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Neurogenic shock may be caused by injury. Neurogenic shock is

Below the level of spinal cord injury.

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Lecture by Dr. E. Kern USA about Empty Nose Syndrome (Russian)

Installation of a synthetic suburethral loop UroSling for men

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I just want to show you that the problem is real. It is mentioned in the International Rhinological Society, the American Rhinological Society, and the Mayo Clinic. I first heard about it probably about 15 years ago, then I read about it, it was first described in Europe probably in the late 18th century - correction - in the late 17th or early 18th century by an autologger, Gilles de Amsterdam. This woman had reconstructive surgery six months ago that didn't make her feel any better, she had been on allergy therapy for two years with no benefit, and here you can see - I'm sorry, I'm sorry I can't show you this - but this is a psychological assessment. These are, in my opinion, the four main functions of the nose - the four primary functions of the nose. And whether it saturates the inhaled air with moisture is part of the respiratory function. And secondly, when we remove functional tissue, what happens? This is the rabbit model, this is the work of Judy Tria and Tom McCarthy in our laboratory, this is the preparation of the rabbit, we are instilling Indian ink, we started experimenting with Indian ink yesterday. This is real time, see how Indian ink moves through ciliary activity to the natural opening of the maxillary sinus in rabbit preparation. So here's the second point. The first thought is that the mucous membrane is an organ of the nose. This is no longer respiratory epithelium, this is skin! So, there is no more mucociliary transport, it has disappeared! Squamous metaplasia has occurred. And it helps me at least think about how we're going to treat these patients. How will we treat these poor patients who come with crusting, bleeding, difficulty breathing, inability to concentrate, sleep problems, depression and some of them with aprosexia. Eric Moore, who is on our staff, looked at these patients. He did this several years ago before he left training. Sometimes when patients say they can't breathe, we insert cotton into their nose, right at the corner of their nasal valve, and sometimes they clutch their chest. And I tell them: - Take a deep breath. - Yes, now I can breathe. It helps patients.

Neurogenic shock

Pathogenesis of cardiovascular disorders

To clearly understand the pathogenetic mechanisms of the development of cardiovascular disorders, it is necessary to dwell on the neuroanatomy of the parts of the nervous system that regulate the activity of the cardiovascular system.

Neuroanatomy

The center of regulation of the cardiovascular system is the nuclei of the same name in the medulla oblongata. This center, in turn, is influenced by impulses from the cerebral cortex and subcortical nuclei. Parasympathetic impulses from the cardiovascular nuclei of the medulla oblongata reach their targets through the fibers of the vagus nerve (n. vagus). Preganglionic fibers form synapses with postganglionic parasympathetic neurons near the myocardium. Peripheral vessels do not have parasympathetic innervation.

Blood pressure regulation is modulated by the activity of supraspinal centers (located in the brain), which send stimulating impulses to spinal sympathetic preganglionic neurons through descending pathways. As a result of spinal cord injury, the descending pathways of the spinal cord are interrupted and the sympathetic neurons located here lose the ability to generate signals from the sympathetic nervous system.

Thus, interruption of the descending pathways of the spinal cord leads to a decrease in the activity of the sympathetic nervous system and the elimination of its antagonistic effect on the parasympathetic part, the impulses of which reach their targets through the intact vagus nerve. A decrease in the activity of the sympathetic nervous system leads to a decrease in blood pressure, loss of normal adaptability of the cardiovascular system and disruption of its reflex regulation.

Clinical picture

Most often, patients with neurogenic shock have low blood pressure, and the patient's skin is warm and dry. These symptoms appear due to inhibition of sympathetic innervation of the cardiovascular system, leading to a decrease in the return of blood from the peripheral vascular bed, a decrease in total peripheral vascular resistance (TPVR) and a disruption in the centralization of blood flow. Patients may experience hyperthermia. In this case, a pronounced loss of heat occurs.

The clinical picture of neurogenic shock and the severity of the patient’s condition largely depends on the level of spinal cord damage. Damage localized above the first thoracic segment of the spinal cord (Th1) leads to the destruction of the spinal cord pathways that control the activity of the entire sympathetic nervous system (regulating the normal functioning of many organ systems, including vital ones - cardiovascular, respiratory and others).

