Post-resuscitation disease (PRD) – the state of the body after clinical death (circulatory arrest), followed by the restoration of the function of organs and systems.
The first who described in detail the condition of the body in the framework of postresuscitation pathology was the Russian scientist, academician of the Academy of Medical Sciences.
About 25% of all deaths are not associated with incurable diseases or senile or destructive changes in the brain. In Europe, about 700,000 are registered annually, and in the United States – 400,000 cases of sudden death.
As a result of resuscitation at the prehospital and hospital stages, in more than half of the cases, it is possible to restore spontaneous circulation. However, 50% of these patients subsequently die, mainly as a result of cardiac or cerebral damage.
The survival rate of patients (the number of survivors after resuscitation of patients who have been discharged from a medical institution) who have undergone circulatory arrest in a hospital setting ranges from 0 to 29% (14% on average), and community-acquired patients from 0 to 40%. The main factor influencing the level of survival is the length of the time interval from the moment of arrest of blood circulation to the onset of CPR. An important prognostic factor for the outcome of the CPR is the primary mechanism for circulatory arrest. At the age of less than 10 years, a higher survival rate than over 10 years; Survival rate does not differ in patients aged 10–70 years and decreases progressively in people older than 70 years.
In the etiology of postresuscitation disease lies the combination of total ischemia with reoxygenation and reperfusion. Re-oxygenation and reperfusion not only eliminate the effects of the primary pathological effects, but also cause a cascade of new pathological changes.
Among the survivors, only 15–20% have a quick recovery of an adequate level of consciousness, the rest go through postresuscitation disease. Patients with a PRB clinic are characterized by a very high mortality rate, reaching 80% during the first half of the post-resuscitation period. In 1/3 of lethal cases, cardiac causes, in 1/3 – dysfunction of various extracerebral organs and 1/3 – neurological (death in a remote period of PSD).
Clinic. Stages PWB:
Stage I(first 6–8 hours) is characterized by instability of the main functions of the body. Tissue perfusion decreases by a factor of 4–5, despite the stabilization of arterial pressure, the phenomena of circulatory hypoxia, lactic acidosis, the content of fibrinogen degradation products (FDP) and soluble fibrin monomer complexes (RCFM) increases.
Stage II(10–12 hours) – the period of temporary stabilization of the main functions of the body and the improvement of the condition of patients. Pronounced disorders of tissue perfusion, lactic acidosis persist, there is a further increase in the FDP level and RKFM significantly increases, fibrinolysis slows down – signs of hypercoagulation. This is the stage of “metabolic storms” with symptoms of severe hyperfermentemia.
Stage III(the end of the 1st – 2nd day) is characterized by a repeated deterioration of the condition of patients according to the dynamics of clinical and laboratory data. Hypoxemia, tachypnea, tachycardia, arterial hypertension develop, in young and middle-aged people there are signs of acute pulmonary injury syndrome or acute respiratory distress syndrome (SOLP / ARDS) with increasing blood shunting.
The signs of DIC are maximally pronounced: thrombinemia, hypercoagulation, an increase in the FDP level against the background of a progressive decrease in fibrinolysis, leading to the development of microthrombosis and blocking of microcirculation. There are lesions of the kidneys, lungs and liver, but all of them are still functional and are reversible with adequate treatment.
Stage IV(3rd – 4th day) is either a period of stabilization and subsequent improvement of the functions of the body with recovery without complications; or a period of further deterioration in patients with an increase in multiple organ failure (STR) due to the progression of the systemic inflammatory response syndrome (SIRS). It is characterized by hypercatabolism, development of interstitial edema of lung tissue and brain, deepening of hypoxia and hypercoagulation with the development of signs of multiorgan failure: bleeding from the gastrointestinal tract, psychosis with hallucinatory syndrome, secondary heart failure, pancreatitis and disorders of the liver.
