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In our country, meningococcal disease has a low endemic and high lethality, with epidemic out breaks; some of them of historical character, like the one happened during the first half of the last century. The action of a group of doctors, pioneers in clinical, research and teaching aspects, together with the health personnel that constituted their team, immersed in a successful public health policy, allowed to consolidate the necessary care of the sick child of this serious pathology, as well as many others, thus enabling the development of a structured and scientific proposal, in the light of the knowledge available at that time. Therefore, after 80 years, it is important to review the various clini cal, pathophysiological and therapeutic aspects, in addition to the hospital and social context, of this successful history of the Chilean public health system.

: Editor's note: From its first issue in 1900 through to the present day, AJN has unparalleled archives detailing nurses' work and lives over more than a century. These articles not only chronicle nursing's growth as a profession within the context of the events of the day, but also reveal prevailing societal attitudes about women, health care, and human rights. Today's nursing school curricula rarely include nursing's history, but it's a history worth knowing. To this end, From the AJN Archives highlights articles selected to fit today's topics and times.This month's article, from the September 1908 issue, describes the nursing management of shock and hemorrhage. Hospital nurses are instructed to employ measures that today would be described as prehospital first aid. The author (a "Graduate of Bellevue Hospital, New York") directs the nurse to "work quickly and quietly, dismiss every one from the room who cannot be of intelligent assistance, and… in no way impart to the patient the serious nature of his or her condition." More than a century later, nursing interventions for shock are considerably more intense and complex, as illustrated in the feature article in this issue, "Assessing Patients During Septic Shock Resuscitation."

At the death of Cardinal Pietro Basadonna in 1684, his personal physician Romolo Spezioli wrote a report describing the disease, circumstances of death and autopsy findings of the illustrious prelate. This document, kept in the Biblioteca Civica at Jesi, is a significant attestation of the medical terminology and diagnostic and therapeutic procedures of the time. Even with the constraints that interpretation of a clinical account dating back over 300 years inevitably imposes, perusal of this report suggests that Cardinal Basadonna's demise could have been due to septic shock, consequent to a urinary infection caused by a bulky bladder stone.

In the late 19th century, it was already known that severe infections could be associated with cardiovascular collapse, a fact essentially attributed to cardiac failure. A major experimental work in the rabbit, published by Romberg and Pässler in 1899, shifted attention to disturbed peripheral vascular tone as the mechanism of hypotension in these conditions. In the first half of the 20th century, great progresses were made in the pathophysiologic understanding of hemorrhagic and traumatic shocks, while researchers devoted relatively little attention to septic shock. Progress in the hemodynamic understanding of septic shock resumed with the advent of critical care units. The hyperdynamic state was recognized in the late fifties and early sixties. The present short review ends with landmark studies by Max Harry Weil, demonstrating the importance of venous pooling, and John H. Siegel, which introduced the concept of deficient peripheral utilization of oxygen, inspiring later work on the microvascular disturbances of septic shock.

Purpose: To define some of the most common characteristics of vascular hyporesponsiveness to catecholamines during septic shock and outline current therapeutic approaches and future perspectives., Methods: Source data were obtained from a PubMed search of the medical literature with the following MeSH terms: Muscle, smooth, vascular/physiopathology; hypotension/etiology; shock/physiopathology; vasodilation/physiology; shock/therapy; vasoconstrictor agents., Results: NO and peroxynitrite are mainly responsible for vasoplegia and vascular hyporeactivity while COX 2 enzyme is responsible for the increase in PGI2, which also contributes to hyporeactivity. Moreover, K+ATP and BKCa channels are over-activated during septic shock and participate in hypotension. Finally, other mechanisms are involved in vascular hyporesponsiveness such as critical illness-related corticosteroid insufficiency, vasopressin depletion, dysfunction and desensitization of adrenoreceptors as well as inactivation of catecholamines by oxidation., Conclusion: In animal models, several therapeutic approaches, targeted on one particular compound have proven their efficacy in preventing or reversing vascular hyporesponsiveness to catecholamines. Unfortunately, none have been successfully tested in clinical trials. Nevertheless, very high doses of catecholamines ( > 5 μg/kg/min), hydrocortisone, terlipressin or vasopressin could represent an alternative for the treatment of refractory septic shock.

