Post-resuscitation disease is a specific condition of the body that occurs after successful resuscitation measures. It is caused by temporary total tissue ischemia and blood flow restoration syndrome. It is manifested by a marked increase in the concentration of blood enzymes, hypoperfusion, a decrease in CBV, the development of disseminated intravascular coagulation, multiple organ failure. It is diagnosed by the presence of appropriate symptoms and circulatory arrest in the recent past. Specific treatment includes hormones, cardiotonics, infusions of saline solutions and blood components, anti-ischemic and nootropic medications.
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For the first time, post-resuscitation disease (PRD) as an independent nosological unit was described by a Soviet scientist, a member of the AMN V. A. Negovsky in 1979. The works of other specialists have expanded and strengthened knowledge about pathology, thereby strengthening the position of resuscitation as a science in the medical world. According to statistical information, more than half of patients who have undergone cardiopulmonary death (CPD) die from acute circulatory insufficiency or changes in the brain caused by global ischemia. The survival rate after successful CPD measures, according to various sources, ranges from 29 to 40%. Post-resuscitation disease occurs in the first hours after the restoration of perfusion, lasts 7-10 days. The prognosis for life worsens in proportion to the time from cardiac arrest to the start of resuscitation.
Post-resuscitation disease develops under the influence of several pathogenetic factors affecting a patient who has undergone clinical death. A complex negative effect on an organism weakened by the disease leads to significant changes in the work of organs and enzymatic systems, which can cause the death of the patient. Among the most important etiofactors of the formation of PRD are:
- Total ischemia. Prolonged insufficient intake of O2 potentiates the death of some cells. First of all, brain damage occurs (post-resuscitation encephalopathy) as the structure most sensitive to hypoxia. There is vascular spasm, compensatory tachycardia, cardiac output decreases, which exacerbates oxygen starvation. Changes occur in the myocardial tissues, skeletal muscles. The processes of myolysis begin with the release of muscle breakdown products into the blood.
- Reperfusion syndrome. Under conditions of hypoxia, tissues enter the anaerobic glycolysis regime, cells are reconfigured to this way of obtaining energy. A sharp restoration of blood flow and the intake of a large amount of oxygen leads to excessive accumulation of its toxic forms, activation of the processes of apoptosis and cell necrosis.
- Internal combustion engine. It is detected in shock conditions, manifested by the formation of microthrombs in the vascular bed. The latter block the lumen of capillaries, worsen microcirculation in tissues, and cause the formation of multiple small ischemic foci. In the future, this, in combination with other factors, provokes multiple organ failure.
- Bleeding. They arise as a delayed result of DIC at a time when the capabilities of the hemostasis system are depleted, the concentration of coagulation factors decreases. The condition is characterized by an almost complete absence in the plasma of substances responsible for the formation of a blood clot. Accompanied by the development of hemorrhagic syndrome.
- Metabolic storm. After the restoration of blood flow in patients, massive changes in the mechanisms of homeostasis regulation are noted. Acidification of the internal environment occurs with a decrease in pH ≤ 7.34, the level of electrolytes, including potassium, calcium and others, decreases. With an active infusion of sodium bicarbonate at the CPD stage, iatrogenic alkalosis can be determined instead of acidosis. A decrease in CBV is detected due to the deposition of part of the blood in the liver, skeletal muscles, and spleen.
Pathogenesis is based on changes that occur as a result of circulatory arrest. The patient develops acute renal failure, secondary septic shock, respiratory failure and CVD, malfunctions of receptor structures. At the autopsy, dystrophic changes in the kidneys are determined, signs of bilateral multi-focal pneumonia are often present in the lungs. A large amount of myoglobin is also detected here. Hemorrhages of varying severity are found in the tissues. The brain may contain dead areas, which indicates the occurrence of an ischemic stroke. In cerebral death (decortication), irreversible changes in the trunk, cervical segments, and cerebral cortex are noted.
Post-resuscitation disease is systematized by stages, each of which corresponds to the time that has elapsed since the restoration of blood flow. There are 5 main stages of the progression of PRD. All of them are characterized by certain transformations in the patient’s condition. There are the following phases of the development of pathological changes:
- Proceeds for 6-8 hours from the time of resuscitation. There is a marked decrease in tissue perfusion (4-5 times less than normal). There are phenomena of circulatory hypoxia – a condition that occurs when there is insufficient pressure in the capillaries.
- It occurs by 10-12 hours of illness. There is a relative stabilization of body functions, a temporary improvement in the condition. There is a shortage of circulating blood volume, tissue blood flow is reduced by 2-3 times. Electrolyte losses increase, mainly K+. The stage has an important prognostic value, allows you to determine the further course and outcome of the pathological condition with a high degree of probability.
- Observed from the second day of the disease. The fibrinolytic activity of plasma slows down, mixed hypoxia is formed due to changes in the properties of hemoglobin and the development of respiratory distress syndrome. There are the first signs of microthrombosis of the capillary network of internal organs. Violations are of a functional nature, there are no irreversible processes.
- A turning point in the course of the disease. It comes by 3-4 days. It may be characterized by a general improvement in the condition or further progression of pathological changes. With an unfavorable outcome, the phenomena of catabolism increase, interstitial pulmonary edema occurs, hydrogenation of the brain. A generalized inflammatory response begins, signs of insufficiency of internal organs are detected.
