Hyperbaric oxygenation in fluid microembolism

Abstract

Because clinicians require objectively demonstrable neurological deficits to confirm a diagnosis, the recognition of embolic events in the nervous system is generally restricted to the effects of ischemic necrosis produced by arterial occlusion. However, magnetic resonance imaging (MRI) has shown that lesser degrees of damage associated with small emboli are common, especially in the mid brain, and are usually clinically silent. They are frequently associated with atheromatous embolism in the elderly, but microembolic debris, such as fat, is common in the systemic venous return of healthy people and generally trapped in the microcirculation of the lung being removed by phagocytosis. However, pulmonary filtration may fail and microemboli may also pass through an atrial septal defect in so-called 'paradoxical' embolism. Studies of bubbles formed on decompression in diving have demonstrated the importance of pulmonary filtration in the protection of the nervous system and that filtration is size dependant, as small bubbles may escape entrapment. Fluid and even small solid emboli, arresting in or passing through the cerebral circulation, do not cause infarction, but disturb the blood-brain barrier inducing what has been termed the 'perivenous syndrome'. The nutrition of areas of the white matter of both the cerebral medulla and the spinal cord depends on long draining veins which have been shown to have surrounding capillary free zones. Because of the high oxygen extraction in the microcirculation of the gray matter of the central nervous system, the venous blood has low oxygen content. When this is reduced further by embolic events, tissue oxygenation may fall to critically low levels, leading to blood-brain barrier dysfunction, inflammation, demyelination and eventually, axonal damage. These are the hallmarks of the early lesions of multiple sclerosis where MR spectroscopy has also shown the presence of lactic acid. Significant elevation of the venous oxygen tension requires oxygen to be provided under hyperbaric conditions. Arterial tension is typically increased ten-fold breathing oxygen at 2 atmospheres absolute (ATA), but this results in only a 1.5-fold increase in the cerebral venous oxygen tension. The treatment of decompression sickness, and both animal and clinical studies, have confirmed the value of oxygen provided under hyperbaric conditions in the restoration and preservation of neurological function in the 'perivenous' syndrome.

Breath-Hold Diving-Related Decompression Sickness with Brain Involvement: From Neuroimaging to Pathophysiology

“…These authors proposed two potential pathways by which DCS in breath-hold diving could induce BBB impairment: one is based on mechanical damage and endothelial dysfunction caused by gas bubbles generated by decompression, and the other is that microbubbles or bubble/platelet aggregates in the postcapillary venules cause stasis of capillary flow, leading to BBB impairment [ 4 ]. Moreover, dysbaric modification of the BBB has been reported by several researchers previously, in different animal models, using several tracers and under different experimental conditions [ 26 , 27 , 28 , 29 ]. Furthermore, it is now known that vascular endothelial cells are vulnerable to diving-related decompression.…”

Efficacy of alogliptin combined with motor imagery under hyperbaric oxygen in diabetic nephropathy with silent cerebral infarction

“…The combination of incretin drugs and GLP-1R may activate adenylate cyclase, upregulate cyclic adenosine monophosphate levels, trigger Ca 2+ inflow, enhance synaptic plasticity, increase neurotransmitter release and improve learning, memory and cognitive function ( 20 , 21 ). Hyperbaric oxygen therapy may increase the oxygen saturation of patients, reduce intracranial pressure, relieve inflammatory reaction and edema degree, decrease infarction size ( 22 ), use ‘reverse steal phenomenon’ to increase blood and oxygen supply in the focal area, increase the mitochondrial membrane permeability of brain cells, reduce neutrophil apoptosis and promote neural functional recovery and regeneration ( 23 ). Thus, it is an effective means to treat cerebral infarction.…”

Spinal Cord Injury in Decompression Sickness: A Case Report

“…As this blood circulates in the cerebral vasculature, much of the oxygen is extracted from this blood by the cortical grey matter, and the remaining is drained by capillary free zone, long veins which supply the white matter of the mid brain and the spinal cord. In this area, any compromise by micro-emboli will cause the hypoxic damage and dysfunction of the blood CNS barrier, leading to inflammation, demyelination leading to physiological or physical axonal dysfunction, also termed as perivenous syndrome 4 . This venous ischaemia of the cord causes myelitis in the cord in most patients with a diagnosis of DCS of the spinal cord.…”