Multiple organ failure (MODS) is the most common cause of death in intensive care units. It is defined as the potentially reversible failure of two or more organs or systems as a result of severe physiological disturbance requiring intervention to maintain homeostasis. What are the causes and symptoms of multi-organ failure? How is MODS treated?
Multiple Organ Dysfunction Syndrome(MODS - Multiple Organ Dysfunction Syndrome) can be primary or secondary. Primary multi-organ failure develops immediately after the action of the damaging factor, while secondary multi-organ failure is the result of the progression of an uncontrolled, generalized inflammatory reaction.
Multiple organ failure - causes
Sepsis is the most common cause of multi-organ failure, accounting for up to 90 percent of MODS cases. It is not known why some patients with sepsis or SIRS (Systemic Inflamatory Response Syndrome) develop MODS. It is assumed that certain genetic predispositions may play an important role in the expression of inflammatory mediators that lead to disruptions in the intercellular communication pathways.
The consequence of this, with a concomitant massive inflammatory response in SIRS or sepsis, is the development of MODS. There are many pathophysiological changes in the course of MODS.
Activated neutrophils, through specific adhesion molecules on their surface, are attached to the vascular endothelium. When this occurs, the contents of the neutrophil cytoplasmic granules are released and the endothelium is damaged. As a result, it becomes permeable, which results in the penetration of leukocytes, macrophages and lymphocytes from blood vessels into the interstitial space, causing organ damage.
At the same time, prothrombotic factors (e.g. tissue factor) activate the complement and clotting systems, which results in the formation of microclots. In addition, small vessel thrombosis develops as an expression of inhibition of fibrinolysis, which results from a reduced concentration of protein C, antithrombin III and an inhibitor of the tissue factor pathway.
The result of low blood pressure and low cardiac output isOrgan hypoperfusion and tissue hypoxia also lead to progressive organ damage. An additional factor triggering the cascade of the inflammatory process is decreased intestinal perfusion with subsequent damage to the intestinal mucosa and the displacement of bacteria colonizing the gastrointestinal tract into the visceral circulation.
Patients with MODS, at the time of diagnosis, usually have a dysfunction of 2-3 systems, with the dominant symptoms being hypoxia, shock and oliguria.
Multiple organ failure - clinical picture and treatment
The most common dominant symptom of multiple organ failure is primary lung injury followed by respiratory failure. The immediate causes are:
- pneumonia
- aspiration of gastric contents
- inhalation of toxins or smoke
- chest injury
- indirect causes include:
- sepsa
- extracorporeal circulation
- pancreatitis
- injuries located outside the chest or increased respiratory effort and damage to the diaphragm.
To minimize the risk of barotrauma, volutrauma and biotrauma, tidal volumes of no more than 6 ml / kg body weight are used in mechanically ventilated patients. and an inspiratory pressure not exceeding 30 cm H2O.
In treatment, it is important to start resuscitation and circulation at the right time.
Cardiovascular dysfunction causes an impairment of the transport and delivery of oxygen to tissues, resulting in damage to other organs. It results from generalized peripheral vasodilation associated with the local release of endothelial nitric oxide and a reduction in cardiac output and ventricular filling. The consequence of inadequate oxygen supply and tissue hypoxia is increasing metabolic acidosis and an increase in blood lactate concentration.
Decreased cardiac output may be a major marker of disease progression and, together with diastolic failure, is associated with a poorer prognosis. May be accompanied by oliguria and confusion. Patients often develop tachycardia in response to inflammatory mediators and increased sympathetic nervous system activity. Increased capillary permeability causes peripheral edema and hypovolemia, while in the lungs, due to increased capillary permeability, gas exchange is impaired.
Venous blood saturation and lactate measurements are routinely performed to determine and equalize the oxygen debt. It is of particular importance in the first 6 hours of septic shockthe use of inotropic positive drugs and fluid resuscitation, which significantly reduces organ failure and mortality.
Acute renal failure is a relatively common component of multi-organ failure with a multifactorial etiology. It is an independent risk factor, increasing the mortality rate to 45-70% with the coexistence of the septic process. Significant increases in mortality are seen when renal failure is combined with respiratory failure.
