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Biomedical subjects

J Tibballs

Publications and source records attributed to J Tibballs.

At least 55 records · Page 3Linked to original sources
PubMed1998

Ultrasound screening for hepatocellular carcinoma (HCC) in cirrhosis: the evidence for an established clinical practice.

Improvement in our current knowledge of epidemiology, natural history and treatment modalities form the background to generalize the use of ultrasound screening in cirrhosis. The cumulative probability of developing cancer is extremely high in cirrhotics and allows to focus screening programs on a well defined risk group thus maximizing cost-effectiveness. This review article highlights scientific evidences in favour of a generalized practice of US screening.

Carcinoma, Hepatocellular↗
PubMed1998

Accuracy of two pulse oximeters at low arterial hemoglobin-oxygen saturation.

OBJECTIVE: To evaluate the performance of two pulse oximeters in the measurement of arterial hemoglobin saturation in hypoxemic children. DESIGN: Prospective, repeated-measures observational study. SETTING: A 16-bed pediatric intensive care unit in a children's tertiary hospital. PATIENTS: Sixty-six patients with arterial saturation of <90%. INTERVENTIONS: Three arterial blood samples were taken from each subject during a 48-hr period. Pulse oximeter measurements of arterial saturation were compared with arterial saturation determined by cooximetry. MEASUREMENTS AND MAIN RESULTS: Arterial saturation was measured using one or both pulse oximeters (SpO2) and compared with the arterial hemoglobin saturation determined by cooximetry (SaO2). Sixty-two subjects were studied, using the Ohmeda pulse oximeter giving 185 data points (78 with saturations <75% [defined by the average of pulse oximeter and cooximeter]); 53 subjects were studied, using the Hewlett-Packard pulse oximeter yielding 155 data points (60 with saturations <75%). SpO2 ranged from 24% to 94%. Bias and precision of the Ohmeda pulse oximeter were -2.8% and 4.8% >75% and -0.8% and 8.0% <75%. Bias and precision of the Hewlett-Packard pulse oximeter were -0.5% and 5.1% >75% and 0.4% and 4.6% <75%. Intrapatient regression coefficient (r) for the differences between pulse oximeter and cooximeter was 0.58 for the Ohmeda and 0.59 for the Hewlett-Packard. Regression coefficients for predicting change in cooximeter value given a change in the Ohmeda pulse oximeter were 0.59 and 0.71 <75% and >75%, respectively. Similar coefficients for the Hewlett-Packard pulse oximeter were 0.50 and 0.70, respectively. CONCLUSION: The performance of the Ohmeda pulse oximeter deteriorated below an SpO2 of 75%. The Hewlett-Packard pulse oximeter performed consistently above and below an SpO2 of 75%. The ability of both pulse oximeters to reliably predict change in SaO2 based on change in pulse oximetry was limited. We recommend measurement of PaO2 or SaO2 for important clinical decisions.

Child↗
PubMed1998

The effects of antivenom and verapamil on the haemodynamic actions of Chironex fleckeri (box jellyfish) venom.

The efficacy of antivenom and verapamil against Chironex fleckeri (box jellyfish) venom was investigated in monitored mechanically ventilated piglets. Chironex fleckeri tentacle extract alone, a mixture of tentacle extract with antivenom, and verapamil before tentacle extract were administered intravenously to groups of animals. Tentacle extract caused severe systemic hypotension, cardiac dysrrhythmias, pulmonary hypertension, haemolysis and hyperkalaemia. These effects were prevented by pre-incubation of tentacle extract with antivenom. Verapamil did not prevent any effect of venom, exacerbated cardiovascular collapse and increased mortality. We conclude that antivenom neutralizes the cardiovascular, haemolytic and hyperkalaemic effects of box jellyfish venom. Verapamil does not prevent any of these effects and is contra-indicated for treatment of envenomation.

Animals↗
PubMed1998

An evaluation of a new analyser for inhaled nitric oxide administration.

