The Australian litigation landscape - oral and maxillofacial surgery and general dentistry (oral surgery procedures): an analysis of litigation cases.

BACKGROUND: There are persistent concerns about litigation in the dental and medical professions. These concerns arise in a setting where general dentists are more frequently undertaking a wider range of oral surgery procedures, potentially increasing legal risk. METHODS: Judicial cases dealing with medical negligence in the fields of general dentistry (oral surgery procedure) and oral and maxillofacial surgery were located using the three main legal databases. Relevant cases were analysed to determine the procedures involved, the patients' claims of injury, findings of negligence and damages awarded. A thematic analysis of the cases was undertaken to determine trends. RESULTS: Fifteen cases over a 20-year period were located across almost all Australian jurisdictions (eight cases involved general dentists; seven cases involved oral and maxillofacial surgeons). Eleven of the 15 cases involved determinations of whether or not the practitioner had failed in their duty of care; negligence was found in six cases. Eleven of the 15 cases related to molar extractions (eight specifically to third molar). CONCLUSIONS: Dental and medical practitioners wanting to manage legal risk should have regard to circumstances arising in judicial cases. Adequate warning of risks is critical, as is offering referral in appropriate cases. Preoperative radiographs, good medical records and processes to ensure appropriate follow-up are also important.

A novel bedside communication tool.

Effective communication between patients, their families, their carers and health care professionals is paramount to the delivery of high quality care. Addressing the ideas, concerns and expectations of these groups may improve their healthcare experience. We propose that opening a new channel of communication between patients, families, carers and healthcare professionals on the wards would improve the delivery of healthcare. We present a novel written communication aid- the Care Communication Aid (CCA), with preliminary data from secondary and tertiary healthcare trials demonstrating its efficacy and shortcomings, and the reaction of both recipients and providers of healthcare to this novel approach.

Palliative care, double effect and the law in Australia.

Care and decision-making at the end of life that promotes comfort and dignity is widely endorsed by public policy and the law. In ethical analysis of palliative care interventions that are argued potentially to hasten death, these may be deemed to be ethically permissible by the application of the doctrine of double effect, if the doctor's intention is to relieve pain and not cause death. In part because of the significance of ethics in the development of law in the medical sphere, this doctrine is also likely to be recognized as part of Australia's common law, although hitherto there have been no cases concerning palliative care brought before a court in Australia to test this. Three Australian States have, nonetheless, created legislative defences that are different from the common law with the intent of clarifying the law, promoting palliative care, and distinguishing it from euthanasia. However, these defences have the potential to provide less protection for doctors administering palliative care. In addition to requiring a doctor to have an appropriate intent, the defences insist on adherence to particular medical practice standards and perhaps require patient consent. Doctors providing end-of-life care in these States need to be aware of these legislative changes. Acting in accordance with the common law doctrine of double effect may not provide legal protection. Similar changes are likely to occur in other States and Territories as there is a trend towards enacting legislative defences that deal with the provision of palliative care.

Behavioral and physiological responsivity, sleep, and patterns of daily cortisol production in infants with and without colic.

To describe the behavioral and physiological responses associated with colic, the responses of 20 two-month-old infants with and 20 without colic were studied during a physical examination. Parents kept a diary of infant behaviors (including crying and fussing) for 3 days following the visit. Using Wessel, Cobb, Jackson, Harris, & Detwiler criteria, colic was defined as fussing/crying for 3 hr or more on each of the 3 days. Behavioral data coded by "blind" observers showed that during the physical exam, colic infants cried twice as much, cried more intensely, and were more inconsolable than were control infants. Despite these behavioral differences, heart rate, vagal tone, and cortisol measures indicated no appreciable difference in physiological responsivity for the two groups. At home, parents collected saliva cortisol samples at wakeup, midmorning, midafternoon, and evening for 2 days. In a finding similar to that shown by the laboratory data, the colic and control infants did not have different levels of daily average cortisol. These laboratory and home data provide no evidence of greater responsivity in the physiological substrate of difficult temperament for colic infants and are consistent with evidence of similarity in temperament once colic is resolved. At home, compared with control infants, colic infants did display a blunted rhythm in cortisol production. By diary, they also slept about 2 hr less per day than did control infants. Nighttime sleep was still significantly different when fussing/crying was statistically controlled. These data suggest that colic might be associated with a disruption or delay in the establishment of the circadian rhythm in activity of the hypothalamic-pituitary-adrenocortical axis and associated sleep-wake activity.

