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Biomedical subjects

R R Pearson

Publications and source records attributed to R R Pearson.

12 recordsLinked to original sources
PubMed1992

Effects of treatment with dexamethasone on recovery from experimental cerebral arterial gas embolism.

Dexamethasone is often recommended as an adjunct to recompression in the treatment of serious central nervous system decompression accidents. We studied the effects of prophylactic and therapeutic administration of dexamethasone combined with hyperbaric treatment in anesthetized dogs that were subjected to carotid air embolism and a brief episode of arterial hypertension. To assess recovery we measured somatosensory evoked potential (SSEP) amplitude, intracranial pressure, brain water, and cerebral blood flow. Three groups were studied: pre-air treatment (dexamethasone 1 mg/kg 3-4 h before carotid air embolism, and 1 mg/kg immediately after air embolism); post-air treatment (2 mg/kg immediately after air embolism); and control (equivalent volumes of saline pre- and post-air). There was a slight improvement in SSEP early in the course of hyperbaric therapy in the pre-air treated group; the post-air group never differed from control. No differences in intracranial pressure or brain water were found among groups. No blood flows below those lethal to neurons occurred in treated animals but 4 of 7 control animals had low flows. Although prophylactic treatment with dexamethasone produces some improvement in recovery, we cannot confirm that dexamethasone is an effective adjunct to recompression when administered therapeutically.

Animals↗
PubMed1992

Comparison of two recompression profiles in treating experimental cerebral air embolism.

The standard treatment for cerebral arterial gas embolism (CAGE) is an initial recompression to 6 atm abs on air for 30 min followed by oxygen breathing at 2.8 and 1.9 atm abs. It has been suggested that initial recompression to 2.8 atm abs on O2 may be as beneficial, thus avoiding potential treatment complications associated with the deeper depth. To test this hypothesis, we measured the recovery of the somatosensory evoked potential (SEP) following air embolism in anesthetized, ventilated cats. Air was infused into the carotid artery in increments of 0.08 ml until the SEP amplitude was reduced to less than 10% of the baseline value for 15 min. Three groups were studied. A control group (n = 10) received no further treatment after SEP suppression. The second group (6 atm abs/HBO] (n = 8) was compressed to 6 atm abs on air for 30 min followed by O2 breathing at 2.8 atm abs for 100 min. The third group (HBO) (n = 8) was compressed to 2.8 atm abs on O2 for 130 min. The control group recovered 28.8 +/- 18.2% (mean +/- SD) of the baseline amplitude, whereas the 6 atm abs/HBO group recovered 48.6 +/- 22.6%, and the HBO group recovered 62.0 +/- 20.3%. An analysis of variance revealed that only the HBO group had significantly (P less than 0.01) better recovery than the control group. There was no significant difference in SEP recovery between the 2 treatment groups. These results suggest that treating CAGE at 2.8 atm abs with O2 is a viable alternative to the current therapy.

Animals↗
PubMed1989

Cerebral perfusion deficits in dysbaric illness.

Decompression sickness (DCS) is usually categorised as type I (mild; peripheral pain, non-neurological) or type II (serious; neurological). Type II is regarded as predominantly a spinal cord disease with infrequent cerebral involvement. Cerebral perfusion was studied by injection of 99Tcm-hexamethylpropyleneamine oxime and single photon emission tomography in 28 divers with confirmed incidents of DCS and cerebral arterial gas embolism (CAGE). Cerebral perfusion deficits were present in all 23 cases of type II DCS and in all 4 cases of CAGE. No deficits were present in the single case of type I DCS. Type II DCS should be recognised as a diffuse, multifocal, central nervous system disease.

Adolescent↗
PubMed1988

99Tcm-HMPAO single photon emission tomography in the diagnosis of cerebral barotrauma.

Cerebral barotrauma, or the neurological manifestation of the "bends", is a relatively common disease of divers and aviators. To date, however, no-one has succeeded in demonstrating a cerebral or spinal cord lesion in vivo following a decompression incident, despite the presence of definitive clinical signs and symptoms of central nervous system involvement. This paper describes the use of 99Tcm-labelled hexamethylpropyleneamine oxime (99Tcm-HMPAO) with single photon emission tomography in a study of three individuals involved in driving accidents. All three suffered cerebral barotrauma during decompression and all exhibited clinical signs and symptoms of dysbarism to a varying degree. Imaging was performed at time intervals ranging from 2 h to several days following the incidents. The results showed well defined cerebral ischaemic lesions in all three subjects. We conclude that 99Tcm-HMPAO imaging provides a significant advance in locating and demonstrating cerebral lesions following barotrauma and will contribute greatly to our understanding of the pathophysiological processes involved.

Adolescent↗
PubMed1988

Central nervous system decompression sickness: latency of 1070 human cases.

Many aspects of central nervous system (CNS) decompression sickness (DCS) are poorly understood, including the temporal pattern of its presentation and the pathogenic mechanisms involved in the development of the disease. Using case histories and clinical series published in the literature and retrieved from treatment center records, this study is an attempt to define the interval between surfacing from a hyperbaric exposure and the onset of symptoms of CNS DCS. The results of 1070 cases of human CNS DCS were included in the study. The results show that the disease generally occurs rapidly: over 50% became symptomatic within 10 min of returning to 1 ATA, and in only 15% of cases was the onset of symptoms delayed for more than 1 h. Cerebral DCS had a more rapid onset than spinal cord disease: 50% of cerebral cases became apparent within about 3 min and a similar proportion of spinal cord cases within about 9 min from surfacing. The influence of these results on the diagnosis and treatment of dysbaric illness, on the safety of certain diving practices, and on possible pathogenic mechanisms is discussed.

Central Nervous System Diseases↗
PubMed1988

Carbon monoxide poisoning: forgotten not gone!

Carbon monoxide causes one third of all poisoning deaths in Britain. In this paper a modern scheme for the assessment and management of victims of carbon monoxide poisoning is outlined, the importance of the direct cellular toxicity of carbon monoxide and the rationale behind hyperbaric oxygen therapy are discussed, and a list of currently available hyperbaric facilities is given.

Carbon Monoxide Poisoning↗
PubMed1979

Diving accidents.

Explore the source record for details and available documents.

Accident Prevention↗
PubMed1978

Decompression sickness or cold injury?

This paper reports two cases involving divers who presented with painful hands and were treated for decompression sickness. Although treatment was successful, their symptoms and diving history suggest non-freezing cold injury, the so-called immersion hand, rather than decompression sickness. For long exposures or cases where the diver may have inadequate insulation, thermal protection of hands is recommended even in water as warm as 16 degrees C.

Adult↗