I.

General Data
The patient is E.B.C., a 44-year old Filipino male, residing in Molino, Cavite. He
is single and Roman Catholic. He was born on August 31, 1974 in Tacloban, Leyte. He
was admitted on February 14, 2017 at Ospital ng Maynila Medical Center. This is his
second admission in this institution.

II. Chief Complaint

Bilateral loss of vision with L hemisensory loss

III. History of Present Illness

The patient is a known hypertensive since 2016 with HBP of 200/100 mmHg and
UBP of 130/80 mmHg and is maintained on Losartan 50 mg OD and Amlodipine 5 mg
OD with reported fair compliance.
4 hours PTA, the patient experienced blurring of vision, which he described as
bilateral and progressive.
3 hours and 40 minutes PTA, he then experienced pins and needles sensation
on his left foot ascending to his whole left body within a span of 10-15 minutes. When it
reached the face, he said that he cannot feel on his left side anymore and described the
sensation as “pangangapal ng kalahati ng katawan.” At this time also, he said that there
is complete loss of vision and his visual field was black. This is associated with dizziness
but there was no noted headache, weakness or loss of consciousness. There was also
no note of vomiting. The patient said that the hours prior to the manifestations of
symptoms were uneventful and he just sat all day, except for a missed anti-hypertensive
medication (Losartan 50 mg) earlier that morning. After screaming for help, he was
rushed by his neighbors to the nearest hospital.
2 hours PTA, the patient was rushed to the ER of MetroSouth Hospital in Cavite
where he claimed to have a blood pressure reading of 200 be given sublingual Clonidine
with unrecalled dosage and unrecalled relief of hypertension. He was then referred to
OMMC due to lack of vacant room for admission.
1 hour and 10 minutes PTA, patient regained full vision but still has left
hemianesthesia when he arrived at OMMC. He was then subsequently admitted.

IV. Past Medical History

The patient has no known allergies to food or drugs. He claimed that he has complete
immunization, including Hepatitis A.

Medical:
 July 2016 – Hypertension and stroke (Right-sided hemiplegia and
hemianesthesia without loss of consciousness) – OMMC – given Captopril
(unrecalled dose and frequency), Citicoline (500 mg TID, discontinued after 2
months), Losartan (50 mg OD), Amlodipine (5 mg OD) and Aspirin (unrecalled
dose, OD); rTPA not done; still undergoing rehabilitation (physical therapy) up to
present

Surgical:
 none

V. Family History

1
 Both parents are deceased already. His mother died at the age of 69 (2010) after
her fourth episode of stroke. She was also chronically hypertensive. According to the
patient also, their mother had an unrecalled heart condition. His father died at the age of
45 (1995) due to complications of tuberculosis. He is the third in the family and he has 4
other siblings. The eldest is 54 years old, female, with no medical illness; second is 47
years old, male, hypertensive; fourth is 43 years, male, with alleged migraine headache;
and the fifth is 42 years old, female, also with alleged migraine headache. The patient
also has two children, both male, aged 25 and 18 years, both of whom have no medical
illnesses.
Aside from stroke and hypertension and migraine, the patient has no family
history of diabetes, tuberculosis, cancer, vasculitis, rheumatic heart disease, and blood
disorders. He did not report of any experience of headache in the past also. History of
heart disease, such as atrial fibrillation, cannot be ruled out as the patient cannot recall
what the “heart condition” of the mother was.

