Neurogenic shock is an acute circulatory failure that occurs due to a sudden loss of sympathetic regulation of vascular tone when the nervous system is damaged. The most characteristic signs of pathology are hypotension, relative bradycardia, hyperemia and hyperthermia of the skin of the extremities. Severe shock is accompanied by respiratory and consciousness disorders, neurological disorders. Diagnosis is carried out according to clinical examination, blood tests, hemodynamic monitoring, CT and MRI of the affected areas. Shock relief is carried out by means of intensive therapy, an important place is given to early surgical correction.
ICD 10
R57.8 Other types of shock
General information
The epidemiology of neurogenic shock is difficult to assess, since it is based on limited statistical data and depends on the clinical criteria used. Compared with other types of circulatory insufficiency, this type of shock is considered the most rare. With injuries of the cervical spine, an emergency condition is registered in 19-29% of patients, exceeding the indicators for the thoracic and lumbar sections (7 and 3%, respectively). The frequency of shock in intracranial disorders remains unknown. The gender-age structure usually corresponds to that of spinal injuries, half of all cases occur at the age of 16 to 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 usually occur when the craniospinal tract is affected above the Th6 level, including the brain stem. The primary process is associated with direct destruction of nerve pathways, the secondary process is caused by vascular and electrolyte shifts, edema. Shock reactions are caused by two groups of reasons:
- Organic. Severe spinal and spinal tract injuries (automobile, sports, firearms) are a common cause of the neurogenic process. Cerebral disorders include traumatic brain injuries, strokes, subarachnoid hemorrhages. Among other factors, pronounced cerebrospinal hypertension, transverse myelitis, Guillain-Barre syndrome and other peripheral neuropathies were noted.
- Functional. In some cases, circulatory disorders are caused by functional disorders. Shock can occur against the background of deep anesthesia, epidural anesthesia, intense pain syndrome. The role of toxic damage to the autonomic system, the influence of certain medications, and severe psychoemotional trauma is noted. Hypothalamic-pituitary-adrenal insufficiency is recognized as a separate cause.
Specific risk factors are described for the pediatric contingent. Circulatory insufficiency is the result of birth trauma, child abuse. Shock-related fractures and dislocations of the upper cervical segments of the spine are more common in patients with trisomy 21 (Down syndrome), skeletal dysplasia, 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 the capacity of the vascular bed, a decrease in venous return and cardiac output. The daily rhythm of blood pressure fluctuations is lost, hypotension and reflex bradycardia occur, hyperreactivity of peripheral adrenoreceptors joins.
Cardiogenic mechanisms are caused by an increased release of catecholamines associated with dysfunction of the posterior hypothalamus against the background of intracranial pathology. Increased concentrations of hormones trigger direct myocardial damage in the form of selective necrosis. Cardiac dysfunction is manifested by a decrease in ejection, an increase in pre- and post-loading, 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 in traumatic lesions of central structures is accompanied by secondary hypocorticism. In stressful situations, this can lead to a decrease in systemic vascular resistance, a drop in heart contractility, hypovolemic or hyperdynamic shock. Changes in the concentration of endogenous vasopressin were noted, but its role in this situation still needs to be studied.
Classification
According to the mechanism of development, neurogenic shock is a kind of distributive (distributive), in which relative hypovolemia is noted. Taking into account the prevailing processes, it proceeds in three pathogenetic variants: vasodilatory, cardiogenic, neuroendocrine. The generally accepted clinical classification of shock includes several degrees of severity:
- I (compensated). Perfusion of vital organs is preserved. The general condition is of moderate severity, consciousness is clear, the patient is slightly inhibited. Systolic blood pressure exceeds 100 mm Hg.
- II (subcompensated). There is a gradual depletion of compensatory capabilities. The patient’s condition is severe, there is a slowness, the skin is pale. Blood pressure decreases to 90-80 mm Hg, breathing becomes more frequent, becomes shallow.
- III (decompensated). Compensatory mechanisms cannot maintain adequate perfusion. The condition is extremely severe, characterized by adynamia, the level of consciousness is sopor. The skin is pale, acrocyanosis is present. The blood pressure level drops below 70 mm Hg, the pulse is threadlike, determined only on the main arteries. Anuria develops.
- IV (irreversible). The damage is irreversible, and multiple organ failure is typical. The patient is in terminal condition, the skin is grayish in color with a marble pattern, stagnant spots. Blood pressure is below 50 mm Hg or is not detected, pulse and breathing are barely noticeable. Pupils dilate, reflexes and reaction to pain stimuli are absent.
Neurogenic shock symptoms
The clinical picture and severity of pathology are largely determined by the localization of the primary defect. Circulatory insufficiency may occur against the background of a complete (with impaired sensory-motor function) or partial neurological deficit. The focus above the Th1 segment disrupts the sympathetic regulation of many internal organs. Damage below C5 is accompanied by diaphragmatic breathing, and above C3 – its stopping. With a decrease in the level of damage, the severity of violations decreases.
The hemodynamic profile of the vasodilator variant of neurogenic shock is considered as “warm and dry”: peripheral vasodilation is complemented by hypotension with increased pulse pressure, relative bradycardia, redness, 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 often occurs when moving from a lying position to an upright one. Priapism is detected in men.
