Postresuscitation encephalopathy is a component of post-resuscitation disease, which is manifested by a number of neurological and psychological disorders. It is characterized by damage to the tissues of the central nervous system. The clinical picture is diverse, the main symptoms include hyperkinesis, visual disturbances, frontal ataxia, amenative delirious psychoses and convulsive seizures. Pathology is diagnosed on the basis of clinical data and the results of imaging examination (CT and MRI). Specific treatment: barbiturates, drugs that improve microcirculation, calcium channel blockers, antioxidants, cell membrane stabilizers.
G93.1 Anoxic brain lesion, not classified elsewhere
Today, postresuscitation encephalopathy is considered a common phenomenon that occurs in every case of a temporary stop or a significant decrease in perfusion in the brain. The cause of the condition is the high sensitivity of neurons to hypoxia. The degree of severity of clinical manifestations varies from their complete absence (the brain has great adaptive capabilities) to a detailed picture of damage to a particular area of nervous tissue.
Pathology is observed not only after clinical death, but also in people who have suffered a terminal condition of another origin: trauma, asphyxia, severe blood loss, a prolonged episode of hypotension. It is based on oxygen starvation and violation of all metabolic processes. A certain role in the formation of negative transformations is played by a metabolic storm, including the volume release of “shock” hormones. Changes occur at the molecular, cellular, tissue, organ, zonal and systemic levels of the organization, can be reversible and irreversible. The causes of GM damage include:
- Complete stop of blood circulation. Occurs at the moment of cardiac arrest (asystole) or against the background of ventricular fibrillation, when the myocardial fibers contract separately, ineffectively. Similar conditions develop in acute coronary pathology, injuries, intoxication of endogenous or exogenous origin, senile degradation of the organs of the blood supply system, mechanical asphyxia, etc.
- Reduced perfusion. A sharp and prolonged weakening of blood flow in the control structures is the result of vascular pathology (collapse), shock states, loss of 50-60% of BCC due to hemorrhage from large arteries. When the pulmonary trunk or hollow veins are damaged, the volume of extravasate rarely exceeds 300-400 ml, but blood pressure decreases almost instantly, which leads to cerebral oxygen starvation.
- Ischemic stroke. It can occur both independently and against the background of resuscitation measures. In the latter case, the obstruction of the feeding artery is a consequence of increased thrombosis at the first stage of the DIC syndrome. It is characterized by limited necrosis of brain tissues, focal symptoms, indicating a violation of the function of a certain area of the central nervous system.
Hypoxia leads to the formation of regional ischemia. Tissues experience oxygen starvation, suffer from a lack of nutrients. Energy resources are quickly exhausted, lactate, lysosomal enzymes and acyl coenzymes accumulate. Electrolytes and water are redistributed between cells and the intercellular space. Free radicals are intensively formed. At the organ level, this is manifested by swelling and edema of cerebral structures, an acute violation of their function.
In the postresuscitation period, the processes of reoxygenation and recycling are observed. The work of nervous structures is restored unevenly. Nitrogen monoxide, new free radical compounds, is formed in the intercellular fluid and cells. There is a repeated violation of the distribution of calcium ions. The nucleic and protein metabolism changes. In addition to the above, the work of the central nervous system is negatively affected by endogenous intoxication with cytotoxic products and metabolic acidosis. All this provokes disruptions in the work of the receptor apparatus, violations of the synthesis and functionality of neurotransmitters, disconnection of connections between neurons.
Postresuscitation encephalopathy can be separated using several principles. A classification is known by the time that has elapsed since the development of the hypoxia episode (early stage, period of acute manifestations, recovery period), prevailing syndrome (cerebellar, stem, neurasthenic, intellectual-mnestic, apallic). The most common is systematization based on the degree of recovery of the central nervous system:
- Complete. In turn, it is divided into fast and delayed. In the first case, the work of the central NS returns to normal within a day from the moment the pathology is stopped, in the second it takes 2-3 days. The final normalization of neurological parameters and psyche occurs within a few months. Further, postresuscitation encephalopathy disappears completely without residual phenomena.
- With a minor defect. The work of the central nervous system is restored to a level that allows self-care and minimal labor activity. The patient does not need to stay in a neuropsychiatric hospital, can live independently. There are residual disorders affecting physical abilities and quality of life (decreased intellectual development, myasthenia gravis, moderate coordination disorders).
- Partial. Vital functions are restored, but a person cannot take care of himself, work productively, adapt to living in society. The patient needs constant care and supervision of medical personnel. Such conditions include decortication, apallic syndrome, significant changes in the musculoskeletal system and thinking abilities.
- Interrupted. Rapid recovery with subsequent deterioration, resumption of neurological and mental disorders. It often ends with permanent disability of the patient or his death. Regression may occur after a few weeks or months have passed since discharge. The maximum registered term is 2 years. The nature of such phenomena remains unexplored. Experts suggest that the role of the provoking factor is played by increased psychological stress.
- Temporary partial. After resuscitation, the patient’s condition improves somewhat, but there is no recovery of consciousness. The existing disorders lead to human death or brain death (vegetative state), when the mechanisms that support the life of the body continue to function, but the cerebral cortex dies. The prognosis is unfavorable. The fatal outcome occurs after 1-3 months from congestive pneumonia, bedsores, infection.
