JIMENEZ, Joseph M.

Neurology Preceptorial
2019A March 2, 2018
University of the East
Ramon Magsaysay Memorial Medical Center, Inc.
#64 Barangay Dona Imelda, Aurora Boulevard Quezon City 1113

DEPARTMENT OF NEUROLOGY
Neurology II: A.Y. 2017-2018
Preceptor: Dr. Encarnacion

NAME: JIMENEZ, Joseph M.

Date of Admission: December 30, 2017
Date of Interview: February 4, 2018

Patient Profile

Patient LM is a 47 year old, Filipino, female, left-handed, married, and living in Pasig City admitted for
the first time in UERM.

Source and Reliability

The patient’s sister and husband with fair reliability.

Chief Complaint

Loss of consciousness of 16 hours duration.

History of Present Illness

Patient LM is a known hypertensive (2010) with poor compliance prescribed with Valsartan and
Clonidine (Catapres) unrecalled doses. She would only take Catapres when symptomatic and her
usual BP is 160/120 mmHG.

Sixteen hours prior to admission, the patient was apparently well when she suddenly lost
consciousness and was unarousable while visiting their meatshop in Nueva Ecija. She was
immediately brought to a nearby clinic where she was given an unrecalled medicine sublingually and
was advised to go to a hospital. No other eyewitnesses were available to elicit history.

In the interim, her husband noted twitching up and down movements of the right hand. She arrived at
a private hospital where she had a CT angiogram which showed a ruptured aneurysm. The family
opted to have the patient admitted in a hospital in Pasig. She was placed on oxygen mask and was
transferred.

Nine hours prior to admission, the patient was still unconscious when they arrived at RMC and had an
X-ray which revealed dentures lodged in her throat. She was then rushed to UERM due to lack of
materials in RMC.

Hours prior to admission, he was admitted in UERM and was scheduled for surgery at 11pm Dec.30,
2017.

The patient had no trauma, fever, and neck pain.

JIMENEZ, Joseph M. Neurology Preceptorial
2019A March 2, 2018
Temporal Profile

Medical History

The patient is a known hypertensive diagnosed on 2010 with poor compliance. She had a prior
vehicular accident where she had a scar on her left knee. No prior surgeries and no known allergies.
No use of anticoagulants.

Family History

Father has hypertension and diabetes while the mother is alive and well. All five siblings are
diagnosed with hypertension.

Social and Environmental History

The patient is married with 4 children (3 girls and 1 boy). She was born on Nueva Ecija and currently
resides in Pasig City. She is a college undergraduate (2nd yr) and took BS Midwifery.

The patient’s husband denies any alcohol intake, illicit drug use, and tobacco smoking.

Review of Systems

(+) hypertension with uncontrolled BP usually 160/120 mmHg

(+) cough and sputum

Physical Examination

GENERAL SURVEY The patient is obtunded with a GCS score of 10 spontaneous eye
opening, no verbal response, and localizes to pain. She is bedridden
with PEG tube and tracheostomy tube. She is mostly asleep and not
in distress.

VITAL SIGNS Temperature: 37.1 C

JIMENEZ, Joseph M. Neurology Preceptorial
2019A March 2, 2018

BP: 150/100 mmHg (right arm)

PR: 79
RR: 25
O2 sat.: 89-97%

SKIN, HAIR, NAILS Unremarkable

HEENT Postoperative scar on the right frontotemporal area with a total of 12

staples.
Tracheostomy tube with greenish discharge.

CHEST AND LUNGS Labored breathing. No apnea. Tracheostomy. Vesicular breath

sound heard on lung fields.

CARDIOVASCULAR Adynamic precordium. Distinct heart sounds. PMI at left parasternal

border. (+) s3 gallop. No cyanosis. CRT < 2 sec. No edema.
Symmetrical bounding regular pulses.

ABDOMEN Abdomen is flat. Normoactive bowel sounds at 18/min. Tympanic

upon palpation. No guarding and tenderness. No aortic pulsations.
PEG tube on LUQ.

MUSCULOSKELETAL Unremarkable

Mental Status Exam

GCS 10 with spontaneous eye opening, no verbal response and localizes to pain with tracheostomy.
She is unable to follow commands. Judgement, fund of knowledge, insight, and ability to perform
learned functions cannot be assessed. Other areas cannot be assessed.