Damage localized in the spinal cord segments starting from the first thoracic and below only partially disrupts the activity of the sympathetic nervous system. The severity of the manifestations of neurogenic shock decreases along with a decrease in the localization of spinal cord pathology. For example, damage to the upper thoracic segments is accompanied by a more severe clinical picture than, for example, damage to the conus of the spinal cord (at the level of the thoracolumbar junction of the spine).

Neurogenic shock can accompany both complete (lack of motor and sensory functions below the level of injury) and incomplete (partial impairment of spinal cord functions below the level of injury) neurological deficits due to injury.

According to S. Popa et al., all patients with complete neurological deficit due to spinal cord injury (ASIA A or B) have bradycardia, 68% of them have arterial hypotension, the correction of which in 35% of patients requires the introduction of vasopressors, and in 16%, severe bradycardia is observed, turning into asysitolia (cardiac arrest). In contrast, patients with incomplete neurological deficit due to spinal cord injury (ASIA C or D) have bradycardia in 35 - 71% of cases and only a few of them have arterial hypotension requiring vasopressor support, and cardiac arrest very rarely develops.

Differential diagnosis

The diagnosis of neurogenic shock should be made after excluding other critical conditions with a similar clinical picture. Neurogenic shock must be differentiated from other types of shock, in particular hypovolemic. In patients with severe trauma, low blood pressure may be due to ongoing bleeding. Thus, it is tactically correct to first exclude hemorrhagic shock in the patient. Key diagnostic criteria for neurogenic shock are hypotension, bradycardia, neurological dysfunction, and warm and dry skin of the patient.

Treatment

Treatment tactics in the emergency department

Attention! The information is intended for students and current professionals in the field of medicine, is not a guide to action and is presented for additional education.

The initial examination and treatment tactics for suspected neurogenic shock do not differ from those when providing care to injured patients and include emergency diagnosis and correction of life-threatening disorders.

(lat. n.vagus) begins to dominate. The leading clinical signs of neurogenic shock in spinal cord injury are arterial hypotension and bradycardia. In terms of the frequency of injuries to the spinal cord, the cervical region is in the lead, then the level of the thoracolumbar junction of the spine, less often the thoracic region and even less often the level of the lumbar spine (damage to the cauda equina). Neurogenic shock must be differentiated from spinal shock, defined as areflexia below the level of spinal cord injury.

Neurogenic shock

Pathogenesis of cardiovascular disorders

Neuroanatomy

Clinical picture

Differential diagnosis

Treatment

Treatment tactics in the emergency department

Attention! The information is intended for students and current professionals in the field of medicine, is not a guide to action and is presented for additional education.

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An excerpt characterizing Neurogenic shock

