ndersen er an - Gundersen Health System

gundersen lutheran alcohol detoxification protocol
decrease absorption by up to 70%. 30 Hence, enteral replacement
of thiamine in a patient with WE is inadequate.
At the blood-brain barrier, thiamine is transported by both
passive and active carrier-mediated mechanisms. 31 At normal plasma
concentrations, thiamine influxes into the brain almost entirely via
the carrier-mediated process at a rate essentially equal to that of
thiamine turnover. However, by creating a large plasma:central
nervous system concentration gradient, thiamine stores can be
readily replaced within the brain by passive transport alone. As
enteral absorption of thiamine is limited, IV or IM administration
should be used to obtain adequate plasma concentrations. 30
Several studies by Cook, Thomson, and colleagues 29,30,32-35
support the use of a much higher dosage of parenteral thiamine
than what has been traditionally utilized. They have recommended
that patients who are at risk or who have clinical evidence of
WE receive a minimum dosage of 500 mg of IV thiamine 3 times
daily for 3 days. When there is an effective response, thiamine
should be continued at 250 mg IV daily for an additional 3 to 5
days, or until clinical improvement ceases. Traditional dosages of
100 mg to 200 mg of thiamine per day were found to be insufficient
to replete thiamine stores, improve clinical findings, or prevent
permanent neurologic damage or death. The estimated mortality
for inadequately treated WE is 20%. 30,32 Moreover, almost 80%
of patients with untreated or undertreated WE develop Korsakoff
syndrome, a permanent disorder of anterograde and retrograde
amnesia with confabulation as a prominent feature. 12
Identifying patients with WE or who are at high risk of
developing WE is difficult. Nineteen percent of patients with
WE have none of the classic triad of symptoms at presentation.
Only 29% have ocular abnormalities, while only 23% have gait
incoordination and truncal ataxia at presentation. 1 Adding to the
difficulty is that acute alcohol intoxication and alcohol withdrawal
can also cause mental status changes and ataxia, and indeed these
abnormalities are often attributed to intoxication or withdrawal
without consideration of WE.
Several protocols have been developed in an attempt to better
identify, and therefore treat, patients with high likelihood of WE.
Caine et al use criteria of 2 of the classic triad of symptoms (mental
status changes, ocular abnormalities, incoordination of gait/trunk
ataxia) and presence of dietary deficiencies. 36 The Royal College of
Physicians guidelines are to treat “all patients with any evidence of
chronic alcohol misuse and any of the following: acute confusion,
decreased conscious level, ataxia, ophthalmoplegia, memory
disturbance, hypothermia with hypotension…, [and] patients
with delirium tremens…” with thiamine 500 mg IV 3 times daily.
Other at-risk patients receive prophylactic thiamine dosing of 250
mg IV daily for 3 to 5 days. 30
Significant magnesium deficiency is common in chronic
alcoholics, and adequate replacement is also vital in treatment
of WE. Magnesium serves as a cofactor required for normal
functioning of several key thiamine-dependent enzymes of
carbohydrate metabolism and neurochemical transmission.
Studies by Traviesa demonstrated that patients with WE may
well be unresponsive to parenteral thiamine administration if
hypomagnesemia is present. 37-39 Therefore, patients at high risk
of WE should have magnesium levels measured and aggressively
corrected, as well.
Gundersen Lutheran’s current inpatient alcohol detoxification
protocol includes administering 100 mg of thiamine daily for 3
days and gives the option of enteral, parenteral, or IM routes.
There are no specific criteria on the current protocol to identify
individuals who are at high risk or who manifest symptoms of
WE and therefore would potentially benefit from higher doses of
thiamine. Most of the alcohol detoxification patients, unless they
are experiencing severe withdrawal symptoms requiring higher
dosages of IV ativan, do not have IV access routinely placed. The
majority of these patients are receiving enteral thiamine rather
than IM as the alternative route of administration.
The case report presented here demonstrates that an updated
alcohol detoxification protocol could prompt earlier identification
and treatment of patients with WE. Although this patient
had definite improvements in his overall condition during
hospitalization, at discharge he demonstrated memory deficits
that were consistent with Korsakoff syndrome. Whether earlier
administration of higher dosages of IV thiamine would have
changed his outcome is unknown. However, WE is considered
a medical emergency, and therefore outcome is affected not
only by adequate amounts of thiamine replacement but also by
the timeliness of the administration. To this end, optimally the
protocol would direct that the first dose of high-dosage thiamine
be given while the at-risk patient is in the emergency department.
CONCLUSIONS
Wernicke encephalopathy is a neuropsychiatric condition of
thiamine deficiency that is under-diagnosed and often undertreated.
Specifically, oral thiamine is not absorbed to an extent
sufficient to replace thiamine stores in WE and should not be used.
High IV or IM dosages are required to attain serum levels high
enough for passive transport across the blood-brain barrier.
We propose a new alcohol detoxification protocol that identifies
high-risk patients or those demonstrating signs of WE to receive
parenteral thiamine 500 mg 3 times daily for a minimum of 3
days. In addition, baseline and daily magnesium levels should be
monitored and replaced if necessary.
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