VI. Personal and Social History

The patient is a two-year vocational college course graduate. He has been
unemployed since his stroke last year. He previously worked as a seaman (1999-2008)
and as a part time school bus driver while waiting for the renewal of his contract (1999-
2016). He was a smoker since 1992 and stopped only last year after he had a stroke (14
years). He smoked 2 packs a day, amounting to 28 pack-years. He was also an
alcoholic beverage drinker since 1992, consuming approximately 1 liter per month, and
only stopped last year after he developed a stroke. He denied illicit drug use.
He usually eats thrice a day, consuming ½ cup rice per meal, with usual viand of
fried egg, some vegetables and meat. He is also fond of eating fatty and salty foods, as
well as using condiments such as soy sauce and fish sauce when eating his meal. He is
also fond of drinking carbonated drinks, usually everyday. His water intake daily
amounts to approximately 1-2 liters.
The patient usually wakes up at around 4 am and sleeps at 8 to 10 pm. He has
no abnormalities in sleeping or waking up except for “loud snoring” which was noticed by
his previous wife. He reported to be well rested in the morning.
The patient usually urinates 5 times daily, with clear to yellow-colored urine
without dysuria, hematuria or polyuria. He defecates 1-3 times daily, formed, brown and
with no associated difficulty.
The patient had two sexual partners but currently, he is living with his siblings in
their house in Molino, Cavite. His two sons are with their moms, respectively.

VII. Review of Systems

General
(+) weight gain
Skin
(-) rashes, (-) petecchiae, (-) bruising

HEENT
(-) use of eyeglasses (-) blurring of vision (-) eye pain (-) tinnitus (-) hearing loss (-)
vertigo (-) rhinorrhea (-) hoarseness (-) dysphagia (-) sore throat
Neck
(-) nape pain (-) lymphadenopathy
Respiratory

2
 (-) dyspnea (-) cough and colds
Cardiovascular
(-) syncope (-) palpitation (-) PND (-) orthopnea
Gastrointestinal
(-) tenderness (-) diarrhea (-) constipation (-) vomiting
Genitourinary
(-) nocturia (-) hematuria (-) dysuria (-) polyuria (-) urethral discharge (-) incontinence
(-) abnormal vaginal bleeding (-) itchiness (-) foul discharge (-) dyspareunia
Musculoskeletal
(-) joint pain (-) joint swelling
Neurologic
(-) loss of consciousness (-) tremor (-) seizures (-) traumatic brain injury (-) headache
Hematologic
(-) bruising (-) epistaxis (-) melena (-) hematochezia (-) petecchiae (-) purpura (-)
bleeding
Endocrine
(-) heat intolerance (-) cold intolerance

VIII. Physical Examination

General Survey:
The patient is conscious, coherent, oriented to three spheres and not in
respiratory distress.

Vital signs
Temperature: 37.1oC (tympanic)
Pulse rate: 78 bpm (radial)
Respiratory rate: 18
Blood pressure: 140/100 mmHg

Anthropometrics
Weight: 65 kg
Height: 152.4 cm
BMI: 27.98 kg/m2 (overweight)

Skin: His skin has brown complexion, smooth, warm to touch, dry but with good turgor.
He has no pallor, jaundice nor plethora. There were no petecchiae, purpura, and
ecchymosis.

Head: Hair was black, coarse in texture and equally distributed. The scalp has no
dandruff and has no other lesions. The skull was symmetric, and head is proportional to
the body without noted lesions. There was no noted tenderness, mass, other lesions, but
asymmetry was noted, with mild drooping of the right face.

Eyes: Visual acuity: 20/200 on both eyes, however, not reliable at this time due to
administration of Tropicamide. He has intact visual fields. The eyes were symmetric with
no proptosis. The eyebrows were symmetric, with equal distribution of hair, and no
scaliness. Eyelids are symmetric, with no ptosis, lid lag or periorbital edema. There was
no excessive tearing, discharge or inflammation of the lacrimal apparatus noted. The
upper and lower palpebral conjunctivae were pinkish and bulbar conjunctivae were
transparent. Sclerae were anicteric. Smooth cornea (+) arcus senilis. The lenses were

3
clear. Both pupils were dilated (8-10 mm, OU) due to Tropicamide administration. Both
were unresponsive to light and accommodation. She has intact extraocular movements,
uniform convergence and no nystagmus. There was positive red orange reflex on
fundoscopy, as well as narrowing of retinal vessels but no hemorrhages, cotton wool
spots, nor optic disc edema.

