EMERGENCY MEDICINE

CASE PRESENTATION
Desiree Go & Mark Prado
Post-Graduate Intern
August 29 September 4, 2016

Objectives
To classify the proper triage classification of the case.
To identify the salient points in the primary survey.
To formulate appropriate differentials.
To formulate an initial management plan.
To recognize salient points in the secondary survey.
To plan proper management.

General Information
Patients Name: L.V
Age: 66 years old
Sex: Female
Address: Prk. Boulevard, Bacolod City
Status: Married
Religion: Roman Catholic

Chief Complaint

Vomiting

INITIAL VITAL SIGNS (1023H)

BP = 120/60mmHg
CR = 89 bpm
RR = 26 cpm
T = 37.0 C
O2 Sat. = 98%
GCS = 6 ( E1 V1 M4)

TRIAGE FINDINGS AND

CLASSIFICATION
Level 2- Emergent
Altered Mental Status (Stuporous)
Vomiting
GCS = 6 ( E1 V1 M4)

[Conditions that are a potential to life limb or

function, requiring rapid medical intervention or
delegated acts.]

Primary Survey
Stuporous
A Patent airway, non-conversant
B Tachypneic (26cpm), O2 sat = 98% to room air
C Normotensive with BP=120/60 mmHg, adynamic
precordium, distinct S1 and S2, regular rate, irregular
rhythm, weak peripheral pulses, capillary refill <2 seconds,
dry, warm skin
D No disabilities, GCS6 (E1V1M4)
E No significant events or exposure

 Allergies
- None
Medications
- Metoprolol 50mg/tab 1 tab OD
- Amlodipine 10mg/tab 1 tab OD
- Aspirin 80mg/tab tab OD
- Simvastatin 20mg/tab 1 tab OD
All medications were taken with poor compliance

 Past Medical Illness

(+) Hypertension for more than 20 years with poor compliance to
maintenance medications
(-) Diabetes Mellitus
(-) Bronchial Asthma
Previously diagnosed to have atrial fibrillation with rapid ventricular response for a
chief complaint of chest tightness last 2015, treated in CLMMRH OPD
Cardiomegaly was also noted on previous Chest Xray PA (2015)

Last Meal
- 08/26/16, 07:00H
Events
- No significant events or exposure

INITIAL INTERVENTION (11:00H)

37 minutes after admission

Heplock inserted
12 lead ECG
CBG- 208mg/dl
Appraised for intubation: Folks were still undecided and
refused intubation

12 Lead ECG Result

Initial Diagnosis
Cardioembolic Stroke;
Premature Ventricular Contractions in Bigeminy

Referred to IM Service for admission

1hour 22 minutes after
admission

Additional (STAT) Work-up

Cranial CT scan plain
Troponin I
Chest Xray PA
Creatinine
Serum Potassium, Calcium

Patient intubated
2 hours and 7 minutes after admission
Clinical findings:
Decreased level of consciousness : GCS 6 (E1V1M4)
HR: 40 - 55bpm

MV Settings:
FiO2: 100%
TV: 400ml
BUR: 20cpm
AC Mode
ABG I hr post attachment to mechanical ventillator

ABG Result:

REASSESSMENT
3 hours and 37 minutes after admission

BP = 110/60 mmHg
CR = 76 bpm
RR = assisted
Temp. = 36.6 C
O2 Sat. = 99%

REASSESSMENT
12 hours and 7 minutes after admission

BP = 140/100 mmHg
CR = 83 bpm
RR = assisted
Temp. = 36.5 C
O2 Sat. = 99%

REASSESSMENT
15 hours and 55 minutes after admission

BP = 140/100 mmHg
CR = 83 bpm
RR = assisted
Temp. = 36.5 C
O2 Sat. = 99%

Patient expired
21 hours and 20 minutes after admission

HR: 0
CR: 0
BP: 0
ECG Tracing: asystole

 #### hypoxic enceph

Acute ischemic vs. CVA bleed
Prob cardio embolic in origin

SECONDARY SURVEY
14 hours prior to admission
Generalized body weakness
Vomiting of previously ingested food
3 episodes: glass/episode
Non-projectile, non-billous vomitus

Slurring of speech, no facial asymmetry

1 hour prior to admission

Altered mental status (unarousable)

Past Medical History

(+) Hypertension for more than 20 years with poor compliance to maintenance
medications:
- Metoprolol 50mg/tab 1 tab OD
- Amlodipine 10mg/tab 1 tab OD
- Aspirin 80mg/tab tab OD
- Simvastatin 20mg/tab 1 tab OD
Previously diagnosed to have atrial fibrillation with rapid ventricular response for a chief
complaint of chest tightness last 2015, treated in CLMMRH OPD
Cardiomegaly was also noted on previous Chest Xray PA (2015)

