The Story of Blood for Shock Resuscitation: How the Pendulum Swings.

Whole blood transfusion (WBT) began in 1667 as a treatment for mental illness, with predictably poor results. Its therapeutic utility and widespread use were initially limited by deficiencies in transfusion science and antisepsis. James Blundell, a British obstetrician, was recognized for the first allotransfusion in 1825. However, WBT did not become safe and therapeutic until the early 20th century, with the advent of reliable equipment, sterilization, and blood typing. The discovery of citrate preservation in World War I allowed a separation of donor from recipient and introduced the practice of blood banking. During World War II, Elliott and Strumia were the first to separate whole blood into blood component therapy (BCT), producing dried plasma as a resuscitative product for "traumatic shock." During the 1970s, infectious disease, blood fractionation, and financial opportunities further drove the change from WBT to BCT, with few supporting data. Following a period of high-volume crystalloid and BCT resuscitation well into the early 2000s, measures to avoid the resulting iatrogenic resuscitation injury were developed under the concept of damage control resuscitation. Modern transfusion strategies for hemorrhagic shock target balanced BCT to reapproximate whole blood. Contemporary research has expanded the role of WBT to therapy for the acute coagulopathy of trauma and the damaged endothelium. Many US trauma centers are now using WBT as a front-line treatment in tandem with BCT for patients suffering hemorrhagic shock. Looking ahead, it is likely that WBT will once again be the resuscitative fluid of choice for patients in hemorrhagic shock.

Albumin for Prehospital Fluid Resuscitation of Hemorrhagic Shock in Tactical Combat Casualty Care.

Optimal fluid resuscitation on the battlefield in the absence of blood products remains unclear. Contemporary Combat medics are generally limited to hydroxyethyl starch or crystalloid solutions, both of which present significant drawbacks. Obtaining US Food and Drug Administration (FDA)-approved freeze-dried plasma (FDP) is a top casualty care research priority for the US Military. Interest in this agent reflects a desire to simultaneously expand intravascular volume and address coagulopathy. The history of FDP dates to the Second World War, when American expeditionary forces used this agent frequently. Also fielded was 25% albumin, an agent that lacks coagulation factors but offers impressive volume expansion with minimal weight to carry and requires no reconstitution in the field. The current potential value of 25% albumin is largely overlooked. Although FDP presents an attractive future option for battlefield prehospital fluid resuscitation once FDA approved, this article argues that in the interim, 25% albumin, augmented with fibrinogen concentrate and tranexamic acid to mitigate hemodilution effects on coagulation capacity, offers an effective volume resuscitation alternative that could save lives on the battlefield immediately.

The ebb and flow of fluid (as in resuscitation).

Since the early 1960's "resuscitation" following major trauma involved use of replacement crystalloid fluid/estimated blood loss in volumes of 3/1, in the ambulance, emergency room, operating room and surgical intensive care unit. During the past 20 years, MAJOR paradigm shifts have occurred in this concept. As a result hypotensive resuscitation with a view towards restriction of crystalloid, and prevention of complications has occurred. Improved results in both civilian and military environments have been reported. As a result there is new focus on trauma surgical involvement in all aspects of trauma patient management, focus on early aggressive surgical approaches (which may or may not involve an operation), and movement from crystalloid to blood, plasma, and platelet replacement therapy.

Towards hemostatic resuscitation: the changing understanding of acute traumatic biology, massive bleeding, and damage-control resuscitation.

During the past decade there has been a profound change in the understanding of postinjury coagulation. Concurrently, new data suggest that a resuscitative strategy to minimize large volumes of crystalloid while recreating whole is associated with reduced morbidity and mortality. This article outlines the history of resuscitation and transfusion practices in trauma, the changing understanding of coagulation and inflammation, and clinical data driving changes in resuscitative conduct. Finally, the current state of the science suggests future basic science and clinical investigation that will drive changes in transfusion and resuscitation in severely injured military personnel and civilian patients.

Alfred Blalock. Surgeon, educator, and pioneer in shock and cardiac research.

Alfred Blalock (1899-1964) was a pioneer American surgeon who made significant advances in the knowledge and treatment of hemorrhagic and traumatic shock as well as in the palliative treatment of congenital heart disease, particularly tetralogy of Fallot. This historical note reviews highlights in the life and accomplishments of Alfred Blalock, noted academic surgeon and researcher. Blalock originated from Culloden, Georgia and attended Georgia Military College, the University of Georgia, and Johns Hopkins Medical School. He finished his surgical training at Vanderbilt University where he remained ultimately as professor of surgery until 1941 when he became the Chairman and Professor of Surgery at Johns Hopkins Medical School. His research in shock saved many soldiers' lives in World War II. In 1944 he performed the first subclavian-pulmonary artery shunt for tetralogy of Fallot with the support of the superb pediatric cardiologist Helen Taussig and the great technical help of Viven Thomas. Hundreds of operations followed. He educated and trained an incredible cadre of cardiovascular surgeons. He passed away in Baltimore, Maryland, on September 15, 1964.