From the hall, Berg ran into the living room with a floating, impatient step and hugged the count, kissed the hands of Natasha and Sonya and hurriedly asked about his mother’s health.
– How is your health now? Well, tell me,” said the count, “what about the troops?” Are they retreating or will there be another battle?
“One eternal god, dad,” said Berg, “can decide the fate of the fatherland.” The army is burning with the spirit of heroism, and now the leaders, so to speak, have gathered for a meeting. What will happen is unknown. But I’ll tell you in general, dad, such a heroic spirit, the truly ancient courage of the Russian troops, which they – it,” he corrected himself, “showed or showed in this battle on the 26th, there are no words worthy to describe them... I’ll tell you, dad (he hit himself on the chest in the same way as one general who was talking in front of him hit himself, although a little late, because he should have hit himself on the chest at the word “Russian army”) - I’ll tell you frankly that we, the leaders, “Not only should we not have urged the soldiers or anything like that, but we could forcefully hold back these, these... yes, courageous and ancient feats,” he said quickly. – General Barclay, before Tolly, sacrificed his life everywhere in front of the army, I’ll tell you. Our corps was placed on the slope of the mountain. You can imagine! - And then Berg told everything that he remembered from the various stories he had heard during this time. Natasha, without lowering her gaze, which confused Berg, as if looking for a solution to some question on his face, looked at him.
– Such heroism in general, as shown by Russian soldiers, cannot be imagined and deservedly praised! - Berg said, looking back at Natasha and as if wanting to appease her, smiling at her in response to her persistent gaze... - “Russia is not in Moscow, it is in the hearts of her sons!” Right, dad? - said Berg.
At this time, the countess came out of the sofa room, looking tired and dissatisfied. Berg hastily jumped up, kissed the countess's hand, inquired about her health and, expressing his sympathy by shaking his head, stopped next to her.
– Yes, mother, I will truly tell you, difficult and sad times for every Russian. But why worry so much? You still have time to leave...
“I don’t understand what people are doing,” said the countess, turning to her husband, “they just told me that nothing is ready yet.” After all, someone needs to give orders. You'll regret Mitenka. Will this never end?
The Count wanted to say something, but apparently refrained. He stood up from his chair and walked towards the door.
Berg at this time, as if to blow his nose, took out a handkerchief and, looking at the bundle, thought, sadly and significantly shaking his head.
“And I have a big request to ask you, dad,” he said.
“Hm?..” said the count, stopping.
“I’m driving past Yusupov’s house now,” Berg said, laughing. “The manager, I know, ran out and asked if you would buy something.” I went in, you know, out of curiosity, and there was just a wardrobe and a toilet. You know how Veruschka wanted this and how we argued about it. (Berg involuntarily switched to a tone of joy about his well-being when he began talking about the wardrobe and toilet.) And such a delight! comes forward with an English secret, you know? But Verochka wanted it for a long time. So I want to surprise her. I saw so many of these guys in your yard. Give me one, please, I’ll pay him well and...
The Count frowned and gagged.
- Ask the countess, but I don’t give orders.
“If it’s difficult, please don’t,” said Berg. – I would really like it for Verushka.
“Oh, go to hell, all of you, to hell, to hell, to hell!” shouted the old count. - My head is spinning. - And he left the room.
The Countess began to cry.
- Yes, yes, mummy, very difficult times! - said Berg.
Natasha went out with her father and, as if having difficulty understanding something, first followed him, and then ran downstairs.
Petya stood on the porch, arming the people who were traveling from Moscow. Pawned carts still stood in the yard. Two of them were untied, and an officer, supported by an orderly, climbed onto one of them.
- Do you know why? - Petya asked Natasha (Natasha understood that Petya understood why his father and mother quarreled). She didn't answer.
“Because daddy wanted to give all the carts to the wounded,” said Petya. - Vasilich told me. In my opinion…
“In my opinion,” Natasha suddenly almost screamed, turning her embittered face to Petya, “in my opinion, this is such disgusting, such an abomination, such... I don’t know!” Are we some kind of Germans?.. - Her throat trembled with convulsive sobs, and she, afraid to weaken and release the charge of her anger in vain, turned and quickly rushed up the stairs. Berg sat next to the countess and kindly and respectfully consoled her. The Count, pipe in hand, was walking around the room when Natasha, with a face disfigured by anger, burst into the room like a storm and quickly walked up to her mother.
- This is disgusting! This is an abomination! - she screamed. - It can’t be that you ordered.
Berg and the Countess looked at her in bewilderment and fear. The Count stopped at the window, listening.
- Mama, this is impossible; look what's in the yard! - she screamed. - They remain!..
- What happened to you? Who are they? What do you want?
- The wounded, that's who! This is impossible, mamma; this doesn’t look like anything... No, Mama, darling, this is not it, please forgive me, darling... Mama, what do we care about what we’re taking away, just look at what’s in the yard... Mama!.. This can’t be !..
The Count stood at the window and, without turning his face, listened to Natasha’s words. Suddenly he sniffed and brought his face closer to the window.
The Countess looked at her daughter, saw her face ashamed of her mother, saw her excitement, understood why her husband was now not looking back at her, and looked around her with a confused look.
- Oh, do as you want! Am I disturbing anyone? – she said, not yet suddenly giving up.
- Mama, my dear, forgive me!
But the countess pushed her daughter away and approached the count.
“Mon cher, you do the right thing... I don’t know that,” she said, lowering her eyes guiltily.
“Eggs... eggs teach a hen...” the count said through happy tears and hugged his wife, who was glad to hide her ashamed face on his chest.
- Daddy, mummy! Can I make arrangements? Is it possible?.. – Natasha asked. “We’ll still take everything we need…” Natasha said.
The Count nodded his head affirmatively at her, and Natasha, with the same quick run as she used to run into the burners, ran across the hall to the hallway and up the stairs to the courtyard.
People gathered around Natasha and until then could not believe the strange order that she conveyed, until the count himself, in the name of his wife, confirmed the order that all carts should be given to the wounded, and chests should be taken to storerooms. Having understood the order, people happily and busily set about the new task. Now not only did it not seem strange to the servants, but, on the contrary, it seemed that it could not be otherwise, just as a quarter of an hour before it not only did not seem strange to anyone that they were leaving the wounded and taking things, but it seemed that it couldn't be otherwise.
All the household, as if paying for the fact that they had not taken up this task earlier, busily began the new task of housing the wounded. The wounded crawled out of their rooms and surrounded the carts with joyful, pale faces. Rumors also spread in the neighboring houses that there were carts, and the wounded from other houses began to come to the Rostovs’ yard. Many of the wounded asked not to take off their things and only put them on top. But once the business of dumping things had begun, it could not stop. It didn't matter whether to leave everything or half. In the yard lay untidy chests with dishes, bronze, paintings, mirrors, which they had so carefully packed last night, and they kept looking for and finding an opportunity to put this and that and give away more and more carts.
“You can still take four,” said the manager, “I’m giving away my cart, otherwise where will they go?”
“Give me my dressing room,” said the countess. - Dunyasha will get into the carriage with me.
They also gave away a wardrobe wagon and sent it two houses away to pick up the wounded. All the household and servants were cheerfully animated. Natasha was in an enthusiastically happy revival, which she had not experienced for a long time.
-Where should I tie him? - people said, adjusting the chest to the narrow back of the carriage, - we must leave at least one cart.
- What is he with? – Natasha asked.
- With the count's books.
- Leave it. Vasilich will clean it up. It is not necessary.
The chaise was full of people; doubted about where Pyotr Ilyich would sit.
- He's on the goat. Are you a jerk, Petya? – Natasha shouted.
Sonya kept busy too; but the goal of her efforts was the opposite of Natasha’s goal. She put away those things that should have remained; I wrote them down, at the countess’s request, and tried to take with me as many as possible.

