CARDIOVASCULAR JOURNAL OF AFRICA • Vol 23, No 9, October 2012
AFRICA
e11
to reveal the cause of superwarfarin ingestion. In our case, the
patient’s history was remarkable, implying suicidal intentions as
the motive behind ingestion of this drug.
The diagnosis of superwarfarin toxicity should be suspected
in any patient who has a history of drug abuse or depression, has
a depressive mood and/or presents with a markedly prolonged
PT, PTT and INR levels and severe deficiency of vitamin
K-dependent clotting factors, with a transient or no response
to standard doses of vitamin K therapy. Since superwarfarins
may lead to relative vitamin K deficiency, biochemical assays
including plasma vitamin K, PIVKA-II (protein-induced in
vitamin K absence, a measurement of the non-carboxylated
proteins) levels, decreased urinary Gla (g-carboxyglutamic acid)
levels should be carried out. Increased vitamin K 2,3-epoxide
levels, increased plasma vitamin K epoxide-to-vitamin K ratio
(
used to detect vitamin K deficiency) may also support this
diagnosis. In our case, we detected markedly prolonged PT, PTT
and INR levels, together with a deficiency of vitamin K and
related factors (factors II, VII, IX, and X).
The treatment modalities of superwarfarin poisoning are
administration of vitamin K
1
,
fresh frozen plasma, prothrombin
complex concentrate and recombinant factor VIIa.
8
For cases
in which recent ingestion of superwarfarin is certain, syrup
of ipecac and charcoal may be given to decrease subsequent
absorption of the drug into the circulation. The standard treatment
of superwarfarin toxicity is administration of large doses of
vitamin K. There are multiple forms of vitamin K: vitamin K
1
(
phylloquinone) is an active vitamin K that is typically produced
by green plants. Vitamin K
2
(
menaquinone) is a group of
compounds made by intestinal bacteria. Vitamin K
3
(
menadione)
is the parent compound lacking the necessary side chain and is
inactive
in vitro
.
Vitamin K
1
is recommended for the treatment
of superwarfarin toxicity.
Management of patientswith superwarfarinpoisoning involves
prolonged administration of high doses of vitamin K
1
.
The oral
route is preferred to intramuscular or intravenous injection
to avoid haematoma formation. Intravenous administration is
preferred only if severe bleeding is present, due to the risk of
an anaphylactic reaction with this route of administration.
8
If
the patient is actively bleeding or at high risk of bleeding, fresh
frozen plasma infusions are given to replace deficient vitamin
K-dependent coagulation factors.
In our case, since the patient had a history of ingesting
superwarfarin for five days and was admitted to the emergency
department with epigastric pain, gingival bleeding and melena
concomitant with extended coagulation parameters (PT, aPTT,
INR), vitamin K
1
and fresh frozen plasma infusions were
administered intravenously for prolonged periods of time.
Despite this intensive therapy, his INR level regressed to the
normal range only after three months.
Conclusion
Superwarfarin ingestion can be a serious problem, resulting in
life-threatening bleeding. Although awareness of the condition
has increased, its incidence is not decreasing. The prevalence
of superwarfarin poisoning should be determined in every
country, considering these recently published cases. Supervision
of rodenticide usage and education of people who deal with
rodenticides in their homes or workplaces are also necessary.
Further studies are needed in order to achieve faster and more
accurate diagnosis of this condition.
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