Case

Presentation
Marianne Angelina R. Lorenzo
Post-Graduate Intern
BOOZE TIL YOU
OOZE
OBJECTIVES
1. To present a history and physical examination of a patient with an
upper GI bleeding
2. To understand the approach to diagnosis of patients presenting with
UGIB and come up with differential diagnoses
3. To discuss Portal hypertension as a complication of liver cirrhosis and
its management
26/M
Solsona, Ilocos Norte
Roman Catholic
2nd hospital admission
90% reliability
hematemesis
 HISTORY OF PRESENT ILLNESS
Diagnosed case of Liver Cirrhosis Child Pugh C (March 2021)
Take home medications
• Omepraazole 40mg/tab OD
• Propranolol 20 mg BID
• BCAA 1 sachet OD
• Lactulose 30cc ODHS
Advised alcohol cessation
Ideally for EGD but procedures were on hold that time due to OR lockdown.
Still
Ideally advised for EGD but was undecided until lost to follow-up.
for EGD
Lost to follow-up
 HISTORY OF PRESENT ILLNESS
INTERIM

• uncompliant to medications
• still involves in alcohol
drinking spree sessions
(~1/2 bottle of gin 2-3x/week)
• (+) icteric sclera
• (-) episodes of melena,
Ideally for EGD
hematemesis, abdominal pain,
Lost to follow-up
seizures and tremors
 HISTORY OF PRESENT ILLNESS
INTERIM 6 DAYS
PTA

• binge drinking with his

friends

Ideally for EGD

Lost to follow-up
 HISTORY OF PRESENT ILLNESS
6 DAYS 2 DAYS
INTERIM
PTA PTA

(+) nausea
(+) dizziness
(+) generalized body weakness
(+) insomnia
• Stopped drinking alcohol.
• Denies melena, hematemesis,
Ideally for EGD
abdominal pain, seizures and tremors
Lost to follow-up
 HISTORY OF PRESENT ILLNESS
6 DAYS 2 DAYS 1 DAY
INTERIM
PTA PTA PTA

• Still with nausea, dizziness, generalized

body weakness, insomnia
• (+) episodes of retching and eventually
vomiting (coffee-ground vomitus 4x ~
100cc per bouts)
• No consult done nor medications taken
Ideally for EGD
Lost to follow-up
 HISTORY OF PRESENT ILLNESS
6 DAYS 2 DAYS 1 DAY FEW HRS
INTERIM
PTA PTA PTA PTA

