J Hall

Royal Brisbane Hospital, Brisbane, Queensland, Australia

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Publications (7)9.21 Total impact

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    ABSTRACT: Serial procalcitonin is reported to be useful to titrate duration of antibiotic therapy in the non critically ill patient with pneumonia. The aim of this study was to examine the relationship between antibiotic therapy and serial serum procalcitonin concentrations in a cohort of critically ill septic patients and examine for any differences between culture positive (CP) and culture negative (CN) sepsis. Seventy-five critically ill patients with suspected sepsis were enrolled in this prospective observational study. Serial procalcitonin and C-reactive protein assays were measured on days one, three, five, seven, 10 and 14. The mean duration of antibiotic therapy was similar in the two groups (10.4 +/- 5.1 (CP) vs. 8.4 +/- 5.1 (CN) days, P = 0.09). Serum procalcitonin concentrations were significantly higher at baseline in the CP than the CN group (14.9 +/- 22.9 vs. 6.8 +/- 21.5 ng/ml, P = 0.04). During the study period, serum concentrations of procalcitonin and C-reactive protein declined in both groups. Serum procalcitonin consistently remained higher in the CP group (P < 0.05) and did not return to normal values. In the CN group, procalcitonin concentrations fell below 0.5 only on day 10. There was no significant difference in C-reactive protein profile between the two groups. Four patients in the CP group (11%) had relapse of sepsis. The mean procalcitonins in the relapsed subgroup were lower than those in the remission subgroup (P = 0.02). Therapy for proven or presumed infections was associated with declining serum procalcitonin and C-reactive protein in critically ill septic patients. The marked variability and overlap in plasma profile of these markers between CP and CN sepsis makes it difficult to define a nadir plasma concentration at which one can recommend discontinuation of antibiotic therapy.
    Anaesthesia and intensive care 01/2009; 37(1):20-6. · 1.30 Impact Factor
  • T J Morgan · B Venkatesh · A Beindorf · I Andrew · J Hall ·
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    ABSTRACT: Fluids balanced to avoid acid-base disturbances may be preferable to saline, which causes metabolic acidosis in high volume. We evaluated acid-base and bio-energetic effects of haemodilution with a crystalloid balanced on physical chemical principles, versus crystalloids causing metabolic acidosis or metabolic alkalosis. Anaesthetised, mechanically ventilated Sprague-Dawley rats (n=32, allocated to four groups) underwent six exchanges of 9 ml crystalloid for 3 ml blood. Exchange was with one of three crystalloids with strong ion difference (SID) values of 0, 24 (balanced) and 40 mEq/l. Controls did not undergo haemodilution. Mean haemoglobin concentration fell to approximately 50 g/l after haemodilution. With SID 24 mEq/l fluid, metabolic acid-base remained unchanged. Dilution with SID 0 mEq/l and 40 mEq/l fluids caused a progressive metabolic acidosis and alkalosis respectively. Standard base excess (SBE) and haemoglobin concentration were directly correlated in the SID 0 mEq/l group (R2 = 0.61), indirectly correlated in the SBE 40 mEq/l group (R2 = 0.48) and showed no correlation in the SID 24 mEq/l group (R2 = 0.003). There were no significant differences between final ileal values of CO2 gap, nucleotides concentration, energy charge, or luminal lactate concentration. SID 40 mEq/l crystalloid dilution caused a significant rise in subcutaneous lactate. In this group mean kidney ATP concentration was significantly less than controls and renal energy charge significantly lower than SID 0 mEq/l and control groups. We conclude that a crystalloid SID of 24 mEq/l provides balanced haemodilution. Bio-energetic perturbations with higher SID haemodilution may be more severe and need further investigation.
    Anaesthesia and intensive care 05/2007; 35(2):173-9. · 1.30 Impact Factor
  • B Venkatesh · R H Mortimer · B Couchman · J Hall ·
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    ABSTRACT: It is unclear whether a random plasma cortisol measurement and the corticotropin (ACTH) test adequately reflect glucocorticoid secretory capacity in critical illness. This study aimed to determine whether these tests provide information representative of the 24 hour period. Plasma cortisol was measured hourly for 24 hours in 21 critically ill septic patients followed by a corticotropin test with 1 microg dose administered intravenously. Serum and urine were analysed for ACTH and free cortisol respectively. Marked hourly variability in plasma cortisol was evident (coefficient of variation 8-30%) with no demonstrable circadian rhythm. The individual mean plasma cortisol concentrations ranged from 286 +/- 59 nmol/l to 796 +/- 83 nmol/l. The 24 hour mean plasma cortisol was strongly correlated with both random plasma cortisol (r2 0.9, P < 0.0001) and the cortisol response to corticotropin (r2 0.72, P < 0.001). Only nine percent of patients increased their plasma cortisol by 250 nmol/l after corticotropin (euadrenal response). However, 35% of non-responders had spontaneous hourly rises > 250 nmol/l thus highlighting the limitations of a single point corticotropin test. Urinary free cortisol was elevated (865 +/- 937 nmol) in both corticotropin responders and non-responders suggesting elevated plasma free cortisol. No significant relationship was demonstrable between plasma cortisol and ACTH. We conclude that although random cortisol measurements and the low dose corticotropin tests reliably reflect the 24 hour mean cortisol in critical illness, they do not take into account the pulsatile nature of cortisol secretion. Consequently, there is the potential for erroneous conclusions about adrenal function based on a single measurement. We suggest that caution be exercised when drawing conclusions on the adequacy of adrenal function based on a single random plasma cortisol or the corticotropin test.
