Multiple organ failure is the simultaneous or sequential defeat of several systems with the initial predominance of symptoms of failure of one of them. The defining signs are cyanosis, shortness of breath, edema, anuria, hypotension, shock. The diagnosis is established on the basis of the clinical picture, laboratory and hardware examination data. Specific treatment: support of respiration and cardiac activity, stabilization of hemodynamics, elimination of pathogenetic factor (fight against infection, correction of metabolic disorders, restoration of CBV, normalization of hemostasis), artificial and natural detoxification.
J96 I52 K72 N17
Multiple organ failure (MOF) is a pathology that occurs mainly in patients of intensive care units. It was first described as an independent nosological unit in 1973, before that it was considered a combination of two or more unrelated disorders. The frequency of occurrence is about 5-10% of the total number of patients. Mortality in this group is approaching 60%. Patients who have malfunctions in the work of three organs are more likely to die. The condition develops 3-5 days after the successful restoration of cardiac activity, with severe combined injuries, poisoning, endotoxicosis. The development is based on the syndrome of a systemic inflammatory response.
Multiple organ failure occurs as a result of pathological changes occurring in the body after cardiac arrest and subsequent restoration of the heart. In addition, it can form against the background of severe polytrauma, infectious and toxic shock, sepsis, peritonitis. It develops more often if one of the organs involved in the process was previously affected by chronic pathology or changed as a result of exposure to a primary factor (lung contusion in an accident, decreased myocardial contractility in acute coronary syndrome). The number of these factors include:
- The effect of inflammatory mediators. In response to damage, vascular endothelial cells begin to synthesize biologically active substances: interleukins, cytokines, nitric oxide, interferons, tumoral necrotizing factor. Under the influence of these components, there is a change in the permeability of the vascular wall, the tone of the circulatory system, the work of macrophage immunity. In conditions of physiological disorders, inflammatory mediators have an excessive effect, lead to the development of edema, pronounced dilation or constriction of blood vessels, the appearance of an inflammatory reaction.
- Microcirculatory failures. With extensive injuries, blood sequestration occurs with the formation of hypovolemia. This causes a decrease in cardiac output, the formation of microthrombs, deterioration of perfusion in tissues and organs, relative ischemia. The reperfusion mechanism also plays a certain role in the development of MOF, in which changes occur associated with the restoration of adequate blood flow (oxygen, calcium, ion paradox).
- Infectious and septic effects. It is observed both with volumetric bacterial processes and with any other serious diseases. In the first case, sepsis is the result of flora entering the blood from the focus of inflammation. In the second case, microorganisms penetrate into the systemic bloodstream from the intestine, the permeability of the wall of which increases with exhaustion. Cytokine production is stimulated and a systemic inflammatory reaction develops.
- The phenomenon of “double blow”. It is caused by the therapeutic effect on the victim, leading to an aggravation of MOF. Active infusion of plasma-substituting solutions is the cause of reperfusion syndrome, a massive antibacterial effect aimed at combating sepsis increases the toxic load on the excretion systems. All this negatively affects the severity of the patient’s condition.
Multiple organ destruction has several mechanisms of development, the main of which is ischemic organ damage. Some of the cells die off, the rest go into anaerobic glycolysis mode. The main damage occurs when the blood flow is restored. During this period, a large number of free radicals are formed, causing peroxide oxidation of tissues. The second pathogenetic mechanism is intensive thrombosis at the initial stage of DIC syndrome. The resulting microemboles disrupt the patency of the capillary network, which increases ischemia.
Edema as a result of increased vascular permeability leads to the accumulation of fluid in the abdominal cavity, increased intraabdominal compression. There is a mechanical compression of the abdominal organs, the lifting of the diaphragm with limited mobility of the lungs. There is an increase in intra-thoracic pressure, a decrease in the working space of the heart. The outflow of blood from the brain is disrupted. The central nervous system is involved in the process, cerebral edema develops with the appearance of neurological symptoms.
MOF is divided into groups based on the results of the assessment of the activity of organs and systems, the general condition of the patient. For this purpose, the Apache II or D. Marshall scale, created in 1995 specifically for working with patients suffering from multiple organ failure, can be used. In practice, the method of A. L. Levit, presented in 2000, is more relevant. According to him, each of the systems can be in a compensated, subcompensated or decompensated state. Multiple organ failure is defined as severe with decompensation of two systems, as extremely severe – with significant changes in three organs. The assessment is carried out separately for each body.
- Compensation. The body functions with minor deviations from the norm, a complete failure of any system does not occur. The changes are progressing rapidly. In fact, the compensatory stage does not refer to MOF as such, but to its precursors. Correction of the condition at this stage allows to prevent severe ischemic tissue damage. The duration of the stage depends on the initial condition of the patient and can range from several hours to 3-5 days.
- Subcompensation. Moderate changes requiring medical correction. Patients at this stage often need the introduction of relatively small doses of inotropic agents, auxiliary respiratory support, a single intake of diuretics. In the absence of assistance, the duration of the subcompensation period reaches 1 day.
- Decompensation. Severe changes in the structure of organs, complete or partial violation of their function. There are signs of damage to several systems. The patient is in an extremely serious condition. Intensive therapy with the use of high-tech life support techniques is required. Ventilation, infusion of pressor amines, detoxification with the use of devices such as “artificial kidney” are shown.
The clinical picture depends on the presence of lesions of certain structures. Usually, signs of changes on the part of the respiratory system come to the fore. There is shortness of breath, diffuse cyanosis, inclusion of auxiliary muscles in the process of inhalation, sweating, psychomotor agitation. Patients who are able to move independently occupy a forced sitting position with their hands resting on the bed. Later, activity is replaced by inhibition, depression of consciousness.