• Still with episodes of retching

• 1 episode of coffee-ground vomitus ~50
cc
• (+) progressing generalized body
weakness, easy fatigability and dizziness
• (-) melena, abdominal pain, seizure,
Ideally for EGD
tremors, change in sensorium
Lost to follow-up
 REVIEW OF SYSTEMS
GENERAL: (-) fever, (-) anorexia, (+)weight loss
SKIN, HAIR, NAILS: (-) itchiness, (-) color change, (-) rashes, (-) texture changes, (-) changes in the hair (-) abnormal nail
growth
HEENT:
• (-) blurring of vision, (-) doubling of vision, (-) photophobia, (-) redness, (-) itchiness, (-) lacrimation, (-) deafness, (-)
tinnitus, (-) ear discharge, (-) otalgia, (-) epistaxis, (-) nasal discharge, (-) obstruction, (-) anosmia, (-) sinus pain
PULMONARY: (-) shortness of breath, (-) hemoptysis
CARDIAC: (-) chest pain, (-) nocturnal dyspnea, (-) orthopnea, (+) palpitations, (-) syncope, (-) leg swelling
GASTROINTESTINAL: (-)constipation, (-)diarrhea, (-) dysphagia
GENITOURINARY: (-) urinary frequency, (-) urgency, (-) dysuria, (-) hematuria, (-) flank pain
MUSCULOSKELETAL: (-) muscle pain (-) joint pains
NEUROLOGIC: (-) loss of consciousness, (-) abnormalities of sensation, (-) motor dysfunction or weakness or paralysis
ENDOCRINE: (-) heat/cold intolerance, (-) palpitations, (-) polydipsia, polyphagia, polyuria
HEMATOLOGIC: (-) bruising, (+) pallor
PAST MEDICAL HISTORY
• Chronic Alcohol Liver Disease (October 2020) - with several OPD
consults
• March 2021: Hypovolemeic Shock resolved secondary to Upper
Gastointestinal Bleeding probably secondary to bleeding
esophageal varices vsportal gastropathy secondary to Liver
Cirrhosis Child Pugh C Secondary to Chronic Alcoholic Liver
Disease; Acute Kidney Injury - resolved.- with series of blood
transfusions
• (-) surgery
• (-) allergies
FAMILY HISTORY
• (+) HTN (maternal)
• (-) DM
• (-) Asthma
• (-) PTB
• (-) Liver Dses
• (-) Kidney Dses
• (-) Malignancy
PERSONAL AND SOCIAL HISTORY
• Construction worker
• Smoker 5 pack years (stopped in 2020)
• Alcohol beverage drinker consuming 1/2-1 bottle of gin everyday
for 10 years
• Denies use of illicit drugs, IV drug injections
• Sexual History: Denies having in a relationship, denies sexual
activity
 PHYSICAL EXAMINATION
GENERAL SURVEY Conscious, coherent, not in cardiopulmonary distress
Vital Signs: BP: 100/60 mmHg (supine & upright) CR: 137 bpm
RR: 20cpm T: 36.5C SpO2: 99% at room air
Anthropometrics: Wt: 65 kg Ht: 1.62 m BMI: 24.6 (Overweight -
Asia Pacific)
SKIN (+) palmar palor, no palmar erythema, no active dermatoses, no
cyanosis, no bruises, with good skin turgor, warm to touch
HEENT No gross head lesions or deformities;
icteric sclera, pale palpebral conjunctiva, no eye discharge or
erythema.
No gross ear deformities, intact gross hearing
No ear/nasal discharge; moist lips and buccal mucosa, no active
gum/mucosal bleeding or lesions;
No cervical lymphadenopathies, no neck vein engorgement
 PHYSICAL EXAMINATION
THORAX AND No chest wall deformity, with tattoo on upper anterior chest 10x5 cm
LUNGS (+) spider angioma;
Symmetric chest wall expansion, no retractions, clear breath sounds
CARDIOVASCULAR Adynamic precordium, tachycardic, regular rhythm, PMI at 5th ICS
MCL, no heaves, no thrills, no murmurs
BREAST No gynecomastia
ABDOMEN Globular, nondistended, no active lesions, no surgical incisions, no
caput medusae, no bulging flanks, normoactive bowel sounds,
tympanitic, Liverspan at 14 cm midclavicular line, obliterated
Traube space, soft, nontender, liver edge palpated, no fluid
wave shift, no CVA tenderness
RECTAL No skin tags, no mass palpated, no hemorrhoids, good sphincteric
tone, yellow to brown fecal material on tactating finger, no blood
EXTREMITIES Full and equal pulses, Pale nail beds, No clubbing, No thenar
atrophy, CRT <2secs. (-) edema
 PHYSICAL EXAMINATION
NEURO GCS: 15 (E4V5M6)
Mental Status: Alert, coherent oriented to time, place and person
CN I: Not assessed
CN II: Pupils 2-3 mm, equal and briskly reactive to light; (+) direct and
consensual pupillary light reflexes
CN III, IV, VI: Full extraocular muscle movements, (-) ptosis
CN V: Intact masseter strength, intact corneal reflexes, Intact facial
sensation in the entire face
CN VII: No facial asymmetry, paralysis
CN VIII: Intact gross hearing
CN IX, X: Intact swallowing, no secreti
CN XI: Shrugs shoulders
CN XII: Tongue in midline, no atrophy, no fasciculations

Motor: Good tone and muscle bulk, 5/5 strength on all extremities
Sensory: 100% on all extremities
DTR: 2+ on all extremities
No dysdiadochokenesia
Gait: Tandem
Others: No babinski, no clonus, no tremors, no asterixis
 SALIENT FEATURES
SUBJECTIVE
26/M
Liver cirrhosis Child Pugh C (March
2021)
Binge alcohol beverage drinker
(+) nausea, dizziness, generalized
body weakness, insomia
Weight loss, palpitations
Retching
Hematemesis
(-) Melena, abdominal pain, seizure,
tremors, change in sensorium
OBJECTIVE
Tachycardia
(+) palmar pallor
(+) icteric sclera
(+) pale palpebral conjunctiva
(+) spider angioma
(+) hepatomegaly (liverspan 14 cm
MCL)
Obliterated traube space
(-) palmar erythema, gynecomastia,
caput medusae, thenar atrophy,
abdominal tenderness, fluid wave
shift, melena on examining finger,
tremors, asterixis
 PRIMARY WORKING IMPRESSION

Upper Gastrointestinal Bleeding probably

secondary to Mallory Weiss Tear vs Bleeding
Esophageal Varices secondary to Liver Cirrhosis
secondary to Chronic Alcohol Liver Disease
 APPROACH TO
GASTROINTESTINAL BLEEDING
OVERT GIB OCCULT GIB

hematemesis
symptoms of blood loss or
melena anemia such as
hematochezia lightheadedness, syncope,
angina, or dyspnea;
or with iron-deficiency
anemia or a positive fecal
occult blood test on routine
testing

Harrison's Principles of Internal Medicine 20th edition

 APPROACH TO
GASTROINTESTINAL BLEEDING
UPPER GIB LOWER GIB
Hematemesis Hematochezia

