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DAVAO DOCTORS HOSPITAL

Department of Internal Medicine

Data Base Submission


In partial fulfillment of the requirements in Internal Medicine

Submitted by
Nallathambi, Aiswarya Bharathi
General Data: Patient S, D, a 43-year old Male, News Reporter based in the Philippines, born
on Sept 30, 1974, Catholic, Married, residing in Nova Tierra Village, Lanang who came in with
left sided body weakness, was admitted in this institution on 10/24/2017 at 3.31 pm

History of present illness: The patient is a 43 year old male with premorbid activities of daily
living independent, not on any maintenance medications as verbalized by the patient.

 About 3 months prior to admission, the patient had onset of headache, throbbing and
pulsatile, in the occipital region, with a pain scale of 5-6/10, triggered by working long
hours covering the Marawi city war, as claimed by the patient. The intensity of the
headache waxed and waned. No associated fever/nausea/seizures noted.
 1 month prior to admission, patient noted to have exertional shortness of breath, after
climbing one flight of stairs. No intervention done. No medications taken. In the interim
patient went to Singapore and there were recurrent episodes of headache. He was given
Codeine and Panadol by the clinic at his firm.
 21 days prior to admission, as he was working in his office, he had sudden loss of
consciousness, while he was working, fell and hit his head on the front. He was
transported to Singapore General Hospital by his paramedics, where his BP was noted to
be elevated with a systolic BP of 206. Upon arrival, he had unrecalled episodes of
projectile vomiting with associated severe headache, left sided body weakness and
dysarthria. He was immediately admitted, given IV labetalol. A CT scan of brain revealed
Right Thalamic bleed, CT angiogram was unremarkable.
 During the next several days, his management included control of blood pressure and
other symptoms. He was initially started on Mannitol and weaned off, blood pressure
controlled by several oral antihypertensives after that. His blood pressure was difficult to
control. He was given maximum doses of Amlodipine, Hydralazine, Enalapril, Atenalol.
BP trend was erratic and still hypertensive. He was also started on Prazosin 2TDS – noted
with occasional SBP drips to 90+.
 13 days prior to admission, while in the hospital, he also developed aspiration
pneumonia, started on Tazocin, improved and later on taken off IV. His blood and urine
cultures were negative. He also had exertional SOB, He was also noted to be snoring
quite loudly, ordered to have sleep study done and diagnosed with Obstructive Sleep
Apnea. During this time the patient had several intervals of loss of consciousness, lasting
from minutes to hours.
 1 week prior to admission, patient showed severe left sided neglect, hemiplegic left, both
upper and lower extremities, non ambulatory with dysarthria. No loss of consciousness.
The patient’s family was keen to fly the patient back home for treatment.
 1 day prior to admission, patient had a repeat CT scan which showed resolution of the
bleed, his BP was stable and he was declared safe to fly, with discharge medications of
Prazosin 2mg/tab, Hydralazine HCl. 25 mg/tab, Furosemide 40 mg/tab, KCl 600 mg/tab,
Atorvastatin 40 mg/tab, Amlodipine 10 mg/tab, Metformin HCl 500 mg/tab, Omeprazole,
Atenolol, Bisacodyl suppository PRN for no bowel movt, Lactulose syrup, Paracetamol
1 g/tan PRN for pain/fever and Codeine phosphate PRN for pain for 7 days.
 On the day of admission, patient was transported to Changi Airport, transferred from
stretcher to business class seat with safety precautions and then transported directly to our
institution upon arrival in the Philippines.

Past medical history: Although patient was not officially diagnosed with hypertension, he had
his blood pressure checked 2 years ago, which revealed elevated systolic BP of >200mmHg, but
he refused to seek consult. He was given Losartan by his brother in law who’s a doctor, without
prescription, but he was non-compliant to medications. He also did not get his blood sugar tested
until his admission in the first hospital. He’s non asthmatic, no TB exposure, had no previous
hospitalizations or surgeries. He has history of recurrent headaches – described as throbbing and
pulsatile – in the occipital region, started approximated 3-4 months prior, self medicated with
Panadol or sometimes given Codeine in the firm he worked with. The patient did not have any
known allergies to food or medication.

Family history: Patient has a positive family history of hypertension on the paternal side. His
father died of stroke and his brother died of hypertensive crisis. Patient’s father also has Diabetes
Mellitus. No family history of Bronchial asthma, tuberculosis or cancer.

