Where we stand
Missouri Resident Poster Competition 1999
Mary M. Klix M.D.
St. John's Medical Center
in women on oral contraceptives:
we should not just blame the pill
A 31-year-old female with a 2-day history of a throbbing,
occipital headache, presented to the emergency room. She developed
nausea and vomiting several hours after the headache began. Her
medical history included irritable bowel syndrome and polycystic
ovary disease. Her only medication was oral contraceptives which she’d
been taking for 3 years. Family history was negative for
thrombophilia or related disorders. Physical exam was unremarkable,
as was the neuro exam. The PT & PTT were normal. Cranial CT scan
revealed a right transverse and sigmoid sinus thrombosis.
The patient was started on heparin, decadron and phenytoin and
admitted to the hospital. On day 3, she became unresponsive with
fixed, dilated pupils. She was intubated and repeat CT revealed
acute cerebral edema obliterating all ventricles. The interventional
radiologist was able to use intracranial urokinase to lyse the
superior sagittal sinus and bilateral transverse sinus thromboses.
Venous flow markedly improved. On hospital day eight, she was
extubated, was able to speak and follow simple commands.
Lab investigation of the patient’s hypercoagulable state
revealed: Normal, nonfasting homocysteine levels; low Protein C
& S Activity, (she’d received one dose of warfarin on day 2);
heterozygosity for the Factor V Leiden mutation; negative lupus
anticoagulant and negative prothrombin promoter gene mutation.
There are many known predisposing factors for thrombophilia. In
young women who wish to begin OCP therapy, a careful medical and
family history should be obtained. If they later present with
unusually located thromboses, underlying risk factors should be
sought. Congenital heparin cofactor 2, Protein C & S
deficiencies; activated protein C resistance, (some due to Factor V
Leiden); prothrombin promoter gene mutation; antiphospholipid
syndrome: lupus anticoagulant: sticky platelet syndrome; tissue
plasminogen activator defects and others can cause patients to be
more susceptible to thrombophilia. We can evaluate for many of these
factors, but some values are altered by anticoagulants. Protein C
and S are among these, and they are significantly reduced within 48
hours of beginning warfarin therapy. Factor V Leiden, conversely, is
detected by DNA analysis, and is unchanged by drug therapies.
Patients who are heterozygous for this mutation, which is believed
to be part of the most common known risk factor for venous
thrombosis, (present in as much s 15% of the population), increase
their risk of a significant event by 5 to 10 times that of the