In the second hour, the four Rostov carriages, loaded and stowed, stood at the entrance. The carts with the wounded rolled out of the yard one after another.
The carriage in which Prince Andrei was carried, passing by the porch, attracted the attention of Sonya, who, together with the girl, was arranging seats for the countess in her huge tall carriage, which stood at the entrance.
– Whose stroller is this? – Sonya asked, leaning out of the carriage window.
“Didn’t you know, young lady?” - answered the maid. - The prince is wounded: he spent the night with us and is also coming with us.
- Who is this? What's your last name?
– Our very former groom, Prince Bolkonsky! – sighing, answered the maid. - They say he is dying.
Sonya jumped out of the carriage and ran to the Countess. The countess, already dressed for the trip, in a shawl and hat, tired, walked around the living room, waiting for her family in order to sit with the doors closed and pray before leaving. Natasha was not in the room.

is an acute circulatory failure that occurs due to a sudden loss of sympathetic regulation of vascular tone due to damage to the nervous system. The most characteristic signs of the pathology are hypotension, relative bradycardia, hyperemia and hyperthermia of the skin of the extremities. Severe shock is accompanied by disturbances in breathing and consciousness, and neurological disorders. Diagnosis is carried out based on clinical examination, blood tests, hemodynamic monitoring, CT and MRI of the affected areas. Shock relief is carried out using intensive care, and early surgical correction is important.