Stage V(5–7 days or more) develops only with an unfavorable course of PRP: progression of inflammatory suppurative processes (pneumonia, often abscess, suppuration of wounds, peritonitis in operated patients, etc.), generalization of infection – the development of septic syndrome, despite early implementation adequate antibiotic therapy. At this stage, the lesion of parenchymal organs is already degenerative and destructive.
The most frequent variant of the course of PRB is postanoxic encephalopathy, which develops to varying degrees in all patients undergoing circulatory arrest.
Post-toxic (post-resuscitation) encephalopathy is a brain lesion capable of progressive development after anoxic short-term exposure. This is a combination of neurological and mental disorders observed at all stages of the post-toxic period, formed against the background of reperfusion of the brain after a prolonged arrest of blood circulation.
There are 3 types of recovery of neurological status in the post-toxic period:
- Recovery occurs after a short (3 hours) period of lack of consciousness and is characterized by rapid normalization of adequate mental activity within 24 hours after clinical death in the majority (70%) of patients.
- After overcoming the acute pathological condition, 50% of patients develop neurosis-like syndrome, short-term seizures, neurocirculatory dystonia, and dispersed small focal symptoms (prolapse).
- Delayed recovery of CNS functions. Impairment of consciousness (somnolance, stupor, coma of varying degrees) can last for many days and depends on the development of brain edema. It is in patients with type 3 recovery of CNS functions that pronounced neurological manifestations develop in the long-term period (2-3 months). The most frequent manifestation (in 63.6%) is a neurosis-like non-psychotic syndrome in the form of asthenia and irritable weakness. Of the mental disorders of a psychotic nature, intellectual-mental disorders are the most frequent (15.6%).
Pathophysiology of postanoxic encephalopathy
Damage to neurons in PRB is multifactorial in nature and develops both at the time of circulatory arrest, during CPR, and during the restoration of independent blood circulation:
- period of ischemia-anoxiaat the time of lack of blood circulation in the period of clinical death (no-flow);
- period of hypoperfusion-hypoxiawith artificial maintenance of blood circulation in the process of CPR (low-flow), since the level of cardiac output (SV) reaches only 25% of the initial;
- reperfusion period, consisting of successively developing phases: no-reflow, next, then the phase of hyperemia and subsequent global and multifocal hypoperfusion.
In this case, the vast majority of neuronal damage processes do not occur at the time of circulatory arrest or CPR, but during reperfusion.
Stages of cerebral perfusion after restoration of independent blood circulation in the post resuscitation period:
- The initial development of multifocal lack of reperfusion (no-reflow phenomenon).
- The transient global hyperemia stage develops at the 5–40th minute of spontaneous circulation. The mechanism of its development is associated with vasodilation of cerebral vessels by increasing the intracellular concentration of Na + and adenosine and reducing the intracellular pH and the level of Ca 2+. The duration of cerebral ischemia determines the duration of the stage of hyperemia, which in turn is heterogeneous in different regions of the brain.
- The stage of prolonged global and multifocal hypoperfusion develops from 2 to 12 hours post-resuscitation period. The rate of cerebral glucose metabolism is reduced to 50%, but global brain oxygen consumption returns to a normal (or higher) level. Vasospasm, edema, sludging of erythrocytes and excessive production of endothelin, decreases cerebral venous PO2 to a critical level (less than 20 mm).
A coma within 48 hours or more is a predictor of poor neurological outcome. If 72 hours after the blood circulation has stopped, the neurological deficit is ≤ 5 points on the Glasgow scale, in the absence of a motor reaction in response to painful stimulation or pupillary reflex, this is a predictor of the development of a persistent vegetative state in all patients.
Plasma concentration of neuron-specific enolase (NSE) > 22 µg / l (80% sensitivity and 100% specificity), which is determined during the I-st week after a circulatory arrest, is associated with the development of persistent coma.
Astroglial protein level S-100 > 0.7 µg / l in the first 24 hours of the post-resuscitation period is associated with a poor neurological outcome.
