Page 88 - JSOM Spring 2025

FIGURE 2 Photo taken from the Mar Mikhael district near the immediately due to the abrupt change in light from the hallway
Charles Helou highway, looking into the port (ground zero). Between to LED-lit kitchen. Of note, there were no neurologic signs or
the highway and the grain silo, where the cranes are, were located the symptoms that indicated brainstem herniation, based on John’s
majority of various supply wharehouses/containers for goods such as
hospital supplies, food, and miscellaneous items—all destroyed. normal level of consciousness, normal vital signs, and absence of
Cushing’s response. Nevertheless, this acute neurologic change
raised my suspicion that John’s condition was more serious than
previously thought because throughout my training, we were
always taught that the “eyes are the gates to the brain.” My
index of suspicion for neurologic impairment increased.

I immediately consulted the team leader and Battalion surgeon
via teleconsultation. The patient’s history, proximity to the blast,
medical events over the last few days, and current presentation
were reported. Following our discussion, I created a 2-week
patient care plan involving local neurologic consultation, daily
vital signs checks, a thorough medical history review alongside
my Battalion surgeon, and further MACE evaluations.

While implementing the care plan, I assessed and tested for
several differential diagnoses. I began with nutritional and
metabolic derangements (e.g., hypoglycemia, hyponatremia). I
then assessed for structural and functional lesions (e.g., cranial
nerve palsy, vascular injury, traumatic eye injury) with cranial
nerve, motor, and sensory exams. There were no signs of cra-
nial nerve III palsy, gait abnormalities, dermatome changes, or
Photo by ZJL. focal weakness. I also considered sympathomimetic poisoning
and anticholinergic poisoning due to the nature and compo-
nents (i.e., ammonium nitrate) of the blast. The most danger-
ous differential diagnosis at the time, owing to the operational
environment and limited resources, was a focal lesion within
5
Military Acute Concussion Exam (MACE) and head, eye, ears, the brainstem, such as a hemorrhage or ischemic infarct, or an
nose, and throat (HEENT) exams and ensured the health and expanding posterior communicating artery aneurysm that was
well-being of the team. On examination, personnel from the compressing the third cranial nerve. However, in those early
team closest to the blast had ruptured tympanic membranes, moments with limited information, my most likely differential
conductive hearing loss, and blood and debris within their ex- diagnosis was that this was related to post-blast exposure to
ternal auditory canals. Those furthest from the blast had no chemicals, such as anticholinergic poisoning.
acute signs of trauma and performed similarly to their baseline
pre-deployment MACE scores even though they were perceived Informed by physical examination findings and the Battalion
to have been exposed to more of the direct blast wave. surgeon’s guidance, I encouraged the patient to rest, check his
glucose levels, undergo laboratory evaluation, and consume ap-
Over the next few weeks, we lived out of our trucks on the propriate amounts of water. No laboratory abnormalities were
Beirut airport’s tarmac, operating on a reverse schedule (night- noted. Eventually, a Lebanese neurology team evaluated him
time operations) to assist in regional humanitarian relief ef- at a private hospital, where they ordered a head CT scan and
forts. During this time, one of my teammates began to show CT angiography of the head and neck, which showed no evi-
symptoms of what first appeared to be fatigue or performance dence of intracranial hemorrhage, ischemic stroke, large vessel
exhaustion from the prolonged operations. The patient will be occlusion, or intracranial aneurysm. To further investigate, the
referred to as “John” for anonymity. neurology team requested a brain MRI scan with gadolinium
contrast to evaluate the parenchyma and bony structures.
Clinical Findings
Diagnosis
John displayed cognitive lapses that had not been evident
prior to the blast, such as forgetting where he was or why The MRI scan revealed a significant abnormality. The patient’s
he was performing a task. For example, during a workout he pituitary gland was shrunken, as evidenced by fluid accumula-
stopped what he was doing and looked around the room as if tion in the sella turcica. While I was initially uncertain about
he had forgotten where he was. At that moment, my concern the etiology and severity of John’s condition, after this MRI
for his well-being escalated, and I implemented daily check-ins finding, and due to the uncertainty surrounding the cause
regarding his mental state, sleep-wake cycle, and hydration. (acute or incidental), it was clear that his pathology was out
During these check-ins, I asked John how he had slept the of my scope of practice as an 18D. The new MRI finding, pro-
night before, whether he felt anything out of the ordinary, and gressive symptoms over the past few weeks, and focal neuro-
other questions pertinent to a review of neurologic systems. logic deficit (anisocoria) ultimately led me to advise our team
leader to medically evacuate John.
After several days of assessments, a new symptom of unilateral
anisocoria emerged. One pupil was roughly 4mm larger than the I remember my team leader looking at me, relying entirely on
other, and the dilated pupil was unreactive to light. It stood out my clinical judgment to inform his command decision. This

86 | JSOM Volume 25, Edition 1 / Spring 2025