An initially unknown “John Doe” male presented to the emergency department (ED) via emergency medical services (EMS) with concern for stroke. He lived in a boarding home and was found unresponsive in a common bathroom by new housemates who called 911. They reported that the patient appeared well when he came home from work. About 6 hours later, they found the bathroom door locked and pried it open to find the patient unresponsive. There also was a report of a possible history of substance abuse. Upon EMS arrival, the patient was tachycardic in the 150s with a blood sugar of 254. His initial blood pressure was 76/52. EMS reported that the patient was combative and altered with a possible right-sided facial droop. They called for a medical command to administer 5 mg of IM midazolam to better control the patient so that treatment could be started. En route to the emergency department, he received 200 mL of intravenous normal saline solution. On arrival to the ED, the patient’s vitals were as follows: heart rate of 95 beats per minute, respiratory rate of 17 breaths per minute, blood pressure was 129/76 mmHg, 96.3 degrees F rectal temperature, 97% saturation in room air, and blood sugar of 309.
Given the facial droop and concern for stroke, a “Stroke Alert” was initiated. The doorway exam showed a subtle right-sided facial droop and left-sided weakness of the upper and lower extremities. Per protocol, he went directly for a noncontrast CT brain. The CT showed old small lacunar infarcts without definite acute findings. His physical exam found mild tachycardia, clear though shallow lungs, a non-distended soft abdomen without masses, and a lethargic sensorium that was resistant to care. His neurological exam was notable for PERRL and EOMI, no gag reflex, subtle right-sided nasolabial flattening, left upper extremity held in hemiplegic appearance with immediate drop to the bed, decreased spontaneous left leg motor, and a positive right Babinski reflex. Right-sided motor and all sensation were intact. Ocular confrontation did not suggest visual field cuts. He was mute and did not appear to understand or follow commands. His Glasgow Coma Scale was 9, and he had a NIH stroke scale of 20.
His last known well time was more than 6 hours prior to arrival in the ED. As such, he was not a candidate for acute thrombolysis. Further workup included a computed tomography angiography (CTA) of the head and neck which showed no large vessel occlusion, significant stenosis, or aneurysm. The CT also noted that the thoracic aorta and aortic arch vessels were patent and normal in caliber. Chest X-ray was unremarkable including normal mediastinal contours. Labs were notable for BUN 32 mg/dL, creatinine 6.2 mg/dL, blood sugar 309 mg/dL, lactic acid 5.6 mg/dL, CK 3985U/L, WBC 19 × 109/L, and hemoglobin 9.7 g/L. Urinalysis showed cloudy urine with 2 + glucose, 3 + blood, 3 + protein, 6–15 WBCs, and cellular casts. PT/INR was 16.5/1.42 and PTT was 31.6. Toxicology was positive for benzodiazepines (administered by EMS).
The patient received 300 mg of rectal aspirin. Based on the above labs and imaging, the patient was admitted with the following diagnoses: acute stroke, acute kidney injury, lactic acidemia, rhabdomyolysis, severe sepsis, and UTI. At this point, the hospital received identification for the patient from a coworker. He was noted to be 58 years old with a history of hypertension.
Approximately 2.5 hours after the presentation, his blood pressure was noted to be 194/76, then 220/137. Fifteen minutes later, his blood pressure dropped to 83/64 without medication intervention. The patient’s abdomen was noted to be distended, and he remained hypotensive despite fluid resuscitation. A CT abdomen/pelvis with IV contrast was ordered which showed a large abdominal aortic aneurysm and large retroperitoneal hematoma, findings highly suspicious for a ruptured AAA. Emergent transfer to a higher medical center was arranged for endovascular surgery.
A repeat CTA of the chest/abdomen/pelvis at the receiving hospital showed a stable retroperitoneal hematoma and aneurysm that extended to the iliac arteries with extensive plaque calcification. The thoracic aorta was found to be normal in appearance. MRI brain showed a large area of diffusion restriction in the right occipital lobe favoring acute/subacute infarction with associated mass effect and partial effacement of the occipital horn of the right lateral ventricle. Additional scattered foci of diffusion restriction were favored to be embolic in etiology per the radiology report. There was a concern for the proximal embolic source (cardiac or aortic arch), but they were unable to identify the source of the embolic shower. Hypercoagulable studies were unrevealing. They intubated him after specialty evaluation. The endovascular infrarenal aorta to iliac bifurcation surgery went well. He received a tracheostomy and gastrostomy due to continued poor neurologic examinations. He was able to follow commands and mouth words. He remained with left-sided weakness. Bubble study echocardiogram was unremarkable except for LVH and trace multi-valve regurgitation. He had a normal ejection fraction. An MRI done 5 days after the presentation showed evidence of multiple diffuse strokes. He had acute/early infractions of the right occipital, and bilateral cerebellar and cerebral hemispheres. Radiologic impression favored embolic origin due to the diffuse bilateral involvement. Notably, this patient was noted to have some scattered atherosclerotic plaques in the aortic arch, but there was no evidence of aneurysm in the thorax. Additionally, there was no evidence of atrial fibrillation at any point during the patient encounter.
