Platelets are derived from the bone marrow megakaryocyte precursor, which contains loose granules and dense granules. Their average life expectancy is approximately 7 to 14 days. Thrombocytes have a variety of biological activities and functions. They are also extremely sensitive inflammatory cells that play an important role in the inflammatory response. Platelets have been preliminarily recognized as able to sense damage to vessel endothelium. Increasing recent evidence suggests that platelets have an indispensable role in regulating inflammatory responses [8,9,10]. The platelet concentration reflects the production and decay of thrombocytes, which decreases when peripheral blood platelets are destroyed; this decrease also stimulates compensatory hyperplasia of the bone marrow megakaryocytes to produce more platelets [11]. The platelet concentration will increase when the primary disease is under control. Because the platelet concentration can reflect the relationship between the consumption and generation of platelets in the body to some degree, it also shows early changes in conditions. Therefore, to a certain extent, platelet concentration, which can provide an early and sensitive indicator of illness severity and prognosis, also indirectly reflect the body’s ability to respond to disease.
Shock refers to a pathological process characterized by the reduction of the body’s effective circulation blood volume, tissue perfusion deficiency, cellular metabolic disorders, and functional impairment. The essence of burn-related shock is hemorrhagic shock. A major goal of the initial management of burn injuries is to replace extracellular fluid loss in proportion to the % TBSA of the burn. For large burns, intravenous (i.v.) fluid therapy is required to avoid the life-threatening consequences of hypovolemic shock; to this aim, a number of resuscitation formulae have been proposed [12]. Our study found that patients who were successfully resuscitated from shock had a higher platelet concentration level than others. Due to the lack of effective blood volume and hemoglobin, patients who suffer resuscitation failure will experience pathophysiological deterioration and instability of the internal environment. As delayed resuscitation, tissue ischemia, hypoxia reperfusion injury, and acute infection promote the activation of the coagulation system, platelet activation factor (PAF) is released, resulting in further decreases in the number of platelets.
Sepsis and multiple organ dysfunction syndrome (MODS) caused by sepsis are the principal reasons for death in burn patients [13]. Several studies have shown variation in the rates, mortality, and characteristics of patients with MODS according to the type of patients, sample size, definition, and involved organs. In many burn centers, MODS is still a leading cause of death in patients with severe burns [14]. Due to the strong and persistent stress stimulation after severe burns combined with platelet adhesion and aggregation, active substances such as PAF, prostaglandin G2 (PGG2), prostaglandin H2 (PGH2), and thromboxane A2 (TXA2), which are released by platelets, produce complex biological effects. These active substances, which can strengthen the inflammatory response, affect the regulation of blood flow, change vasodilator levels and permeability, and alter the coagulation state, resulting in the contraction of blood vessels, the aggregation of inflammatory cells, and the release of a large number of inflammatory mediators. To a certain extent, these changes can endanger the survival of cells and lead to organ failure. As a result, the excessive production of platelets is a sign of poor prognosis. PAF was directly involved in shock, sepsis, and organ failure. Changes in peripheral platelet concentration indicate that the rapid decline in platelet concentration is related to multiple organ failure (MOF).
Sepsis refers to systemic inflammatory response syndrome (SIRS) caused by infection, which is a serious complication of shock, burns, trauma, infection, and major surgery. In sepsis, abnormal platelet activation and neutrophil paralysis is well recognized. Platelet activity is characterized by the contribution to disseminated intravascular coagulation (DIC) and the enhanced inflammation response [15]. Severe burns complicated with sepsis are an important cause of MODS [16]. Most organ damage occurs during the first week post-burn; additional damage may occur within 4 weeks post-burn, but the rate of organ damage slows in the third week. The pathogenesis of sepsis is complex and has not yet been fully elucidated; however, it includes infection, inflammation, tissue damage, and dysfunctions of the immune system, blood coagulation, metabolism, neuroendocrine system, and immunologic regulating network. Thrombocytopenia is one characteristic of sepsis that increases the risk of death [17]. Research proves that thrombocytopenia is associated with sepsis, prolonged hospital stays, and increased mortality [18]. The present study found statistically significant differences between patients with septic shock and those with non-septic shock on day 3 and day 5, yet there were no significant differences between these patients on the day of injury. This difference suggests that platelet concentration is an early indicator of septic shock. As an indicator of diffuse intravascular coagulation, thrombocytopenia is related to inflammatory mediators [19]. Treating the primary disease and providing anti-infective therapy are more effective than simply correcting the platelet concentration. A downward trend in platelet concentration is more informative than whether the platelet concentration is within the normal range. This report shows that platelet concentration is associated with reductions in the mortality rate and that the degree of decrease in the platelet concentration is positively correlated with the severity of sepsis [20]. Consequently, observing the daily changes in platelet concentration and considering them as a sign of the progress of anti-inflammatory treatment offers important guiding significance.
The previous analysis shows that platelet concentration can provide an objective and sensitive early indicator of severe burn patients’ condition and outcome. The reasons are as follows: A platelet’s life cycle is short and very few platelets are stored in the marrow, because the platelet concentration changes during the early stages of disease, which can sensitively show the severity of a patient’s condition. Platelets play an important role in the inflammatory response; therefore, the degree of the inflammatory response is associated with the platelet concentration. Disease progression is associated with the risk of reducing the platelet concentration, and reduced platelet concentration may also lead to the exacerbation of disease. They are connected and influence each other.