Acute Vision Loss in a Patient With Atrial Fibrillation

Case Study

A rapid response event was initiated for a patient for acute onset change in vision. On prompt arrival of first responders, the patient was found to be a 64-year-old female with a known history of atrial fibrillation, anticoagulated with apixaban, type 2 diabetes mellitus, hypertension, and coronary artery disease for which she had received coronary artery bypass graft one year before. She was admitted to the hospital two days before for management of alcohol-induced pancreatitis and was still not feeling well enough to tolerate any oral intake, including any oral medications. The patient had been doing well neurologically until 30 min before the rapid response was initiated, which was when she had developed an acute onset change in vision.

Vital Signs

Temperature: 98.5 °F, axillary
Blood Pressure: 148/89 mmHg
Heart Rate: 115 beats per min – telemetry showed atrial fibrillation
Respiratory Rate: 14 breaths per min
Pulse Oximetry: 98% oxygen saturation on room air

Focused Physical Examination

A quick exam showed a thin elderly appearing female in mild distress. Cranial nerve exam showed pupils were equal and reactive to light and accommodation. Bilateral visual field defects were present, which were consistent with homonymous hemianopia with macular sparing. Other cranial nerves were intact. Gross sensations, strength, and coordination were intact. Cognition was intact on a focused exam. A cardiovascular exam revealed tachycardia with an irregularly irregular rhythm; no carotid bruits were present on auscultation.

Interventions

A cardiac monitor and pacer pads were attached immediately. Bedside blood glucose was done which showed a capillary glucose level of 154 mg/dL. The National Institutes of Health Stroke Scale (NIHSS) was administered, and the patient scored three based on complete bilateral hemianopia. Stat complete blood count (CBC), electrolyte panel, and coagulation profile were ordered. Electrocardiogram (EKG) was obtained and showed atrial fibrillation. Computed tomography (CT) of the head was ordered and obtained emergently, which did not show any acute intracranial bleed. CT angiogram of the head and neck were negative for any major vascular occlusions. An emergent consult was obtained from stroke neurology, and it was decided to administer tPA given the patient’s disabling persistent neurological deficit. The patient was transferred to the intensive care unit for systemic thrombolysis and subsequent monitoring.

Final Diagnosis

Embolic posterior cerebral artery ischemic stroke secondary to atrial fibrillation.

Ischemic Stroke

Stroke is the sudden onset of focal neurologic deficits associated with dysfunction of the central nervous system (brain, retina, or spinal cord) because of either ischemia or hemorrhages. It is associated with clinical or radiological findings of permanent injury to neurological tissues. It can be broadly defined as either ischemic or hemorrhagic. Ischemic stroke is the more common subtype and accounts for 80% of the cases (see Table 41.1 for causes of stroke). It is caused by reduced blood flow to cerebral parenchyma resulting in an infarct of neural tissue. Hemorrhagic stroke, in contrast, is caused by the extravasation of blood into the brain parenchyma or the subarachnoid space because of the rupture of a blood vessel. Hemorrhagic strokes constitute approximately 20% of all strokes. Transient ischemic attacks are a separate entity and constitute transient, focal neurological deficits without clinical or radiological evidence of infarction.

Table 41.1

Causes of ischemic stroke

Cause	Mechanism
Thrombosis	• Large vessel diseases • Atherosclerosis – affects extracranial and intracranial vessels • Arterial dissection – affects extracranial and intracranial vessels • Vasculitis – affects extracranial and intracranial vessels • Fibromuscular dysplasia – affects extracranial vessels • Moyamoya syndrome – affects intracranial vessels • Small vessel diseases • Lipohyalinosis and fibrinoid degeneration • Atheroma formation
Embolism	• Cardiac source • Atrial fibrillation, sustained atrial flutter • Mechanical heart valve • Atrial or ventricular thrombus • Infective endocarditis • Non-infective endocarditis (lupus, marantic endocarditis) • Atrial myxoma • Atrial or left ventricular aneurysm • Patent foramen ovale • Arterial source • Aortic atheroma • Aortic root aneurysm • Cryptogenic – unknown source of embolism
Systemic hypoperfusion	• Shock – any cause, but more commonly with cardiogenic shock • Severe anemia
Hypercoagulability	• Sickle cell disease • Polycythemia vera • Essential thrombocytosis • Hypercoagulable disorders – prothrombin gene mutation, APLS, protein C/S deficiency, Factor V Leiden, antithrombin III deficiency • Heparin-induced thrombocytopenia