A 49-year old female without any co-morbidities presented to the emergency department (ED) with seizures. On arrival, she was in a postictal state.
She had recently visited a local hospital with complaints of severe dysmenorrhea and low back pain. The attenders informed us that she was very sleepy and weak at that time, was treated for pain and given tranexamic acid, and sent home. The next day, she had one episode of Generalized Tonic-Clonic Seizure, and she arrived in our ED in a postictal phase. She vomited twice in the ED.
Her vitals were as follows:
- Blood pressure (BP): 160/100 mmHg.
- Heart rate (HR): 22/min
- Peripheral capillary oxygen saturation (SPO2): 98% on room air
- General Random Blood Sugar (GRBS): 233 mg/dl
- Glasgow Coma Scale (GCS): E2V5M6
Her examination was as follows:
- The patient was drowsy but arousable.
- Pupils bilateral reacting to light. No anisocoria.
- CNS examination could not be completed as the patient was drowsy.
- A normal pattern of breathing. The respiratory examination was normal.
- The abdomen was soft, symmetric, and non-tender without distention.
Point-of-care ultrasound (POCUS) showed a flap in the abdominal aorta. (See Figure 1 and 2 for transverse and longitudinal views of the aorta, respectively) Upon this finding, cardiac surgery and neurology consultations were sought.
Image shows transverse section of the abdominal aorta showing a flap.
Image shows abdominal aorta showing a flap.
The laboratory results were as follows:
- D-dimer: 1192 ng/ml
- Haemoglobin (Hb): 10 g/dl
- The international normalized ratio (INR): 1.25
- Platelets: 260000 per mcL
- Total leucocyte count (TLC): 22000 cells/mm3
- Creatinine :1.6 mg/dl.
Meanwhile, the patient was suffering multiple seizure-like episodes, characterized by staring, deviation of the mouth, and irregular limb movements, but these episodes lasted for few minutes and ended without the postictal phase. The patient was drowsy but obeyed commands and did not have any recollection of those few minutes.
Head computed tomography (CT) showed no infarct or bleeding. It was normal.
CT angiogram and aortogram revealed that the patient had Stanford Type A aortic dissection with the flap extending to the entire left subclavian artery, with severely occluding filling defects and thrombosis of the false lumen into bilateral common carotid arteries (See Figure 3, 4 and 5). On the other end, the dissection extended to the common iliac arteries (See Figure 6).
Image shows CT Aortogram showing bilateral common carotid artery filling defects
Image shows ascending and descending aortic dissection
Image shows dissection of the common iliac artery before bifurcation.
Initially, the patient was treated symptomatically by anti-epileptics and analgesics. After the cardio-thoracic and vascular surgeon consultations, we decided to airlift the patient to a higher centre as our hospital was tertiary care and there were no grafts for the urgent repair of the extensive aortic dissection. We intubated the patient for secure transportation. However, we learned that the patient expired in the higher centre before reaching the operating room.
Before I shed light on the important part of this discussion, I know that the outcome of this case was unfortunately grave. However, I chose this case because of it.
In this case, the patient had low back pain in her previous hospital visit. However, she was sent home with symptomatic management, implying that it could have been addressed more carefully. She visited our ED one day later, and POCUS let us diagnose the dissection in 15 minutes, which was confirmed by a CT aortogram within 40 minutes. After consultations and finding the available facility, we airlifted the patient to a higher centre for urgent repair, but the patient could not make it to the operating room.
We all know acute aortic dissection is the most common life-threatening disorder affecting the aorta. Over the first several hours, the mortality rate increase up to 1% per hour; therefore, early intervention is critical (1). In our case, the involvement of bilateral carotid arteries caused seizure-like episodes and altered mental status. Also, studies show that patients with similarly located dissections may experience neck pain, transient ischemic attacks (TIA), cerebral ischemia, transient monocular blindness and subarachnoid haemorrhage (SAH) but not seizure(2). In our case, the global hypo-perfusion caused recurrent TIAs, which resembled seizure-like clinical episodes. That’s why emergency physicians should be vigilant about the underlying causes of seizure-like activities, even if altered mental status similar to postictal state is present, especially if the patient does not have a history of seizures and the complaints are unclear. Keep the aortic dissection in mind as a differential. Also, I cannot stress the use of POCUS in the ED enough. It is a game-changer, and in our case, it detected a lethal disease successfully.
- Never ignore back pain that does not subside after adequate pain management.
- POCUS is always a game-changer. It saves a lot of time and lives, as in my case.
- Seizures or not, you must keep a high suspicion for lethal vascular diseases. Remember the basics: If unclear, go back to history.
- Once you confirm an aortic dissection, never delay treatment because time = life.
- Never ever send a patient back home unless you are completely sure about the cause of the presenting symptom. Over investigating is ok when compared to under investigating, when it might cost a life.
References and Further Reading
- Braverman AC. Acute aortic dissection: clinician update. Circulation. 2010;122(2):184-188. doi:10.1161/CIRCULATIONAHA.110.958975
- Debette S, Grond-Ginsbach C, Bodenant M, et al. Differential features of carotid and vertebral artery dissections: the CADISP study. Neurology. 2011;77(12):1174-1181. doi:10.1212/WNL.0b013e31822f03fc
One thought on “Seizure: Lethal Dissection”
Good one Doctor !
Way to go,,,,all the best