We examined the ability of a new combined nitric oxide (NO)/nitrogen dioxide (NO2) electrochemical analyser (PrinterNOx, Micro Medical Limited, Chatham, Kent, England) to measure NO and NO2 concentrations. The PrinterNOx was compared to a chemiluminescence analyser (42H, Thermo Environmental Instruments Inc, Franklin MA, U.S.A.). NO and NO2 were generated in a standard ventilator circuit using a paediatric ventilator (900C, Siemens Elema, Sweden) connected to an artificial lung (260li, TTL Test Lung, Michigan Instruments, MI, U.S.A.). Forty-four paired NO measurements ranging from 2.56 ppm to 74.6 ppm and 50 paired NO2 measurements ranging from 0.0 ppm to 5.39 ppm were obtained. For the measurement of NO the PrinterNOx showed a tendency to overestimate the chemiluminescence analyser. Regression analysis showed a close relationship between the two analysers with r2 = 0.9981 and a regression equation of y = 1.1658 x +0.0197. In the more clinically important range of 0-25 ppm, r2 increased to 0.9996 with a regression equation of y = 1.1984 x -0.4657. Conversely the PrinterNOx underestimated the chemiluminescence analyser for the measurement of NO2. The regression equation describing this relationship was y = 0.879 x -0.0447 (r2 = 0.9993). We conclude that the PrinterNOx is of sufficient accuracy to be of clinical use in the administration of NO.

Anesthesiology↗
PubMed1998

The cardiovascular, coagulation and haematological effects of tiger snake (Notechis scutatus) venom.

The cardiovascular, coagulation and haematological effects of Tiger Snake (Notechis scutatus) venom were investigated in anaesthetized, mechanically ventilated dogs. Intravenous infusion of venom caused dose-related systemic hypotension, low cardiac output, pulmonary hypertension and raised pulmonary artery occlusion pressure. These effects occurred within several minutes of venom administration but recovered over 30 to 40 minutes. They were accompanied by prolongation of prothrombin and activated partial thromboplastin times and by depletion of serum fibrinogen. Fibrin degradation products were not detected. Thrombocytopenia and leucopenia were observed within minutes of venom administration but recovered over 30 to 40 minutes. The mechanism of systemic hypotension is probably pulmonary vascular obstruction and coronary ischaemia caused by disseminated intravascular coagulation, although the existence of a myocardial depressant in venom or release of vasoactive substances by venom cannot be excluded.

Animals↗
PubMed1998

The cardiovascular, coagulation and haematological effects of tiger snake (Notechis scutatus) prothrombin activator and investigation of release of vasoactive substances.

The cardiovascular, coagulation and haematological effects of prothrombin activator from Tiger Snake (Notechis scutatus) venom were investigated in anaesthetized mechanically ventilated dogs. Infusion caused dose-related systemic hypotension, marked decreases in cardiac output and stroke volume, marked increases in pulmonary artery pressure, pulmonary artery occlusion pressure and pulmonary vascular resistance. Effects occurred within several minutes but abated over 30 to 40 minutes. Evidence of procoagulation included prolongation of prothrombin and partial thromboplastin times and depletion of serum fibrinogen. Thrombocytopenia and leucopenia occurred. All effects were prevented by prior administration of heparin but none by inhaled nitric oxide. Oesophageal echocardiography during infusion identified thrombi within the heart, right ventricular dilatation and dyskinesia. Electrocardiography suggested myocardial ischaemia. Pulmonary thromboemboli were identified histologically post mortem. Cardiovascular effects of the activator were not due to a variety of endogenous substances as indicated by use of antagonists to platelet activating factor and thromboxane A2 indomethacin, dexamethasone, serotonin, ketanserin, histamine, promethazine and ondansetron. Tiger Snake prothrombin activator causes bilateral ventricular failure by thrombotic obstruction of the pulmonary vasculature and possibly by coronary ischaemia.