The mortality rate of septic shock remains high. The guidelines of the Surviving Sepsis Campaign were published in 2004 and were revised in 2008. Steroid therapy is prominent in the guidelines but remains controversial. In this review, steroid therapy for septic shock is discussed with various landmark papers.

Infectious disease has been a leading cause of death in humans since the first recorded tabulations. From Hippocrates and Galen, to Lister, Fleming and Semmelweiss, this article reviews the notable historical figures of sepsis research. The early descriptions and theories about the etiology (microbial pathogens), pathogenesis (toxins and mediators), and treatment of sepsis-associated disease are also discussed.

The ability to diagnose and treat infectious diseases and handle infectious disease outbreaks continues to improve. For the most part, the major plagues of antiquity remain historical footnotes, yet, despite many advances, there is clear evidence that major pandemic illness is always just one outbreak away. In addition to the HIV pandemic, the smaller epidemic outbreaks of Legionnaire's disease, hantavirus pulmonary syndrome, and severe acute respiratory syndrome, among many others, points out the potential risk associated with a lack of preplanning and preparedness. Although pandemic influenza is at the top of the list when discussing possible future major infectious disease outbreaks, the truth is that the identity of the next major pandemic pathogen cannot be predicted with any accuracy. We can only hope that general preparedness and the lessons learned from previous outbreaks suffice.

Objectives: To review the history of clinical use of corticosteroids with particular reference to adjunctive therapy for severe pediatric sepsis and, in this context, to provide an overview of what is known, what is not known, and what research questions are particularly relevant at this time., Data Source: Literature review using PubMed, cross-referenced article citations, and the Internet., Conclusions: The history of corticosteroid use in clinical medicine has been colorful, noisy, and always controversial. Therapeutic corticosteroid indications that initially seemed rational have frequently been refuted on closer, rigorous clinical trial inspection. Although it may be prudent to provide stress-dose steroids to children with septic shock who are clinically at risk for adrenal insufficiency (chronic or recent steroid use, purpura fulminans, etomidate or ketoconazole administration, hypothalamic, pituitary, adrenal disease), the safety and efficacy of stress-dose steroids as general adjunctive therapy for pediatric septic shock have not been established. Glucocorticoid administration does add potential risk to critically ill children. In particular, although adjunctive corticosteroids may hasten resolution of unstable hemodynamics in septic shock, this may occur at the metabolic cost of hyperglycemia. Clinical practice that fosters innovative therapy (off-label use) over research probably represents bad medical and social policy. Accordingly, pediatric critical care researchers have a responsibility to generate pediatric-specific evidence-based medicine for adjunctive corticosteroid therapy for severe sepsis in children.

In the time it has taken medicine to develop the techniques to describe the circulatory changes of severe infections, both pattern and process have been profoundly influenced by the use of intravenous fluids, vasopressors, antibiotics, steroids, mechanical ventilation and haemoflltration. Constant features of severe sepsis include a reduction in peripheral vascular tone on both the arterial and venous sides of the circulation, a defect in oxygen utilisation resulting in lactic acidosis, and varying degrees of myocardial dysfunction. These events have a temporal progression, the precise pattern observed depending on the tempo of the infection, the influence of therapeutic manoeuvres, the age and comorbidities of the patient, and the time the observations are made in the course of events. Early sepsis is accompanied by a decrease in systemic vascular resistance and a metabolic acidosis. The clinical picture includes fever, tachycardia, tachypnoea, respiratory alkalosis and an increased cardiac output with warm, dry peripheries and a bounding pulse. Advanced sepsis involves varying degrees of venous and myocardial contractile failure, and is characterised by progressive acidaemia, respiratory failure and marked sympathetic adrenergic activation. In the absence of vigorous fluid resuscitation, the cardiac output is decreased and the patients are cold, clammy peripherally shut down, and frequently confused, obtunded or comatose. In infections with a silent primary focus (predominantly involving Gram-negative organisms), this stage is frequently the first to attract the attention of attending staff. Late sepsis is characterised by profound acidaemia, vascular hypo-responsiveness, multiple organ failure and death.

