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combination therapy is initiated with both BAL and CaNa2 EDTA; the BAL may
be discontinued in many cases after 2 to 3 days, but CaNa2 EDTA is continued
for 5 days. For symptomatic patients or those with high BLLs (>69 mcg/dL),
CaNa2 EDTA should always be started 4 hours after BAL due to the risk of
worsening lead encephalopathy when CaNa2 EDTA is given alone in these
patients. Provide adequate hydration to promote urine output. Symptomatic
children without frank encephalopathy should receive chelation therapy with a
combination of BAL for 3 to 5 days and CaNa2 EDTA for 5 days. Supportive care
includes close monitoring for signs of encephalopathy and, again, maintenance of
urine flow. In the event of BAL or CaNa2 EDTA shortage, succimer may be an
adequate substitute, although the evidence in support of its use for severe
intoxication or encephalopathy is purely observational.
Patients with encephalopathy require combination chelation therapy with
higher-dose CaNa2 EDTA and BAL for 5 days, as well as intensive supportive
care. Fluid therapy is critical to achieve adequate urine flow to excrete the lead–
chelate complexes; however, fluid overload can exacerbate cerebral edema.
Seizures commonly occur in acute encephalopathy and should be controlled
with anticonvulsant drugs (see Chapter 72 Seizures ). Hypothetical concerns have
been raised about the use of phenobarbital in lead encephalopathy (i.e.,
synergistic disturbances in porphyrin metabolism), but its clinical use has not
been associated with any noticeable deleterious effect. Recent advances have
been made in the management of cerebral edema and increased intracranial
pressure (see Chapter 122 Neurosurgical Emergencies ), but have not been
evaluated in controlled fashion in the context of lead encephalopathy.