Animals↗
PubMed1997

Generation of nitrogen dioxide during nitric oxide therapy and mechanical ventilation of children with a Servo 900C ventilator.

OBJECTIVE: To determine the combinations of nitric oxide (NO), oxygen (O2), minute ventilation (MV) and total gas flow (TGF) which generate toxic concentrations of nitrogen dioxide (NO2) during mechanical ventilation with a Servo 900C ventilator. DESIGN: The measurement of NO2 generated with NO (20, 40, 60, 80, 100 ppm) and O2 [fractional inspired oxygen (FIO2) 0.21, 0.4, 0.6, 0.9] during mechanical ventilation with MVs of 2.5, 5.0 and 7.5 l/min and TGFs from 2 to 14 l/min. SETTING: Laboratory of intensive care unit in paediatric tertiary hospital. RESULTS: Toxic concentrations of NO2 (> 5 ppm) were generated in the ventilator circuit when NO was 80 ppm or 100 ppm in FIO2 of 0.6 or 0.9 with MVs of 2.5, 5.0 and 7.5 l/ min; and with 80 ppm NO in FIO2 of 0.6 at all TGFs from 2.0 to 13.6 l/min and MVs of 2.5, 5.0 and 7.5 l/min (TGF/MV 0.3-5.4). NO2 1.5-2.6 ppm was generated with 40 ppm NO in FIO2 of 0.6, TGFs 2.1-13.7 l/ min, and MVs 2.5, 5.0 and 7.5 l/min (TGF/MV 0.3-5.5). NO2 0.9-0.6 ppm was generated with 20 ppm NO in FIO2 of 0.6, TGFs 2.5-13.8 and MVs 2.5, 5.0 and 7.5 (TGF/MV 0.3-5.5). NO2 generation was not affected significantly by the TGF/MV ratio. CONCLUSIONS: The generation of NO2 in the ventilator circuit is directly proportional to concentration of NO and O2 and inversely proportional to the TGF and MV but uninfluenced by the TGF/MV ratio. NO 80 ppm, but neither 20 nor 40 ppm in FIO2 of 0.6, generates toxic NO2 irrespective of TGF, MV or the TGF/MV ratio.

Child↗
PubMed1997

Eucalyptus oil poisoning among young children: mechanisms of access and the potential for prevention.

We studied unintentional paediatric eucalyptus oil poisoning to identify potential intervention strategies. The epidemiology of paediatric eucalyptus oil poisoning in Victoria was determined by analysis of four databases. The sequence of events preceding ingestion was examined by a telephone survey involving 109 parents or guardians of children under five years involved in an actual or suspected ingestion of eucalyptus oil. Such children were identified prospectively from all callers during a nine-month period to the Victorian Poisons Information Centre and those presenting to the emergency departments of the participating hospitals of the Victorian Injury Surveillance System. Eucalyptus oil was a leading agent associated with hospitalisation for poisoning among Victorian children aged under five years. In the telephone survey, 90 incidents were found to involve vaporiser solutions, 15 eucalyptus oil preparations, and the remainder other eucalyptus-oil-containing products of a medicinal nature. Regardless of the type of product, 74 per cent gained access via a home vaporiser unit, most frequently placed at ground level. Although amounts ingested are usually small, the reported range of toxic doses is wide, necessitating at least a medical assessment following ingestion. Potential countermeasures identified in a consultative workshop included: discontinuing the use of eucalyptus oil as a therapeutic agent; confirmation that vaporiser-well residues are nontoxic; removal of barriers to product reregistration following safety-related modifications; improved child-resistant closures; discouraging vaporiser use for respiratory infections among young children; and development and dissemination of protocols for treatment of suspected ingestion.

Child, Preschool↗
PubMed1997

Monitoring nitric oxide: a comparison of three monitors in a paediatric ventilator circuit.

