The effete in the heat: heat-related hospital presentations during a ten day heat wave.

BACKGROUND: Severe heat-related illness can result in hospitalisation and possibly death. These illnesses are potentially preventable; in Australia high environmental temperatures are common. AIMS: To identify (i) possible risk factors for hospital attendance with heat-related illness during a heat wave, (ii) problems with diagnosis and therapy, (iii) issues in prevention, and (iv) areas for further study. METHODS: A retrospective descriptive survey from four major teaching hospitals in Adelaide, South Australia (SA), was conducted during a ten day period of exceptional heat in February 1993, in order to review all emergency department presentations (i.e. deaths, casualty treatment or hospital admissions) with a heat-related illness as determined by attending doctors' documentation. Demographic, clinical, management and outcome data were collected. RESULTS: Ninety-four patients were classified as having a heat-related illness of whom 78% had heat exhaustion. Eighty-five per cent were age 60 years or over; 20% came from institutional care; 48% lived alone; 30% had poor mobility. Peak presentation followed high daily temperatures for four consecutive days. Severity was related to pre-existing cognitive impairment, diuretic use and presenting temperature, heart rate, blood pressure, plasma sodium and plasma creatinine. Treatment tended to be non-standardised. Mortality was 12%. Seventeen per cent required a more dependent level of residential care upon discharge. CONCLUSION: Problems were identified in accuracy of diagnosis and appropriate intervention. Awareness of the risk factor profile is needed among health workers, to ensure early preventative strategies. Populations to target for future prevention include elderly people (including those in institutional care), patients with cognitive impairment and patients taking diuretics, multiple medication and/or with other severe co-existing illnesses. Treatment could be more standardised.

Effects of adrenalectomy on responses mediated by dopamine D-1 and D-2 receptors.

The effects of surgical adrenalectomy were investigated on behavioural responses produced by the selective D-1 agonist, SK&F 38393, alone, and in combination with the D-2 agonist, quinpirole (LY171555). Further, stereotyped responses to apomorphine and LY171555 were assessed following treatment with either the D-1 or the D-2 antagonists, SCH 23390 and raclopride, respectively. There was no difference between sham-adrenalectomized (sham) and adrenalectomized (ADX) groups in responses to SK&F 38393. Although concomitant stimulation of both receptor subtypes increased the incidence of stereotyped sniffing behaviour, there was no difference in the magnitude of this effect between the sham and ADX groups. Raclopride reduced LY171555-induced sniffing and hypothermia less in ADX rats than in sham controls, which was consistent with the hypothesis that adrenocortical hormones affect D-2 receptor responsiveness. SCH 23390 had a greater inhibitory effect on LY171555 responses, but a smaller effect on apomorphine responses in the ADX group compared with their sham controls. It is concluded that the amplified D-2-stimulated response observed in ADX rats may be more dependent on tonic D-1 receptor activation than the control D-2 response of shams.

Adrenocortical hormone status affects responses to dopamine receptor agonists.

The effects of altered adrenocortical hormone status were investigated on hypothermic and behavioural responses elicited following systemically administered apomorphine or LY171555. Hormonal status was modified by surgical adrenalectomy, followed by subsequent replacement therapy with corticosterone, and by chronic corticosterone treatment of intact rats, followed by its withdrawal. The incidence of stereotyped sniffing produced by both apomorphine and LY171555 was increased in the adrenalectomized group and decreased following replacement therapy and in intact rats treated with chronic corticosterone, compared with sham-operated animals and saline-treated controls, respectively. Withdrawal of chronic corticosterone treatment in intact rats reversed the effects of the chronic treatment on dopamine-mediated responses. Similar changes were observed in hypothermic responses to the two dopamine agonists. Striatal D-1 and D-2 dopamine receptor concentration and affinity were unaffected by adrenal hormone modification suggesting that corticosterone may act at a site distal to the dopamine receptor to bring about the observed changes in dopamine-mediated behavioural responsiveness.

The effects of selective dopamine receptor agonists and antagonists on body temperature in rats.

Body temperature was measured at repeated time intervals following the administration of various dopamine agonists and antagonists. The D-1 and D-2 receptor agonist, apomorphine, produced dose-dependent hypothermia. This effect was inhibited by the D-2 receptor antagonist, spiroperidol. Stimulation of D-2 receptor by LY171555 produced dose-dependent hypothermia, which was attenuated by pretreatment with spiroperidol and not altered by the D-1 receptor antagonist SCH23390. The D-1 receptor agonist, SK&F38393 had no effect on body temperature. SCH23390 administered alone produced initial hyperthermia and subsequent hypothermia. When administered with apomorphine, SCH23390 both attenuated and potentiated the hypothermic response, depending on the dose and time of administration of each drug. The results suggest that dopamine receptor agonists induce hypothermia by stimulation of the D-2 receptor subtype.