- Manifests by 5-7 days. Volumetric septic processes are diagnosed: pneumonia, sepsis, internal abscesses. Antibacterial therapy is ineffective. The cause of infection is suppression of immunity due to prolonged hypoxia. Encephalopathy of toxic origin is maximally manifested, multiple organ failure is aggravated, metabolic products accumulate in the blood. The death of the patient occurs after 1-5 days. The cause of death is the defeat of several vital systems, infectious and toxic shock, sepsis.
There are many clinical signs of post-resuscitation disease that indicate negative changes. At the initial stage, the patient has symptoms of shock: a marbled skin tone, a sharp decrease in blood pressure up to undetectable values, compensatory tachycardia, pupil dilation. As a rule, the patient is in a deep coma. There is no consciousness, motor activity. Reflexes are sharply suppressed or completely turned off. Muscle tone is reduced.
In the future, changes in the heart rate are detected due to a lack of electrolytes and ischemic damage to the CCC. Conduction blockages, arrhythmias are possible, which manifests itself in the form of an irregular, fragmentary pulse. Blood pressure may remain reduced or return to normal. Hemodynamics is often supported by medical methods. The signs of cardiac and respiratory insufficiency are visually distinguishable – diffuse cyanosis and acrocyanosis, which persist even during artificial lung ventilation.
When examining a patient, a small petechial rash is sometimes found, which indicates the development of hemorrhagic syndrome. There may be signs of internal or external latent bleeding, including vomiting of “coffee grounds”, stools of the “melena” type, progressive hypotension, tachyarrhythmia, a decrease in Hb, Ht, pallor of the skin. In the presence of changes on the part of the liver, the mucous membranes and body coverings acquire a yellowish color. Kidney damage is characterized by a sharp decrease in diuresis or a complete absence of urine. With severe changes in the central nervous system, unconsciousness, coma persists.
Among the complications of PRD is brain death, in which somatic functions are preserved, but the central nervous system undergoes irreversible changes. Such patients go into a vegetative state with no hope of recovery. The diagnosis is confirmed by the results of electroencephalography. A serious consequence of stopping blood flow is multiple organ failure, in which two or more body systems fail. In most cases, the kidneys, hepatobiliary apparatus, lungs, heart, and brain are destroyed. Massive hemorrhages may appear, in which the death of the patient occurs from acute blood loss.
The diagnosis is established on the basis of clinical, laboratory and hardware studies of the work of the patient’s vital organs. The condition is determined by an anesthesiologist-resuscitator in tandem with specialists of another profile (neurologist, cardiologist, nephrologist, etc.), representatives of the laboratory and functional diagnostics service. Usually there are no diagnostic difficulties. Use methods such as:
- Physical examination. It allows you to identify the external signs of PRD, to identify obvious disorders associated with changes in heart rate, a decrease in blood pressure, deterioration of breathing in the lungs. Therapeutic measures begin according to the results of the primary medical opinion. Other methods of examination are used after the fact, in parallel with intensive therapy.
- Laboratory. In the patient’s blood, an increase in the concentration of certain enzymes (LDH, alkaline phosphatase, CK) is detected. There are changes in the electrolyte and gas composition, an increase in hematocrit of more than 36-48%. With the development of renal insufficiency, the level of urea and creatinine increases. The protein content decreases.
- Hardware methods. Evidence of brain death is an isoelectric line on the EEG. Heart damage leads to the appearance on the cardiograph film of signs of myocardial ischemia and arrhythmias of various types: extraordinary deformed ventricular complexes, unequal intervals “R-R”, small-wave or large-wave fibrillation, depression or elevation of the “ST” segment. When performing sonography, necrotic areas in the internal organs may be detected.
Post-resuscitation disease requires a number of medical procedures aimed at restoring vital functions and brain function. Of significant importance are general measures, which become especially important during the long-term stay of the patient in an unconscious state. Recovery measures include:
- General methods. Relevant for resuscitation patients of any profile. Careful care is required with daily washing and changing the position of the body every 2 hours. Areas of skin maceration are treated with camphor alcohol or specialized dermatoprotective agents. In the absence of AKI, a full-fledged protein diet, abundant drinking is indicated. Failure to comply with these requirements entails the development of pressure sores, deepening intoxication, increasing the load on the immune system, increasing the risk of sepsis.
- Drug therapy. It is aimed at protecting tissues from hypoxia, improving perfusion, stimulating the work of the heart, brain. Such groups of drugs as cardiotonics, pressor amines, antihypoxants, means that improve microcirculation, antispasmodics, nootropics are used. Mandatory infusion therapy using colloidal and crystalloid solutions is indicated.
- Operational methods. These include, conditionally, hemodialysis, which is necessary to remove toxic metabolic products. In case of renal insufficiency, plasmapheresis is performed to eliminate excessive volumes of water containing metabolic products. Full-fledged operations intended for the treatment of PRD have not been developed.
Prognosis and prevention
Post-resuscitation disease has an unfavorable prognosis for the patient’s life. During the first half of the year, about 80% of people who have undergone prolonged hypoxia die. Among patients who received help immediately after cardiac arrest, this indicator is significantly lower. The cause of death is neurological and heart diseases, chronic respiratory failure. Some of the survivors undergo posthypoxic encephalopathy, in which mental abilities deteriorate. Prevention consists in timely initiation of CPD, minimization of the period of absence of blood flow, full-fledged medical support at all stages of the recovery process, starting from its first minutes.