The predictive power of narrative data in occupational therapy evaluation.

OBJECTIVE: This study examined whether adding the Canadian Occupational Performance Measure (COPM) to existing occupational therapy evaluation measures used in a subacute skilled nursing facility unit enhanced the accuracy of therapists' predictions of the functional status of clients at discharge. METHOD: This study utilized a prospective comparison design. Two independent predictive variables were developed using the standard Functional Independent Measure (FIM), and an enhanced FIM that included narrative information from the Canadian Occupational Performance Measure (FIM/COPM). These variables were subsequently compared with the actual FIM discharge (DFIM) scores for 31 clients. The primary author (D.S.) gathered data from chart review and conducted the statistical analysis. The data were analyzed using descriptive correlations (Pearson r) and comparison statistics (Wilcoxon signed rank test). RESULTS: Comparison statistics (Wilcoxon signed rank test) revealed a statistically significant difference between the standard FIM predictive score and the discharge FIM score. No statistically significant difference was found between the FIM/COPM predictive score and the discharge FIM score. These findings suggest that predictive scores based solely on information attained from the standard FIM resulted in less accuracy in outcome predictions. Correlational analyses further supported these conclusions. CONCLUSION: The findings support the study hypothesis that use of the COPM in combination with the FIM enhances accuracy in prediction of outcomes for rehabilitative services for persons in adult physical disabilities settings.

Delivery and expression of fluid shear stress-inducible promoters to the vessel wall: applications for cardiovascular gene therapy.

In atherosclerosis, endothelial cells at sites of stenosis experience elevated levels of shear stress. We have constructed a series of shear stress-inducible transcription units (SITUs) expressing the luciferase reporter gene and determined their activation by fluid shear stress in transfected endothelial cells. Chimeric promoters were constructed that comprised basal transcription factor-binding sites coupled to a shear stress response element (SSRE). We have used consensus binding sites for transcription factors NF-kappaB, Ap1, Sp1, Oct1, and Egr-1/Sp1 in either the presence or absence of the previously defined "GAGACC" SSRE. The response of the promoters to shear stress was determined after transfection into human umbilical vein endothelial cells (HUVECs). After transient transfection into HUVECs, fluid shear stress activated the promoters by between two- and eightfold. The most responsive SITUs comprised an overlapping Sp1/Egr-1-binding site linked to a TATA box with (SP5) or without (SP7) the GAGACC SSRE. Instillation of SP5 DNA in vivo into the left carotid artery of rabbit and subsequent generation of a stenosis using a mechanical wire occluder caused a 10-fold upregulation of luciferase reporter gene expression at the site of vessel occlusion. These vectors show promise for therapeutic gene expression at sites of occlusive vascular disease.

Dampening of the cortisol response to handling at 3 months in human infants and its relation to sleep, circadian cortisol activity, and behavioral distress.

The decrease in responsiveness of the hypothalamic-pituitary-adrenocortical (HPA) system is marked over the first months of life. Seventy-eight healthy infants (44 girls), 7 to 15 weeks old, were given a laboratory mock physical examination. Salivary cortisol samples were collected pre- and postexamination and at home. Behavioral state during the examination and home sleep/wake activity were measured. Subjects younger than 11 weeks showed an increase in pre- to postexamination cortisol, while older subjects did not. Further, there was no decrease in behavioral distress to the examination with age. Infants who showed an early- morning peak (EMP) in home cortisol levels were significantly older and were likely to be those who slept through the night. However, the presence of an EMP was not associated with a lack of cortisol response to the examination. The decrease in cortisol responsiveness witnessed around the age of 3 months is presumably due to other processes associated with age, and not with the expression of the day-night rhythm in basal cortisol.

Prevention of intra-coronary thrombosis in the anaesthetised dog: the importance of thromboxane A2 and thrombin.

