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 1960ís 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 ětoxinsî 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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| 1. | Maintenance of vascular competence by adequate fluid replacement to
ensure blood flow to vital organs |
| 2. | Use of vasopressors to support blood pressure |
| 3. | Maintenance of the airway and provision of adequate oxygenation |
| 4. | Appropriate use of antimicrobial agents to treat potential and/or
identified bacterial infection. |
| 5. | Management of multiple organ failure |
| 6. | Treat congestive heart failure |
| 7. | Dialysis p.r.n. |
| 8. | Use of agents to reduce intracranial pressure |
| 9. | Appropriate antibiotics if bacterial infection is present |
| 10. | Treatment of anemia, if present |
| 11. | Counteract toxin presence with appropriate anti-toxin medications,
as available at the time (e.g. anti-endotoxin antibody, anti-tumor
necrosis factor) |
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In effect, a major intensive care effort should be undertaken in
consultation with appropriate specialists. |
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