ICD-10

R57.8 Other types of shock

General information

The epidemiology of neurogenic shock is difficult to assess because it is based on limited statistical data and depends on the clinical criteria used. Compared to other types of circulatory failure, this type of shock is considered the rarest. For injuries of the cervical spine, an emergency condition is registered in 19-29% of patients, exceeding the figures for the thoracic and lumbar spine (7 and 3%, respectively). The incidence of shock in intracranial disorders remains unknown. The gender-age structure usually corresponds to that for spinal injuries; half of all cases occur between the ages of 16 and 30 years, with an 8-fold predominance in men.

Causes

The development of pathology is mediated by acute damage to the central nervous system - primary or secondary. Hemodynamic changes typically occur when the craniospinal tract is affected above the Th6 level, including the brainstem. The primary process is associated with direct destruction of nerve pathways, the secondary process is caused by vascular and electrolyte changes, edema. Shock reactions are caused by two groups of reasons:

Organic. A common cause of the neurogenic process is severe injuries to the spine and spinal tract (automobile, sports, gunshots). Cerebral disorders include traumatic brain injury, stroke, and subarachnoid hemorrhage. Other factors include severe cerebrospinal fluid hypertension, transverse myelitis, Guillain-Barré syndrome and other peripheral neuropathies.
Functional. In some cases, circulatory disorders are caused by functional disorders. Shock can occur against the background of deep anesthesia, epidural anesthesia, or intense pain. The role of toxic damage to the autonomic system, the influence of certain medications, and severe psycho-emotional trauma is noted. Hypothalamic-pituitary-adrenal insufficiency is recognized as a separate cause.

Specific risk factors have been described for the pediatric population. Circulatory failure is the result of birth injuries and child abuse. Shock-related fractures and dislocations of the upper cervical spine are more common in patients with trisomy 21 (Down syndrome), skeletal dysplasias, and juvenile idiopathic arthritis.

Pathogenesis

There is no single mechanism for the development of neurogenic shock. Against the background of damage to the structures of the central nervous system, there is a loss of sympathetic innervation of the cardiovascular system with an increase in vagal influence. This is accompanied by systemic vasodilation, a sharp increase in vascular capacity, and a decrease in venous return and cardiac output. The daily rhythm of blood pressure fluctuations is lost, hypotension and reflex bradycardia occur, and hyperreactivity of peripheral adrenergic receptors occurs.

Cardiogenic mechanisms are caused by increased release of catecholamines associated with dysfunction of the posterior hypothalamus against the background of intracranial pathology. Increased concentrations of hormones trigger direct damage to the myocardium in the form of selective necrosis. Cardiac dysfunction is manifested by a decrease in output, an increase in pre- and afterload, which are not compensated by reflex tachycardia. Hemodynamic instability is aggravated by an increase in pressure in the pulmonary capillaries with an increase in hypoxic phenomena.

Neuroendocrine mechanisms are involved in the development of shock changes. Insufficiency of the hypothalamic-pituitary-adrenal system with traumatic damage to the central structures is accompanied by secondary hypocortisolism. In stressful situations, this can lead to a decrease in systemic vascular resistance, a decrease in cardiac contractility, and hypovolemic or hyperdynamic shock. Changes in the concentration of endogenous vasopressin have been noted, but its role in this situation still requires study.

Classification

According to the mechanism of development, neurogenic shock is a type of distributive shock, in which relative hypovolemia is noted. Taking into account the prevailing processes, it occurs in three pathogenetic variants: vasodilator, cardiogenic, neuroendocrine. The generally accepted clinical classification of shock includes several degrees of severity:

Idegree (compensated). Perfusion of vital organs is maintained. The general condition is moderate, consciousness is clear, the patient is slightly inhibited. Systolic blood pressure exceeds 100 mm Hg.
IIdegree (subcompensated). There is a gradual depletion of compensatory capabilities. The patient's condition is serious, lethargy is noted, the skin is pale. Blood pressure drops to 90-80 mm Hg, breathing quickens and becomes shallow.
IIIdegree (decompensated). Compensatory mechanisms cannot maintain adequate perfusion. The condition is extremely serious, characterized by adynamia, the level of consciousness is stupor. The skin is pale, acrocyanosis is present. The blood pressure level drops below 70 mm Hg, the pulse is thread-like, determined only in the main arteries. Anuria develops.
IVdegree (irreversible). The damage is irreversible, and multiple organ failure is typical. The patient is in a terminal condition, the skin is grayish in color with a marbled pattern and stagnant spots. Blood pressure is below 50 mm Hg or undetectable, pulse and breathing are barely noticeable. The pupils dilate, reflexes and reactions to painful stimuli are absent.