(-) Diabetes Mellitus

(-) Bronchial Asthma
(-) No previous hospitalization or surgeries
(-) No known food and drug allergies

Family History
(+) Hypertension in the paternal side
Personal and Social History
Not a cigarette smoker
Not an alcoholic drinker
Denies illicit drug use

Review of Systems
Unable to assess due to decreased sensorium

SECONDARY SURVEY

Physical Examination
General Survey: Examined a stuporous
patient, not in respiratory distress with the
following vital signs:
BP: 120/60 mmHg
PR: 89 bpm
GCS 6 ( E1 V1 M4)

RR: 26 cpm
T: 36 C per axillae

Physical Examination

Head: no deformities; black and gray hair, equally distributed with no bald areas

Eyes: symmetric, anicteric sclerae, anisocoric pupils: (OD: 5mm dilated; OS:
1- 2mm pinpoint pupils), non-reactive to light and accommodation, firm
and equal by digital palpation test,

Ears: symmetric, no deformities, no discharges

Nose: nasal septum midline, moist nasal mucosa

Mouth: dry lips, no mucosal ulcers, pink gums, incomplete dentition without
dentures, dry tongue without lesions, uvula at midline

Physical Examination
Neck: supple, no lymphadenopathies, non-palpable thyroid gland,
unengorged neck veins
Chest and Lungs: equal chest expansion, clear, equal breath
sounds bilaterally
Heart: adynamic precordium, distinct S1 and S2, regular rate,
irregular rhythm, no murmurs, no thrills or heaves

Physical Examination
Abdomen: soft, normoactive bowel sounds, no
bruits, tympanitic except over area of liver
dullness
Back: no abnormal curvatures of the spine, no
lesions
Extremities: no edema, ROM not assessed,
weak peripheral pulses, CRT <2 sec

Physical Examination
Neurologic Exam:
Cerebral: stuporous
Cerebellar: unassessed due to decreased sensorium

Physical Examination

Neurologic Exam:

Sensory: unassessed due to decreased sensorium

Motor: no involuntary movements, no atrophy

5/5 2/5
0/5 2/5

Physical Examination

Neurologic Exam:
Cranial Nerves:

CN 1: unassessed due to decreased sensorium

CN 2,3: anisocoric pupils: (OD: 5mm dilated;

reactive to light and accommodation

CN 3,4,6: unassessed due to decreased sensorium

CN 5: unassessed due to decreased sensorium

CN 7: unassessed due to decreased sensorium

CN 8: unassessed due to decreased sensorium

CN 9,10: (+) gag reflex and swallowing reflex

CN 11: unassessed due to decreased sensorium

CN 12: unassessed due to decreased sensorium

OS: 1- 2mm pinpoint pupils), non-

Working Diagnosis:
Cardioembolic Stroke;
Cardiac Dysrhythmias T/C Acute Coronary
Syndrome

INTERVENTION

Venoclysis: Heplock

Labs:
- CBC
- CBG
- ABG
- Serum Ca, K
-Creatinine
- ECG 12 Leads
-Chest X-ray PA
-Cranial CT scan-Plain
- Troponin - I

Medications:

Atorvastatin 40mg/tab 1 tab OD HS

Metoclopramide 10mg/amp 1 amp IV q8h for
vomiting
Captopril 25mg/tab tab TID
ISMN 60mg/tab 1/2tab ODHS
Trimetazidine 35mg/tab 1 tab BID
Omeprazole 40mg/tab 1 tab ODAC
Lactulose 30cc ODHS hold for BM >3x

Special Orders:
Attach to cardiac monitor
MIO Q shift
Limit OFI <1L per day
Admit to SCU - NI
O2 at 4lpm via NC

Laboratory work-ups:

Exam Name

Result

BUN

Interpretation

Creatinine

97

53.04-114.92 mmol/L

Normal

Potassium

2.2

3.3-4.6 mEq/L

Decreased

Calcium

1.22

1.14-1.35 mmol/L

Normal

Troponin I

70.13

Normal

CT Scan- Plain (8/27/16)

Acute Infarction, involving the right
middle cerebral and posterior cerebral
arterial territories
Hydrocephalis with subependymal
seepage, leftward subfalcine, right
uncal, descending transtentorial and
tonsillar herniations, secondary.
Atherosclerotic internal carotid and
vertebral arteries.