Vapiprost (GR32191, a TxA2 antagonist), r-hirudin, aspirin, ticlopidine and aspirin plus ticlopidine were examined for their ability to prevent electrically-induced thrombosis in an artificially stenosed coronary artery in the anaesthetised dog. Drugs or vehicle were administered prior to a 2 h period of electrical damage which was followed by a further 2 h observation period. In all vehicle-treated animals, blood flow markedly declined with onset of the damaging current; 80% completely occluded. All treatments reduced the incidence of complete occlusion to a similar extent. Vapiprost and r-hirudin also largely prevented the decline in blood flow both during and following the damage period whilst aspirin and ticlopidine, either alone or in combination were much less effective. With r-hirudin treatment, marked cyclic changes in flow occurred throughout the experiment; these were abolished by administration of vapiprost. In this dog model, TxA2 and thrombin appear to work in concert to produce coronary thrombosis, ADP being of minor importance. The superior effect of vapiprost over aspirin suggests a beneficial role for endogenous prostacyclin.

Overwhelming postsplenectomy sepsis twenty-two years after operation risks management and prevention.

A new case of fatal postsplenectomy sepsis occurring 22 years after operation for splenic rupture is described. There are now 30 published cases in which this complication occurred 10 or more years after operation. The microorganism responsible for the vast majority of cases is Streptococcus pneumoniae. The causative pathogen identified in the present case was a Viridans Streptococcas, Strep. sanguis, an opportunistic, low virulence pathogen. The clinical presentation of this patient is characteristic of the syndrome of overwhelming postsplenectomy infection and exemplifies the dramatic suddenness with which it develops.

Coexistence of hereditary spherocytosis and beta-thalassemia: case report of severe hemolytic anemia in an American black.

The first reported case of hereditary spherocytosis (HS) and beta-thalassemia in an American black is presented. The diagnosis rested on clinical presentation, family history and specialized laboratory findings. The tendency toward hemolysis of spherocytes and thalassemia red cells may explain the severity of anemia in this patient. The clinical course of these coexistent diseases and the role of splenectomy in relieving the hemolytic component caused by hereditary spherocytosis are described. A detailed review of the literature on HS and beta-thalassemia is also included.

Thromboxane (Tx) A2 receptor blockade and TxA2 synthase inhibition alone and in combination: comparison of anti-aggregatory efficacy in human platelets.

1. The present study has compared the relative anti-aggregatory effect of various compounds which interfere with thromboxane (Tx) A2-dependent aggregation of human platelets in whole blood in vitro. These included the cyclo-oxygenase inhibitor aspirin, the TxA2 synthase inhibitor dazoxiben, the TxA2 (TP-) receptor blocking drug GR32191 and two compounds, R.68070 ((E)-5-[[[(3-pyridinyl) [3-(trifluoromethyl)phenyl]-methylen] amino]oxy] pentanoic acid) and CV-4151 [E)-7-phenyl-7-(3-pyridyl)-6-heptenoic acid), which possess both TP-receptor blocking and TxA2 synthase inhibitory activities in the same molecule. 2. GR32191, R.68070 and CV-4151 all antagonized aggregation to the TxA2 mimetic U-46619, with pA2 values of approximately 8.2, 5.4 and 4.8 respectively. This effect was specific, platelet aggregation induced by adenosine 5'-diphosphate (ADP) being unaffected by concentrations up to 10, 1000 and 300 microM respectively. In contrast, neither aspirin nor dazoxiben exhibited any measurable TP-receptor blocking activity. 3. The rank order of potency (pIC50) for inhibition of TxA2 formation in serum was R.68070 (7.4) greater than CV-4151 (6.9) greater than dazoxiben (5.7) greater than aspirin (5.3). In addition, all four drugs abolished collagen-induced platelet TxA2 formation. In contrast, GR32191 produced no consistent inhibition of TxA2 formation in either system up to concentrations of 10-30 microM. 4. The specificity of R.68070, CV-4151 and dazoxiben for TxA2 synthase was indicated by their ability to increase serum levels of prostaglandin E2 (PGE2) and PGD2 in parallel with decreases in TxA2 formation. This profile was not observed with aspirin or GR32191. However, high concentrations of R.68070 (100,microM) and CV-4151 (1000 microM) necessary for maximum TP-receptor blocking activity, produced substantially smaller increases in PGE2 and PGD2, consistent with an aspirin-like effect of these compounds upon cyclo-oxygenase. With dazoxiben (1000 microM), PGE2 and PGD2 levels remained elevated. 5. Aspirin inhibited collagen-induced platelet aggregation, the effect correlating with inhibition of TxA2 formation. Dazoxiben, whilst also achieving maximal inhibition of TxA2 formation, produced significantly less inhibition of aggregation than aspirin. In contrast, GR32191 (0.1-1O microM), at concentrations specific for TP-receptor blockade, produced a significantly greater antagonism of collagen-induced platelet aggregation than aspirin. This additional effect of GR32191 was absent in platelets pretreated with aspirin, indicating the probable involvement of an endogenous anti-aggregatory cyclo-oxygenase product in response to collagen stimulation. 6. R.68070 and CV-4151 also inhibited collagen-induced aggregation, with very high concentrations of R.68070 (100 microM) producing an effect equivalent to that of GR32191. 7. In contrast, the combination of GR32191 with either dazoxiben, R.68070 or CV-4151, at concentrations specific for TxA2 synthase, produced a synergistic inhibitory effect upon collagen-induced platelet aggregation which was greater than that achieved with either aspirin or any of the compounds used alone. Pretreatment of platelets with aspirin reversed this synergistic effect, consistent with it being dependent upon the formation and action of anti-aggregatory prostaglandins. 8. In conclusion, the present study has confirmed the superior platelet inhibitory profile of a combination of a TP-receptor blocking drug and a TxA2 synthase inhibitor to that of either activity alone. However, the maximum inhibitory effect of the currently available compounds, R.68070 and CV4151, which possess both activities in the same molecule, appears to be no greater in vitro than that obtained with the potent TP-receptor blocking drug, GR32191. This most probably reflects the inhibition by R.68070 and CV-4151 of platelet cyclo-oxygenase at the concentrations required for effective TP-receptor blockade which results in a reduction in the formation of anti-aggregatory prostanoids.