Cranial Nerves
CN I – cannot be assessed
CN II – (+) ROR
CN II, III – Left eye (-) direct reflex (+) consensual reflex
Right eye (+) direct reflex (-) consensual reflex
CN III, IV, VI – primary gaze midline upon eye opening which shifts to the right
CN V – no response on light touch on the left side of the face on V1, V2, and V3. Right face intact
light touch
CN VII – no drooping of eyelids. Able to raise eyebrows, wrinkle forehead, close eyelids, and frown
CN VIII – cannot be assessed
CN IX, X – intact gag reflex (suction)
CN XI – unable to follow commands
CN XII – unable to assess due to mandibular fracture

Motor exam
Strength: LUE 1/5
RUE 3/5
LLE 1/5
RLE 1/5
Tone: normal tone on both LE and UE.

Sensory exam
Localizes to pain on RUE.
Does not respond to pain and light touch on LUE, LLE, and RLE
JIMENEZ, Joseph M. Neurology Preceptorial
2019A March 2, 2018
Reflexes
Present bilateral Babinski reflex. Present grasping reflex.

DTRs:
Biceps, brachioradialis, and patellar - +2

Cebellar and Meningeal

Cannot be assessed

CASE DISCUSSION
Primary Impression: INTRACRANIAL HEMORRHAGE SECONDARY TO A RUPTURED
ANEURYSM

SUBJECTIVE
47, female
Known hypertensive (poor compliance)
Family history of hypertension
16 hour loss of consciousness
OBJECTIVE
BP: 160/120 mmHg right (usual BP)
Obtunded, mostly asleep
GCS 10 spontaneous eye opening, no verbal
response, localizes to pain
No direct and consensual pupillary response on
the left eye
Intact direct and consensual pupillary response
on the right eye
No response to light touch on the left face
No response to light touch on LUE, LLE, RLE
Unable to follow commands
1/5 muscle strength on LUE, LLE, RLE
3/5 muscle strength on RUE
Present bilateral Babinski reflex
Grasping reflex

Symptoms alone are not specific enough to distinguish ischemic from hemorrhagic stroke. However,
generalized symptoms, including nausea, vomiting, and headache, as well as an altered level of
consciousness, may indicate increased intracranial pressure and are more common with hemorrhagic
strokes and large ischemic strokes. Seizures are common in hemorrhagic than in ischemic type. The
progression of the clinical symptoms are faster in an ischemic stroke which takes minutes.

ICH is the second most common form of stroke after infarct (15%-30% of strokes are ICH), but the
most deadly (In Adams, this is the third most common cause of stroke, following cerebral embolism
and thrombotic disease). Unlike ischemic infarct: smooth progressive onset over minutes to hours,
often with severe headache, vomiting and alterations in level of consciousness. Unenhanced CT scan
of the brain is the initial diagnostic study of choice

The volume of hematoma correlates highly with morbidity and mortality. Kothari method:
(length x width x height) / 2 is a fast and simple method of estimating the volume of intracerebral
hemorrhage. The clot enlarges in at least 33% of cases within the first 3 hours of onset. Most
common site is the putamen and adjacent internal capsule.

The vessel that ruptures, giving rise to the hemorrhage are usually small, deep penetrating
nonbranching end arteries that arise directly from much larger arteries like:
 Middle cerebral artery (lenticulostriate going to the
 putamen)
 Anterior choroidal artery, anterior cerebral artery
JIMENEZ, Joseph M. Neurology Preceptorial
2019A March 2, 2018

 Posterior cerebral artery, posterior communicating artery

 Cerebellar arteries, basilar artery

The outcome of ICH depends largely on patient age, hematoma size, location, presence of ventricular
hemorrhage, and Glasgow Coma Scale score
 Age - the higher the age group, the poorer the outcome
 Volume of the hematoma - the greater the volume of the hematoma, the greater the increase
in ICP. In small hematomas, you may not be required to operate, that’s why there’s that 30cc.
However, if it’s 100cc, it doesn’t matter whether you operate or not because the prognosis will
still be poor
 Location - the more midline the position, the poorer the diagnosis. Subcortical> Putaminal>
Thalamic > Pontine (worst hemorrhage)

Patients with ICH will never go back to normal. The purpose of surgery is to try to prevent them from
dying. You will have to accept the fact that the patient will have a neurologic deficit.

