Ep 122: 45-Year-Old Healthy Man with Loss of Consciousness

This episode presents a healthy 45-year-old who loses consciousness while playing tennis and is found to have focal neurologic findings. We discuss the initial evaluation and acute therapeutic interventions.

Transcript

[upbeat intro music]

[Dr. Handy] Hi, everyone. Welcome
back to Harrison's Podclass.

We're your co-hosts. I'm Dr. Cathy Handy.

[Dr. Wiener] And I'm Dr. Charlie
Wiener, and we're joining

you from the Johns Hopkins
School of Medicine.

[music continues]

Welcome to episode 122:

a 45-year-old healthy man
with loss of consciousness.

Cathy, today's patient is
a 45-year-old healthy man

who takes no medications.

He's playing tennis, and while doing that,

he develops a severe headache, collapses,

and he loses consciousness.

EMS is called by his colleagues,

and on their initial evaluation,

they find that his blood
pressure is 170/80.

His heart rate is 75. His
heart rate is regular.

He's got respirations of 14 per minute

and an oxygen saturation of 98%.

They immediately transport him
to the emergency department,

where he is found to be
arousable now but somnolent.

He's confused, and he has some
notable left-sided weakness.

His vital signs are otherwise
essentially unchanged,

and he's afebrile.

His spouse arrives soon thereafter,

and she reports that the patient

has not reported feeling unwell,

and he's not been limited in
any of his activities recently.

Everything was normal, as
far as she was concerned.

[Dr. Handy] Okay, the list of things

that can cause sudden loss of
consciousness is pretty short.

The preceding headache,

the focal neurologic
deficits make this sound

like it's potentially a
subarachnoid hemorrhage, or SAH.

That would be very much
a medical emergency.

[Dr. Wiener] Let's talk about
some of those other possibilities.

An ischemic stroke comes
to mind, for example.

[Dr. Handy] There are many
things on the differential,

and we're going to get a
STAT CT scan of his head,

which would be diagnostic of
the subarachnoid hemorrhage

but let's talk about
some of the other things.

So meningitis is a possibility

but given he's not had
any prodrome or no fevers,

I don't think that that is likely.

Thunderclap headaches can mimic
a subarachnoid hemorrhage,

but they don't typically cause
true loss of consciousness

as we heard about in this case.

And that would be a
diagnosis of exclusion.

Also, he has no prior
risk factors for stroke

and no evidence of AFib,
a major risk factor.

So I think an embolic or a
thrombotic stroke is less likely.

Depending on the location
of the hemorrhage,

they can definitely cause
a focal cranial nerve

or motor deficits, and we did hear about

focal neural symptoms on his exam.

[Dr. Wiener] Okay, well, as you requested,

he's whisked quickly to the CT scanner,

and he's found to have, as you suggested,

an aneurysm of the right
middle cerebral artery

with a subarachnoid and
intraventricular blood.

He goes for embolization,

and afterwards he seems
more alert and is oriented.

[Dr. Handy] Okay, so that's diagnostic.

More than 95% of patients
with subarachnoid hemorrhage

have enough blood to be visualized

on a high-quality, non-contrast CT scan

that's obtained within 72 hours.

If the scan fails to
establish the diagnosis

of subarachnoid hemorrhage,

and no mass, lesion, or
obstructive hydrocephalus is found,

a lumbar puncture should be performed

to establish the presence
of subarachnoid blood.

Lysis of the red blood cells

and subsequent conversion
of hemoglobin to bilirubin

stains the spinal fluid
yellow within 6-12 hours.

This xanthochromic spinal fluid peaks

in intensity at 48 hours,

and it can last for one to four weeks,

really depending on the amount
of blood that's present.

[Dr. Wiener] Before we
get to the question,

let's talk a little bit
about the epidemiology

of subarachnoid hemorrhages.

[Dr. Handy] Excluding head trauma,

the most common cause of
subarachnoid hemorrhage

is rupture of a saccular aneurysm.

Autopsy and angiography studies have found

that about 2% of US adults
harbor intracranial aneurysms.

So that's a prevalence of
about 4 million people.

The aneurysm will rupture,

producing a subarachnoid hemorrhage,

in about 25-30,000 cases per year.

Also, remember from a
prior Podclass episode

that patients with
polycystic kidney disease

have a higher prevalence
of cerebral aneurysms, too.

[Dr. Wiener] And rupture can
be fatal, often, correct?

[Dr. Handy] The overall mortality rate

for aneurysmal subarachnoid
hemorrhage is about 35%

with around 1/3 of these
patients dying immediately

and prior to hospital admission.

So obviously, that is very severe.

Of those who survive,
more than half are left

with clinically significant
neurologic deficits because of

the initial hemorrhage, or
delayed neurologic deficit.

[Dr. Wiener] And finally, tell me more

about these saccular
aneurysms that you mentioned

and the pathophysiology
that leads to rupture.

Why do they rupture?

[Dr. Handy] Saccular aneurysms
occur at the bifurcations

of the large to medium-size
intracranial arteries.

Rupture is into the subarachnoid
space in the basal cisterns

and sometimes into the
parenchyma of the adjacent brain.

Approximately 85% of aneurysms occur

in the anterior circulation,
mostly on the circle of Willis.

About 20% of patients
have multiple aneurysms,

many at mirror sites bilaterally.

Now, as an aneurysm develops,

it typically forms a neck with a dome.