GR32191, a highly potent and specific thromboxane A2 receptor blocking drug on platelets and vascular and airways smooth muscle in vitro.

1. The thromboxane A2 (TP)-receptor blocking activity and specificity of action of GR32191 ([1R-[1 alpha(Z),2 beta,3 beta,5 alpha]]-(+)-7-[5-([1,1'-biphenyl] -4-ylmethoxy)-3-hydroxy-2-(1-piperidinyl)cyclopentyl]-4-heptoni c acid has been evaluated in human platelets and various smooth muscle preparations, both vascular and non-vascular, from a range of species including man. 2. Utilising a platelet counting method to assess aggregation the drug was found to antagonise, in a surmountable manner, human platelet aggregation produced by the TP-receptor agonists, U-46619, EP171 and SQ26655, in whole blood and physiological buffer, with pA2 values of approximately 8.3 and 8.7 in the two media respectively. In the presence of GR32191 the rate of aggregation induced by U-46619 was slowed. 3. The effect of GR32191 upon U-46619-induced platelet shape change and aggregation in platelet-rich plasma was evaluated utilising a turbidometric technique. Both shape change and aggregation were antagonised by GR32191. At relatively high concentrations of the drug a slowing of aggregation and shape change to U-44619 was seen and an unsurmountable antagonism became apparent. 4. The action of GR32191 upon human platelets was specific with platelet aggregation induced by adenosine 5'-diphosphate, platelet activating factor, vasopressin and adrenaline and the inhibitory effects of prostacylin (PGI2), prostaglandin D2 (PGD2) and N-ethylcarboxamide-adenosine (NECA) being unaffected by concentrations of the drug as high as 10 microM. Furthermore, at concentrations of up to 100 microM, the drug itself produced no shape change or aggregation, of human platelets. 5. GR32191 also specifically and potently antagonised in a competitive, surmountable manner the contractile actions of U-46619 upon human vascular smooth muscle and antagonised U-46619-induced contractions of vascular and airways smooth muscle preparations from rat, dog, guinea-pig and rabbit with varying potency. This is discussed in terms of possible heterogeneity of TP-receptors. 6. GR32191 therefore represents a highly potent and specific TP-receptor blocking drug. This profile of action, coupled to its long duration of effect in man described elsewhere, make it an ideal drug tool for elucidating the physiological and pathophysiological role of thromboxane A2.

Circadian variations in hepatic glutathione content, gamma-glutamylcysteine synthetase and gamma-glutamyl transferase activities in mice.