Personal and social history: Patient has history of smoking, during his college years, although
he quit 2 years later, when he was in his late 20s, with an average of 2 pack years. Patient has
occasional alcohol intake(1 bottle of beer, with the frequency of less than once a month). Patient
has no known food or drug allergies. Patient’s regular diet consisting of fatty food, meat and
vegetables. He had been a news reporter for almost 20 years, he described his job as a stressful
one, with no fixed work hours. The most recent stressful event as described by him was his
coverage of the Marawi city war prior to going to Singapore for a fellowship program. Around
this time, he is supposed to have developed throbbing pulsatile headache, along with insomnia.
He was one of the 16 journalists chosen from all over the world to attend the Honorary
Fellowship of Journalism in Singapore. He resided in Singapore for 3 months with colleagues,
with whom he had good relationships. He was sexually active before leaving for Singapore.

Review of systems:

General: No weight loss, No weakness

Skin: No rashes, No itchiness, No discoloration, No brittle nails

HEENT: Head: Recurrent headaches, No dizziness, No trauma, No lightheadedness.

Eyes: No blurred vision, No redness, No cataracts, No lacrimation.


Ears: No hearing deficiencies, No tinnitus, No vertigo, No discharge.

Nose: No frequent colds, No nasal obstruction, No nasal discharge. Throat: No bleeding gums,
No dentures, No soreness, No tonsillitis.

Neck: No swollen glands, No goiter, No stiffness.

Breast: No gynecomastia.

Respiratory: (+) 2 pillow orthopnea, No paraoxysmal nocturnal dyspnea, No cough, No


hemoptysis, No wheezing, No history of TB (+) Shortness of Breath upon climbing 1 flight of
stairs, for the last few months.

Gastrointestinal: No dysphagia, No heartburn, No nausea, No vomiting, No changes in bowel


habits, No abdominal pain, No hemorrhoids, No melena, No hematochezia.

Peripheral vascular: No varicose veins, No leg cramps, No cyanosis, No swelling with redness
or tenderness.

Genitourinary: No dysuria, No frequency of urination, No urgency, No nocturia, No hematuria,


No previous urinary tract or sexually transmitted infections.

Musculoskeletal: No joint pains, No arthritis, No gout, No stiffness, No weakness, No limitation


of motions. Psychiatric: No nervousness, No mood changes, No depression, No previous
psychiatric treatment.

Neurologic: No dizziness. No changes in speech or orientation, No numbness or loss of


sensation, No seizures.

Hematologic: No anemia, No easy bruising or bleeding, No previous blood transfusion.

Endocrine: No thyroid problems, No excessive sweating, No heat or cold intolerance.

Physical Examination: Patient was awake, alert, not in respiratory distress with 15 on
GCS(E4V5M6). Patient’s vital signs at the ER were Blood pressure of 128/79 mmHg,
Respiratory rate 19 cpm, pulse rate of 80 bpm, temperature of 36°c, oxygen saturation of 100%.
He weighs 83 kg and has a height of 167 cm. Patient’s BMI is 29.8 kg/sq.m(overweight).

On physical examination, patient’s skin was warm to touch, no lesions, no scars, no pallor was
noticed. For the head and neck, patient’s head was normocephalic, atraumatic, with no alopecia.
Pink palpebral conjunctiva, anicteric sclera was noted, pupils constricting to 3mm, equal and
reactive to light. Wax partially obscuring both ear canals and intact tympanic membrane. Nasal
mucosa was pink with midline septum, No sinus tenderness, No alar flaring. Pink oral mucosa
with poor dentition, no bleeding gums, tongue deviated to the right, No tonsil enlargement were
noted. Trachea is midline, No neck vein engorgement, No cervical lymphadenopathy, No thyroid
enlargement.

The Chest on examination had no retractions, equal chest expansion, no scars, no lesions with
equal tactile fremitus in both lung fields. Resonant on percussion in both lung fields. Clear breath
sounds were heard upon auscultation. No adventitious sounds were appreciated.

During Cardiovascular exam, upon inspection, precordium was adynamic and point of maximal
impulse was not visible but palpable at 5th ICS about 7cm from midsternal line, no heaves or
thrills were palpable. Upon auscultation, regular heart rate and rhythm was appreciated with,
distinct S1 and S2 heard. No S3 or S4 heard. No murmurs appreciated.

Abdomen was non-distended with no scars, lesions or ascites with normoactive bowel sounds
upon auscultation. Abdomen was tympanic upon percussion. No hepatosplenomegaly, no masses
and No tenderness were noted upon palpation.

No lesions or deformities were noticed during physical examination of the extremities. There
were full peripheral pulses on all four extremities. Hands and feet were warm to touch, no
bipedal edema noted.

Upon Neurological examination, for the mental status examination, the patient was conscious,
coherent, oriented to time, place and person. He had euthymic mood and appropriate affect. He
had no auditory or visual hallucinations, no delusions, no suicidal or homicidal ideation. Patient
had difficulty articulating; reduced speech volume. Attention span decreased.