The arterial internal
elastic lamina disappears

at the base of the neck of the aneurysm,

and connective tissue
replaces smooth muscle cells.

The site of rupture is
most often the dome.

Aneurysm size and site are important

in predicting the risk of rupture.

Those that are greater than
seven millimeters in diameter

and those at the top of the basilar artery

and at the origin of the
posterior communicating artery,

or the PCA, are at
greater risk of rupture.

[Dr. Wiener] Okay, well, great.
I think that's phenomenal

background on subarachnoid hemorrhage.

And you called what was going to happen

but let's talk a little
bit about management.

So the question asks,

all of the following
therapeutic interventions

are indicated in this patient, except?

A. catheter-directed aneurysm repair;

B. oral nimodipine;

C. pneumatic lower extremity compression;

D. prophylactic lumbar drainage;

and E. therapeutic hyponatremia.

[Dr. Handy] Okay, so the first
part of this question was

understanding that what was
happening was a subarachnoid

hemorrhage, and now we're
talking about the therapeutic

interventions that would be
indicated in that scenario.

So the answer is E.

So hyponatremia is one of
the four dreaded causes

of delayed neurologic deficit

after a subarachnoid hemorrhage.

Hyponatremia may be profound,

and it can develop quickly
in the first two weeks.

There's both natriuresis
and volume depletion

with subarachnoid hemorrhage

so that patients become both
hyponatremic and hypovolemic.

Both atrial natriuretic peptide

and brain natriuretic peptide have a role

in producing this cerebral
salt-wasting syndrome.

The hyponatremia may
contribute to cerebral edema,

which is the last thing
that these patients need.

Typically, the hyponatremia clears

over the course of one to two weeks,

and in the setting of
subarachnoid hemorrhage

should not be treated with
free water restriction

as this may increase the risk of stroke.

[Dr. Wiener] You mentioned
that hyponatremia is one of

the four dreaded causes of
delayed neurologic deficits.

What are the other three?

[Dr. Handy] We're going to
talk a little bit about that

in the context of the answers,

but they're aneurysm
re-rupture, hydrocephalus,

and delayed cerebral ischemia.

[Dr. Wiener] Okay, well, let's
go through the true answers

to help us manage a patient
with subarachnoid hemorrhage.

[Dr. Handy] So first,
if the patient survives,

but the aneurysm is not obliterated,

the rate of re-bleeding is
20% in the first two weeks,

30% in the first month, and
about 3% per year afterwards.

Therefore, repair of the aneurysm

is in order to prevent re-bleeding.

At many centers, definitive
repair is carried out

within 24 hours of the
bleed in all patients

who are stable enough to
tolerate the procedure.

An aneurysm can be
clipped by a neurosurgeon

or coiled by the endovascular surgeons.

Recent studies have demonstrated

that endovascular techniques
such as coiling or stenting

have better results than
surgical approaches.

However, these interventions
may not be available,

or the patient's anatomy
may not be amenable

to an endovascular approach.

So surgical clipping is
still utilized in some cases.

There are reliable data showing

that specialized aneurysm
treatment centers

can improve mortality rates.

[Dr. Wiener] Option B was
nimodipine. What is its role?

[Dr. Handy] I mentioned delayed
cerebral ischemia, or DCI.

So this remains a leading cause
of morbidity and mortality

following aneurysm,
subarachnoid hemorrhage.

Treatment with the calcium
channel antagonist nimodipine

improves outcome perhaps by
preventing ischemic injury

rather than reducing
the risk of vasospasm.

Symptomatic cerebral
vasospasm can also be treated

by increasing the cerebral
perfusion pressure

by raising mean arterial pressure

through plasma volume expansion

and the judicious use of
IV vasopressor agents.

Raised perfusion pressure
has been associated

with clinical improvement
in many patients,

but high arterial pressure
may promote re-bleeding

in unprotected aneurysms.

Euvolemia should be targeted

as significant hypervolemia can lead

to cardiopulmonary complications.

As I mentioned in the
context of hyponatremia,

hypovolemia should be strictly avoided.

[Dr. Wiener] Okay, and I presume

that pneumatic compressions prevent PE.

[Dr. Handy] Yeah, these
patients are at risk of PE,

or pulmonary embolism.

And DVT prophylaxis with
heparin can be initiated

within one to two days
following endovascular treatment

but not immediately.

So that would be indicated
to start sooner than that.

[Dr. Wiener] And finally,
prophylactic lumbar puncture?

[Dr. Handy] Yeah, this was new to me,

but a recent trial of
prophylactic lumbar drainage

after subarachnoid hemorrhage,

even with normal intracranial pressure,

improved outcomes and decreased the rates

of secondary infarction at six months.

[Dr. Wiener] Okay, so the
teaching points, which are many

in this case, is that
subarachnoid hemorrhage typically

arises in unsuspected situations

of an unknown asymptomatic
intracerebral aneurysm.

If the patient survives the hospital,

they benefit from immediate intervention

to stabilize the aneurysm,

and then avoid delayed cerebral ischemia

caused by re-bleeding,
hyponatremia, hydrocephalus,

or delayed cerebral ischemia.

[Dr. Handy] And we have this
question and more questions

like it in Harrison's Review Questions.

And then you can also check
out the Harrison's chapter

on subarachnoid hemorrhage
for more information.

Visit the show notes for
links to helpful resources,

including related chapters

and review questions from Harrison's.

And thank you so much for listening.

If you enjoyed this episode,
please leave us a review

so we can reach more
listeners just like you.

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