Admitting Conference

Abejo, Jerika D.
Bona, Henry Jr.,
Clinical Clerk
 General Data - M.R
- 87 y/o
- male
- Married
- Farmer
- Zone 5 San Felipe, Naga City

Source and Reliability

Chief
- Body weakness
Complaint:
History of
2 weeks PTA - Pt. noted body weakness bilateral lower
Present extremities
Illness - Unable to walk
- No consult was done
- No medications taken.

- Persistence of symptoms
Few hours - Associated with aphasia
PTA - Consulted at BMC ER
Past Medical
History  (-) HPN
 (-) DM
 (-) cardiac dse.
 (-) lung dse.
Family
History (-) HPN
(-) DM
(-) Cardiac dse.
(-) Lung dse
Personal and
Social History

- Non-smoker
- Non-alcoholic drinker
Review of Systems
General: (-) dizziness, (-) weight loss, (-) fever
Skin: (+) dryness, (-) rashes (-) lesions
HEENT: (-) headache; (-) nape pain; (-) blurring of vision; (-) epistaxis;

(-) difficulty of swallowing, (-) tinnitus, (-) bleeding gums

Neck: (-) pain, (-) swelling, (-) lumps, (-) stiffness
Respiratory: (-) wheeze (-) cough, (-) difficulty of breathing
Cardiovascular: (-) chest pain, (-) palpitation, (-) dyspnea, (-) orthopnea
GIT: (+) loss of appetite; (-) abdominal pain, (-) diarrhea, (-) vomiting
GUT: (-) dysuria, (-) hematuria, (-) urinary frequency, (-) urinary
incontinence
MSK: (-) muscle pain, (-) joint pain
Reproductive: (-) penile, discharge, (-) pain
Neuro: (-) seizure, (-) fainting episode
 General:Patient is awake, aphasic and not in cardiorespiratory distress.
Physical
Exam Vital signs: BP- 170/100 mmhg Temp: 36.3 RR:18 cpm PR: 91 bpm
SpO2: 98%

Skin: poor skin turgor,

HEENT:
Head: The skull is normocephalic/atraumatic with black hair, evenly
distributed. No dandruff noted. No tenderness upon palpation.

Eyes: White sclera, pink palpebral conjunctivae. Pupils 2mm-3mm equally

reactive to light and accommodation, both with direct and consensual reaction.
Good extraocular muscle movement. No nystagmus or lid lag.
Physical Exam
Ears: Normal and symmetric. No lesions. No tenderness. Poor
hearing acuity in both ears.
Nose: Symmetric, patent on both nasal vestibules. No bleeding. No
sinus tenderness.
Throat (and mouth): Lips are slightly dry. Oral mucosa is pink. No
ulcers or nodules noted. Tongue not deviation
Neck: Trachea midline. No lymphadenopathy noted. No visible
jugular neck veins. No tenderness.
Physical Exam Thorax and Lungs: Symmetric lung expansion with good excursion. No
intercostal/subcostal/suprascapular retractions noted. No deformities like
kyphoscoliosis. Lungs are resonant. Normal tactile fremitus. Hyperresonant upon
percussion. Breath sounds vesicular; no adventitious sounds noted.

Cardiovascular: Adynamic precordium with no observable heaves and thrills.

Carotid upstrokes are brisk, without bruits. Normal rate and regular rhythm. PMI at
5th ICS MCL.

Abdomen:round, soft, nontender with no visible masses, striae, dilated veins, and
ecchymosis. With no visible pulsation. Bowel sounds are normoactive and tymapic
in percussion in all quadrants. No palpable masses were noted.

Extremities: Full range of motion in the upper extremities. 3/5 in both lower
extremities. No evidence of deformity. No bipedal edema noted.
 Neurologic:
Patient is awake, aphasic, obeys simple commands.
Physical Exam Cranial nerves I- not tested
II-XII grossly intact.
Motor: normal bulk, strength 5/5 on both upper extremities, 3/5 on both lower
extremities
Sensory: grossly normal and symmetrical on light touch, temperature, and
pain. Gait not tested.
Salient
Features:
- 87 y/o
- Male
- Farmer
- decreased appetite
- Body weakness bilateral on lower extremities
Clinical -Cerebrovacular disease probably infarct
- Hypertension
Impression
  Admitted at medical annex
 Inserted NGT for feeding (OTF 1600 kcal in 6 equal feeding)
 IVF PNSS 1 L for 12 hours
 Dx:
- CBC w/ PC
Day 0 (er) - FBS, Lipid Profile
- Na, K, BUN, Crea
- 12 L ECG
- CXR APL
- Stat Plain Cranial CT scan
  Tx:
- Lactulose 30cc before bedtime
- Rosuvastatin 10mg, 1 tab 2x/day
- Omeprazole 40 mg/IV once a day