The cardiogenic form of shock is manifested by hypotension, palpitations, bradycardia in such a situation is extremely rare. Peripheral vessels narrow, systemic venous resistance increases, the skin becomes cold and moist. Myocardial dysfunction is accompanied by a decrease in cardiac output, a drop in shock volume, dizziness, pallor. Central venous pressure is normal or elevated.
Arterial hypotension in the neuroendocrine variant of shock does not respond well to vasopressor infusions. Hemodynamic signs of vascular insufficiency are reduced CVD and peripheral resistance, shock volume and cardiac output. A distinctive feature can be considered low baseline cortisol levels. A corticotropin stimulation test often leads to an increase in its concentration, but this does not exclude the presence of shock.
Neurogenic disorders can persist for 1-6 weeks. Vegetative dysreflexia, low blood pressure at rest and orthostatic hypotension are not uncommon during the chronic phase – after the successful resolution of shock reactions. Vegetative instability is often manifested by episodic hypertension, hyperemia of the skin, sweating and tachycardia.
Complications
Neurogenic hemodynamic disorders combined with other injuries, in the absence of timely recognition and relief, are characterized by a life-threatening course with the development of multiple organ failure, fatal outcome. The loss of central control over the function of the respiratory muscles leads to a deepening of respiratory disorders, cardiogenic variants of pathology are accompanied by pulmonary edema, takotsubo cardiomyopathy.
Sharp and prolonged hypotension can provoke secondary ischemic damage to the brain and spinal cord, which further exacerbates neurological deficits. Microcirculatory disorders mediated by hemodynamic instability potentiate thrombotic complications that increase the risk of pulmonary embolism, acute coronary syndrome, and cerebral circulatory insufficiency.
Diagnostics
Taking into account the potential danger of 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 insufficiency, especially in the presence of pronounced progressive refractory hypotension. The following methods of laboratory and instrumental control help in this:
- Blood tests. A detailed picture of peripheral blood, coagulogram data, and plasma electrolyte composition are obtained. Determine the concentration of cortisol, markers of myocardial necrosis (troponins, myoglobin, creatine phosphokinase). It is extremely important to evaluate arterial and venous blood gases, the results of which reveal hypoxemia, hypercapnia, acidosis.
- Hemodynamic monitoring. Hemodynamic parameters can be examined by non-invasive or invasive methods. The first include blood pressure measurement, pulse oximetry, ECG, plethysmography. Cardiac output is measured using echocardiography with Dopplerography, methods based on thermodilution. Tissue perfusion can be judged by the amount of diuresis. Invasive monitoring is performed through a central venous or arterial catheter.
- Tomographic methods. They are necessary to establish the causes of hemodynamic instability, to 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 careful supervision.
Diagnostic lumbar puncture with cerebrospinal fluid analysis, neurophysiological studies (encephalography, neuromyography) are of no small importance. A neurologist differentiates vascular insufficiency with hypovolemic, hemorrhagic, obstructive shocks. It is necessary to exclude the presence of congestive heart failure, sepsis, massive PE. Patients need an emergency consultation with a traumatologist and a neurosurgeon.
Treatment
Conservative therapy
The urgent condition requires timely relief according to the principles of resuscitation and intensive care. In case of injuries to the cervical spine, immobilization with a collar is performed to prevent further damage to the spinal cord. In parallel, measures aimed at stabilizing systemic hemodynamics and tissue perfusion are being implemented:
- Infusion support. To restore vital functions and prevent secondary ischemic processes, the main efforts are directed to the relief of hypotension. First–line therapy is infusion of saline solutions for rapid recovery of BCC. With concomitant hemorrhagic shock, crystalloids are combined with colloidal solutions to retain fluid in the vascular bed.
- Inotropes and vasopressors. If liquid resuscitation did not lead to the elimination of the symptoms of shock, second–line drugs are used – inotropic (dobutamine), vasopressor agents (dopamine, adrenaline). To improve spinal cord perfusion, in the first week after spinal injury, it is recommended to maintain average blood pressure at the level of 85-90 mm Hg.
- Holinoblockers. Treatment of severe hemodynamically significant bradycardia is carried out with cholinolytics – atropine, glycopyrrolate. An alternative can be adrenomimetics (isadrin), methylxanthines (theophylline, aminophylline). The latter are indicated for cases of resistant bradycardia.
The presence of neurological deficiency requires decongestant therapy with corticosteroids, but prolonged 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 disorders, the patient is transferred to a ventilator. In the long-term period, in order to restore functional capabilities, comprehensive rehabilitation is necessary.
Surgical treatment
Surgery may be required for traumatic injuries complicated by bruising and compression of nerve structures. To eliminate direct pressure on brain tissues, reduce the severity of shock and prevent secondary lesions, spinal segments are stabilized, open or closed reposition, decompression is performed. Any deterioration of neurological functions requires urgent surgical correction, early intervention reduces the need for a ventilator, reduces the duration of hospital stay.
Experimental treatment
Current research is aimed at preventing secondary neurogenic damage, exploring new ways to restore neurons, 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, thyrotropin-releasing hormone is being investigated. 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 injuries with complete neurological deficiency pose a clear threat to life. Delays in operational correction worsen an already very serious prognosis. Even after hemodynamic stabilization of the patient, vegetative dysregulation persists for a long time, there is a risk of secondary complications and a decrease in the quality of life. Preventive measures are reduced to timely diagnosis of neurological pathology, early and full-fledged therapy of systemic disorders.