Modern principles of intensive care
Therapy of the post-resuscitation period is carried out according to the following principles: extracranial and intracranial measures.
1. Since the level of cerebral blood flow becomes dependent on the level of mean arterial pressure, it is recommended to ensure hypertension in the first 15–30 minutes after resuscitation (GARDEN 37 ° C).
4. Maintenance of normoglycemia (4.4–6.1 mmol / l). Hyperglycemia is associated with a poor neurological outcome.
5. Maintaining the hematocrit level within 30–35%. Conducting mild hemodilution, reducing blood viscosity, which significantly increases in the microvasculature due to ischemia.
6. Control of seizure activity by the introduction of benzodiazepines.
The modern concept of cerebral resuscitation is presented in the figure.
- Pharmacological methods.At the moment, in terms of evidence-based medicine, there are no effective and safe methods of pharmacological effects on the brain during the resuscitation period. It is advisable to use perftoran: reduces swelling of the brain, the severity of postresuscitation encephalopathy and increases the activity of the cerebral cortex and subcortical structures, contributing to the rapid exit from a comatose state.
- Physical methods. Hypothermia is the most promising method of neuroprotective protection of the brain.
The therapeutic effect of hypothermia is provided by the implementation of the following mechanisms:
- preservation of ATP pool and improvement of glucose utilization by brain tissue;
- inhibition of destructive enzymatic reactions;
- suppression of free radical reactions and inhibiting the accumulation of lipid peroxidation products;
- reduction of intracellular mobilization of Ca 2+;
- protection of lipoprotein plasticity of cytoplasmic membranes;
- decrease in consumption of O2v regions of the brain with low blood flow;
- reduction of intracellular lactate acidosis;
- inhibition of biosynthesis and production of excitotoxic neurotransmitters;
- reduction of neutrophil migration in ischemic zones;
- reducing the risk of cytotoxic and vasogenic edema of the brain.
It was found that a decrease in body temperature of 1 ° C on average reduces the rate of cerebral metabolism by 6-7%.
According to the current recommendations of the European Resuscitation Council of 2005, unconscious patients who underwent circulatory arrest, it is necessary to ensure that the body is hypothermic to 32–34 ° C for 12–24 hours.
Rehabilitation in the clinic “Seasons”
The duration of a comatose period can be from several weeks to 12-16 months or more. There are several options for getting out of coma. The most favorable is the situation in which there is a restoration of personal characteristics with the presence of productive contact. The completion of intensive therapy and the connection of modern methods of physical rehabilitation allows one to overcome the neurological deficit and gradually restore consciousness and the patient’s physical activity, in some cases sufficient for elementary self-care and a gradual return to the social environment. The degree of recovery of neurological functions may be different.
It is also possible to exit from the coma into the so-called state of “small consciousness”, which is also called the vegetative state. This is a collective term that combines a number of neurological syndromes (akinetic mutism, appalichesky syndrome, “electro-functional silence” and
Treatment of patients with a persistent or chronic vegetative state consists in carrying out a set of rehabilitation measures, preventing and treating complications, and caring.
Neurorehabilitation consists of polymodal stimulation aimed at activating sensitive, motorized analyzers, restoring speech production and
Equilibrium – the ability to maintain the orientation of the body and its parts with respect to the surrounding space. It depends on the continuous flow of visual, vestibular and somatosensory (proprioceptive) impulses and its integration at the level of the brainstem and cerebellum. Equilibrium disorders result from damage to the central or peripheral vestibular structures, cerebellum, or sensory pathways that provide proprioception. Such disorders usually manifest at least one of two clinical symptoms: dizziness or ataxia …
Increased systolic blood pressure over 140
Cerebral Palsy (CP)
The main methods of physical rehabilitation are built in our clinic in such a way that they have an impact on controlling the movement of the body as a whole and its components – straightening the body against gravity and simple targeted movements, which, by training using special techniques, form friendly movements – dynamic stereotypes, – allowing to perform the function of movement and self-service …