[Historical vision of shock]. / Visión histórica del shock.

The concept of shock and its close relationship with that of stress dates back to the experiments of Hans Selye initiated in 1936 at McGill University in Montreal, with whom I collaborated between 1939 and 1942. It was demonstrated that the General Adaptation Syndrome begins with an Alarm Reaction, which consists of a Stage of Shock and one of Counter-Shock, followed by a Stage of Adaptation and finally a Stage of Exhaustion. My Ph.D. thesis concluded that shock was due to an adrenal insufficiency postulating that active metabolic processes drain the body of certain essential compounds the lack of which causes shock. My interest in the role of the glucose metabolism in shock led me to work with Bernardo Houssay in 1942 at the Institute of Physiology of the University of Buenos Aires and in 1944 with C.N.H. Long at Yale University. There I developed a method for the induction of hemorrhagic shock in the guinea pig with 94% lethality; curiously, the administration of 200 mg of ascorbic acid prevented death. Upon my return to Buenos Aires, these results were confirmed and moreover, it was demonstrated that the administration of cortisone led to 40% survival of the animals while desoxycorticosterone had no effect. At the time, no explanation was available but to-day, half a century later, this Symposium should be able to explain the mechanisms leading to death by hemorrhagic shock.

Vision historica del shock / Historical vision of shock

El concepto de shock y su estrecha relación con el de stress surgió a partir de los trabajos de Hans Selye iniciados en 1936 en la Universidad de McGill en Montreal, con quien colaboré entre 1939 y 1942. Se demonstró que el síndrome general de adaptación se inicia con la reacción de alarma, compuesta por una etapa de shock y una de contra-shock, seguida de la etapa de resistencia y finalmente de la de agotamiento. Mi tesis doctoral concluía que el shock se debía a una insuficiencia suprarrenal aguda postulándose que procesos metabólicos activos hacían desaparecer compuestos esenciales para la sobrevida. Mi interés en la relación del shock con los hidratos de carbono me llevó en 1942 a trabajar con Bernardo Houssay en el Instituto de Fisiología de la Universidad de Buenos Aires y luego en 1944 con C.N.H. Long en la Universidad de Yale. Allí desarrolé un método para inducir el shock hemorrágico en el cobayo con una letalidad del 94 por ciento; llamativamente, con la administración de 200 mg de ácido ascórbico se prevenía la muerte. Al trasladarme definitivamente a Buenos Aires, estos resultados se confirmaron y además se consiguió un 40 por ciento de sobrevida con cortisona mientras que la desoxicorticosterona carecía de efecto. En aquel entonces no tuvimos explicación para la muerte por shock hemorrágico, pero hoy, medio siglo más tarde, de este Simposio debería surgir el mecanismo involucrado. (AU)

Vision historica del shock / Historical vision of shock

El concepto de shock y su estrecha relación con el de stress surgió a partir de los trabajos de Hans Selye iniciados en 1936 en la Universidad de McGill en Montreal, con quien colaboré entre 1939 y 1942. Se demonstró que el síndrome general de adaptación se inicia con la reacción de alarma, compuesta por una etapa de shock y una de contra-shock, seguida de la etapa de resistencia y finalmente de la de agotamiento. Mi tesis doctoral concluía que el shock se debía a una insuficiencia suprarrenal aguda postulándose que procesos metabólicos activos hacían desaparecer compuestos esenciales para la sobrevida. Mi interés en la relación del shock con los hidratos de carbono me llevó en 1942 a trabajar con Bernardo Houssay en el Instituto de Fisiología de la Universidad de Buenos Aires y luego en 1944 con C.N.H. Long en la Universidad de Yale. Allí desarrolé un método para inducir el shock hemorrágico en el cobayo con una letalidad del 94 por ciento; llamativamente, con la administración de 200 mg de ácido ascórbico se prevenía la muerte. Al trasladarme definitivamente a Buenos Aires, estos resultados se confirmaron y además se consiguió un 40 por ciento de sobrevida con cortisona mientras que la desoxicorticosterona carecía de efecto. En aquel entonces no tuvimos explicación para la muerte por shock hemorrágico, pero hoy, medio siglo más tarde, de este Simposio debería surgir el mecanismo involucrado.

The bacterial factor in hemorrhagic shock.

After a century of research on hemorrhagic shock, traumatic shock, septic shock and burn shock, it is known that all of the states lead to cellular injury and death through the same common pathways. Methods for blocking these pathways may ameliorate all of these conditions.