Ears: Ears are symmetrical, normoset, non-tender and has no lesions. There was no ear
discharge. Otoscopy revealed intact, pearl grey tympanic membrane with cone of light
pointing towards the anteroinferior direction. There was no inflammation. There was no
cerumen seen. The external acoustic meatus was intact and has no deformities or
inflammation. The patient has no lateralization upon Weber test. Air conduction is
greater than bone conduction on both ears upon Rinne test. Intact gross hearing

Nose: The external nose was in midline and has no skin lesions. Alae were symmetric
and retractable without flaring. Both vestibules were patent with presence of hair. Middle
and inferior turbinates were symmetric and pinkish. Nasal mucosa was pinkish and
moist. There was no polyp seen. Nasal septum was at midline, with no perforation.
Frontal and maxillary sinuses were non-tender. There was a slightly shallow nasolabial
fold on the right side.

Mouth and Throat: The patient has no halitosis. His lips were moist and pinkish, and,
have no ulcers, bleeding or discoloration. Gums were pinkish without bleeding,
ulcerations or swelling. Teeth were intact except for a few dental caries. Oral mucosa
was pinkish and has no ulcerations. Tongue was in midline, pinkish, and with no
ulcerations, fasciculation, deviation or bleeding. Uvula and soft palate were not deviated
and rise symmetrically.

Neck: The neck is symmetric, with no noted skin lesions. There was no jugular vein
distention and JVP = 7 cm at 30o. There were no palpable and tender lymph nodes.
Trachea was in midline. Thyroid gland was not palpable.

Chest and Lungs: APL ratio was 1:2. There was no scar in the chest area. He was
eupneic. He has symmetric chest rise. Chest area was non-tender. Chest expansion
was symmetrical. Tactile fremiti were symmetric throughout. Both lung fields were
resonant. Lung fields have normal breath sound (vesicular on the peripheries,
bronchovesicular over the sternum and between scapulae, and bronchial over trachea).
No adventitious sounds were heard.

Heart: The patient has adynamic precordium with no bulging and visible pulsation. There
was no heaves. PMI was located at 5th ICS, left midclavicular line with a diameter of 2
cm. S1>S2 at apex, S2>S1 at base. There were no S3 and S4 gallops. There was no
murmur. There was no pericardial friction rub

Abdomen: the patient has globular abdomen with inverted umbilicus. There were no
superficial vein dilatation, no visible pulsations. The patient had normoactive bowel
sounds at 12 per minute. No bruits were heard over the aorta, renal and iliac arteries.
Abdomen is tympanitic over most areas. Liver has a span of 5 cm right midclavicular
line. Traube’s space is intact and there was no CVA tenderness.

Genito-urinary: deferred

4
Peripheral Vascular and Extremities
The patient has pinkish nail beds with capillary refill time of < 2 seconds. Peripheral
pulses are grade 2 on all sites. There is no edema, varicosities, deformities noted on all
extremities. He has (-) Homan sign. Passive ROM on all extremities was full but active
ROM on the right upper and lower extremities were decreased due to weakness. He has
no pressure ulcers on the back or the extremities. There are no other lesions noted. He
has no CVA tenderness.

Neurological exam:
Mental Status
The patient is alert and conscious. He was oriented to time, place, person. He was
responsive to questions. Speech is fluent and words are clear. Thought processes are
coherent and insight is good.

