. Although the initial lung injury score was not predictive of ARDS, the initial plasma surfactant protein-B was predictive (area under the curve = 0.77 [0.63 to 0.90], nonparametric receiver-operating characteristic analysis). In this cohort, plasma surfactant protein-B was particularly predictive of ARDS when applied to patients suffering a direct lung insult (area under the curve = 0.87 [0.72 to 1.02]), with a sensitivity of 85% (95% CI: 55 to 98%) and specificity of 78% (40 to 97%) at a cutoff of 4,994 ng/ml.

Acute Disease↗
PubMed2000

Lung function, permeability, and surfactant composition in oleic acid-induced acute lung injury in rats.

Although acute lung injury (ALI) is associated with inflammation and surfactant dysfunction, the precise sequence of these changes remains poorly described. We used oleic acid to study the pathogenesis of ALI in spontaneously breathing anesthetized rats. We found that lung pathology can occur far more rapidly than previously appreciated. Lung neutrophils were increased approximately threefold within 5 min, and surfactant composition was dramatically altered within 15 min. Alveolar cholesterol increased by approximately 200%, and even though disaturated phospholipids increased by approximately 30% over 4 h, the disaturated phospholipid-to-total phospholipid ratio fell. Although the alveolocapillary barrier was profoundly disrupted after just 15 min, with marked elevations in lung fluid ((99m)Tc-labeled diethylenetriamine pentaacetic acid) and (125)I-labeled albumin flux, the lung rapidly began to regain its sieving properties. Despite the restoration in lung permeability, the animals remained hypoxic even though minute ventilation was increased approximately twofold and static compliance progressively deteriorated. This study highlights that ALI can set in motion a sequence of events continuing the respiratory failure irrespective of the alveolar surfactant pool size and the status of the alveolocapillary barrier.

Albumins↗
PubMed1999

Partitioning lung and plasma proteins: circulating surfactant proteins as biomarkers of alveolocapillary permeability.

1. The alveolocapillary membrane faces an extraordinary task in partitioning the plasma and lung hypophase proteins, with a surface area approximately 50-fold that of the body and only 0.1-0.2 micron thick. 2. Lung permeability is compromised under a variety of circumstances and the delineation between physiological and pathological changes in permeability is not always clear. Although the tight junctions of the epithelium, rather than the endothelium, are regarded as the major barrier to fluid and protein flux, it is becoming apparent that the permeability of both are dynamically regulated. 3. Whereas increased permeability and the flux of plasma proteins into the alveolar compartment has dire consequences, fortuitously the flux of surfactant proteins from the airspaces into the circulation may provide a sensitive means of non-invasively monitoring the lung, with important implications for treatment modalities. 4. Surfactant proteins are unique in that they are present in the alveolar hypophase in high concentrations. They diffuse down their vast concentration gradients (approximately 1:1500-7000) into the circulation in a manner that reflects lung function and injury score. Surfactant proteins vary markedly in size (approximately 20-650 kDa) and changes in the relative amounts appear particularly diagnostic with regard to disease severity. Alveolar levels of surfactant proteins remain remarkably constant despite respiratory disease and, unlike the flux of plasma proteins into the alveolus, which may reach equilibrium in acute lung injury, the flux of surfactant proteins is unidirectional because of the concentration gradient and because they are rapidly cleared from the circulation. 5. Ultimately, the diagnostic usefulness of surfactant proteins as markers of alveolocapillary permeability will demand a sound understanding of their kinetics through the vascular compartment.

Animals↗
PubMed1999

Measurement of tidal volume by using transthoracic impedance variations in rats.

The application of impedance pneumography for monitoring respiration in small animals has been limited by problems with calibration. With improved instrumentation, we describe the calibration of tidal volume in anesthetized rats. The detection of changes in voltage, reflecting the electrical impedance variations associated with respiration, was optimized by using disposable adhesive silver-silver chloride electrodes, advanced circuitry, and analog-to-digital recording instrumentation. We found a linear relationship between change in impedance and tidal volume in individual rats (R2 >/= 98%), which was strongly influenced by rat weight. Consequently, a calibration equation incorporating change in impedance and rat weight was derived to predict tidal volume. Comparison of the predicted and true tidal volumes revealed a mean R2 >/= 98%, slopes of approximately 1, intercepts of approximately 0, and bias of approximately 0.07 ml. The predicted volumes were not significantly affected by either frequency of respiration or pulmonary edema. We conclude that impedance pneumography provides a valuable tool for the noninvasive measurement of tidal volume in anesthetized rats.