The dysfunction of the digestive system in patients with MODS leads to the occurrence of diarrhea in patients due to developing food intolerance. It results from impaired regional blood flow, gastrointestinal motility and abnormalities of its bacterial microflora.
In order to reduce the risk of bleeding from the upper gastrointestinal tract, stress ulcer prophylaxis, early diagnosis and treatment of infections as well as improved resuscitation procedures are used. It is also recommended to use parenteral nutrition. In the presence of slow peristalsis, prokinetic drugs are used.
Acute liver failure is associated with cholestasis and increased blood bilirubin levels. Additionally, it is possible to observe an increase in transaminases, protein C, α1-antitrypsin and a decreased level of albumin. The most common symptoms of the nervous system are disturbances of consciousness resulting from hypoxia and hypotension. In addition, the following may appear:
- encephalopathy
- metabolic disorders
- brain swelling
- decreased brain perfusion and brain microcirculation.
Polyneuropathy and myopathy as well as concomitant peripheral demyelination and axonal damage are not uncommon. It should be remembered that coma due to encephalopathy correlates with increased mortality. In the case of lesions in the blood, leukocytosis is the most common pathology. It is also possible to have mild anemia associated with bone marrow suppression and ischemia. Moreover, thrombocytopenia is one of the markers of multi-organ failure. It results from intravascular consumption and decreased platelet production associated with bone marrow suppression and can also be induced by heparin.
Disseminated intravascular coagulation (DIC) is very common in patients with multiple organ failure, characterized by a prolonged blood clotting time, thrombocytopenia, and low levels of fibrinogen and protein C, resulting in bleeding and anemia. This leads to hypoxiatissue and organ damage. In the course of DIC, prophylaxis of deep vein thrombosis is recommended.
Immune system dysfunction is manifested by impaired delayed hypersensitivity reactions, decreased production of antibodies, and abnormal lymphocyte responses. This can lead to infection with virulent microorganisms.
Early treatment with targeted antibiotics is essential to reduce mortality in acute sepsis. Also, selective decontamination of the gastrointestinal tract with non-absorbing antibiotics reduces the colonization of the upper gastrointestinal tract and reduces the risk of pneumonia associated with mechanical ventilation. Multiorgan failure negatively affects 4 major neuroendocrine axes:- first, disturbance of the hypothalamic-thyroid axis leads to the low T3 syndrome, and decreased thyroxine secretion correlates with increased mortality
- secondly, there is a relative vasopressin deficiency in septic shock
- third, in the case of the glucose-insulin axis, hypoglycaemia is often associated with relative insulin resistance due to the secretion of pro-inflammatory cytokines and hyperglycaemic hormones; strict glycemic control reduces multi-organ failure
- fourthly, cytokines affect the hypothalamic-pituitary-adrenal axis, which leads to an increase in the concentration of cortisol in the blood plasma, however, it should be remembered that the level of cortisol may be inadequate, due to the presence of adrenal insufficiency, the use of low doses of glucocorticosteroids is recommended only in septic shock unresponsive to the administration of vasopressors
To sum up, the essence of treating multi-organ failure is a therapy that supports every failing organ. In order to establish an adequate treatment in the shortest possible time period, the patient's clinical condition is monitored regularly and individual organs are monitored either invasively or non-invasively. Proper diagnosis enables appropriate causal treatment, appropriate care and support for damaged organs in the intensive care unit.
Special attention is given to patients with sepsis - they require urgent antibiotic administration and infection control, including surgical treatment.
It should not be forgotten that patients with impaired defense mechanisms are at increased risk of developing sepsis and MODS. These include patients undergoing chemotherapy, the elderly, burns, multi-organ injuries, diabetes, chronic insufficiencykidneys and / or liver, people with respiratory support or with catheters.
Multiple organ failure - prognosis
The risk of death in the course of multiple organ failure increases with the number of systems failing and with the severity and duration of the failure. It is worth knowing that the dysfunction of each subsequent organ increases the risk of death by as much as 15%. About a third of deaths occur within the first 48 hours, and 80% of those with MODS die within 14 days.
There are some unfavorable prognostic factors, including acute disease, acidosis, old age, infection with resistant organisms, and an impaired immune response. Patients who survive require prolonged and intensive care and rehabilitation - after 6 months only 50% of them return to their usual activities.
