The association between streptococci and scarlet fever was confirmed by Alphonse Dochez and George and Gladys Dick in the early 1900s.Also in 1884, the worlds first convalescent home for people with scarlet fever was opened at Brockley Hill, Stanmore, founded by Mary Wardell.Nil Filatov (in 1895) and Clement Dukes (in 1894) described an exanthematous disease which they thought was a form of rubella, but in 1900, Dukes described it as a separate illness which came to be known as Dukes disease, Filatovs disease, or fourth disease. However, in 1979, Keith Powell identified it as in fact the same illness as the form of scarlet fever which is caused by staphylococcal exotoxin and is known as staphylococcal scalded skin syndrome.Scarlet fever serum from horses blood was used in the treatment of children beginning in 1900 and reduced mortality rates significantly.In 1906, the Austrian pediatrician Clemens von Pirquet postulated that disease-causing immune complexes were responsible for the nephritis that followed scarlet fever.Bacteriophages were discovered in 1915 by Frederick Twort. His work was overlooked and bacteriophages were later rediscovered by Felix dHerelle in 1917. The specific association of scarlet fever with the group A streptococci had to await the development of Lancefields streptococcal grouping scheme in the 1920s. George and Gladys Dick showed that cell-free filtrates could induce the erythematous reaction characteristic of scarlet fever, proving that this reaction was due to a toxin.
Care is directed to the dysfunctional organs (dialysis for the kidneys, mechanical ventilation for lungs dysfunction).Mortality rates have been decreasing in the United States. This is likely due to the rapid identification and treatment of the CS. Some studies have suggested that this possibly related to the increased use of coronary reperfusion strategies, like heart stents. Nonetheless, the mortality rates remain high. Multi-organ failure is associated with higher rates of mortality. Signs and symptoms
The presentation is the following:
Anxiety, restlessness, altered mental state due to decreased blood flow to the brain and subsequent hypoxia. Low blood pressure due to decrease in cardiac output. A rapid, weak, thready pulse due to decreased circulation combined with tachycardia. Cool, clammy, and mottled skin (cutis marmorata) due to vasoconstriction and subsequent hypoperfusion of the skin. Distended jugular veins due to increased jugular venous pressure. Oliguria (low urine output) due to inadequate blood flow to the kidneys if the condition persists. Rapid and deeper respirations (hyperventilation) due to sympathetic nervous system stimulation and acidosis. Fatigue due to hyperventilation and hypoxia. Absent pulse in fast and abnormal heart rhythms. Pulmonary edema, involving fluid back-up in the lungs due to insufficient pumping of the heart. Causes
Cardiogenic shock is caused by the failure of the heart to pump effectively. It is due to damage to the heart muscle, most often from a heart attack or myocardial contusion. Other causes include abnormal heart rhythms, cardiomyopathy, heart valve problems, ventricular outflow obstruction (i.e. systolic anterior motion (SAM) in hypertrophic cardiomyopathy), or ventriculoseptal defects.