The Mini-Mental Status Examination

Orientation Able to identify weather, date, day, month, and year 5/5

Able to acknowledge admission to room, Ospital ng Maynila, 5/5

floor, city, country

Registration Able to repeat three objects: baso, unan, lapis 3/3

Attention and Able to perform serial 7 correctly: 93, 86, 81, 89, 82 3/5
calculation

Recall Able to remember all three objects 3/3

Language Able to name two objects: ruler, ballpen 2/2

Able to repeat “wala nang pero pero pa” 1/1
Able to follow three-step command: kunin ang papel, itupi sa 3/3
gitna, i-abot sa akin
Able to copy design (clock) 0/1
Able to write a sentence 0/1
Able to follow written command 1/1

TOTAL 26/30
Normal: 26-30; Normal adjusted: 24-28
Patient: no dementia

Cranial nerves

Cranial Nerve/s Assessment

I Able to determine the scent of coffee in both nasal orifice

II, III Patient’s VA on both eyes was 20/200 due to administration of

5
 Tropicamide. There was no pupillary light reflex bilaterally. Visual
field is intact upon confrontation test

III, IV, VI EOM muscles intact

V (+) corneal reflex in both eyes

Motor: Temporal and masseter muscles strength intact
Sensory: Can distinguish blunt and sharp objects from the left
forehead, cheek and jaw area

VII Motor – (+) asymmetry when smiling, left lip drooping but symmetric;
dysarthric with difficulty in fully moving his lips.
raising of both eyebrows were symmetric
Sensory – able to distinguish taste in anterior 2/3

VIII intact gross hearing

IX, X Gag reflex present, uvula in midline, no hoarseness in voice noted

XI Strength of SCM and trapezius muscles (R- 3/5; L-5/5)

XII Tongue in midline, no atrophy noted, moves freely from front to back
and side-to-side

Motor system
The patient The patient has atrophied muscles on both proximal and distal right upper
and lower extremities. There was slight resistance to passive movement on the left
upper and lower extremities but the right upper and lower extremities were flaccid.

Muscle Movement RIGHT LEFT

Finger abduction 1/5 5/5

Finger adduction 1/5 5/5

Opposition of thumb 1/5 5/5

Grip 1/5 5/5

Wrist extension 2/5 5/5

Wrist flexion 2/5 5/5

Elbow extension 3/5 5/5

Elbow flexion 3/5 5/5

Shoulder abduction 3/5 5/5

Shoulder adduction 3/5 5/5

6
 Hip flexion 4/5 5/5

Hip extension 4/5 5/5

Knee flexion 5/5 5/5

Knee extension 5/5 5/5

Plantar dorsiflexion 5/5 5/5

Plantar flexion 5/5 5/5

Deep Tendon Reflexes

DTR RIGHT LEFT

Biceps 3+ 2+

Triceps 3+ 2+

Knee 3+ 3+

Ankle 4+ 2+

(+) clonus of right ankle

Primitive Reflexes
(+) Babinski reflex

Coordination and Gait

Cannot assume a sitting position from supine position
Not able to perform pronator drift and Romberg test as the patient has right sided body
weakness

Sensory Examination:

PRIMARY MODALITIES RIGHT LEFT

TESTED

Light Touch Upper: 100% Upper: 60%

Lower: 100% Lower: 60%

Crude Touch Upper: 100% Upper: 60%

Lower: 100% Lower: 60%

Proprioception Able to detect position of Not able to detect position of

big toe big toe

Pain Upper: 100% Upper: 60%

Lower: 100% Lower: 20%

7
 Discrimination Upper: 100% Upper: %
Lower: 100% Lower: %

Vibration Not assessed Not assessed

Temperature Not assessed Not assessed

Higher sensory functions: (-) astereognosis (-) agraphesthesia

Cerebellar
There was no fasciculations, tics, athetosis, hemiballismus, chorea, dystonia, intentional
tremors and asterixis. He was able to do rapid alternating movements upper extremities
and lower extremities on the left side; able to follow finger-to-nose test using the left arm;
able to do heel to shin test using the left leg and heel.