Symptoms of neurogenic shock

The clinical picture and severity of the pathology are largely determined by the location of the primary defect. Circulatory insufficiency can occur against the background of complete (with impaired sensory-motor function) or partial neurological deficit. A lesion above the Th1 segment disrupts the sympathetic regulation of many internal organs. Damage below C5 is accompanied by diaphragmatic breathing, and above C3 it stops. As the level of damage decreases, the severity of the disorders decreases.

The hemodynamic profile of the vasodilator variant of neurogenic shock is considered “warm and dry”: peripheral vasodilation is complemented by hypotension with increased pulse pressure, relative bradycardia, redness, and warming of the skin of the extremities. After spinal injuries, it is possible to notice a difference in the tone of the vascular network above and below the affected segments. Orthostatic hypotension without reflex tachycardia is common when moving from a supine to an upright position. In men, priapism is detected.

The cardiogenic form of shock is manifested by hypotension and rapid heartbeat; bradycardia in this situation is extremely rare. Peripheral vessels constrict, systemic venous resistance increases, and the skin becomes cold and moist. Myocardial dysfunction is accompanied by a decrease in cardiac output, a drop in stroke volume, dizziness, and pallor. Central venous pressure is normal or increased.

Acute and prolonged hypotension can provoke secondary ischemic damage to the brain and spinal cord, which further aggravates neurological deficits. Microcirculatory disorders mediated by hemodynamic instability potentiate thrombotic complications, increasing the risk of pulmonary embolism, acute coronary syndrome, and cerebrovascular insufficiency.

Diagnostics

Considering the potential danger of the pathology, an urgent examination of the patient is carried out in the intensive care unit. Before establishing a diagnosis of neurogenic shock, it is recommended to exclude other causes of circulatory failure, especially in the presence of severe progressive refractory hypotension. The following methods of laboratory and instrumental control help with this:

General and biochemical blood tests. A detailed picture of peripheral blood, coagulogram data, and plasma electrolyte composition are obtained. The concentration of cortisol and markers of myocardial necrosis (troponins, myoglobin, creatine phosphokinase) are determined. It is extremely important to evaluate arterial and venous blood gases, the results of which reveal hypoxemia, hypercapnia, and acidosis.
Hemodynamic monitoring. Hemodynamic parameters can be studied using non-invasive or invasive methods. The first include blood pressure measurement, pulse oximetry, ECG, plethysmography. Cardiac output is measured using Doppler echocardiography, thermodilution-based methods. Tissue perfusion can be judged by the amount of diuresis. Invasive monitoring is carried out through a central venous or arterial catheter.
Tomographic methods. Necessary to establish the causes of hemodynamic instability and detect concomitant injuries that pose a danger to the patient. CT scanning allows you to assess the condition of the spine, brain, and internal organs. MRI diagnostics are more informative for spinal injuries. In patients with shock reactions, tomography should be performed under close supervision.

Diagnostic lumbar puncture with cerebrospinal fluid analysis and neurophysiological studies (encephalography, neuromyography) are of no small importance. A neurologist differentiates vascular insufficiency from hypovolemic, hemorrhagic, obstructive shocks. It is necessary to exclude the presence of congestive heart failure, sepsis, and massive pulmonary embolism. Patients need emergency consultation with a traumatologist and neurosurgeon.