Day 0 (er) - Neuro vital sign every hour

- Vital signs every 2 hours
- Bed side precaution
- Turn patient side to side every 2 hours
- WOF: change in sensorium
  S > aphasia, body weakness
 O > GCS 11 (E4, V1, M6)
> 3/5 bilateral lower extremities
A > CVD prob Infarct
Day 1 P > IVF and diet as ordered
> follow up lab result
Facilitate plain cranial ct scan
Monitor vital every 4 hours
Wof: decrease sensorium
  S > day 2 post stroke
 O > GCS 10 (E4, V1, M5)

Day 2 2-3 mm ERTL

Aphasic
Body weakness
Day 3
CASE
  an abrupt onset of a neurologic deficit that is attributable to a
Cerebrovascular focal vascular cause
 Cerebrovascular diseases include some of the most common and
disease devastating disorders: ischemic stroke and hemorrhagic stroke
 second leading cause of death worldwide

Stroke Sudden onset of focal (global) neurologic deficit

due to an underlying vascular pathology

Transient Ischemic Attack Transient episode of neurogenical dysfunction

caused by a focal brain, spinal, or retinal ischemia,
without evidence of infarction (normal cranial
imaging) in which symptoms typically last less
than an hour
ISCHEMIC HEMORRHAGIC
- Deficit maximal at onset - headache, vomiting, SBP>220
- Atherothrombotic stroke: mmhg, impaired consciousness
usually during sleep and evolution of focal deficits
- Cardioembolic stroke: sudden over a period of minutes to hour
onset of maximal deficits (<5 - Hypertensive ICH: develops over
min) with rapid improvement of 30-90 minutes
initially massive symptoms - Anticoagulant-induced ICH: may
evolve for as long as 24-48 hours
 Cerebral ischemia caused by a reduction in blood flow that lasts
longer than several seconds
Neurologic symptoms are manifest within
seconds because neurons lack glycogen
Transient Ischemic Attack (TIA) all neurologic signs and symptoms resolve
within 24 hour without evidence of brain
infarction on brain imaging
 may arise from emboli to the brain or from in
situ thrombosis of an intracranial vessel
hypoxic-ischemic encephalopathy the constellation of cognitive sequelae that
Types of cvd? ensues in global hypoxia-ischemia causes
widespread brain injury
Focal ischemia caused by thrombosis of the cerebral vessels
or infarction themselves or by emboli from a proximal arterial
source or the heart
Intracranial hemorrhage caused by bleeding directly into or around the
brain
produces neurologic symptoms by producing a
mass effect on neural structures, from the toxic
effects of blood itself, or by increasing intracranial
pressure
  Acute occlusion of an intracranial vessel causes reduction in blood
flow to the brain region it supplies
 decrease in cerebral blood flow to zero causes death of brain
Ischemic tissue within 4–10 min

Stroke  values <16–18 mL/100 g tissue per minute cause infarction within
an hour
 values <20 mL/100 g tissue per minute cause ischemia without
infarction unless prolonged for several hours or days
  ischemic but reversibly dysfunctional tissue surrounding a core
Ischemic area of infarction
Penumbra
  Two distinct pathways:
Focal Cerebral 1.a necrotic pathway in which cellular cytoskeletal breakdown is
rapid, due principally to energy failure of the cell
Infarction
2.an apoptotic pathway in which cells become programmed to die
  first goal is to prevent or reverse brain injury

Treatment:  airway,breathing, and circulation (ABCs), and treat hypoglycemia

or hyperglycemia
Acute Ischemic  emergency noncontrast head CT scan to differentiate between
Stroke ischemic stroke and hemorrhagic stroke
figure 446-1
medical mgt
of stroke and
tia
 1. Medical support - immediate goal is to optimize cerebral
improve perfusion in the surrounding ischemic penumbra
clinical 2. IV thrombolysis

outcome 3. Endovascular revascularization

4. Antithrombotic treatment
fall within six 5. Neuroprotection
categories: 6. Stroke centers and rehabilitation.
figure 446-2
cascade of
cerebral
ischemia
Table 446-1
admin of IV
for acute
ischemic
stroke
Table 446-2
causes of
ischemic
stroke
  Hypertension, coagulopathy, sympathomimetic drugs (cocaine,
INTRACEREBRAL methamphetamine), and cerebral amyloid angiopathy cause the
majority of these hemorrhages.
HEMORRHAGE
Table 446-4
Causes of
intracranal
hemorrhage