Meningeal
(-) nuchal rigidity (-) Kernig sign (-) Brudzinski

IX. Salient Features and Approach to Diagnosis

Pertinent Positive Pertinent Negative

 44 years old Filipino male  no loss of consciousness
 chief complaint of transient bilateral  no vomiting
loss of vision and left hemisensory  unestablished family history of
loss heart disease or palpitation
 hypertensive with HBP of 200/100  no family history of diabetes,
mmHg vasculitis
 fair to poor compliance to  denies illicit drug use
medications (Losartan 50 mg OD,  no history of syncope, palpitation
Amlodipine 5 mg OD, and Aspirin  no tremors, seizures
OD)  no history of traumatic brain injury
 sudden blurring of vision followed  no history of headache
by total loss of bilateral vision  no dementia
followed by regaining of vision after  no loss of consciousness
2-4 hours  no Babinski and clonus on the left
 gradual right hemisensory loss side
described as “pangangapal”
 with associated dizziness
 already had a stroke 6 months prior
to admission, involving left
hemiparesis and hemisensory loss
with left sided facial drooping nad
dysarthria; no loss of
consciousness when attack
happened
 with strong family history of stroke,
hypertension and migraine
 smoker of 28 pack-years
 alcoholic beverage drinker

8
 fond of eating high salt high fat diet
with daily carbonated drinks
 positive for weight gain
 awake, conscious, coherent,
oriented to three spheres
 BP of 140/100 mmHg
 Patient is overweight
 Decreased active ROM of right UE
and LE but full passive and active
ROM of left UE and LE
 positive for red orange reflex on
fundoscopy with retinal vessel
narrowing on both eyes
 bilaterally dilated eye due to
administration of
mydriatic/cycloplegic
 intact visual fields
 loss of sensation on left face
 asymmetric smile with right side
drooping of lip
 left upper and lower muscle groups
were atrophied and
hypotonic/flaccid, with the arm
being more flaccid than the leg
 gross weakness of the right side of
the body, more prominent on the
arm
 hyperactive reflexes with clonus on
right ankle
 cannot assume sitting or standing
position
 unable to distinguish crude and fine
touch as well as pain and
proprioception on the left side of
the body

9
Approach to Diagnosis

The chief complaint of the patient was used as the pivot point for this case. With the development of bilateral loss of vision,
differentials such as central retinal artery occlusion, transection of the optic chiasm, or other lesions pertaining to the visual pathway
will come into mind. But with the eventual development of left hemisensory loss, several other causes will eventually replace these
differentials. Seizures, migraine, metabolic causes, mass lesion, or stroke may all give rise to the sensory symptoms experienced by
the patient.

10
X. Differential Diagnoses

1. Seizure
Seizure is associated with the imbalance in the excitatory (increase) and inhibitory
(decrease) signals to the neurons, resulting in abnormal firing. Seizure, when focal or
localized to a specific area in the brain, may produce localized symptoms. In this case,
considering the patient had hemisensory loss, seizure of the parietal lobe may be
suspected. However, other functions of the parietal lobe should have been lost in the
patient, particularly resulting in hemineglect and other parietal symptoms. Moreover,
localization to this area will not explain the bilateral loss of vision, unless the seizure
involved either occipital lobe (visual cortex) or temporal lobe (optic radiation).
RULED OUT

2. Migraine
It has been said that the pathology in migraine headache results in alternating
vasodilation and vasoconstriction of cerebral blood vessels, resulting in fibrosis or
damage of the vessel wall, increasing the risk for clotting or occlusion, hence mimicking
stroke. Several cases of migraine headache causing stroke-like symptoms have been
reported. Moreover, the patient has family history of migraine headache (although not
clinically diagnosed). However, in the case of the patient, factors that make migraine
headache causing stroke-like symptoms include the epidemiology of migraine, which is
more common in women; and, the absence of symptoms of migraine in the patient.
RULED OUT