Analog-Digital Conversion↗
PubMed1998

Respiratory mechanics and surfactant in the acute respiratory distress syndrome.

1. Although abnormalities in pulmonary surfactant were initially implicated in the pathogenesis of the acute respiratory distress syndrome (ARDS) 30 years ago, most subsequent research has focused on mediators of the parenchymal acute lung injury (ALI) and the associated increase in alveolocapillary permeability. 2. Surfactant is essential for normal breathing and the severity of ALI correlates with surfactant dysfunction and abnormalities in surfactant composition; however, no relationship has been shown with respiratory system compliance. In neonates and most animal models, respiratory system compliance will directly reflect the elastic properties of the lung. However, the greater vertical height of the chest wall in adults, in combination with the increase in lung density due to ALI, results in dependent collapse of alveoli. Because simple, global measurement of compliance is strongly influenced by the volume of aerated lung, alternative measures of respiratory mechanics may reflect surfactant dysfunction. 3. Using a dynamic, volume-dependent model of respiratory mechanics to indirectly reflect this heterogeneous inflation, we have found direct relationships with surfactant composition in patients with ARDS. A failure of surfactant to increase surface tension in large alveoli may also explain why lung overdistension occurs at relatively low pressures. Furthermore, surfactant dysfunction will exaggerate heterogeneous lung inflation, augmenting regional overinflation, and is essential for ALI secondary to repetitive opening and closing of alveoli during tidal ventilation. 4. Ventilation-induced ALI has also been shown to result in massive increases in pro-inflammatory cytokines within the lung. Because ALI itself fails to compartmentalize cytokines, with spillover into the systemic circulation resulting in distant organ dysfunction, surfactant dysfunction may have widespread implications.

Adult↗
PubMed1998

Clearance of Clara cell secretory protein 16 (CC16) and surfactant proteins A and B from blood in acute respiratory failure.

Surfactant proteins A and B (SP-A and SP-B) enter the circulation in a manner that acutely reflects changes in pulmonary function in patients with acute respiratory failure (ARF). There is a small but significant gradient in SP-A and SP-B from arterial to mixed venous (A-V) blood, and since we have detected both proteins in urine, the kidney may be a major site of their systemic clearance. Clara cell secretory protein 16 (CC16), which leaks from the respiratory tract, is known to be freely eliminated by the kidney. Lung plasma protein levels will depend on the rates of both protein entry into and clearance from plasma. In order to study the limiting variable determining these levels, we compared plasma CC16, SP-A, and SP-B in matching A-V blood samples from 37 ARF patients with indices of lung dysfunction and glomerular filtration rate (GFR) (of plasma cystatin C and creatinine). Cystatin C, CC16, SP-A, and SP-B were reduced in mixed venous plasma (all p < 0.001) and their A-V gradients were directly related to their arterial levels (all p < 0.03). Whereas CC16, SP-A, and SP-B reflected blood oxygenation (all p < 0.05), only SP-A and SP-B were related to lung injury score (LIS) (both p < 0.05). In contrast, whereas the clearances of both CC16 and cystatin C were related to that of creatinine (p < 0.02 for both), the clearances of SP-A and SP-B were not. Our study confirms that all three lung proteins are acutely cleared from the circulation of patients with ARF (half-lives < 18 min), and we conclude that whereas the plasma concentration of CC16 depends on GFR, plasma concentrations of SP-A and SP-B reflect lung function independently of this variable.

Acute Disease↗
PubMed1998

Haemolysis associated with continuous venovenous renal replacement circuits.

Extracorporeal circuits can cause haemolysis resulting in an increase in plasma-free haemoglobin (PFHb). High pressures and clots within the circuit have been identified as factors increasing the likelihood of haemolysis. Continuous venovenous haemodiafiltration (CVVHD) is associated with high circuit pressures as the pump-driven circuit clots over a period of time. PFHb was measured during CVVHD to determine if circuit life, maximum circuit pressure or the clotting of the haemofilter was associated with evidence of haemolysis. Circuit life up to 50 hours, circuit pressures or haemofilter clotting had no significant effect on PFHb. There was a small rise in PFHb in the circuits lasting beyond 50 hours. CVVHD circuits can be run up to 50 hours without concern for haemolysis.