Concentration – able to say serial 7’s, spell world, months of year.

Presents with left sided neglect.

Memory – Remote past intact; Recent past impaired; Immediate memory intact

Cranial nerve exam

I – Able to smell; Olfaction intact

II – Pupils are equally reactive to light; Peripheral vision towards left impaired

III, IV, VI – EOM impaired towards the left; left lateral palsy

V – Facial sensation to the left impaired

VII – Facial asymmetry; Loss of nasolabial fold on the left

VIII – Able to hear; No sensorineural/conductive hearing loss


IX & X – Gag reflex not assessed

XI – Able to shrug shoulders against resistance on the right side only, No movement on the left

XII – Tongue deviation to the right

Motor and Sensory

Motor strength

Motor Right Left


strength

UE 5/5 0/5

LE 5/5 0/5

Sensory

Sensory Right(UE & LE) Left(UE & LE)

Kinesthesia Intact Impaired

Light touch Intact Impaired

Pain Intact Impaired

2 pt Intact Impaired
discrimination

Gait and Reflexes

Non ambulatory;Requires max assistance sitting.

Reflexes

(-) Babinski’s
(-) Kernig’s

(-) Brudzinski’s

Rhomberg’s test not performed.

Deep Tendon Reflexes

2+ on Triceps, Biceps, Patellar, Achilles and Plantar on the Right side and 0 on all reflexes on
the Left side.

Salient features

PERTINENT POSTIVES PERTINENT NEGATIVES


Left sided body weakness (-) Fever
Pulsatile headache (-) Chest pain
Vomiting (-) GI complaints
Uncontrolled hypertension (-) Seizures
Diabetes Mellitus (-) Cognitive impairment
Family history of stroke (-) AV hallucinations
Family history of hypertensive crisis

Loud Snoring

Pertinent Neuro Findings

Recent past memory – impaired


Dysarthria
Left lateral palsy
Facial asymmetry
Loss of nasolabial fold, L
Tongue deviation to L
Hemiplegia, L UE & LE
Muscle strength (0/5) on Left UE and LE
Sensory deficit L UE; LE

Admitting Impression:

 Cerebrovascular Accident, Intranial Hemorrhagic Stroke secondary to uncontrolled


hypertension, right thalamic bleed; diabetes mellitus type II, Essential hypertension;
obstructive sleep apnea

Discussion

Stroke

The clinical term for acute loss of perfusion to a vascular territory of the brain, resulting in
ischemia and a corresponding loss of neurologic function. Typically manifest with the sudden
onset of focal neurologic deficits, such as weakness, sensory deficit, or difficulties with
language.

Classification of Stroke

Ischemic Stroke

 Thrombotic
 Embolic

Hemorrhagic Stroke

 Intraparenchymal
 Subarachnoid

History

Symptoms include the following:

 Sudden numbness or weakness of face, arm, or leg, especially on one side of the body
 Sudden confusion, difficulty in speaking or understanding
 Sudden deterioration of vision of one or both eyes
 Sudden difficulty in walking, dizziness, and loss of balance or coordination
 Sudden, severe headache with no known cause

A focused medical history aims to identify risk factors for atherosclerotic and cardiac disease,
including hypertension, diabetes mellitus, tobacco use, high cholesterol, and a history of
coronary artery disease, coronary artery bypass, or atrial fibrillation.
Common signs of stroke include the following: Acute hemiparesis or hemiplegia , Complete or
partial hemianopia, monocular or binocular visual loss, or diplopia, Dysarthria or aphasia
Ataxia, vertigo, or nystagmus, sudden decrease in consciousness

In younger patients, elicit a history of recent trauma, coagulopathies, illicit drug use (especially
cocaine), migraines, or use of oral contraceptives. Establishing the time the patient was last
normal is especially critical when thrombolytic therapy is an option.

If the patient awakens with the symptoms, then the time of onset is defined as the time the
patient was last seen without symptoms. Family members, coworkers, or bystanders may be
required to help establish the exact time of onset, especially in right hemispheric strokes
accompanied by neglect or left hemispheric strokes with aphasia.

If the patient is a candidate for thrombolytic therapy, a thorough review of the inclusion and
exclusion criteria must be performed. The exclusion criteria largely focus on identifying risk of
hemorrhagic complication associated with thrombolytic use.

Goal of Physical/Neuro Exam

 Assessing the airway, breathing, and circulation (ABCs)


 Defining the severity of the patient's neurologic deficits
 Identifying potential causes of the stroke
 Identifying potential stroke mimics
 Identifying comorbid conditions

Lab Exams

Laboratory evaluation of the patient with ischemic stroke should be driven by comorbid illnesses
as well as the potential acute stroke.

