CLINOCOPATHOLOGIC CONFERENCE II

CLINICAL PROTOCOL
GROUP C-3

MEMBERS:

Deganos, Shara Mae Duloguin, Carlo Eggyboy

Delacruz, Mikhael Ecija, Clyde joshua
Delacruz, Reena Edera, Janelle
Delos Angeles, Carlo Escuro, Wendy
Delos Reyes, Eric Bim Feliciano, Patricia
Domigpe, Janeth Figueroa, Ralph
Domingo, Kressel Anne Fong, Henreed
Duenas, Keith Gaca, Klent

General Data: EO, a 68- year old male, Filipino, from Rizal Province, and a
diagnosed case of atrial fibrillation was admitted for the second time in a
government hospital.

Clinical Impression: Myocardial Infarction

I. HPI with pertinent Physical examination and Laboratory findings:

Upon Admission CBC ANEMIA

Creatinine ELEVATED
BUN ELEVATED
Serum NORMAL
Electrolytes (Na,
K, Cl)
CK-MB (7-25 U/L) ELEVATED
Troponin ELEVATED
12-Lead ECG NO ST ELEVATION AND LATERAL WALL
ISCHEMIA
PT & PTT NORMAL
FECALYSIS BLACK & WATERY STOOL WITH (+)
 OCCULT BLOOD TEST
Chest X-ray PNEUMONIA
1ST HOSPITAL CBC HEMOGLOBIN: (N: 140-180 g/L)
DAY
DECREASED
= 117 g/L
HEMATOCRIT: (N: 0.40-0.54%)
DECREASED
= 0.36%
RBC COUNT: (N: 4.7-6.1 X1012/L)
DECREASED =
3.8
PLATELET COUNT: (N: 150-450 X109/L)
= 213
BUN (N: 2.5-6.4 mmol/L)
ELEVATED = 32.2 mmol/L

CREATININE ELEVATED: 374.6

(N: 53-115umol/L)
COAGULATION PROTIME (N: 11.8-14.6 sec)
PANEL
PROLONGED = 16.2 sec

TROPONIN I (N: 0.02-0.06)

ELEVATED = 5.529
2ND HOSPITAL FECALYSIS (+) MELENA
DAY
3RD HOSPITAL FECALYSIS (+) MELENA
DAY
FBS (N: 4.1-5.9mmol/L)
TOTAL LIPID TOTAL CHOLESTEROL (N:0-5.2mmol/L)
PROFILIE
HDL (N:0-1.5mmol/L)
 LDL (N:1.89-3.09mmol/L)
VLDL (N:0-1.0mmol/L)
TRIGLYCERIDES (N: 0-2.26 mmol/L)
TROPONIN I (N: 0.02-0.06)
ELEVATED = 3.194
4TH HOSPITAL FECALYSIS (+) MELENA
DAY
CBC HEMOGLOBIN: (N: 140-180 g/L)
DECREASED
= 113 g/L
HEMATOCRIT: (N: 0.40-0.54%)
DECREASED
= 0.35%
RBC COUNT: (N: 4.7-6.1 X1012/L)
DECREASED =
3.6
PLATELET COUNT: (N: 150-450 X109/L)
= 238
TROPONIN I (N: 0.02-0.06)
ELEVATED = 3.984
5TH HOSPITAL URINALYSIS NORMAL
DAY
TPAG TOTAL PROTEIN(N:64-82g/L)
NORMAL =69.97 g/L
ALBUMIN(N:34-50g/dL)
NORMAL =34.97 g/dL
GLOBULIN(N:23-35g/dL)
NORMAL =35 g/dL
A/G RATIO(N:1.1-1.6)
NORMAL =1.15
AST/SGOT (N:15-37U/L) ELEVATED = 42U/L
 ALT/SGPT (N:30-65U/L) ELEVATED = 67 U/L
BILIRUBIN TOTAL BILIRUBIN (N:3-17umol/L)
NORMAL = 8.5
DIRECT BILIRUBIN (N:0.0-3.0umol/L)
NORMAL = 2.0
INDIRECT BILIRUBIN (N:3-114umol/L)
NORMAL = 4.206.5