The patient presented with a sever loss of consciousness with no evidence of headache or focal
neurologic deficits (no source). This correlates to the severity of the bleed. If this was an infarct, a
sudden weakness would present but rather an ICH is a more likely diagnosis. The location could be
putaminal or subcortical, being the most common areas of first stroke with the risk factor of
uncontrolled BP. The PE also corresponds in where there is bilateral Babinski reflex, irregular
respiration, and the gaze is preferred to the side of the clot.

Differential diagnosis:
Brain Neoplasm could present with the symptoms but the temporal profile does not coincide. The
progression of the symptoms are too fast. A mass in the cranium would present usually in an insidious
manner and most commonly with seizure or headaches. The appearance of the focal neurologic
deficit t was abrupt suggesting the etiology of stroke more likely.

Meningitis is another differential but the absence of nuchal rigidity makes it highly unlikely. There was
also no fever. Do lumbar tap to rule out (if not increased ICP) or CT will show inflamed meninges.

Subdural hematoma is commonly associated with trauma which is absent, making this diagnosis
unlikely.

Diagnostic tests:
CBC – to check for leukocytosis
Coagulation studies – PT and aPTT to identify coagulopathies
Serum electrolytes and osmolality – to rule out electrolyte imbalance and maintenance
Blood glucose – to rule out hypoglycemia
ECG – help diagnose heart problems and identify etiology
Lumbar tap – obtain opening pressure and to evaluate CSF for SAH (presence of RBCs)

CT scan noncontrast– to rule out hemorrhagic vs ischemic stroke. High sensitivity and specificity.
MRI or CT angiography– higher sensitivity and specificity. For negative CT and lumbar tap.

Plan:
First step is to identify if the patient is indeed in a stroke. It is important to rule out metabolic diseases
and other etiologies. The second step is to determine the pathophysiology of the stroke to initiate the
correct treatment.
Criteria for stroke include temporal profile of the clinical syndrome is sudden and the evolution of the
neurologic disturbance is in relation to the patient’s medical status. The patient is a known
JIMENEZ, Joseph M. Neurology Preceptorial
2019A March 2, 2018
hypertensive that is non-compliant and has a strong predisposition to stroke. Another criterion is the
evidence of a focal neurologic sign (hemiparesis). Check the risk factors and rule out stroke
mimickers.
If the criteria is in line with stroke, a CT scan is requested because it has good sensitivity and fast
diagnostic imaging to rule out hemorrhage. Also request for ECG to help diagnose etiology and treat
any heart problems if present.

Management:
Hemorrhagic Stroke
Medical treatment includes:
 Determine the cause of the bleeding (CT)
 Controlling the blood pressure – rapid reduction to 140-160 is not recommended
o Use of beta blockers or ACE/ARBs is recommended
 Stopping any medication that could increase bleeding.
 Measuring and controlling the pressure within the brain
 Maintenance of adequate ventilation
 Selective use of controlled hyperventilation to a pCO2 of 25-30mmHg
 Monitor ICP with use of mannitol
o Osmolality 295-320 mosm/kg
o Na 145-150mEq
 Limit IV infusion to normal saline

Definitive treatments are:

Surgery — Surgical management of cerebral aneurysms, in which a clip is placed across the neck of
the aneurysm, is an effective and safe procedure. However, risks associated with surgical aneurysm
treatment include new or worsened neurologic deficits caused by brain retraction, temporary arterial
occlusion, and intraoperative hemorrhage
 Clipping of Aneurysm
 Excision of AVM
 Evacuation of Hematoma
 Hemicraniectomy (decompression)

Endovascular therapy using Coil embolism - The Guglielmi electrolytically detachable coil system was
introduced in the early 1990s. Platinum coils are inserted into the lumen of the aneurysm. A local
thrombus then forms around the coils, obliterating the aneurysmal sac. The procedure is often, but not
invariably performed under general anesthesia. Complications of endovascular coiling include
thromboembolism and intraprocedural aneurysm rupture.
 Coiling or Embolization, especially for AV
 malformations
 Radiosurgery – deliver a high dose radiation to the lesion which will incite endovascular
proliferation which will clot the vessel and obliterate the AVM; this has less morbidity than
open surgery but the clotting takes 3-5 years and patients may come back with rebleed
• Gamma Knife base – With a cobalt content, and emits gamma rays
• LINAC – uses x-rays as an ionizing variation to control AV malformations