Complications
Although most people infected with yellow fever experience only a mild infectious illness and do not progress to the period of intoxication, up to 50% of those living in endemic areas who develop hemorrhagic manifestations and hepatorenal disease die of overwhelming multiorgan failure after an average of 7 to 10 days despite intensive care management.[15][2]
Patients with no prior immunity traveling to endemic areas are more likely to die, and case fatality rates for travelers who progress to the period of intoxication can be as high as 89%.[15]
15% to 25% of patients develop some degree of hepatorenal dysfunction, generally believed to be triggered by significant cytokine dysregulation caused by viral cytotoxic effects resulting in disseminated intravascular coagulation, tissue anoxia, oliguria, and shock.[2]
The degree of transaminitis correlates with prognosis.
Common in the toxic phase of the disease and characterized by petechiae, ecchymoses, or overt bleeding from the gums, nose, mucosae, or phlebotomy sites.
Common in the toxic phase and often highly refractory to fluids and pressor support.
In the toxic phase, coma, stupor, and agitated delirium have been described. This seems to be part of the cytokine storm and not an indication of a true viral encephalitis.
Indicates cytolytic activity in the toxic phase. Intensive care monitoring and supportive care is the mainstay of therapy in this phase.
Indicates circulatory collapse and autonomic dysregulation. Intensive care monitoring and supportive care is the mainstay of therapy in this phase.
Rare complication in the toxic phase. Intensive care monitoring and supportive care is the mainstay of therapy in this phase.
Mimics toxic phase of natural disease. Extremely rare (<1:1,000,000) complication but potentially fatal and more commonly reported in recent years. It is associated with older age and immunodeficiency.[48][49]
There is a theoretical risk of increased vaccine-related adverse events in patients with genetic or therapy-induced (i.e., CCR5 inhibitor therapy such as maraviroc) absence of CCR5 chemokine receptors.
Uncommon (1:58,000) complication likely due to intolerance of the gelatin in the vaccine.[48]
While the toxic hepatorenal syndrome is generally reversible in surviving patients, hypotension-induced renal tubular acidosis may rarely result in hemodialysis-dependent renal failure.
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