Simultaneous measurements of nitric oxide (NO) (0-80 ppm) using a chemiluminescence monitor and two electrochemical monitors were performed during simulated paediatric mechanical ventilation. The mean difference (bias) between the chemiluminescence (Model 42H Thermo Environmental Instruments Inc) and an electrochemical monitor (Pulmonox Research and Development Corp) was 0.52 +/- 6.52 ppm (SD). The 95% confidence limits of the mean difference were 3.00 to -1.96 ppm and the limits of agreement between the two techniques were 13.56 to -12.52 ppm. The mean difference between the chemiluminescence monitor and another electrochemical monitor (NOxBox, Bedfont Scientific Inc) was -7.27 +/- 4.29 ppm. The 95% confidence limits of the mean difference were -9.02 to -5.56 ppm and limits of agreement of the two techniques were -16.13 to 1.55 ppm. These results suggest that electrochemical monitors may be used to guard against potentially toxic concentrations of NO (greater than 20 ppm). However they do not suggest that either of the electrochemical monitors may be used with confidence in lieu of the chemiluminescence monitor to regulate NO at low clinical NO levels (1-5 ppm).

Child↗
PubMed1996

Teaching hospital medical staff to handwash.

OBJECTIVE: To increase the frequency of handwashing by medical staff. DESIGN: a prospective study of handwashing before and after patient contact. SETTING: A paediatric intensive care unit in a tertiary hospital. PARTICIPANTS: 61 intensive care unit medical staff and visiting medical staff. INTERVENTIONS: A five-phase behaviour modification program:(i) unobtrusive observation for four weeks to obtain a baseline handwashing rate (ii) overt observation for five weeks (preceded by written advice); (iii) overt observation continued for four weeks with performance feedback; (iv) all observation and feedback discontinued for seven weeks; and (v) unobtrusive observation for five weeks to obtain a residual rate. RESULTS: 939 patient contacts were observed. The baseline handwashing rates before and after patient contact were 12.4% and 10.6%, respectively. During overt observation, the respective rates increased and plateaued at 32.7% and 33.3%, but increased further (to 68.3% and 64.8%) during the period of performance feedback. The residual handwashing rates, observed unobtrusively seven weeks after the cessation of performance feedback, were 54.6% before and 54.9% after patient contact.

Attitude of Health Personnel↗
PubMed1995

Clinical effects and management of eucalyptus oil ingestion in infants and young children.

OBJECTIVE: To determine the symptoms and signs of eucalyptus oil poisoning in infants and young children, to estimate the toxic dose and to recommend management strategies. DESIGN AND SETTING: Retrospective analysis of case histories of children admitted to the Royal Children's Hospital, Melbourne, between 1 January 1981 and 31 December 1992 with a diagnosis of eucalyptus oil poisoning. MAIN OUTCOME MEASURES: Demographic data, circumstances of ingestion, doses, clinical effects, management, complications and duration of hospital stay. RESULTS: 109 children (mean age, 23.5 months; range, 0.5-107) were admitted; clinical effects were observed in 59%. Thirty-one (28%) had depression of conscious state; 27 were drowsy, three were unconscious after ingesting known or estimated volumes of between 5 mL and 10 mL, and one was unconscious with hypoventilation after ingesting an estimated 75 mL. Vomiting occurred in 37%, ataxia in 15% and pulmonary disease in 11%. No treatment was given for 12%. Ipecac or oral activated charcoal was given for 21%, nasogastric charcoal for 57%, and gastric lavage without anaesthesia for 4% and under anaesthesia for 6%. All patients recovered. Hazardous treatment and overtreatment were common. For 105 children, mean hospital stay was 22 hours (range, 4-72 h) and for 13 patients mean intensive care unit stay was 18 hours (range, 4-29 h). In 27 patients who ingested known doses of eucalyptus oil, 10 had nil effects after a mean of 1.7 mL, 11 had minor poisoning after a mean of 2.0 mL, five had moderate poisoning after a mean of 2.5 mL and one had major poisoning after 7.5 mL (P = 0.0198). CONCLUSIONS: Ingestion of eucalyptus oil caused significant morbidity in infants and young children. Significant depression of conscious state should be anticipated after ingestion of 5 mL or more of 100% oil. Minor depression of consciousness may occur after 2-3 mL. Airway protection should precede gastric lavage.