3. Metabolic
Several metabolic disturbance may cause transient loss of vision and sensory loss but
the most common include disturbance in blood sugar levels and electrolyte levels.
Hypoglycemia and hyperglycemia have been noted to cause transient loss of vision and
paresthesias due to its effect on neuronal metabolism. However, these conditions are
highly unlikely in the patient as according to the history, the patient was well-fed before
the development of his symptoms, and that he has no risk factors such as diabetes.
Moreover, these are also associated with loss of consciousness, and generalized
weakness, which did not happen to the patient.
RULED OUT

4. Mass Lesion
Mass lesions, such as tumors, hematomas, abscess, cysts, etc. when compressing
certain sites in the brain, may produce localizing symptoms, such as what the patient
manifested. A compressing lesion of the thalamus, internal capsule or occipital lobe may
produce these symptoms experienced by the patient. However, due to the acuteness of
the event, a lesional compression is highly unlikely unless the lesion has been present in
that area for a long time now, which could have allowed it to grow and compress the
adjacent areas. However, this should have been symptomatic too.
RULED OUT

4. Stroke

11
Stroke is the most common cause of localizing lesions such as hemisensory loss.
Obstruction or hemorrhage in the thalamic perforators may cause hemisensory loss;
obstruction or bleed in the parietal cortex may produce hemisensory loss; obstruction in
the occipital lobe or even up to the level of retinal artery, may produce visual loss.
Obstruction of the different vascular territories can very well explain the symptoms in this
patient. Moreover, almost all of the risk factors for the development of stroke are present
in the patient. These include sex, genetics, hypertension, previous stroke, sedentary
lifestyle, smoking, and use of alcoholic beverage. Moreover, the acuteness of the
symptom development highly points out to a vascular pathology rather than other
pathologies.
CANNOT BE RULED OUT

XI. Working Impression

Acute Kidney Injury secondary to Acute Uric Acid Nephropathy to consider to be on top
of Chronic Uric Acid Nephropathy; Gouty Arthritis

XII. Localization

Pathology: Ischemic Stroke, most probably Lacunar Infarct

The consideration that this stroke is ischemic more than hemorrhagic is supported by the
fact that there are no symptoms of increasing intracranial pressure, which is a sign that a
hemorrhagic process occurred, considering the Monroe-Kellie hypothesis. Although the
patient is severely hypertensive when the episode occurred, which is the most common
cause of hemorrhagic stroke, the symptoms do not point to lesions in the most common
site of hemorrhagic stroke, which is the putamen. Moreover, chronic undiagnosed
hypertension may produce lipohyalinosis of vessels, particularly small vessels such as
the perforators, which may eventually result in infarction of the supplied organ. Of the
ischemic types, the lesion is most likely thrombotic, because there are no heart
abnormalities, which can rule out cardioembolic stroke. Although TIA cannot be ruled out
unless 24 hours have passed already, with the severity of symptoms and the eventual
resolution of the vision loss without resolution of hemianesthesia, TIA is highly not likely.
In this case, a lacunar stroke is considered due to the abrupt onset and maximal
presentation of symptoms during the first hour of the vascular event.

Levelization: Subcortical

In this case, a peripheral lesion is not considered because the lesion involved almost the
whole left side of the body of the patient, wherein peripheral lesions usually are regional
if not focal in distribution. Between cortical and subcortical, subcortical is highly favored
because there are no cortical symptoms such as loss of consciousness, aphasia,
memory, attention and calculation disorders, and intact higher cortical sensory functions,
such as those that control graphesthesia and stereognosis. Therefore, the lesion is
highly likely subcortical.

Lateralization: Right subcortical area

Since the manifestation is a left hemisensory loss, the lesion most likely is on the right
subcortical area of the patient.

12
Localization: Right Thalamus with possible involvement of the occipital lobe

Since the patient presented with pure sensory stroke, the most likely location is the
thalamus. The lesions can be explained well by an infarct of the ventroposteromedial
and ventroposterolateral nuclei of the thalamus, wherein sensory input from the face and
body are being relayed, respectively, before going to the cortex. Internal capsule lesion
is possible however, it presents more with a mixed or sensorimotor stroke or a pure
motor stroke. Brainstem lesions are highly unlikely due to absence of brainstem sign or
crossed hemiplegia and ipsilateral cranial nerve dysfunction.

