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In the United States, more than 1 million burn injuries occur every year. Although the survival from burn injury has increased in recent years with the development of effective fluid resuscitation management and early surgical excision of burned tissue, the mortality of burn injury is still high. In these fire victims, progressive pulmonary failure and cardiovascular dysfunction are important determinants of morbidity and mortality. The morbidity and mortality increases when burn injury is associated with smoke inhalation. Smoke inhalation and pneumonia increase mortality of burn patients by 20 and 40%, respectively [], suggesting that the pulmonary involvement is a very important risk factor in burn trauma. Our group and others have reported various factors that are involved in pathophysiology of acute lung injury (ALI) in burn, including coagulopathy [, ]. It was earlier described that burn injury is associated with a hypercoagulable state []. The coagulopathy seen in these burn patients is associated with marked depletion of a major endogenous regulator of blood coagulation, antithrombin []–[]. In the present chapter, we will discuss a possible role of antithrombin in the pathophysiology of ALI induced by combined burn and smoke inhalation and review the therapeutic approaches.

Anemia is one of the most common problems suffered by critically ill patients and occurs early during their intensive care unit (ICU) stay. Despite alternatives, blood transfusion is still the most common treatment of anemia in ICUs around the world. In the last decade, a number of studies have observed the transfusion practices in North America and Europe. These studies have also provided information regarding the efficacy and the negative consequences of blood transfusion therapy.

The decision process leading to red blood cell (RBC) transfusion should be based as much as possible on available evidence. Risks and benefits of transfusion as well as the risks attributable to anemia must be taken into account. In this chapter, we will discuss what prompts pediatric intensivists to prescribe a RBC transfusion, what should guide this decision, and what is missing to really make a decision based on an evidence-based approach.

Thrombocytopenia is a common feature in intensive care patients. Similar to other settings in which thrombocytopenia may occur, the decrease in platelet count may be caused by impaired production, increased consumption, or enhanced degradation of these cells. In this chapter, we will discuss the epidemiology and differential diagnosis of a decreased platelet count in critically ill patients, First, we will briefly introduce platelet function and platelet vessel wall interaction in the normal situation and during severe infection and/or inflammation.

Hemostasis monitoring is becoming increasingly important in the management of bleeding patients in the operating room (OR) and the intensive care unit (ICU) in order to improve outcome and reduce costs of treatment. It has been shown in cardiac surgery that frequent reassessment of the coagulation status and transfusion according to well-structured algorithms reduced blood loss and blood component use when compared with transfusion regimens based on clinician discretion [, ]. Routine laboratory based coagulation tests (e.g., prothrombin time [PT]/interna-tional normalized ratio [INR], activated partial thromboplastin time [aPTT], fibrin-ogen) measure clotting times and factors in recalcified plasma after activation with different coagulation activators. Platelet numbers are given to complete overall coagulation assessment. Although the values obtained by routine coagulation testing are accurate, standardized, and have been used for a long time, their use has been questioned in the assessment of a severely bleeding patient because values are measured in plasma, no information on platelet function is available, and there is a time delay of 30–60 min from sampling to obtaining the results.

Exsanguination is still a major cause of death in severely injured patients []. Trauma-associated bleeding diathesis, overt at admission to the trauma unit, correlates with the severity of trauma and mortality [, ]. Sufficient hemostatic management is critical to the successful resuscitation of the severely injured patient, second in importance only to adequate ventilation. Despite intense efforts to elucidate the pathomechanism and control the process, trauma-associated coagulopathy remains a challenge in the treatment of trauma patients. In this light, monitoring of hemostasis should confirm and specify the clinical diagnosis of bleeding diathesis, guide goal-directed therapy, and possibly predict consecutive transfusion requirements at admission. The present chapter reviews routine laboratory tests and viscoelastic point-of-care hemostasis monitoring as a means of hemostasis monitoring in the emergency setting, as well as relevant pathomechanisms, and therapeutic approaches.

The major complication associated with the use of warfarin is bleeding due to excess anticoagulation. The risk of major bleeding episodes in patients treated with warfarin is related to the degree of anticoagulation. An exception to this general rule is retroperitoneal hemorrhage, which may be more common in patients taking anticoagulants, even when levels are within the therapeutic range []. Intracranial hemorrhage (ICH) is the most serious and lethal complication of antithrombotic therapy. Over one-half of patients with warfarin-associated ICH die within the first 3 months, a substantially higher mortality rate than that of spontaneous ICH in those not receiving anticoagulants [, ].

Gender-based differences in patient response to injury/disease have long been recognized both in clinical and experimental settings [, ]. Despite this, some remain skeptical on the role of gender in the overall outcome of patients [, ]. From an analysis of more than 150,000 trauma patients, it was concluded that male patients are at higher risk of death as compared to female patients following blunt trauma []. Similarly, other studies have also indicated that females are more resistant to sepsis as compared to males [, ]. However, gender was not found to be a significant factor in the outcome of trauma patients in some other studies [, ]. Thus, the role of gender in the outcome of trauma patients remains somewhat controversial. In contrast, the findings from experimental studies clearly indicate that gender plays a critical role in the host response to major injury [, ]. These studies have shown that immune and cardiovascular functions are suppressed following trauma-hemorrhage in mature males, ovariectomized and aged females, while both immune and cardiac functions are maintained in proestrus females under those conditions [, , , ]. Similarly, liver functions following trauma-hemorrhage were depressed in males, but were maintained in proestrus females. Moreover, the survival rate of proestrus females subjected to sepsis after trauma-hemorrhage is significantly higher than age-matched males or ovariectomized females. In this chapter, we will review studies delineating the potential mechanisms by which male and female sex hormones influence immune and other organ functions following trauma-hemorrhage.

There are obvious anatomical, physical, and genetic differences between men and women that have always been a central focus of human life. Such differences have become the target of humor, politics, and legal issues and many other aspects of the human experience. At the same time, though receiving less notoriety, there are also striking sex-related differences in the presentation, outcomes, and responses to many disease processes and therapies.

Whether gender influences the outcome of severe sepsis remains a matter of debate. Because many confounding variables may affect observed associations between gender and mortality, high-quality statistical analyses are essential to carefully adjust the two groups of patients. About 55% to 65% of patients with sepsis have chronic co-morbidities associated with immune dysfunction (e.g., chronic renal failure, diabetes mellitus, human immunodeficiency virus [HIV] infection, and alcohol abuse), which increase the susceptibility to sepsis []. Genetic polymorphisms that affect the susceptibility to infection and/or the severity of the systemic response to infection [] may lead to variability among individuals and between males and females []. Access to healthcare, another determinant of the incidence and outcome of sepsis, varies according to age, ethnic group, and gender, although a recent study conducted in the USA found only relatively small quality-of-care differences between males and females or across income groups compared to the gap for each subgroup between observed and desirable quality of health care []. Here, we review the data on the existence of, and reasons for, associations between gender and outcome of severe sepsis (Fig. 1).