Treatment of neurogenic shock

Conservative therapy

An urgent condition requires timely relief according to the principles of resuscitation and intensive care. For injuries to the cervical spine, collar immobilization is performed to prevent further damage to the spinal cord. In parallel, measures are being taken to stabilize systemic hemodynamics and tissue perfusion:

Infusion support. To restore vital functions and prevent secondary ischemic processes, the main efforts are aimed at stopping hypotension. First-line therapy is infusion of saline solutions to quickly restore blood volume. With concomitant hemorrhagic shock, crystalloids are combined with colloid solutions to retain fluid in the vascular bed.
Inotropes and vasopressors. If fluid resuscitation does not eliminate the symptoms of shock, second-line drugs are used - inotropic (dobutamine), vasopressor agents (dopamine, adrenaline). To improve spinal cord perfusion, it is recommended to maintain mean blood pressure at 85-90 mmHg in the first week after spinal injury. Art.
Anticholinergics. Treatment of severe hemodynamically significant bradycardia is carried out with anticholinergics - atropine, glycopyrrolate. An alternative can be adrenomimetics (isadrin), methylxanthines (theophylline, aminophylline). The latter are indicated for cases of resistant bradycardia.

The presence of neurological deficit requires decongestant therapy with corticosteroids, but long-term use of hormonal agents is not recommended due to the high risk of complications. Based on the clinical situation, antibacterial, hemostatic and neuroprotective correction is additionally prescribed. In case of respiratory problems, the patient is transferred to mechanical ventilation. In the long term, comprehensive rehabilitation is necessary to restore functionality.

Surgery

Surgery may be required for traumatic injuries complicated by contusion and compression of nerve structures. To eliminate direct pressure on brain tissue, reduce the severity of shock and prevent secondary lesions, stabilization of the vertebral segments, open or closed reposition, and decompression are carried out. Any deterioration in neurological functions requires urgent surgical correction; early intervention reduces the need for mechanical ventilation and shortens the length of hospital stay.

Experimental treatment

Current research is aimed at preventing secondary neurogenic damage, exploring new ways to restore neurons, and regenerate lost connections in the brain and spinal cord. For this purpose, the use of antioxidants, apoptosis blockers, and calpain inhibitors is being considered. The effect of naloxone and thyrotropin-releasing hormone is being studied. The use of stem cells and gene therapy is considered a promising direction.

Prognosis and prevention

Cases of severe neurogenic shock caused by spinal injuries or cerebral lesions with complete neurological deficit pose a clear threat to life. Delays in surgical correction worsen an already very serious prognosis. Even after hemodynamic stabilization of the patient, autonomic dysregulation persists for a long time, and there is a risk of secondary complications and decreased quality of life. Preventive measures come down to timely diagnosis of neurological pathology, early and complete treatment of systemic disorders.

Neurogenic (vasogenic) shock is a decrease in tissue perfusion due to loss of vascular-motor tone of the peripheral arterial network. The loss of vasoconstrictor impulses causes an increase in vascular volume and reduces venous return and cardiac output.

Etiological information

Neurogenic shock is predominantly the result of damage to the spinal tissue due to fractures of the cervical or upper thoracic spine, when there is a break in the sympathetic regulation of peripheral arterial-venous tone.
In some cases (for example, when it spreads to the spinal tissue), neurogenic shock may develop while maintaining the integrity of the vertebrae.
Penetrating injuries in the spinal cord can also become causative factors for such a pathological condition.
Sympathetic impulses to the heart, which typically increase heart rate and contractility, and impulses to the adrenal medulla, which are responsible for increasing the release of catecholamines, are interrupted by high spinal cord injury. In this case, there is an obstacle to the formation of the characteristic reflex tachycardia that occurs with relative hypovolemia as a result of an increase in the volume of the venous bed and loss of vascular motor tone.