As for the transient binocular blindness, infarct of the two lateral geniculate bodies may
also cause the symptom, but according to journals, the most common cause is infarct of
the visual cortex in the occipital lobe. However, with the fast resolution of the symptom, a
transient ischemic attack is also considered. This is one of the most common prelude to
a stroke of the posterior circulation, which supplies the thalamus via the thalamic
perforator branches of posterior cerebral artery.

Localization of right side deficit:

This is most likely the deficit of the previous stroke. Considering all the findings of right
lower facial drooping, right hemiparesis and history of right hemianesthesia without loss
of consciousness and gradual evolution of symptoms, infarct of the posterior limb of the
internal capsule is highly likely. Although his right extremities are somewhat flaccid, this
can still be localized to an upper motor neuron lesion because in the stages of stroke
recovery, the last stage before full recovery is flaccidity of the muscles before it regain
full strength.

XIII. Management

Emergency Room

The first and foremost thing to do in patients who presented with stroke is to provide
emergent supportive care including the ABCs of resuscitation. In the case of the patient,
airway should still be inspected because there is right sided motor deficit even if the left-
side deficit is purely sensory. If the patient is stabilized already, he should be moved to a
stroke unit, if available in the hospital.

The next step which I think is most appropriate for this patient is top exclude common
causes of these symptoms (stroke mimickers). The physician, through careful history
and PE, should ensure that the patient is really having a cerebrovascular accident. Next
is the measurement of neuro vital signs, including level of consciousness, BP, MAP, RR,
temperature, pupillary reaction and oxygen saturation. Oxygen should be given if
saturation is less than 95%. If MAP is greater than 130, the patient’s hypertension
should be treated, otherwise, rapid lowering of BP is contraindicated or not advised.

The next step is to score the patient to classify him to different treatment options. One of
the most important early scoring for this patient is NIHSS. In his case, my score for him
is 10 based on the level of consciousness, deficits on all four extremities, both motor and
sensory, and aphasia. Therefore the patient can be classified as having moderate

13
stroke. This is very important since optimum management will somehow depend on the
score of the patient. Risk factors and comorbidities should be recognized and symptoms
of increased ICP should be ruled out.

The patient is started on 0.9% NSS to run for 8 hours to ensure adequate hydration.

Laboratory Tests

Non-contrast CT of the brain or MRI-DWI as soon as possible should be performed to

localize the lesion and identify the degree of involvement of the different regions of the
brain. This is the confirmatory factor whether the stroke is really ischemic or
hemorrhagic. Other tests that should be ordered for a patient with moderate ischemic
stroke include complete blood count with platelet, so as to assess for possible bleeding
problems in planning for the administration of rt-PA; CBG or FBS and HbA1c to rule out
hypo or hyperglycemia as a cause of these symptoms, to monitor and maintain patient
on euglycemic state; PT/PTT, again, in preparation for rt-PA; serum Na and K, to rule
out these as cause of this event; and, ECG or 24-hour holter monitoring, to rule out
arrhythmia as a cause of cardioembolic stroke. If the setting is really ideal, we can
include lipid profile to check for dyslipidemia.

Pharmacologic Management

Recombinant tissue plasminogen activator is recommended as first line therapy for

ischemic stroke. However, a criteria exists for a patient to be qualified for rt-PA
administration. As for the patient, he met 2/3 inclusion criteria which as >18 years old
and clinical diagnosis of ischemic stroke. However, the last criteria, wherein the onset
should be less than 180 minutes of 3 hours, has not been met by the patient. However,
in the latest guideline, this time period has been extended up to 4.5 hours and with this
the patient is a candidate for rt-PA already. However, contraindications should also be
assessed. In the case of the patient, there is none and the patient is a good candidate
for rt-PA. Some will ask, will this patient benefit from thrombolysis? In a study conducted
by Shobha in 2013, patients with lacunar syndromes still benefit from rt-PA. if the patient
can afford, this can be administered at a dose of 0.9 mg/kg IV over 1 hour with the 10%
of the total dose administered as bolus over 1 minute. Considerations include removal of
all contraptions or securing that there will be no manipulation of the contraptions of the
patient within 24 hours are administration of rt-PA should be done, because this drug
can result in severe hemorrhage.

