Method for neuroprotection of spinal cord under artificial circulation

Abstract

FIELD: medicine.SUBSTANCE: invention relates to cardiovascular surgery, cardiac anesthesiology and neurosurgery. Using a heart-lung machine, controlled hyperoxia of arterial blood is achieved. A partial pressure of oxygen in arterial blood (PaO2) that exceeds physiological parameters is maintained before clamping the thoracoabdominal aorta, during the ischemic stage, in the early reperfusion period, and in the late reperfusion period. The parameters of controlled hyperoxia, including oxygen concentration, exposure duration, and time intervals of exposure, are taken into account depending on the stage of the operation, the duration of ischemia, and the functional state of the patient.EFFECT: reducing the severity of ischemic damage to the spinal cord by maintaining an optimal level of oxygenation of the nervous tissue during critical periods of surgical intervention, and reducing the incidence of paraparesis or paraplegia.1 cl, 1 tbl, 1 ex

Description

[0001] The invention relates to the field of medicine, specifically to cardiovascular surgery, cardiac anesthesiology, and neurosurgery, and can be used in reconstructive and prosthetic surgeries on the thoracic and thoracoabdominal aorta, involving temporary aortic clamping, artificial blood circulation, and the risk of ischemic spinal cord injury. The method is intended for the prevention of ischemic and reperfusion spinal cord injury during the intraoperative and early postoperative periods.

[0002] Ischemic spinal cord injury is one of the most severe, disabling, and socially significant complications of surgical interventions on the thoracic and thoracoabdominal aorta. The incidence of spinal complications, including paraparesis and paraplegia, according to various clinical studies, ranges from 3 to 20%. The risk of their occurrence directly depends on the duration of ischemia, the level and extent of aortic compression, the extent of collateral circulation, and the initial functional state of the spinal cord. Blood supply to the thoracic and lumbar spinal cord is provided by a system of segmental arteries, including the intercostal and lumbar arteries, among which the great radiculomedullary artery (Adamkiewicz artery) plays a key role.Clamping of the thoracoabdominal aorta leads to a sharp decrease in perfusion pressure in the spinal cord basin, disruption of oxygen delivery, development of tissue hypoxia, neuronal energy deficit, and activation of primary and secondary ischemic injury cascades. A method of selective hypothermia and combined organ perfusion protection during aortic surgery is known in the art, where spinal cord neuroprotection is achieved using hypothermia and pharmacological protection (RU 2258513 C2, published 20.08.2005 A61K 31 / 573).

[0003] However, this solution does not provide for targeted management of arterial blood oxygenation levels depending on the stages of ischemic exposure and does not take into account the neuroprotective potential of controlled hyperoxia as an independent protective factor. Other disadvantages of such neuroprotection methods include: the lack of individualized selection of hyperoxia parameters; the lack of control over the partial pressure of oxygen in arterial blood (PaO2) during key periods of spinal cord ischemia and reperfusion; the lack of use of hyperoxia as an independent and controllable neuroprotective factor under artificial circulation; and the inability to adapt the oxygenation regime to the stages of surgical intervention.

[0004] Furthermore, a method for providing local cooling of the brain and spinal cord is known from the prior art, in which neuroprotection of the spinal cord during ischemia is carried out using hardware protection methods, while selective action is used (JP 7543364 B2, published 09 / 02 / 2024, A61F 7 / 00).

[0005] According to another source, a method is known for providing local cooling of the brain and spinal cord, which uses hardware neuroprotection of the spinal cord with a combination of monitoring and physical impact (US 10569064 B2, published 02 / 25 / 2020, A61F 7 / 12).

[0006] The closest to the claimed method is the method for preventing spinal cord ischemia by regulating hemodynamics and neurophysiological monitoring, which involves monitoring the functional state of the spinal cord and correcting systemic hemodynamics to prevent ischemic damage (RU 2277848 C2, published 20.06.2006, A61B 5 / 0484).

[0007] The disadvantages of the identified analogs are the lack of comprehensive application of controlled hyperoxia of arterial blood using an artificial circulation apparatus at specified time intervals before, during and after clamping of the thoracoabdominal aorta.

