General
The exact cause for death from smallpox and certain life-threatening
complications of vaccination is uncertain. Symptom complexes
characteristic of toxic or septic shock were observed in the 1960’s
and before, but little could be done to counteract the symptoms with
the modalities available in those times. Other patients appeared to
suffer hemorrhagic complications that were characteristic of
Disseminated Intravascular Coagulation (DIC). Again, little could be
done as therapy for this condition was in its infancy.
Significant gain in decreased morbidity and prevention of mortality
could result from aggressive application of modern intensive-care
level of treatment. Every effort should be made to apply such
modalities to patients with complications of vaccination that appear
to have as a component toxic or septic shock, or DIC.
This section is not meant as a definitive guide to the diagnosis and
treatment of these shock conditions, but to serve as a reminder that a
major effort should be made in seriously ill patients with
complications of vaccination to apply the best modern technology and
care to reduce morbidity and mortality.
Diagnostic and Clinical Considerations
Septic Shock
The symptom complex of the usually sudden onset of fever, chills,
myalgias, and change in mental status (agitation, irritability,
restlessness, delirium, confusion, or even stupor or coma) should lead
to the diagnosis of septicemia. Tachycardia, tachypnea, hypotension establish
impending or actual shock. End organ failure may supervene as evidenced by
cyanosis (pulmonary), jaundice (hepatic), anuria (renal) and congestive heart
failure (cardiac). With infection of the central nervous system, convulsions,
meningeal signs and focal neurologic signs occur. Adult respiratory distress
syndrome may intervene.
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The laboratory findings include positive cultures from blood and other
sites (in the case of vaccinia, virus or viral antigens may be
detected), leucocytosis with shifts to the left, thrombocytopenia,
hypoxemia, alterations in electrolytes, and reduction in serum
concentrations of iron, glucose, and calcium. Hyperbilirubinemia will
be seen in hepatic failure and signs of renal failure will be detected
in the urine and by azotemia. Imaging studies may be necessary with
pulmonary, central nervous system or abdominal findings.
Consultation with intensivists is strongly advised to establish the
diagnosis and to institute appropriate ICU-level treatment.
Therapeutic Principles
First, use VIG aggressively to reduce the virus load and potentially
to reduce circulating “toxins” of the virus or induced by the virus as
it infects other sites from viremia. Having accomplished that, the
principles of treatment include:
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Maintenance of vascular competence by adequate fluid replacement to
ensure blood flow to vital organs |
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Use of vasopressors to support blood pressure |
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Maintenance of the airway and provision of adequate oxygenation |
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Appropriate use of antimicrobial agents to treat potential and/or
identified bacterial infection. |
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Management of multiple organ failure |
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Treat congestive heart failure |
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Dialysis p.r.n. |
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Use of agents to reduce intracranial pressure |
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Appropriate antibiotics if bacterial infection is present |
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Treatment of anemia, if present |
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Counteract toxin presence with appropriate anti-toxin medications,
as available at the time (e.g. anti-endotoxin antibody, anti-tumor
necrosis factor) |
In effect, a major intensive care effort should be undertaken in
consultation with appropriate specialists.
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