    Anaesthesia and intensive care 05/2005; 33(2):201-9. · 1.30 Impact Factor
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    ABSTRACT: This prospective study evaluated serum procalcitonin (PCT) and C-reactive protein (CRP) as markers for systemic inflammatory response syndrome (SIRS)/sepsis and mortality in patients with traumatic brain injury and subarachnoid haemorrhage. Sixty-two patients were followed for 7 days. Serum PCT and CRP were measured on days 0, 1, 4, 5, 6 and 7. Seventy-seven per cent of patients with traumatic brain injury and 83% with subarachnoid haemorrhage developed SIRS or sepsis (P=0.75). Baseline PCT and CRP were elevated in 35% and 55% of patients respectively (P=0.03). There was a statistically non-significant step-wise increase in serum PCT levels from no SIRS (0.4+/-0.6 ng/ml) to SIRS (3.05+/-9.3 ng/ml) to sepsis (5.5+/-12.5 ng/ml). A similar trend was noted in baseline PCT in patients with mild (0.06+/-0.9 ng/ml), moderate (0.8+/-0.7 ng/ml) and severe head injury (1.2+/-1.9 ng/ml). Such a gradation was not observed with serum CRP There was a non-significant trend towards baseline PCT being a better marker of hospital mortality compared with baseline CRP (ROC-AUC 0.56 vs 0.31 respectively). This is the first prospective study to document the high incidence of SIRS in neurosurgical patients. In our study, serum PCT appeared to correlate with severity of traumatic brain injury and mortality. However, it could not reliably distinguish between SIRS and sepsis in this cohort. This is in part because baseline PCT elevation seemed to correlate with severity of injury. Only a small proportion of patients developed sepsis, thus necessitating a larger sample size to demonstrate the diagnostic usefulness of serum PCT as a marker of sepsis. Further clinical trials with larger sample sizes are required to confirm any potential role of PCT as a sepsis and outcome indicator in patients with head injuries or subarachnoid haemorrhage.
    Anaesthesia and intensive care 09/2004; 32(4):465-70. · 1.30 Impact Factor
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    B Venkatesh · T J Morgan · R J Boots · J Hall · D Siebert ·
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    ABSTRACT: Elevated cerebrospinal fluid (CSF) lactate concentrations in neurotrauma and sub-arachnoid haemorrhage are associated with a poor prognosis. However, in blood-stained CSF, elevated lactate levels may arise from red cell metabolism, even without ischaemia, potentially reducing specificity. This study was undertaken to quantify the erythrocyte contribution to CSF lactate measurements, with and without, exposure to room air. Blood was added to CSF to achieve three different red cell concentrations. The CSF was then exposed at 37 degrees C to either room air or 5% CO2 and 95% oxygen. Vancomycin and gentamycin were added to inhibit bacterial growth. Lactate concentrations and red cell concentrations were measured prior to the addition of blood and 10 minutes, 6 hours and 24 hours later. CSF without the addition of blood was used as a control. In the control specimens there were no increases in CSF lactate concentrations over time, either in air or CO2, whereas all specimens with blood added demonstrated significant increases in lactate at 6 and 24 hours (P < 0.01). The lactate increases in both air and CO2 were correlated directly with red cell counts (R2 = 0.62 to 0.87). At all red cell concentrations, the mean lactate increase was greater in air. Red cells in CSF cause significant increases in lactate concentrations, more so when exposed to air. This should be considered when interpreting lactate in blood stained CSF. Blood-stained CSF specimens for lactate assay should be collected directly from an external ventricular drain rather than a reservoir bag.
    Critical care and resuscitation: journal of the Australasian Academy of Critical Care Medicine 10/2003; 5(3):177-81. · 2.01 Impact Factor
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    ABSTRACT: To detail the biology and diagnostic usefulness of serum procalcitonin in critical illness. A review of articles published in peer reviewed journals from 1990 to 2001 and identified through a MEDLINE search on procalcitonin. Procalcitonin (PCT) is a prohormone of calcitonin. Serum levels are elevated during sepsis and have been identified as a potential marker of infection in critical illness. However, its function and precise source of origin during sepsis remain unclear. The value of estimating serum PCT appears to be in the differentiation of infectious from non-infectious forms of systemic inflammatory response syndrome. A number of studies also point to its usefulness in distinguishing between bacterial and viral meningitis. However, there are a number of non-infectious conditions, where elevations in serum PCT occur, reducing its specificity. Its superiority as a marker of sepsis compared with other acute phase reactants continues to be debated. The utility of serum procalcitonin as a diagnostic test of sepsis is still under evaluation. Moreover, a number of unanswered questions remain regarding the biological role of PCT during sepsis, its target receptors and its protective value to the patient.
    Critical care and resuscitation: journal of the Australasian Academy of Critical Care Medicine 01/2002; 3(4):236-43. · 2.01 Impact Factor