Pathogenetic mechanism

In a mild degree, neurogenic shock proceeds relatively favorably. This condition is observed in shock status caused by functional reasons. In this case, compensatory mechanisms are activated, for which the trigger is a change in the activity of volume receptors, especially the left atrium. Ascending impulse flows stimulate the work of the sympathoadrenal system, this changes the vascular tone towards narrowing, which causes the restoration of the original circulatory state of the blood. In case of severe damage to nerve tissue due to disruption of afferent and efferent conduction of excitations or destruction of associative connections in high regulatory centers, central regulatory mechanisms begin to be blocked. Thus, typical irreversible transformations develop in the peripheral vascular bed, especially in the small-caliber section. Sludge of erythrocytes, thrombosis of capillaries and venules, increased vascular permeability, interstitial swelling, hypoxic state of tissues, and metabolic disorders occur. Everything described above also occurs with another type of shock, and this, in turn, causes multiple organ failure.

Symptomatic picture and diagnosis

The classic symptoms of the pathological process are:

decreased blood pressure;
bradycardia (absence of reflex tachycardia due to interruption of sympathetic impulses);
warming of the extremities (loss of peripheral vasoconstriction);
sensorimotor disorders that indicate spinal cord damage;
a characteristic x-ray picture of a violation of the integrity of the bone tissue of the spinal column.

However, identifying the presence of neurogenic shock can be extremely difficult, since patients with multiple injuries, including damage to the spinal canal, often have brain injury, which usually makes it difficult to identify the causative factor of motor and sensory disorders. In addition to this, combined injuries can lead to hypovolemia and blur the clinical manifestation.

During a physical examination of the victim, the skin is usually dry and warm, the victim’s consciousness is preserved, respiratory functioning is without any disturbances, and the cervical venous vessels are in a collapsed state. In some cases, it is enough to raise the two lower limbs slightly higher than the body of the patient, who is in a horizontal position, and all manifestations of vasomotor shock spontaneously disappear. This test is most effective for shock, which is caused by high anesthesia of the spinal cord.

In the subgroup of patients with spinal cord injury as a result of penetrating wounds, the majority with low blood pressure have hemorrhage (approximately 75%) rather than a neurogenic etiology, and only a portion of them (approximately 6-8%) have classic manifestations of vasomotor shock. A hypovolemic condition must be ruled out before a diagnosis of appropriate shock is made.

Therapeutic measures

After ensuring the patency of the respiratory tract and normalizing ventilation of the lungs, introducing fluid into the body and restoring intravasal volume, systemic blood pressure and perfusion processes often return to normal. The introduction of vasoconstrictor drugs improves the tone of peripheral vessels, reduces the capacity of the vasorus and increases venous return. However, this is only possible after the elimination of the hypovolemic state and appropriate diagnosis. Specific therapy is usually short-term, approximately one to two days.

The duration of pressor maintenance may be consistent with the overall prognosis of improved neurological function. Timely restoration of blood pressure and perfusion processes also helps to improve blood supply to the spinal tissue, prevent the progression of its ischemia and minimize its secondary damage. Restoration of normal hemodynamic processes should precede any surgical attempts to stabilize a spinal column fracture.

Neurogenic shock

Neurogenic shock
[[File: Spinal cord injury in the cervical spine. Closed complicated fracture-dislocation of the C4 vertebra. Contusion and compression of the spinal cord at the level of C4-C5 vertebrae. \|190px\|center\|]]
ICD-10	R 57.8. 57.8.
ICD-9	785
MeSH	D012769	D012769

Neurogenic shock

Definition

Neurogenic shock- a condition of the human body that develops as a result of damage to the spinal cord, during which the conduction of impulses of the sympathetic nervous system is disrupted, and the unlimited tone of the vagus nerve (lat. n.vagus) begins to dominate. The leading clinical signs of neurogenic shock in spinal cord injury are arterial hypotension and bradycardia. In terms of the frequency of injuries to the spinal cord, the cervical region is in the lead, then the level of the thoracolumbar junction of the spine, less often the thoracic region and even less often the level of the lumbar spine (damage to the cauda equina). Neurogenic shock must be differentiated from spinal shock, defined as areflexia below the level of spinal cord injury.

Pathogenesis of cardiovascular disorders

Neuroanatomy

Clinical picture

Differential diagnosis

Treatment

Treatment tactics in the emergency department

Attention! The information is intended for students and current professionals in the field of medicine, is not a guide to action and is presented for additional education.