The next pharmacologic modality for this patient is the use of antiplatelet. In this case,
the patient should be started on Aspirin 325 mg tablet in 4 divided doses during the first
24 hours, followed by tapering to 160 mg/day, then maintenance of 80 mg or 1 tab per
day. This is one protective factor to prevent stroke recurrence.

The patient may also be started on Citicoline 1 g every 12 hours for 3 months. This drug
is a neuroprotectant.

In the initial period, specifically during the first 3 days, the patient should not be given
any anti-hypertensive medications so as to maintain permissive hypertension. We only
need to treat immediately if the SBP is > 220 mmHg, or DBP > 120 mmHg or if the MAP
is >130. In this acute setting, Nicardipine drip may be used to reduce BP because this
drug can easily be titrated. Clonidine and other centrally acting drugs should not be

14
utilized in reducing blood pressure because they cause rapid drop in BP. After the days
of permissive hypertension, the patient may be started on an ACEI or ARB. In this case,
I will prescribe Losartan 50 mg OD.
According to the current recommendations, the patient should also be started on HMG
CoA inhibitor, particularly a moderate intensity therapy, Atorvastatin 40 mg OD.

Non-pharmacologic Management

Basically, in the acute setting, we should perform interventions that will have a
neuroprotective effect on the patient. These include prevention of hypotension,
hyperglycemia, hypoglycemia, hyperthermia and hypoxemia. That is why, monitoring of
the laboratory tests mentioned earlier is important. The patient’s BP should be
maintained on a permissive hypertensive level in the first 5-7 days, preferably 180/105
mmHg. Do not let the BP reach 185 because this will be a contraindication for rt-PA use.
Blood pressure should be monitored every 15 minutes pretreatment. After treatment,
monitoring should be every 15 minutes for 2 hours after starting the infusion of rt-Pa,
every 30 minutes for 6 hours, then every hour for 18 hours.

Blood glucose target is 140-180 mg/dl. a good oxygenation should manifest as 95%
saturation and above. And temperature should be maintained between 33-35 degrees
Celsius.

To prevent recurrence, aside from maintaining the patient on antiplatelet medication,

lifestyle modification should also be performed, particularly in the diet, level of activity
and vices.

For the right sided and left sided deficits, the patient should be started on physical
therapy, speech and occupational therapy, a day after the onset of stroke, at least 5
days a week until recovery.

XIV. Prognosis and Complications

First ever lacunar strokes have low risk of recurrence however in the case of the patient,
he has 10x risk of developing another stroke due to history of recurrence. Moreover,
without being treated with rt-PA, there is a higher chance that the deficit may remain
permanent, particularly if no rehabilitation is initiated. The patient may have contractures.
He is also at risk of having deep vein thrombosis if he does not ambulate soon. He is
also at risk of having pressure ulcers, and even pneumonia.

XV. References

Smith, W., English, J., & Johnston, S. (2015). Cerebrovascular Diseases. In D. Longo,
D. Kasper, J. Jameson, A. Fauci, S. Hauser, & J. Loscalzo, Harrison's principles of
internal medicine. New York: McGraw Hill Medical.
Stroke Society of the Philippines. (2013). Guidelines for the prevention, treatment and
rehabilitation of stroke. Quezon City: Stroke Society of the Philippines.
Huff, J. (2010). Stroke differential diagnosis- mimics and chameleons. FERNE , 1-16.

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