Case Discussion

Stroke
A stroke, or cerebrovascular accident, is
defined as an abrupt onset of a
neurologic deficit that is attributable to
a focal vascular cause.
loss of function varies with location and
extent of damage

STROKE SOCIETY OF THE PHILIPPINES

DEFINITION OF STROKE

Sudden onset of focal neurologic

deficit due to an underlying
neurovascular pathology

TRANSIENT ISCHEMIC ATTACK

A focal (or global) neurological deficit
lasting < 24 hours
Most: lasts <30 mins
transient episode of neurological dysfunction
caused by focal brain, spinal or retinal ischemia,
without evidence of acute infarction in which
symptoms typically last <1hr
Stroke Society of the Philippines

Risk Factors - Nonmodifiable

Age
Gender (women more likely to die)
Race (African Americans)
Heredity

Risk Factors - Modifiable

Diabetes mellitus
Heart disease, atrial fibrillation

Heavy alcohol consumption

Hypercoagulability

Hyperlipidemia

Hypertension
Obesity
OCPs
Physical inactivity
Sickle cell disease
Smoking

CLASSIFICATION OF STROKE
Based on Ictus (Time from stroke onset):

Hyperacute
Acute
Subacute
weeks)
Chronic

(0-6 hours)
(6-72 hours)
(3 days - <3
(>3 weeks)

CLASSIFICATION OF STROKE
Based on Severity (National Institutes of Health Stroke Scale)

1. Level of Consciousness
2. Horizontal Eye Movement
3. Visual field test
4. Facial Palsy
5. Motor Arm
6. Motor Leg
7. Limb Ataxia
8. Sensory
9. Language
10.Speech
11.Extinction and Inattention

Interpretation

CLASSIFICATION OF STROKE
BASED ON PATHOLOGY

1. ISCHEMIC stroke (infarct)

Thrombotic
Lacunar Strokes
Large vessel thrombosis
Hypercoagulable disorders

Embolic
Artery to Artery
Carotid bifurcation, Aortic arch
Cardioembolic

CLASSIFICATION OF STROKE
BASED ON PATHOLOGY
2. HEMORRHAGIC stroke (rupture of artery)

Intracerebral

Subarachnoid

Ischemic Strokes (Thrombotic )

Atherosclerosis is the most common pathology
leading to thrombotic occlusion of blood
vessels.

 Atherosclerotic infarction 30%

Lacunar infarction 25%
<occlusion of small, deep, penetrating arteries

Cardioembolic infarction 20%

Cryptogenic infarction 20%
Those that cannot be explained. There could be several
causes/etiologies.
Sickle cell disease
Protein S or protein C deficiency

Infarction of other unusual cause 5%

Cardioembolism
Embolism of thrombotic material forming on the atrial
or ventricular wall or the left heart valve.
The fragment of thrombus may lyse quickly,
producing only TIA.
Alternatively, the arterial occlusion may last longer,
producing stroke.
Localization of emboli
Frequently in MCA, PCA
Infrequently in ACA

Cardioembolic stroke
Abrupt onset of a neurologic deficit due to occlusion of
cerebral vessels with emboli from a cardiac source.

 20% of all ischemic strokes

Stroke caused by heart disease is due to embolism
of thrombotic material forming on the Atrial/
ventricular walls or the left heart valves
detach and embolize into the arterial circulation

Causes of Cardioembolic
strokes
Atrial fibrillation
Mural thrombus
Myocardial Infarction
Dilated Cardiomyopathy
Valvular Lesions (MS, Mech Valve, Bact.
Endocarditis)
Paradoxical embolus (ASD, PFO)
Atrial Septal Aneurysm
Spontaneous echo contrast

Pathophysiology:
Loss in the supply of oxygen and glucose secondary to
vascular occlusion (thrombus or embolus)
Failure of cerebral circulation from cardiac
decompensation (CHF) or shock
Collapse of energy-producing processes with
disintegration of cell membranes

Cerebral Blood Flow (CBF)

Zero- death of brain tissue within 410 min
<1618 mL/100 g tissue/min cause infarction within
an hour;
<20 mL/100 g tissue/min cause ischemia without
infarction

Normal= (85-100g/min )

Ischemic Penumbra
ischemic but reversibly dysfunctional tissue
surrounding a core area of infarction.
will eventually progress to infarction if no
change in flow occurs
saving it is the goal of revascularization
therapies.