Acute Kidney Injury↗
PubMed1998

The use of antimicrobials in ten Australian and New Zealand intensive care units. The Australian and New Zealand Intensive Care Multicentre Studies Group Investigators.

A prospective standardized collection of clinical, microbiological and pharmaceutical information on antibiotic use was conducted in Australia and New Zealand intensive care units (ICUs) involving 481 consecutive critically ill patients who were receiving antibiotics for any reason while in ICU. Patients had a mean SAPS II score of 34.1 +/- 17.8 with an expected mortality of 15.6% (actual mortality 12%). Of these, 292 (60.8%) were admitted to the ICU within 72 hours of surgery. Among such surgical patients, 233 (79.9%) received antibiotics for "surgical prophylaxis" while in ICU (48% of sample population). The second largest group of patients treated with antibiotics in ICU included those with systemic inflammatory response syndrome and clinical suspicion of infection (38%). Antibiotics were prescribed for the treatment of clinically diagnosed infection in 268 patients. Clinical response was apparent in 62.6% and in most (71%) was achieved in the first 72 hours of treatment. The incidence of antimicrobial-related side-effects was 4%, mostly in the form of diarrhoea or rash (75% of all side-effects). The most commonly prescribed antimicrobials were gentamicin (n = 146), ceftriaxone (n = 98), vancomycin (n = 94) and metronidazole (n = 111). Three times daily prescription of aminoglycosides was uncommon (< 1%). Forty-one patients had a documented infection (positive culture) with a gram-negative organism. Of these, 17 received therapy with a single antibiotic and 24 received therapy with two antibiotics. Despite similar illness severity, there were six deaths in the former group and only two in the latter.

Anti-Bacterial Agents↗
PubMed1998

Surfactant composition reflects lung overinflation and arterial oxygenation in patients with acute lung injury.

Pulmonary surfactant abnormalities have consistently been documented in patients with acute lung injury (ALI), however, there is little evidence directly correlating them to altered respiratory mechanics. To explore this further, surfactant composition was measured in lung aspirate fluid collected on 15 occasions from 10 patients with ALI. The composition was compared with lung aspirate fluid from 11 intubated patients prior to elective cardiac surgery (CS), and bronchoalveolar lavage fluid from 16 normal subjects. In both the ALI and cardiac groups the proportion of disaturated phospholipids (DSP) and phosphatidylcholine was reduced. Plasma levels of surfactant proteins-A and -B (SP-A and -B) were elevated, but were unrelated to alveolar surfactant levels. In the ALI group, and the ALI + CS group, DSP, normalized to the total phospholipid content, sphingomyelin (SPH), and urea, showed strong direct correlations with arterial oxygen tension/inspiratory oxygen fraction (all p < or = 0.01). In the ALI group, normalized DSP was also directly related to the elastance of the positive end-expiratory pressure-induced increase in the end-expiratory lung volume (all p < or = 0.02), and indirect correlations were found with a measure of lung overinflation (%E2; all p < or = 0.01). We conclude that surfactant composition correlates with lung function abnormalities in acute lung injury and cardiac patients, and that both groups had elevated plasma surfactant proteins-A and -B levels, consistent with a concurrent increase in alveolocapillary permeability.

Blood-Air Barrier↗
PubMed1998

Measurement of overinflation by multiple linear regression analysis in patients with acute lung injury.

Strategies to optimize alveolar recruitment and prevent lung overinflation are central to ventilatory management of patients with acute lung injury (ALI). The recent description of overinflation using multilinear regression analysis of airway pressure (Paw) and flow (V') data allows a functional assessment of lung mechanics. However, this technique has not been studied in ALI patients. During 15 positive end-expiratory pressure (PEEP) trials in 10 ALI patients, respiratory elastance was partitioned into volume-independent (E1) and volume-dependent (E2VT) components, where Paw=(E1+E2VT)V+RrsV'+Po; where V is volume, VT is tidal volume, Rrs is respiratory resistance and Po is static recoil pressure at end-expiration (equivalent to total PEEP). Then, %E2 was calculated as (100E2VT)/(E1+E2VT); a measure of lung overinflation when %E2>30%. Alveolar recruitment, assessed as a PEEP-induced increase in V>50 mL at a constant Paw occurred in 14 of 15 trials (299+/-34 mL, mean+/-SEM), but was independent of the degree of lung inflation. Lung overinflation was common (six of 15 clinically set PEEP levels) and occurred despite a dynamic elastic distending pressure (Pel,dyn) <30 cmH2O during 18 of 36 PEEP titrations. During a PEEP titration the resultant %E2 was directly related to delta(peak airway pressure-Po) (rs=0.86, p<0.001) and delta(Pel,dyn-Po) (rs=0.89, p<0.001). The 95% predictive intervals for a 2 cmH2O change in either driving pressure were %E2 values of 30.4-68.1% and 32.8-69.2%, respectively. Single or continuous measurement of %E2 (a measure of lung inflation) is a readily available method for titrating ventilatory parameters. Further, during a positive end-expiratory pressure titration a change in ventilatory driving pressure > or =2 cmH2O is indicative of overinflation.