Present management of shock derives, in part, from the classic investigations of Walter B. Cannon and Alfred Blalock. The intersections of their professional lives as recorded in the professional literature and in personal correspondence suggest that Blalock's pivotal studies of experimental shock were fueled, at least in part, by Cannon's inability to resolve the inconsistencies of the then-popular toxic theory of shock. Cannon appears to have substantially shaped Blalock's thought and work, initially as authority and competitor and later as colleague and friend. Blalock's experimental proof that injury precipitated obligatory locoregional fluid losses, the effects of which could be ameliorated by vigorous restoration of plasma volume, became a cornerstone of shock theory and therapy.

The history of sepsis demonstrates that despite current knowledge about its pathogenesis the definition of sepsis is more contested than ever. However, a definite terminology is necessary to define the entrance criteria for future clinical studies concerning patients with sepsis or septic shock. For this purpose, in 1991 a consensus conference was held in the US, but its recommendations have not found unequivocal acceptance. These recommendations and their historical background are presented and their consequences discussed.

A recently published theory (N Engl J Med 1985;313:1027-30) argues that the famous Athenian epidemic of 430 B.C. was caused by a combination of influenza and toxin-producing staphylococci (the "Thucydides syndrome"). Although it is accepted by some medical authorities, and ostensibly supported by identification of modern cases, the theory's plausibility has not been carefully examined. The authors used an epidemiologic approach supplemented by historical and clinical observations to examine the likelihood that a "Thucydides syndrome" could have caused the Athenian epidemic. Arguing against the influenza theory are epidemiologic and clinical features of the disease, mathematical models of the spread of influenza, and empirical observations of epidemic influenza in premodern populations of known size and crowding. The authors conclude that neither influenza nor a "Thucydides syndrome" could have produced the Athenian epidemic. Epidemiologic features suggest either a zoonotic or vectorborne disease, a disease associated with an environmental source, or a respiratory infection with unusual alternative mechanisms of spread.

This article reviews the history of Toxic Shock Syndrome and its relationship to tampons as well as governmental regulation of the tampon product. The historical antecedents and factors leading to governmental regulation will be addressed.

Objectives: HA-1A, a monoclonal antibody against endotoxin, was thought to be effective in treating patients with Gram-negative sepsis. Because of this possibility, many clinicians felt obligated to use the drug and assumed that its product license application would be approved by the U.S. Food and Drug Administration (FDA). Nevertheless, the efficacy of HA-1A was not conclusively demonstrated by a first clinical trial. The FDA rejected the product license application and requested a second clinical trial, which was suspended after excess mortality was noted in patients treated with HA-1A. This review of the history of the drug was prepared to provide clinicians and sepsis investigators with information about HA-1A and, by extension, the process by which new technology is introduced into critical care practice., Data Sources: Data used to prepare this review were obtained from the author's personal files as well as the computerized MEDLINE database., Study Selection: Studies were selected for their relevance to the history of HA-1A and their relevance to the introduction of potentially useful medical technology., Data Extraction: The author extracted all applicable data., Data Synthesis: Although the first clinical trial of HA-1A suggested that the drug was effective in treating patients with Gram-negative bacteremia with or without shock, further analysis by the FDA indicated a benefit only for bacteremic patients with shock. Furthermore, the original study design was not followed, leading in part to the FDA's refusal of the product license application. Concern also was raised over the issue of identifying which patients should receive HA-1A and the cost of the drug, which would have put it past the reach of some American hospitals and thereby, would have conflicted with the ethical principle of social justice. Finally, the second trial suggested that HA-1A might be harmful., Conclusions: Due to the FDA's action, the issues raised about HA-1A, and the results of the two clinical trials, clinicians should not use the drug. The history of HA-1A provides insights about how new technology is and will be introduced into critical care practice.

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.