PENUMBRA

CORE

ACLS Suspected Stroke Algorithm

F- Facial Weaknesss
A- Arm Drift
S- Speech (Abn)
T-Time

Inclusion criteria
Age: 18 yrs or older

Diagnosis of an ischemic
stroke with neurologic
deficit
Time from onset of
symptoms is within 3
hours

Exclusion criteria
Evidence of intracranial
hemorrhage from CT scan

Exclusion criteria
Active internal bleeding or
acute trauma, such as a
fracture
Clinical presentation suggestive of a Acute bleeding diathesis,
subarachnoid hemorrhage, even
including the following but may
with normal CT
include other manifestations:
Evidence of multilobar infarction in Intraspinal surgery, serious
more than one-third of the cerebral head trauma, or previous
hemisphere on CT
stroke within the past 3
months
History of intracranial hemorrhage Arterial puncture at a noncompressible site within the
past 7 days
Uncontrolled hypertension based on
repeated measurements of > 185
mm Hg systolic pressure or > 110
mm Hg diastolic pressure
Known AV malformation, neoplasm,
or aneurysm
Witnessed seizure at stroke onset

Monitoring BP in Stroke patients eligible for a

fibrinolytic

Differential diagnosis:
Tumor
Gradual progressive course and insidious
onset
Bells palsy
Pure hemifacial weakness including forehead
Trauma
CNS Infections
Fever prior to onset of symptoms

Laboratory testing & Imaging:

CT Scan
Hyperintense/dense(White)
Hemorrhage

Hypointense/dense (Dark)
Infarction

MRI for higher resolution

ECG for cardiogenic stroke
Carotid doppler- degree of stenosis
Transcranial doppler- intracranial sclerosis
2D Echo Left atrial thrombus, aortic arch atheroma

USE OF BRAIN IMAGING

To rule out bleed
To rule out stroke mimickers
To distinguish minor from severe stroke
To confirm localization of stroke

GOALS OF TREATMENT:
Reduce the ongoing neurologic injury
Decrease mortality and long-term disability
Prevent complications
Secondary to
dysfunction

immobility

Prevent stroke recurrence

and

neurologic

6 categories of stroke treatment

(1) medical support,
(2) IV thrombolysis,
(3) endovascular revascularization,
(4) antithrombotic treatment,
(5) neuroprotection, and
(6) stroke centers and rehabilitation

I. MEDICAL SUPPORT

immediate goal is to optimize cerebral perfusion in the surrounding ischemic

penumbra.

preventing the common complications of bedridden patients

Subcutaneous heparin

pneumatic compression stockings

antipyretics and surface cooling

Water restriction and IV mannitol may be used

II. IV Thrombolysis
The National Institute of Neurological Disorders and
Stroke (NINDS) rtPA Stroke Study showed a clear benefit
for IV rtPA in selected patients with acute stroke.

IV

rtPA (0.9 mg/kg to a 90-mg maximum; 10% as a

bolus, then the remainder over 60 min )

Patients treated with IV (rtPA) within 3 hours of

stroke onset are at least 30% more likely to have
minimal or no disability at 3 months
The benefit of IV rtPA for acute ischemic stroke beyond 3
hours from onset is not established

III. Endovascular Revascularization

using thrombolytics via an intraarterial route to
increase
the concentration of drug at the clot and minimize
systemic bleeding complications
Intraarterial administration of a thrombolytic agent for
acute ischemic stroke (AIS) is not approved by the
U.S. FDA); however, many stroke centers offer this
treatment based on these data.

IV. Antithrombotic Treatment

Platelet Inhibition
Aspirin (only antiplatelet agent that has
been proven effective for the acute
treatment of ischemic stroke )
Given 24 and 48 hours after completion of alteplase
therapy
Dose 50-325 mg/day
Reduces long-term death and disability

Anticoagulation
Heparin (no additional benefit over aspirin;

V. Neuroprotection
the concept of providing a treatment that prolongs the
brains tolerance to ischemia
AVOID: 5 H Principle
Hypotension - Aggressive BP lowering is detrimental in acute
stroke
Hypoxemia- Maintain adequate oxygenation
Hyperglycemia- Can increase severity of ischemic injury (eg
lactic acidosis)
Hyponatremia cerebral swelling
Hyperthermia- related to increased metabolic demand, increased
free radical production and enhanced neurotransmitter release

 Neuroprotectants are drugs that:

1. Protect against excitotoxins and prolong

neuronal survival

2. Block the release of glutamate, free

radicals, inflammatory cytokines, and the
accumulation on intracellular calcium cations

Examples: Citicoline, Cerebrolysin, NueroAid

VI. Stroke Centers and Rehab

improves neurologic outcomes and reduces
mortality
includes use of standardized stroke order sets.
early physical, occupational, and speech
therapy.
Prevention of complications of immobility
Pneumonia, DVT and pulmonary embolism,
pressure sores of the skin, and muscle
contractures

Outcomes
Cardioembolic strokes have a worse prognosis and
produce larger and more disabling strokes than other
types.

References:
Harrison's Principles of Internal Medicine 19th
Edition.(P. 2417-2420).USA: McGrawHill Education
ACLS Suspected Stroke Algorithm