[0008] The technical objective of the claimed invention is to develop a method for neuroprotection of the spinal cord, which makes it possible to reduce the severity of ischemic and reperfusion injury to the spinal cord during compression of the thoracoabdominal aorta by means of a controlled increase in the partial pressure of oxygen in arterial blood under conditions of artificial circulation.

[0009] The technical result of the claimed invention is a reduction in the severity of ischemic damage to the spinal cord by maintaining an optimal level of oxygenation of the nervous tissue during critical periods of surgical intervention, increasing the resistance of neurons to hypoxia, reducing the severity of secondary ischemic and reperfusion damage, improving neurological outcomes in the postoperative period, and reducing the incidence of paraparesis and paraplegia.

[0010] The stated technical result is achieved by a method for spinal cord neuroprotection during thoracoabdominal aortic clamping, including connection to a heart-lung machine to maintain high partial pressure of oxygen in the blood and distal perfusion, and monitoring the functional state of the spinal cord. According to the invention, the heart-lung machine is used to achieve controlled hyperoxia of arterial blood, maintaining a partial pressure of oxygen in arterial blood (PaO2) above physiological values ​​prior to clamping the thoracoabdominal aorta, during the ischemic phase. The parameters of controlled hyperoxia, including oxygen concentration, exposure duration, and time intervals, are taken into account depending on the stage of the surgery, the duration of ischemia, and the functional state of the patient.

[0011] Physiological indicators of partial pressure of oxygen in arterial blood (PaO2) are understood to be values ​​of 80-100 mmHg, characteristic of normoxic conditions in patients with standard ventilation and the absence of artificial circulation.

[0012] The ranges of PaO2 values, according to the declared method, are presented in Table No. 1.

[0013] Table No. 1

[0014] Stage of surgical intervention PaO2 range, mmHg Functional purpose Before clamping the thoracoabdominal aorta (pre-ischemic stage) 150-250 Formation of an oxygen reserve in the spinal cord tissue Aortic cross-clamping period (ischemic stage) 400-500 (short-term up to 550) Compensation for decreased perfusion, maintaining oxygen diffusion Early reperfusion period 200-300 Reduction in the severity of reperfusion injury Late reperfusion period 100-150 Smooth transition to physiological normoxia

[0015] The parameters are adjusted based on the dynamics of PaO2, neurophysiological monitoring data and systemic hemodynamic parameters.

[0016] Controlled hyperoxia increases oxygen delivery to ischemic spinal cord structures, improves oxygen diffusion under conditions of reduced perfusion pressure, and enhances neuronal resistance to hypoxic injury. It is combined with neurophysiological monitoring, including recording of somatosensory evoked potentials and motor evoked potentials. Hyperoxia can be used in combination with pharmacological neuroprotective agents. PaO2 is monitored discretely at key moments during aortic clamping and de-clamping. Hyperoxia parameters are adjusted based on the dynamics of neurophysiological parameters.

[0017] The proposed method does not require additional invasive intervention and is easily integrated into existing aortic surgery protocols; it provides a reproducible, controllable, and physiologically sound neuroprotective effect.

[0018] The claimed method of neuroprotection of the spinal cord during compression of the thoracoabdominal aorta is based on the use of the neuroprotective potential of arterial blood hyperoxia under conditions of artificial circulation and allows for increasing the safety of surgical interventions, as well as improving clinical and functional outcomes.

[0019] Example

[0020] An example of the implementation of the method of neuroprotection of the spinal cord using controlled hyperoxia of arterial blood: Patient - V., 66 years old, gender - male.

[0021] Admission date: 19.01.2026. Surgery date: 21.01.2026. Diagnosis Primary diagnosis: Giant thoracoabdominal aortic aneurysm type II according to Crawford. Compression atelectasis of the lower lobe of the left lung. Bilateral hydrothorax. Pericardial effusion.

[0022] Background diagnosis: hypertension stage III, degree 1, risk 4. Fasting hyperglycemia. Concomitant diseases: focal gastritis. Chronic calculous cholecystitis. Degenerative-dystrophic changes in the cervical, thoracic, and lumbosacral spine.

