Conversation 2

A 30 year old man had a motor vehicle accident 3 years ago and sustained a large hematoma across the chest and umbilicus. He was discharged home after two days after undergoing CT scans. At that time his FBC, BUSE, Creatinine, Blood sugar and LFT were all normal.

Two days later he developed gross hematuria. Laboratory tests showed his haemoglobin had dropped to 13gm/dL (haematocrit 36%) from the previous value of 17gm/dL (haematocrit 50%). The WBC count was normal but the platelet count was now very low at 22000/uL (previously 193000).

The hematuria resolved on its own after a few days. A PBF examination showed anisocytosis with occasional schistocytes as well as thrombocytopenia. There were no abnormal WBC. Giemsa staining of blood smears shown no intracellular organisms. The patient was discharged home with the assumption that the low platelets were due to the large subcutaneous hematoma and the anemia was due to the hematuria.

On review one week later, the platelet count was 242000/uL and one month later his haematocrit was 44%.

The patient remained well until one week ago when he felt weak and experienced tunnel vision while standing. He did not lose consciousness. Soon he began to feel very fatigued and presented himself to the hospital. His pulse and BP were normal. He was afebrile. His oxygen saturation was 99% on room air. He was alert, oriented and did not appear ill. Heart, lungs and abdomen were normal. He had an area of erythema on the posterior aspect of the right knee and bruising on both arms. Small areas of petechiae were noted in the areas of erythema and in the left flank.

At this time, his haemoglobin was only 5.8gm/dL with haematocrit 17.5%. WBC count was normal but platelets were very low at 13000/uL. The reticulocyte count was elevated at 16%. The PT and aPTT were both normal. The fibrinogen level was normal. The D-dimer level was markedly increased. Serum haptoglobin was low. Serum LDH was very much elevated. The serum ferritin was high. LFT was normal. The blood urea was raised but the serum creatinine was normal.
Urine examination was positive for blood and protein.

Giemsa staining of blood smears revealed no intracellular organisms.

A screening test for antibodies to B. burgdorferi was done when the patient gave a history of frequent tick bites and this was positive.

He was treated with doxycycline, clindamycin and quinine.

On the third hospital day, the patient had the sudden onset of expressive aphasia, pronator drift of the right arm, and inability to follow complex commands. The remainder of the neurologic examination was normal.

CT angiography of the head and neck revealed normal intracranial and neck vessels with no evidence of intracranial haemorrhage, infarction or any other intracranial lesions.

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