Multiple organ failure with heart damage is manifested by chest pains, hemodynamic instability, accumulation of fluid in soft tissues due to increased plasma proliferation through the vascular wall. Pulmonary edema may occur, accompanied by the appearance of pinkish foam from the mouth. Compensatory tachycardia up to 180 beats / min is detected, later replaced by bradycardia with a decrease in heart rate to 40 and below. At the terminal stage, there is a decrease in sensitivity to inotropic agents and alpha-adrenomimetics.
In the renal-hepatic variety of the disease, the volume of diuresis is noticeably reduced. Then anuria occurs, requiring hemodialysis. Hypoglycemia is detected, which entails disturbances of consciousness. The patient develops ascites, dyspepsia, protein edema. The skin and mucous membranes turn yellow, hemorrhagic rash is possible. After a few hours or days, signs of hepatic encephalopathy are detected: the patient is not aware of his actions, does not understand where he is, what is happening to him.
Gastrointestinal tract lesions are characterized by signs of obstruction caused by mechanical compression of the intestine. Pain, bloating, asymmetry of the anterior abdominal wall, retention of stool and gases, vomiting are determined. There is no tolerance to feeding. It is possible to develop a stress ulcer and intestinal hemorrhage, which is manifested by a decrease in Hb levels, pallor of the patient, a drop in blood pressure, the occurrence or intensification of DIC syndrome with massive blood loss.
With successful cupping, multiple organ damage can result in the development of delayed diseases. In 5% of patients who have re-applied for help in a medical facility, chronic renal failure is diagnosed, approximately 2% of patients experience symptoms of coronary heart disease or have signs of CHF. Pulmonary changes are noted in 3% of cases. In the acute period, ventricular fibrillation is a complication against the background of toxic myocardial damage and tachycardia with a heart rate above 160-180/min. It is possible to damage the conductive system of the heart with the formation of AV blockade. Brain ischemia often leads to a decrease in mental abilities, encephalopathy, paresis, paralysis.
Diagnosis is carried out according to the results of clinical, laboratory and instrumental examination. An anesthesiologist-resuscitator should supervise patients, however, a doctor of any specialty, including an employee of the ambulance team, can conduct an initial examination and establish a preliminary diagnosis for referring a patient to a specialized department. Differential diagnosis is carried out with a combined pathology of several body systems, etiologically unrelated to the mechanisms of development of the disease in question. The full examination program includes:
- Physical examination. During the consultation, the specialist identifies the characteristic external signs of a lesion of a particular organ, determines the presence of subjective complaints. In most cases, symptoms of hemodynamic disorders, cardiac activity and respiration, metabolic changes are detected.
- Blood test. The analyses show a decrease in hemoglobin levels to 60-80 g / l, a drop in glucose to 2.5 mmol / l, an increase in AST, ALT more than twice from normal values, an increase in bilirubin content ≥ 30 mmol / liter. PaO2 is in the range of 64-50, PaCO2 – 56-90 mmHg, pH changes in the acidic side (≤ 7.3).
- Hardware inspection. The main method is constant monitoring of vital functions. Indicators are often within the following limits: SAP < 50 mm Hg (in the absence of medical support), heart rate ≥ 180 or ≤ 40 per minute. Central venous pressure ≥ 14 mm or negative. RR ≥ 5 or ≤ 50 (without ventilator and oxygen therapy). During the radiography of the lungs, darkening is visualized, when performing an abdominal ultrasound, the level of free fluid is revealed.
The therapy is aimed at restoring the CBV, normalizing the rheological properties of blood, supporting vital functions, and preventing delayed consequences. Multiple organ failure should be stopped at the compensation stage, this increases the likelihood of full recovery. The following therapeutic effects are applied to the patient:
All-winter measures: compliance with the strictest bed rest, round-the-clock monitoring with the use of an anesthesiological heart monitor. The indicators of blood pressure, heart rate, RR, saturation, and heart rate are subject to control. Every 4 hours, blood is taken for ABB, daily – for biochemistry and general analysis. To prevent trophic damage to the skin, full-fledged hygienic care is carried out, nutrition is prescribed in accordance with the existing disorders (gentle, liquid, parenteral).
Conservative treatment. Abundant infusions of crystalloid and colloidal solutions are shown. With hypotension, dopamine is injected. With a deficiency of coagulation factors and the presence of DIC syndrome, transfusion of freshly frozen plasma is necessary. Increased thrombosis requires taking acetylsalicylic acid, curantil, heparin. With severe symptoms, antimediatory therapy with ibuprofen, inhibitors of platelet activation factor is performed. Intravenous administration of steroid hormones and antibiotics is recommended.
Surgical treatment. Invasive procedures include extracorporeal detoxification (hemo- and peritoneal dialysis). Open intervention may be required in case of complete failure or necrosis of internal organs (liver, kidneys), as well as intestinal obstruction. Laparocentesis is performed to remove ascitic fluid.
Prognosis and prevention
Multiple organ failure has a favorable outcome at the early start of treatment. As the process progresses, irreversible changes accumulate in the body, increasing the risk of complications. The decompensated form of the disease has an unfavorable prognosis, in 60% of cases it leads to the death of the patient. Prevention consists in preventing MOF. It is necessary to stop the foci of infection, in case of volumetric injuries, to begin a massive infusion at the pre-hospital stage, to eliminate the existing hemodynamic and heart rhythm disorders in a timely manner. An important point is to control the diuresis of a patient being treated in the ICU. The difference between the consumed and excreted liquid should not exceed 100-200 ml per day.