SERUM SODIUM (N: 136-145mmol/L)

ELECTROLYTES
DECREASED: 127 mmol/L
POTASSIUM (N: 3.5-5.1mmol/L)
NORMAL = 4.20 mmol/L
CHLORIDE (N:97-107mmol/L)
DECREASED = 93 mmol/L
CALCIUM (N: 2.12-2.52mmol/L
DECREASED= 1.89
mmol/L
MAGNESIUM (N: 0.69-0.93mmol/L)
DECREASED= 0.52
mmol/L

BUN (N: 2.5-6.4 mmol/L)

ELEVATED = 21.4 mmol/L

6TH HOSPITAL SERUM SODIUM (N: 136-145mmol/L)

DAY ELECTROLYTES
DECREASED: 127 mmol/L
POTASSIUM (N: 3.5-5.1mmol/L)
NORMAL = 4.20 mmol/L
 CHLORIDE (N:97-107mmol/L)
DECREASED = 93 mmol/L
BUN (N: 2.5-6.4 mmol/L)
ELEVATED = 21.4 mmol/L

CREATININE (N: 53-115umol/L)

ELEVATED = 346.2 mmol/L

7TH HOSPITAL Stat ECG ST SEGMENT ELEVATION IN LEADS V1

DAY THROUGH V6 AND LEAD I AND aV L
Stat TROPONIN I (N: 0.02-0.06)
ELEVATED = 5.469
CBC HEMOGLOBIN: (N: 140-180 g/L)
DECREASED
= 83 g/L
HEMATOCRIT: (N: 0.40-0.54%)
DECREASED
= 0.25%
RBC COUNT: (N: 4.7-6.1 X1012/L)
DECREASED =
2.7
PLATELET COUNT: (N: 150-450 X109/L)
= 175
BUN (N: 2.5-6.4 mmol/L)
ELEVATED = 20 mmol/L

CREATININE (N: 53-115umol/L)

ELEVATED = 244.3 mmol/L
 SERUM SODIUM (N: 136-145mmol/L)
ELECTROLYTES
NORMAL: 139 mmol/L
POTASSIUM (N: 3.5-5.1mmol/L)
DECREASED = 2.50
mmol/L
CHLORIDE (N:97-107mmol/L)
ELEVATED = 111 mmol/L

Low Hemoglobin- Decreased in hemorrhage (gastrointestinal and genitourinary)

and anemia. symptoms of low hemoglobin: weakness, shortness of breath,
dizziness, fast, irregular heartbeat, headache, cold hands and feet, chest pain.

Low Hematocrit - Decreased in blood loss (gastrointestinal and genitourinary)

and anemia.
BASIS: Epigastric pain associated with passage of black, tarry stool.

Elevated BUN (Azotemia) - Elevated BUN can also be found as a physiologic

response to decreased renal blood flow which affects the filtration of BUN from
the blood, as well as gastrointestinal hemorrhage, catabolic state tissue
breakdown and sepsis.
BASIS: Epigastric pain and tarry stool

Prolonged PT - coagulation factor deficiency. nephrotic syndrome, disseminated

intravascular coagulation.

Low Sodium- Sodium and water depletion secondary to nephrotic syndrome,

administration of hypotonic fluids, hypoalbuminemia, SIADH, and diuretics.

Low Potassium - Serum depletion secondary to nephrotic syndrome, steroid

therapy and diuretics.
Low Chloride - Can be caused by overhydration, diuretics Can also be due to
hyponatremia, since chloride is the counter ion of sodium. Can also be due to
causes of hyponatremia.