Acute Disease↗
PubMed1997

Endotoxin alters the systemic disposition of nitric oxide synthase inhibitors in the awake sheep.

1. We evaluated the haemodynamic effects and systemic disposition of the nitric oxide synthase (NOS) inhibitor NL-nitro-L-arginine (NOLA) after intravenous (i.v.) administration of two different doses (5 and 20 mg/kg) in awake healthy sheep and awake sheep given a continuous i.v. infusion of endotoxin (lipopolysaccharide, 12 ng/kg per h, i.v., for 18 h). In addition, we determined the systemic disposition of another NOS inhibitor, NL-nitro-L-arginine methylester (L-NAME; 20 mg/kg, i.v.) in awake healthy sheep only. 2. NL-Nitro-L-arginine produced a dose-dependent decrease in heart rate (HR) and cardiac output (CO) together with a dose-dependent increase in mean arterial pressure (MAP) and peripheral vascular resistance (PVR) when compared to baseline. In endotoxic sheep NOLA produced a greater increase in MAP and mean pulmonary arterial pressure (MPAP). 3. In healthy sheep there was a dose-related increase in total body clearance (Cl) of NOLA. The Cl increased from 0.028 L/min after the lower dose to 0.032 L/min after the higher dose. The infusion of endotoxin caused an increase in Cl of NOLA to 0.040 and 0.047 L/min, respectively, and a decrease in plasma slow half-life (t1/2) from 825 to 546 min and from 780 to 453 min, respectively. 4. NL-Nitro-L-arginine methylester was rapidly cleared from the plasma with a slow half-life of approximately 7.5 min and there was a simultaneous appearance of NOLA in the plasma. 5. These results support the view that nitric oxide has a significant role in regulating vascular tone in healthy and endotoxic sheep and indicate that the increases in Cl of NOLA with an increase in its dose and the presence of endotoxin will be important in influencing appropriate dosage regimens in clinical studies.

Animals↗
PubMed1997

Aerosol kinetics and bronchodilator efficacy during continuous positive airway pressure delivered by face mask.

BACKGROUND: Rates of fresh gas flow (FGF) commonly used when continuous positive airway pressure (CPAP) is delivered by face mask theoretically reduce the delivery and availability of therapeutic aerosols. As it may be hazardous for patients with acute respiratory failure to interrupt mask CPAP, the effects of CPAP on aerosol kinetics and bronchodilator efficacy were investigated. METHOD: The effect of CPAP at 10 cm H2O at a FGF rate of 50 l/min on the delivery of technetium labelled aerosol generated from a readily available jet nebuliser was measured using a bench model of spontaneous respiration. In a separate clinical study the bronchodilator responses to incremental doses of nebulised salbutamol were measured in nine stable asthmatic subjects in a random sequence of conventional nebulisation (control) or nebulisation whilst receiving CPAP via a tight fitting face mask. Each patient acted as his or her own control. RESULTS: CPAP significantly reduced total aerosol delivery to the face mask from 6.85 (1.52)% to 1.3 (0.37)% of the initial nebuliser charge. In the clinical study a significant bronchodilator response to nebulised salbutamol was seen during both conventional nebulisation and nebulisation whilst receiving CPAP by face mask. The shape of the dose-response curves and the magnitude of the total increase in the forced expiratory volume in one second (FEV1) was identical for CPAP and control conditions. CONCLUSIONS: Despite a reduction in aerosol presented to the proximal airway, the bronchodilator response to inhaled beta 2 agonists in stable asthmatic subjects was not affected when CPAP was delivered by face mask. Despite a high rate of FGF, nebulised beta 2 agonists are effective when administered in conjunction with CPAP delivered by face mask.

