Case Report

Severe anemia associated with transient ischemic attacks involving vertebrobasilar circulation

Abstract

Transient ischemic attack is one of the most common causes of transient neurologic deficit. Anemic hypoxia results from reduced hemoglobin content with normal arterial oxygen tension and saturation. Anemic hypoxia caused by blood loss or hemolysis has not been considered as an independent factor leading to significant neurologic problems because cerebral homeostasis adjusted by the physiologic regulation in cerebral hemodynamics and oxygenation would meet the brain oxygen requirement in most circumstances even with profound anemia. We report a case of severe anemia associated with transient ischemic attack involving vertebrobasilar circulation.

Transient ischemic attack is one of the most common causes of transient neurologic deficit. It is defined as a brief episode of Neurologic dysfunction caused by focal brain or retinal ischemia, with clinical symptoms typically lasting for less than 24 hours and without evidence of acute infarction [1]. Embolism, large-artery atherosclerosis, pene- trating small-artery disease, and arterial dissection are common etiologies of TIA [2-5]. Anemia is not routinely attributed to TIA; we report a case of severe anemia associated with TIA involving vertebrobasilar circulation.

A 55-year-old man went to our emergency department (ED) with chief complaint of dizziness and general fatigue for 1 day. He had a 3-year history of end-stage renal disease under regular hemodialysis, a history of diabetes mellitus of more than 10 years, and a 5-year history of gout. He was just diagnosed with oxacillin-resistant staphylococcal bacteremia 9 days before presentation in our ED and was under vancomycin treatment. Initial blood pressure was 123/61 mm Hg, pulse rate was 97 beats per min, and body temperature was 37.1?C. Finger-stick testing revealed a blood glucose level of 354 mg/ dL. He claimed that fever had subsided for 1 week and appeared well after antibiotics treatment. Physical examination and neurologic examination revealed generally normal find- ings, and he was mildly pale. Laboratory studies showed the following results: hemoglobin level, 10.3 g/dL; Na, 133 mEq/

L; K, 4.5 mEq/L; Ca, 7.8 mg/dL; ketone, negative; and osmolality, 305 mOsm/kg H₂O. Meclinzine was prescribed for dizziness relief, and observation was suggested. However, the patient’s condition deteriorated 20 hours later. Dysarthria, dysphagia, Gait Ataxia, and decreased level of consciousness were found. Finger-stick testing showed a blood glucose level of 263 mg/dL, and the vital signs were as follows: body temperature of 36.3?C, heart rate of 76 beats per minute, respiratory rate of 23 breaths per minute, and blood pressure of 132/53 mm Hg. Electrocardiogram revealed normal sinus rhythm. Emergency brain computed tomographic scan was arranged immediately, but it did not demonstrate findings of new infarcts. Arterial blood gas showed the following: pH, 7.395; PCO2, 28.0 mm Hg; PO2, 112.0 mm Hg; HCO₃, 16.8

mm/L; and saturation (SAT), 98.2%. Hemoglobin level was

3.2 g/dL. Anemia was corrected soon by blood transfusion; after that, the dysarthria, ataxia, and dysphagia resolved. The level of consciousness was recovered completely to normal. No episode of hypotension was noticed. Posterior TIA was diagnosed. Esophagogastroduodenoscopy confirmed gastric ulcer bleeding. Echocardiography demonstrated normal left ventricular function, absence of left ventricular thrombus, and normal valvular function. Color-coded carotid duplex revealed mild stenosis without hemodynamic change in both carotid branches and reduced blood flow at both extracranial vertebral arteries. transcranial Doppler demonstrated possible diffuse atherosclerosis at both posterior cerebral artery and left vertebral artery. The patient was discharged with no neurologic sequelae under pantoprazole and clopidegrol treatment. No episodes of TIA have recurred, and he has remained free of any neurologic deficit after a 6-month follow-up.

Anemic hypoxia results from reduced hemoglobin content with normal arterial oxygen tension and saturation. Anemic hypoxia caused by blood loss or hemolysis has not been considered as an independent factor leading to significant neurologic problems because cerebral homeostasis adjusted by the physiologic regulation in cerebral hemodynamics and oxygenation would meet the brain oxygen requirement in most circumstance even with profound anemia [6]. We have found only 2 case reports of TIA caused by anemia [7,8]. Tissue dysfunction caused by anemic hypoxia may aggravate disease manifestations in organs with a compromised condition. Although not much is addressed for the brain, it

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is well known for the heart [9,10]. There are 2 possible reasons for Brain hypoxia: reduced cerebral blood flow at both extracranial vertebral artery and severe anemia. Any of these factors may not induce neurologic deficit; however, the combination of these 2 factors may decrease the amount of oxygen available for brain tissue requirement and then result in neurologic impairment.

Our case provides a concept that the coexistence of anemia and vertebral artery insufficiency may be a causative factor of TIA.

Kuang-Yu Hsiao MD Cheng-Ting Hsiao MD Leng-Jye Lin MD

Chi-Jei Shiao MD I-Chuan Chen MD Department of Emergency

Chang Gung Memorial Hospital

Chiayi, Puzih City Chiayi County 613, Taiwan

Chang Gung University College of Medicine

Taoyuan, Taiwan E-mail address: [email protected]

doi:10.1016/j.ajem.2007.05.028

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