Adult↗
PubMed1994

A comparison of syringes to collect blood for analysis of gases, electrolytes and glucose.

We studied the interchangeability of two blood gas syringes (Johns, Hardie Health Care Products Pty Ltd and Marksman, Martell Medical Products Inc) for the collection of blood for the analysis of PCO2, PO2, pH, sodium, potassium and glucose in 71 intensive care unit patients. The interchangeability of these two syringes with a specially designed syringe (Radiometer, Radiometer A/S) for the collection of blood for the analysis of ionized calcium was also studied. Analysis of pH, sodium, potassium and glucose showed no clinically significant differences between samples collected with Johns and Marksman syringes. However, differences in PCO2 and PO2 in samples collected with these syringes may be clinically significant if the PO2 is less than 100 mmHg. There were no clinically significant differences in ionized calcium levels in blood samples collected with Johns, Marksman and Radiometer syringes. We conclude that Johns and Marksman syringes are interchangeable for the collection of blood for the analysis of PCO2, PO2, pH, sodium, potassium and glucose and they are also interchangeable with Radiometer syringes for the collection of blood for ionized calcium analysis.

Adolescent↗
PubMed1993

The role of nitric oxide (formerly endothelium-derived relaxing factor-EDRF) in vasodilatation and vasodilator therapy.

Nitric oxide is widely distributed in the body. It has an important role in the regulation of the circulation and as yet, ill-defined roles in nervous and immune systems. It is derived from L-arginine from a reaction catalysed by a constitutive intracellular enzyme, nitric oxide synthase. It is recognised as the endogenous nitrovasodilator whose action is mimicked by all exogenous nitrovasodilators. After production in the vascular endothelial cell, it diffuses to the smooth muscle cell where it activates the enzyme guanylate cyclase which leads to an increase in cyclic GMP and thence to muscle relaxation. The duration of its action is brief, a few seconds. Disorders of NO metabolism underlie many disease states including endotoxic shock in which prolonged production of nitric oxide may be induced by cytokines. Deficiencies in endogenous production may account for hypertension in various disease states including atherosclerosis and chronic renal failure. NO therapy been used experimentally to successfully treat idiopathic pulmonary hypertension and pulmonary hypertension associated with cardiac and respiratory diseases. However, the long-term benefits have yet to be studied. Administration of NO requires the use of a device to monitor the concentrations of both NO and of NO2. The latter is a noxious agent and a time-related product of the reaction between NO and O2 and is a possible contaminant of preparations of NO. Precautions must be taken to prevent contamination of the work-place atmosphere with NO and NO2. These include gas scavenging and the use of a leak-free system for spontaneous and mechanical ventilation. Using NO in its gaseous form, clinicians have at long last been provided with the means to treat pulmonary hypertension without adversely causing systemic hypotension. The therapy is most suited to short-term use in mechanically ventilated patients. Safe practical long-term NO therapy must await the development of agents which release NO from aerosol preparations.

Humans↗
PubMed1993

An appraisal of techniques for administration of gaseous nitric oxide.

Gaseous nitric oxide (NO) is a potent selective pulmonary vasodilator. When mixed with O2 for more than 10-15 minutes it forms toxic amounts of nitrogen dioxide (NO2). We describe two techniques to administer 20 parts per million (ppm) during mechanical ventilation. A technique using flows of NO and O2 at low pressure to drive a Siemens Servo 900C ventilator provided a constant inspired concentration of NO. Another technique in which NO was added to the inspiratory limb of a Siemens Servo 900C ventilator driven by high pressure oxygen provided a highly variable concentration (9-53 ppm) of inspired NO.

Anesthesia, Inhalation↗