[0023] Name of operation: prosthetic replacement of the thoracoabdominal aorta in the volume of Extent II from the level of Th6 to the infrarenal aorta with a 20 mm Polythese synthetic vascular prosthesis with reimplantation of one pair of spinal arteries at the level of Th8 on a single site, the celiac trunk and the superior mesenteric artery on a single site, the right and left renal arteries using the “button” method under conditions of auxiliary artificial circulation.

[0024] Description of the operation and implementation of the method.

[0025] The surgery was performed with the patient in the right lateral decubitus position. A thoracophrenopararectal approach was performed through the sixth intercostal space on the left, transecting the costal arch and completely cutting the diaphragm. The thoracoabdominal aorta was exposed from the level of the left thoracoabdominal aorta to the infrarenal region. A giant aneurysm of the thoracoabdominal aorta with a maximum diameter of up to 10 cm and up to 7 cm at the level of the visceral arteries was detected intraoperatively. After systemic heparinization, artificial blood circulation was connected. The aorta was clamped. To provide neuroprotection to the spinal cord, the claimed method of controlled arterial hyperoxia was implemented. During ischemic clamping of the thoracoabdominal aorta, the partial pressure of oxygen in arterial blood (PaO2) increased, exceeding physiological values. The maximum recorded PaO2 value was 486 mmHg.Hyperoxia was maintained before applying the proximal clamp throughout the main ischemic stage of aortic reconstruction; in the early reperfusion period after clamp removal. PaO2 was monitored using dynamic arterial blood gas analysis at key stages of the surgery. Transcranial motor evoked potentials from both lower extremities with an amplitude of up to 120 microvolts. H-reflex (Hoffman reflex) - a stable H-reflex was not recorded. Somatosensory evoked potentials - a stable somatosensory evoked potential (P37-N45) was recorded from the right lower extremity with an amplitude of up to 3.5 microvolts. During the surgical intervention, a significant decrease and disappearance of somatosensory evoked potentials (response amplitudes P37-N45) were noted at the stage of iliac artery ischemia, followed by complete recovery.A decrease in the amplitude of motor evoked potentials by more than 50 percent was also noted at the stage of lower limb ischemia, followed by complete recovery.

[0026] Extent II thoracoabdominal aortic reconstruction was performed. After the distal anastomosis was created, the clamp was removed from the infrarenal aorta.

[0027] No neurological complications were observed postoperatively. No signs of ischemic spinal cord injury, including motor or sensory impairment, were detected. The patient was mobilized early. Postoperative mechanical ventilation lasted 6 hours, and the hospital stay was 7 days.

[0028] The given clinical example demonstrates the possibility and effectiveness of using controlled hyperoxia of arterial blood with the achievement of high PaO2 values ​​(up to 486 mm Hg) under conditions of artificial circulation during thoracoabdominal aortic replacement.

[0029] The use of the claimed method made it possible to provide neuroprotection of the spinal cord and prevent the development of ischemic spinal complications.

[0030] The method is applied within the framework of current clinical activity and is accompanied by neurophysiological monitoring, which allows for the evaluation of the effectiveness of the neuroprotective effect and the safety of its use in real operating conditions.

[0031] Based on the above, it can be concluded that the use of the claimed method reduces the risk of ischemic spinal cord injury during reconstructive surgery on the thoracoabdominal aorta and increases the effectiveness of neuroprotection by controlled maintenance of target arterial PaO2 values. It allows for individualized selection of hyperoxia parameters (oxygen concentration, exposure duration, time intervals), and the integration of neuroprotective effects into the standard circuit of the heart-lung machine without significantly complicating surgical intervention.

Claims

A method for neuroprotection of the spinal cord during clamping of the thoracoabdominal aorta, including connection to a heart-lung machine, monitoring the functional state of the spinal cord and correction of systemic hemodynamics, characterized in that controlled hyperoxia of arterial blood is carried out by means of the heart-lung machine, partial pressure of oxygen in arterial blood (PaO2) exceeding physiological indicators is maintained before clamping of the thoracoabdominal aorta, during the ischemic stage, in the early reperfusion period and in the late reperfusion period, wherein the parameters of controlled hyperoxia, including oxygen concentration, exposure duration and time intervals of exposure, are taken into account depending on the stage of the operation, the duration of ischemia and the functional state of the patient.