Glucose and electrolyte tests: Hypoglycemia is the most common electrolyte abnormality that
produces strokelike symptoms. It is easily corrected, and correction leads to rapid resolution of
symptoms. Electrolyte disorders, hyperglycemia, hypoglycemia, and uremia should be
considered as the cause of ongoing mental and physical deficits while pursuing the diagnosis of
stroke.

Complete blood count: CBC provides key information regarding hemoglobin and hematocrit, as
well as platelet count, which is important in fibrinolytic candidates. Additionally, sickle cell
disease, polycythemia, and thrombocytosis increase the risk for stroke.

Prothrombin time (PT) and activated partial thromboplastin time (aPTT) tests: Many patients
with acute stroke are on anticoagulants, such as heparin or warfarin. Treatment decisions, such as
thrombolytic use, require data on coagulation status. An elevated international normalized ratio
(INR) may preclude patients from receiving thrombolytics.

Imaging Studies

CT is the most commonly used form of neuroimaging in the acute evaluation of patients with
apparent acute stroke. Noncontrast CT is very sensitive in detecting intracerebral and
subarachnoid hemorrhage, as well as subdural hematomas. CT is not very sensitive for early
ischemia (<6 h), although several findings can suggest ischemic changes. Loss of the gray-white
matter interface, loss of sulci, and loss of the insular ribbon are subtle signs of early ischemia.

Early mass effect and areas of hypodensity suggest irreversible injury and identify patients at
higher risk of postfibrinolysis hemorrhage. Significant hypodensity on the baseline scan should
prompt a question about the time of onset.Hypodensity in an area greater than one third of the
MCA distribution is considered by many a contraindication for thrombolytics.

CT may demonstrate other causes of the patient's symptoms, including neoplasm, hemorrhagic
stroke, epidural and subdural hemorrhage, aneurysm, abscess, arteriovenous malformation, and
hydrocephalus. CT angiography may demonstrate the location of vascular occlusion. CT
perfusion studies are capable of producing perfusion images and together with CT angiography
are becoming more available and utilized in the acute evaluation of stroke patients.

Treatment

Medical Care

Medical care for AIS occurs on a continuum, beginning in the prehospital setting and ending at
home after discharge.

Stroke centers and organized protocols for the acute and in-house treatment of stroke patients
have been shown to decrease morbidity and mortality associated with stroke.4,5

Emergency medical services (EMS) personnel should begin with the ABCs and, once the
patient's condition is stable, should perform a more directed assessment and administer
supportive treatment. Providing supplemental oxygen when indicated, establishing intravenous
lines, measuring serum glucose, and administering glucose in hypoglycemic patients are
elements of prehospital stroke care.
General Management of Patients with Acute Stroke

FIG– Management of BP in candidates for fibrinolysis

FIG– Management of BP in non candidates for fibrinolysis


Fibrinolytic Therapy

Intravenous t-PA for appropriate patients within 3 hours from symptom onset remains a Class I
recommendation by the American Stroke Association.

Tissue Plasminogen Activators

Recombinant t-PA and streptokinase convert plasminogen to plasmin, which is capable of


hydrolyzing fibrin, fibrinogen and other clotting proteins. Treatment within 3 hours of symptom
onset has led to a 30% increase in the number of patients with little or no neurological deficit in
3 months-1 year

Dose (t-PA): 0.9 mg/g - 10% administered as IV bolus, remainder infused in 1 hour

6% risk of symptomatic cerebral hemorrhage. Giving thrombolytic therapy 6 hours post stroke
showed less benefit and increased risk of bleeding. Exclusion includes minimal neurological
deficits, Very large strokes, Patients older than 80 years , All patients taking oral anticoagulants,
Patients with a history of stroke and diabetes

Cerebral Edema and Increased ICP

Clinical deterioration in large strokes (main branch infarctions of the MCA) occur after several
days of onset, usually worst on the 3rd day. Vasogenic and cellular edema of the necrotic tissue.
Decreased sensorium, anisocoria, Babinski sign.Cerebral Edema and Inc ICP, controlled
hyperventilation, decrease in PCO2 increases pH and cerebral vascular resistance, decrease CSF
pressure

IV Mannitol 1 g/kg initially then 50 g every 2-3 h

Surgical decompression include Hemicraneictomy in large hemispherix strokes, cerebellar


strokes to prevent obstructive hydrocephalus

Stroke Rehabilitation

Use of a body part enhances its representation. Increased use increases the size & /or
excitability of a motor representation. Decreased use decreases the size &/or excitability of a
representation (learned non use). Use itself has an effect but the effect is enhanced by
attempted learning of new skills, attention to task & reward. This forms the basis of
physiotherapy.

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