Early Hyperbaric Oxygen Therapy for Cranial Trauma is More Effective

The main cause of traumatic brain injury is hypoxia

Secondary injury is the main cause of death and disability in traumatic brain injury patients, accounting for more than85% of total disability. Studies have shown that hypoxia is the main cause of cerebral edema. This is determined by the structure and functional characteristics of the human brain:

① although the human brain accounts for only2% of body weight, it consumes more than20% of the total oxygen supply;

② brain tissue does not have the ability to store oxygen and must rely on uninterrupted blood supply;

③ if brain tissue loses oxygen supply for only a few seconds, it can lead to the loss of cell function, and more than 4 minutes can lead to irreversible damage to brain tissue;

④ brain tissue's energy supply is produced only through the action of glucose and oxygen, and the cerebrospinal fluid surrounding brain tissue is full of sugar, so brain tissue is not easily affected by malnutrition causes interruption of energy supply.

Therefore, when brain tissue suffers from trauma, cerebral hemorrhage, cerebral infarction, inflammatory infection, and other diseases cause disruption of brain tissue blood circulation, and blood oxygen supply is hindered, it directly leads to hypoxic edema of brain tissue. Due to the confinement of the skull, once the swelling occurs, it will cause an increase in intracranial pressure, compressing the surrounding tissues and causing other tissue blood circulation disorders, thereby forming a vicious pathological cycle of cerebral edema. Therefore, using all means to timely correct the hypoxia of brain tissue is an important means to sever the vicious cycle of cerebral edema, control the progression of the disease, save the patient's life, and improve the prognosis.

Hyperbaric oxygen therapy can effectively improve cerebral hypoxia

High-pressure oxygen therapy, also known as hyperbaric oxygen therapy (HBOT), is a physical treatment method that involves intermittently exposing patients to pure oxygen within a closed chamber under a pressure usually greater than 1.4 atmospheres. The main mechanism of the HBOT soft chamber for brain injuries can be explained as follows: Under high-pressure conditions, oxygen dissolves rapidly into the bloodstream based on the principles of physics. The amount of dissolved oxygen in the blood is directly proportional to the environmental pressure, and as the pressure increases, the amount of dissolved oxygen in the blood also increases. Research shows that at the commonly used clinical range of 2-3 atmospheres, the amount of physically dissolved oxygen in the arterial blood is approximately 17-21 times higher than at normal atmospheric pressure. Studies have confirmed that under the pressure of 3 atmospheres, the physical dissolved oxygen content in every 100 milliliters of arterial blood is approximately 6.80 ml, which is sufficient to meet the basic oxygen requirements of providing 6.08 ml of oxygen per 100 milliliters of arterial blood needed to sustain vital organs in the human body. In other words, under the pressure of 3 atmospheres during high-pressure oxygen therapy, the basic oxygen needs of the patient's vital organs can be met solely through the physically dissolved oxygen in the blood, without relying on oxygen bound to hemoglobin.

The fundamental principle of high-pressure oxygen therapy contributes to the following therapeutic effects on brain injuries:

Oxygen Delivery: Unlike oxygen bound to hemoglobin under normal atmospheric pressure, physically dissolved oxygen can be directly delivered to the tissue cells as long as the blood flows normally under the propulsion of the heart. This process does not require extra energy consumption, reducing the energy expenditure of damaged brain tissue.
Overcoming Microcirculation Impairment: The small size of oxygen molecules dissolved in the liquid component of the blood allows them to reach oxygen-deprived swollen tissues, even when the capillaries are compressed and red blood cells cannot pass through. This mechanism helps overcome microcirculation disorders caused by brain edema, rapidly relieving tissue hypoxia in the brain.
Increased Oxygen Diffusion Distance: Studies have shown that under the pressure of 3 atmospheres, the increased oxygen content in the liquid component of the blood extends the distance over which each capillary can supply the surrounding tissues threefold. This indicates that high-pressure oxygen therapy compensates for the oxygen supply to brain tissues that have lost blood supply due to microvascular damage by increasing the oxygen diffusion distance within the capillaries.
Anti-Steal Effect: Under high-pressure oxygen conditions, normal tissues undergo appropriate vasoconstriction because they are not oxygen-deprived. However, hypoxic tissues, due to oxygen deficiency and edema, do not experience vasoconstriction, resulting in a significant increase in oxygen supply without reducing blood supply. This clinical effect, known as the "oxygen steal effect," not only facilitates timely and increased oxygen supply to hypoxic brain tissues but also reduces the overall brain water content, directly lowering intracranial pressure and treating brain edema.

From the above explanations, it is evident that high-pressure oxygen therapy plays a crucial role in the treatment of cranial brain injuries and is a promising therapeutic approach. Its mechanism is more precise, targeted, direct, and rapid compared to other clinical methods. Based on existing foundations, clinical research, and practice, the current high-pressure oxygen therapy protocols have been proven to be safe and reliable, without significant toxic side effects.

When can high-pressure oxygen therapy be initiated after cranial brain injuries?

Cranial brain injury itself is a pathological diagnosis, and many diseases can lead to its occurrence. Common causes include traumatic brain injury, cerebral hemorrhage, cerebral infarction, intracranial infection, carbon monoxide poisoning, cardiac arrest, postoperative brain tumor, asphyxia, and more. These injuries can result from direct damage to the brain due to external forces or infections, as well as indirect damage caused by disruption of cerebral blood circulation or systemic hypoxia due to various internal diseases. The etiology is often diverse and complex, with variations in the timing and severity of the condition. Therefore, it requires doctors who have a deep understanding of neurology and expertise in hyperbaric oxygen medicine to evaluate the specific situation of the patient and initiate high-pressure oxygen therapy in a timely and appropriate manner, while excluding absolute and relative contraindications. In many cases, collaboration with medical professionals from various clinical disciplines is necessary to develop comprehensive treatment plans, where high-pressure oxygen therapy is just one component of the combined treatment approach. In principle, as long as the patient is suitable for high-pressure oxygen therapy, initiating treatment as early as possible is preferable. Practical experience has shown that starting high-pressure oxygen therapy within minutes, hours, days, or even weeks after the onset of cranial brain injuries can promptly improve the patient's state of cerebral hypoxia, significantly impacting their prognosis for the better.