Experiments were conducted to determine if the circadian variations previously observed in hepatic reduced glutathione (GSH) concentrations also occurred in the associated enzymatic activities involved in the synthesis (gamma-glutamylcysteine synthetase) and degradation (gamma-glutamyl transferase) of glutathione using male CF-1 mice. All parameters were measured at four hour intervals over a 24-h period under normal (L: 0600-1800 h) and reversed (L: 1800-0600 h) lighting schedules. Circadian rhythms were found in each parameter under both lighting schedules. With GSH content, the rhythms' peak occurred at 0200 h and the nadir at 1400 h under the normal lighting schedule and was reversed (peak: 1800 h; nadir; 0600 h) under reversed lighting. The enzymatic activities also varied in a circadian manner with a phase shift in the peak and nadir occurring with a change in lighting schedule. Liver weight varied in a circadian manner under both lighting schedules with greatest weights occurring at the end of the dark phase. These data show that not only does GSH content vary in a circadian manner but that associated enzyme activities do as well. However, the hepatic enzyme activities did not correlate well with the GSH rhythm and, thus, do not provide a mechanistic rationale for the GSH rhythm.

Resistance and susceptibility to the induction of rat adjuvant disease. Diverging susceptibility and severity achieved by selective breeding.

Rats selected for their ability to develop or resist adjuvant disease were used to establish 2 inbred lines of rat over 20 generations. A resistant line was rapidly established with almost 100% non-responsiveness by the sixth generation. A line showing 100% susceptibility was also established very rapidly but throughout the course of the breeding programme the severity continued to increase in intensity to a level considerably above that to be seen in strains normally considered to be high responders. At the thirteenth generation and beyond, the susceptible line showed a marked sex difference in the secondary lesions, females being more severely affected than the males. The 2 lines of rat were also tested for their ability to develop experimental allergic encephalomyelitis (EAE) in selected generations. There was no clear correlation between the 2 diseases although those animals developing the most severe adjuvant disease also had the most severe EAE.

Differential suppression of experimental allergic diseases in rats infected with trypanosomes.

PVG/c rats, infected 3 days previously with 10(3) Trypanosoma brucei brucei S.42 organisms failed to develop adjuvant disease in response to an intradermal inoculation of mycobacterial adjuvant. By contrast, similarly infected rats, immunized with heterologous brain and spinal cord in Freund's complete adjuvant with pertussis vaccine as a secondary adjuvant, developed clinical signs of allergic encephalomyelitis (EAE) at least as severe as those in uninfected rats. Delayed hypersensitivity reactions to PPD were depressed in trypanosome-infected, adjuvant-injected rats, as were the reactions to myelin basic protein in infected rats developing EAE. There appeared to be no cross-reactivity between trypanosomal antigen and myelin basic protein which could account for the lack of suppression of EAE. It is suggested that the different extent to which autoimmunity is involved in these two experimental allergic diseases may account for the differential suppressive activity of trypanosome infections upon them.

Suppression of rat adjuvant disease by cyclophosphamide pretreatment: evidence for an antibody mediated component in the pathogenesis of the disease.

Cyclophosphamide (Cy), given intraperitoneally at a dose of 100 mg per kg body weight 3 days before adjuvant, was found to abolish the development of adjuvant disease in the PVG/c rat. This treatment, however, enhanced the delayed hypersensitivity responses to purified protein derivative of tuberculin (PPD) developed by these animals. Lower doses of Cy caused a partial inhibition of arthritis which was dose-related. When the time between giving Cy and the injection of adjuvant was increased, a gradual time-dependent recovery of the response was observed. The arthritic response was restored by the passive transfer of 7.6 x 10(7) to 1.5 x 10(8) normal syngeneic spleen cells, although the development of secondary lesions was delayed by 7-14 days. The response could also be restored by the transfer of small amounts of serum from arthritic, but not normal, rats. Large amounts of serum failed to restore the response. Additional evidence that pretreatment with Cy preferentially depleted the B lymphocytes was obtained by the histological examination of the lymphoid tissue. It was also shown that the primary antibody response to sheep erythrocytes was abolished by Cy, but that skin allograft rejection was unaffected. A partial inhibition of the acute inflammatory reaction to carrageenan was observed 3 days after giving Cy. It is suggested that the pathogenesis of adjuvant arthritis involves an immune complex-mediated phase, whihc initiates the joint lesions. Once these lesions have formed, cell-mediated immune mechanisms predominate in the development of the disease. It is not known whether the persistence of immune complexes is necessary to maintain the lesions.