Our results seem to indicate that pretreatment with hyperbaric oxygen can reduce neuropsychometric dysfunction and also modulate the inflammatory response after cardiopulmonary bypass. However, further multicenter randomized trials are needed to clinically evaluate this form of therapy.
Objectives-To investigate and quantify the diVerences in neurological examination findings in patients acutely poisoned with carbon monoxide, between initial assessment at accident and emergency (A&E) departments and subsequently at a hyperbaric unit. Methods-Retrospective case note review of all patients referred to the Hull Hyperbaric Unit for treatment of acute carbon monoxide poisoning between August 1998 and August 1999. Patients who were ventilated or less than 16 years old were excluded because of diYculty in assessing their neurological status. Results-Thirty patients were included for analysis. The mean duration from exposure to assessment in A&E was four hours while patients were reviewed on average three hours later at the hyperbaric unit. Referrals came from 14 diVerent hospitals. A history of loss of consciousness accounted for 70% of referrals. A mean of 3.2 neurological signs per patient was documented in A&E compared with 9.2 at the hyperbaric unit. Seventy nine per cent of abnormal neurological signs were not detected at A&E departments compared with 3% at the hyperbaric unit. The major source of discrepancy was in sharpened Rhomberg's test and heel-toe gait, in 13% of patients examined in A&E departments these signs were recorded as abnormal compared with 90% at the hyperbaric unit. Conclusion-There is a large discrepancy in neurological findings between assessment in A&E departments and the Hull Hyperbaric Unit. A number of factors may account for this including interobserver variation, patient deterioration during transfer, poor documentation, lack of understanding of the sequelae of carbon monoxide poisoning and inadequate examinations. Further research is required to quantify the impact of the various factors that may contribute to the diVerences in neurological findings. (Emerg Med J 2001;18:95-98)
Heart failure (HF) is a chronic condition that is expected to increase in incidence along with increased life expectancy and an aging population. As the incidence of HF increases, the cost to national healthcare budgets is expected to run into the billions. The costs of lost productivity and increased social reliance on state support must also be considered. Recently, acute myocardial infarction (AMI) has come to be seen as the major contributing factor to HF. Although thrombolysis may restore coronary perfusion after an AMI, it may also introduce ischemic reperfusion injury (IRI). In an attempt to ameliorate sustained protein damage caused by IRI, endogenous chaperone proteins known as heat shock proteins (HSPs) are induced as a consequence of the stress of IRI. Recently, hyperbaric oxygen has been shown to induce the production of HSPs in noncardiac tissue, with a resultant protective effect. This current opinion review article suggests a possible role for hyperbaric oxygen, as a technologically modern drug, in augmenting the induction of endogenous HSPs to repair and improve the function of failing hearts that have been damaged by AMI and IRI. In addition, this simple, safe, noninvasive drug may prove useful in easing the economic burden of HF on already overextended health resources.
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