INTRODUCTION: Cerebral venous thrombosis (CVT) has a wide range of presentations. It has a highly variable mode of onset. Its numerous causes and its unpredictable outcomes, make it a diagnostic and therapeutic challenge. Neurological deterioration during an episode of diabetic ketoacidosis is usually assumed to be caused by cerebral edema. However, one should keep in mind that this rare, potentially life threatening complication (CVT), especially in patients predisposed to thrombosis, can be responsible for neurological deterioration.
CASE PRESENTATION: 26-year-old female presented with complaints of nausea, vomiting and abdominal pain of 24 hours duration. Her past medical history included type I diabetes mellitus and history of miscarriage a year ago. Her home medication included insulin and contraceptive patch for the last year. The latter has been switched recently (7 days ago) to progesterone injections to induce and regulate menses. On presentation she was found to be in diabetic ketoacidosis (DKA) The patient was admitted to the medical intensive care unit. She was treated with hydration and with insulin drip.In spite of the fact that acidosis and the blood sugar were controlled, the patient continued to have worsening lethargy that progressed to coma with a Glasgow Coma Scale 3. The patient was then intubated and placed on mechanical ventilation for airway protection. Computerized Tomography (CT) scan of the brain was done . This showed hyper attenuation of the venous sinuses with acute sinusitis affecting ethmoids and bilateral frontal sinuses. Magnetic resonance imaging (MRI) of the brain, magnetic resonance angiogram (MRA) as well as magnetic resonance venogram (MRV) of the brain showed diffuse cerebral venous thrombosis involving the superior sagittal, inferior sagittal, and also the transverse sinuses. Venous infarcts were also noted on the MRI. Patient was treated with Vancomycin, Cefteriaxone , and falgyl. She was also started on heparin to prevent any further thrombosis but later was transferred to an institute with invasive interventional radiology for selective intravenous thrombolysis. The patient had successful thrombolysis. This was proven with a repeat MRV.The patient neurological status recovered gradually but slowly. She was later transferred to an extended care facility to complete her treatment and recovery. Three months later the patient was contacted by us and was found with almost no neurological deficit.
DISCUSSIONS: To our knowledge, cerebral venous thrombosis (CVT) in DKA patients has been reported once in medical literature in a pediatric patient. It is likely that severe dehydration in this adult patient, together with the thrombogenic effect of the progesterone predisposed her to this disease state. CVT is a rare disease entity. A physician is likely to encounter one case during his lifetime. However, consequences could be detrimental if missed. Optimum treatment is not very well defined but expert opinions recommend selective thrombolytic therapy as the treatment of choice.
CONCLUSION: This case illustrates that episodes of acute neurological deterioration in DKA (which is an important state of dehydration) when coupled with another thrombogenic factor (such as hormonal therapy) should raise the suspicion of Cerebral venous thrombosis in addition to cerebral edema. Recognition of this rare entity is critical because the most efficient treatment is local thrombolytic therapy which is available only in certain institutions.
DISCLOSURE: Mohamad Al-Baghdadi, None.