Decreased Platelet - Can occur during sepsis, disseminated intravascular

coagulation and hemolytic-uremic syndrome. It can also be caused by
drug-induced destruction of platelets (e.g. heparin, aspirin, NSAIDS, etc.).

Positive Fecal Occult Blood - Indicative of bleeding in the gastrointestinal tract

(gastritis, gastrointestinal hemorrhage, colitis, and hemorrhoids).

Cardiac Biomarkers Cardiac-specific troponins T and I are highly specific for

myocardial injury and are the preferred biochemical markers for diagnosis of
acute MI.
- Time of initial elevation: 4-6hrs, Times to peak Elevation: 12-24hrs, Time
to return to normal: 72 -96 hrs.

CK-MB isoenzyme is more specific for MI but may also be elevated with
myocarditis or after electrical cardioversion.
- In acute myocardial infarction, the native (tissue) isoforms CK-MB2 and
CK-MM3 are released into the blood.
- In the first 3-4 hours following symptom onset, improved sensitivity for
myocardial infarction detection is achieved.
- Time of initial elevation: 4-8hrs, Times to peak Elevation: 12-24hrs, Time
to return to normal: 72 -96 hrs.

RBC
 indicative of anemia
o maybe due to chronic gastrointestinal bleeding
o manifested in shortness of breath and pale palpebral conjunctiva in
the patient due to decreased O2 delivery

Creatinine
 used to assess renal filtration function
  inversely proportional to glomerular filtration rate
 used to determine sufficiency of kidney function and the severity of kidney
damage and to monitor the progression of kidney disease
o impaired kidneys can lead to multiple chain effects such as
decreased production of hormones (e.g. EPO, renin)

II. Clinical impression based on Physical examination and HPI:

Clinical Impression: Myocardial Infarction
BASIS:
HPI
 2 months prior: Episodes of Chest heaviness lasting about 2 minutes
located in the sternal area precipitated by exertion and stress and
relieved upon rest
 1 week prior: Sudden abdominal pain associated with Chest pain at the
left sternal area characterize as burning sensation radiating to the
back.
 45 minutes prior: Dull but severe substernal pressure that radiated to
his left arm and jaw
PE
 Overweight
 Anxious and Diaphoretic
 With his hand clenched over his chest
 BP: 160/100
 (+) S4 gallop

III. DIFFERENTIAL DIAGNOSIS

Disease: Stable Angina GERD: Cardiac Abdominal

Pericarditis Aortic
Aneurysm

Rule in: (+)chest pain (+) chest pain (+)Stable (+)Sudden

abdominal
 (+)shortness (+) abdominal angina pain
of breath pain
(+)Retrostern (+)Difficulty on
(+)sweating (+) sweating al; often breathing
radiates to
(+)severe (+) burning (+)Diaphoresi
neck, jaw,
substernal sensation s
shoulders or
pressure that
(+) shortness arms, (+)Hypertensi
radiated to the
of breath sometimes on
left arm and
epigastric
jaw
(+)S4 gallop
or mitral
regurgitation
murmur (rare)
during pain;
S3 or rales if
severe
ischemia or
complication
of myocardial
infarction

Rule out: Melena (-) productive (-) Myocardial Melena

cough infection
unpredictable Pain may be
lasting for
pattern of pain localized to
greater than
the front or
30 mins
back of the
chest, often
the
interscapular
region
IV. MAIN CLINICAL DIAGNOSIS (as confirmed by the pertinent lab findings)
 Myocardial Infarction
 PUD

V. CLINICAL CAUSE OF DEATH WITH EXPLANATION OF

PATHOPHYSIOLOGY
- Cardiogenic shock from STEMI and high output failure from anemia secondary
to acute blood loss from PUD.
 Caused by myocardial pump failure due to intrinsic myocardial damage,
extrinsic compression or obstruction to outflow that will lead to low cardiac
output.
 Clinical examples are:
 Myocardial infarction
 Ventricular rupture
 Arrhythmia
 Cardiac tamponade
 Pulmonary embolism