At the exit from the terminal state, the patient is in a deep coma. Later, there is a restoration of the functions for which stem formations are responsible. The patient begins to breathe independently. At first, there is shortness of breath, bradypnea, individual spastic breaths. On average, after 5-6 hours, respiratory activity levels out. There is a reaction of pupils to light, spinal reflexes, cough reflex. Consciousness is restored by gradually reducing the depth of the coma, first to moderate, later to a soporotic state.
After the restoration of consciousness, pronounced psychological defects are revealed: psychomotor and speech arousal, hallucinations, psychoses. It is possible to develop large convulsive seizures, epileptiform syndrome. Visual, auditory and tactile perception is impaired, apraxia occurs. Coordination of movements is changed, weakened. Subsequently, most of these phenomena disappear. Individual signs may persist for a long time or for life.
Evidence of emotional lability (mood swings), muscular asthenia (weakness), apathetic-abusive syndrome (emotional-volitional impoverishment) is found the longest in the patient. Often patients complain of headaches, dizziness, jumps in blood pressure, periodic heaviness behind the sternum, shortness of breath. These phenomena are exacerbated by psychological and emotional overstrain. To one degree or another, permanent residual changes are present in 70% of patients. 20-25% have disorders of the musculoskeletal system (paralysis, paresis).
The main delayed complication of postresuscitation encephalopathy is the regression of convalescence and the return of the disease clinic. It most often occurs on 2-3 or 10 days, but it can develop at 3-4 weeks and later. Presumably occurs as a result of increased stress on not fully recovered nerve tissue. Leads to persistent neuropsychiatric disability. In some cases, only motor functions are affected, mental abilities do not suffer. Regression during the first weeks is registered in 4% of patients, after 4-24 months — in 0.3%.
In the initial hours from the restoration of blood flow, severe pulmonary edema may occur, accompanied by a sharp increase in intracranial pressure. At the same time, a deep coma persists, swelling of the nipples of the optic nerves, anisocoria, nystagmus, hemodynamic instability, tachycardia, followed by bradycardia, is detected. When the thermoregulation center is involved in the process, hyperthermia up to 39-40 ° C is detected, which is not amenable to drug correction. In the absence of treatment, the outcome is the death of the patient.
Postresuscitation encephalopathy is diagnosed by an anesthesiologist-resuscitator. A neurologist or neurosurgeon may be invited to clarify the depth and severity of the lesion. It is necessary to differentiate the condition with hemorrhagic stroke, brain injury received before hospitalization or during resuscitation, cerebral edema. If the symptoms of PE have arisen after discharge from the hospital, a neurologist is engaged in the examination, who, if necessary, directs the patient to re-hospitalization. The following techniques are used to make a diagnosis:
- Physical. There is one or another characteristic clinical symptoms, signs of a decrease in muscle tone or convulsive readiness. Seizures resembling epilepsy are recorded. The picture varies very widely, so the presence of external symptoms alone cannot serve as a basis for making a final diagnosis.
- Hardware. The main methods are computed tomography, electroencephalography and transcranial Dopplerography. CT brain shows signs of hydration or edema, the presence of foci of organic damage. With the help of EEG, the dynamics of intracerebral impulses are determined – usually postresuscitation encephalopathy leads to its weakening. TD allows you to assess the degree of blood filling of the brain and the work of the vascular apparatus. A more informative alternative to the study is isotopic angiography.
- Laboratory. The results of laboratory blood tests reveal a decrease in the hydrogen number of less than 7.3, a violation of the balance of electrolytes. In most cases, there is an increase in potassium concentration, a drop in calcium content. Dissolved gases may be normal if more than a day has passed since the perfusion was stopped. Prior to this, there is an increased CO2 content, an insufficient percentage of oxygen.
Postresuscitation encephalopathy requires step-by-step treatment. In the acute stage, external respiratory support with a ventilator is indicated, the introduction of means to ensure adequate blood flow: pressor amines to stabilize hemodynamics, vasodilators to eliminate the existing cerebral artery spasm. The patient’s head should be at the same level with the body, the leg end is raised. The administration of medications that reduce the energy needs of the brain is shown: sodium thiopental, diazepam. After blood pressure is restored, calcium channel blockers, antioxidants, glucocorticoids are used as stabilizers of cell membranes, hepatoprotectors.
From the 3rd day, a course of nootropic drugs that improve metabolic processes in the nervous tissue begins. The therapeutic regimen includes piracetam and its analogues. Treatment is carried out for 1-1.5 years in courses of 1-2 months. If convulsive seizures persist, the patient should receive antiepileptic drugs. Symptomatic treatment is carried out, selected taking into account residual changes. In case of mental disorders, sedatives, anti-anxiety and sleeping pills are prescribed. A psychiatrist’s consultation is required. Sanatorium-resort recovery is allowed no earlier than 2 months after leaving the critical condition.
Prognosis and prevention
The prognosis of depends on the severity and duration of the pathology. Long-term circulatory arrest causes neurological insufficiency even in cases when resuscitation measures were started on time. A short-term decrease in perfusion without complete cessation of blood flow has a favorable development for the patient. The total mortality rate for 2 years is about 40%. The main proportion of the dead is subjected to severe long-term hypoxic damage.
Prevention consists in constant monitoring of the condition of unstable patients. If there are prerequisites for cardiac arrest, it is necessary to correct the condition in a short time. If resuscitation is still required, from the moment the CCC is resumed, thrombosis is prevented, measures are taken to ensure normal blood supply to the nervous system. Long-term ventilation in the mode of slight hypocapnia is recommended. In clinics equipped with pressure chambers, patients undergo several hyperbaric oxygenation procedures.