Adult↗
PubMed1997

Surfactant replacement therapy in ARDS: white knight or noise in the system?

Although one would predict that surfactant replacement therapy would be effective in acute respiratory distress syndrome (ARDS), a recent large trial proved unsuccessful, possibly reflecting the nature of the surfactant used. Given the importance of the unique proteins in the action of surfactant, these would seem vital components of any exogenous surfactant. The ability to identify patients at risk of ARDS and to characterise their surfactant might allow prophylactic treatment with a nebulised, complementary, tailor-made preparation of surfactant. Advanced cases might undergo bronchoscopic focal lavage to remove plasma proteins and inflammatory mediators prior to focal instillation of surfactant to areas of greatest need. Ventilation regimens might be adjusted both to minimise trauma and to conserve endogenous surfactant.

Adult↗
PubMed1997

Surfactant proteins-A and -B are elevated in plasma of patients with acute respiratory failure.

Surfactant protein-A (SP-A) leaks into the circulation of patients with acute respiratory distress syndrome (ARDS) or acute cardiogenic pulmonary edema (APE) in a manner inversely related to lung function. Since surfactant protein-B (SP-B) is synthesized as a precursor considerably smaller than alveolar SP-A, we investigated whether it enters the circulation more readily. Reactivities consistent with SP-B proprotein (approximately 42 to approximately 45 kD) and the approximately 25 kD processing intermediate were detected in plasma. Plasma immunoreactive SP-B levels were significantly higher in ARDS (8,007+/-1,654 ng/ml [mean+/-SEM], n = 22) and APE (3,646+/-635 ng/ml, n = 10) patients compared with normal subjects (1,685+/-58 ng/ml, n = 33) and ventilated patients with no cardiorespiratory disease (1,829+/-184 ng/ml, n = 7). All groups had plasma SP-B/SP-A ratios approximately 6- to approximately 8-fold higher than in normal lavage or ARDS tracheal aspirate fluid, consistent with protein sieving. During admission, both plasma SP-B and the SP-B/SP-A ratio were inversely related to blood oxygenation (PaO2/FIO2) (p < 0.0001 and p < 0.025, n = 260 from 39 patients; Spearman) and static respiratory system compliance (deltaV/deltaP) (p < 0.0001 and p < 0.01, n = 168 from 25 patients). We describe in detail three patients and conclude that immunoreactive SP-B enters more readily than SP-A, is cleared acutely, and provides a better indicator of lung trauma.

Acute Disease↗
PubMed1996

Continuous renal replacement therapy in critically ill patients: monitoring circuit function.

There is currently no universally accepted method to monitor circuit function or guidelines for circuit replacement during continuous renal replacement therapies (CRRT). The objectives of this study were to diagnose the causes of circuit failure, identify factors responsible for circuit clotting and determine a predictive monitor of circuit function. The CRRT technique used in this study was continuous venovenous haemodialysis (CVVHD). Continuous monitoring of circuit pressures (pre- and post-haemofilter and their difference: the transfilter pressure gradient) was used to diagnose the causes of circuit failure. In circuits ceasing due to clotting, the factors thought to contribute, anticoagulation, haematocrit and platelet count, were measured at the commencement of CVVHD and every eight hours thereafter until circuit failure. Monitors of circuit function, creatinine clearance and plasma to diafiltrate urea ratio were measured every eight hours and compared to the transfilter pressure gradient. During a three-month period data was collected on five consecutive patients (41 consecutive haemofilters). Clotting of the haemofilter (63%) and air detection chamber (7.5%) were the most common identifiable causes of circuit failure. The duration of their circuit life was described using multiple regression analysis, i.e. hours of filter life = -82.8 + (delta platelet count x 0.25) + (delta haematocrit x 3.6) + (circuit flow [ml/min] x 4) R2 = 0.77. A rise in transfilter pressure gradient and a fall in haemofilter function discriminated clotted filters with falling function (decrease in creatinine clearance and urea ratio) from unclotted filters. In any circuit an increase of 26 mmHg or more in the transfilter pressure gradient accurately predicted circuit failure due to clotting and imminent cessation of function. Increases in platelet count, haematocrit, and low circuit flows are important determinants of haemofilter life. The measurement of transfilter pressure gradient across the haemofilter is an accurate bedside monitor of circuit function.

Acute Kidney Injury↗