Melena

Harrison's Principles of Internal Medicine 20th edition

 UPPER GASTROINTESTINAL
BLEEDING

PEPTIC ULCER
DISEASE

EROSIVE DISEASE

MALLORY-WEISS
TEAR

ESOPHAGEAL
VARICES

Harrison's Principles of Internal Medicine 20th edition

 UPPER GASTROINTESTINAL
BLEEDING

PEPTIC ULCER  Nausea

DISEASE  Vomiting of
previously  burning, gnawing, aching epigastric pain
EROSIVE ingested foods  occur 90 mins-3hrs after meal/pain that
DISEASE  Coffee-ground awakens the patient from sleep
emesis/black tarry-  precipitated by food intake
MALLORY- stool
WEISS TEAR  Tachycardia
 Orthostatic
ESOPHAGEAL hypotension
VARICES

Harrison's Principles of Internal Medicine 20th edition

 UPPER GASTROINTESTINAL BLEEDING

Erosions are endoscopically visualized breaks which are confined to the mucosa
PEPTIC ULCER and do not cause major bleeding due to the absence of arteries and veins in the
DISEASE mucosa

EROSIVE The most important cause of gastric and duodenal erosions is NSAID use (~50%)
DISEASE Other potential causes:
 alcohol intake
MALLORY-  H. pylori infection
WEISS TEAR  stress-related mucosal injury

ESOPHAGEAL
VARICES

Harrison's Principles of Internal Medicine 20th edition

 UPPER GASTROINTESTINAL BLEEDING

is a linear mucosal rent near or across the gastroesophageal

PEPTIC ULCER junction that may result to brisk hemorrhage when the tear disrupts
DISEASE a submucosal arteriole

EROSIVE  The classic history is vomiting, retching, or coughing preceding

DISEASE hematemesis, especially in an alcoholic patient.
 Bleeding usually abates spontaneously
MALLORY-
WEISS TEAR
Endoscopy is the best method for diagnosis
ESOPHAGEAL
VARICES

Harrison's Principles of Internal Medicine 20th edition

 UPPER GASTROINTESTINAL BLEEDING

Esophageal varices are dilated submucosal distal esophageal veins connecting

PEPTIC ULCER the portal and systemic circulations.
DISEASE

EROSIVE
DISEASE

MALLORY-
WEISS TEAR

ESOPHAGEAL
VARICES

Harrison's Principles of Internal Medicine 20th edition

 UPPER GASTROINTESTINAL BLEEDING

ESOPHAGEAL VARICES
Esophageal varices are dilated submucosal distal esophageal veins connecting
the portal and systemic circulations.

Prevalence: It is more common in males than in females. Fifty percent of

patients with esophageal varices will experience bleeding at some point.

https://www.ncbi.nlm.nih.gov/books/NBK448078/

Endoscopy is the best method for diagnosis

 Hemoglobin 70 (L)
CBC Hematocrit 0.21 (L)
RBC 2.11 (L)
MCV 99.20
MCHC 33.50
RDW 16.20 (H)
WBC 12.98 (H)
Segmenters 0.88 (H)
Lymphocyte 0.09 (L)
Monocyte 0.03
Eosinophil 0.00 (L)
Basophil 0.00
Platelet 119 (L)
MPV 11.2
PDW 10.5
 CBC 5/26/21 5/31/21
CBC Hemoglobin 70 (L) 106
Hematocrit 0.21 (L) 0.32
RBC 2.11 (L) 3.41
Transfusion
MCV 99.20 94.10
is recommended when the
MCHC 33.50 33.00 hemoglobin drops below 7
RDW 16.20 (H) 19.10 g/dL, based
on a large randomized trial
WBC 12.98 (H) 4.54 showing this restrictive
Segmenters 0.88 (H) 0.45 transfusion
strategy decreases
Lymphocyte 0.09 (L) 0.28 rebleeding and death in acute
Monocyte 0.03 0.21 UGIB compared
with a transfusion threshold
Eosinophil 0.00 (L) 0.06
of 9 g/dL.
Basophil 0.00 0.00 Harrison's Principles of Internal Medicine 20th edition
Platelet 119 (L) 84
MPV 11.2 10.80
PDW 10.5 11.30
Total 9.74 mg/dl
CHILD-PUGH SCORE
Bilirubin (↑9.8x )
Direct 3.04 mg/dl
Bilirubin (↑8.8x)
Indirect 6.70 mg/dl
Bilirubin (↑5.8x)
Albumin 31.38 g/l (↓)

INR 3.03 (↑)

Total 9.74 mg/dl
Bilirubin (↑9.8x ) MELD-Na SCORE
Creatinine 97.18 umol

BUN 12.10 mmol

Albumin 31.38 g/l (↓)

INR 3.03 (↑)

Sodium 133.30 (↓)

Potassium 4.35

eGFR: 92 ml/min/1.73 m²
 WHOLE ABDOMINAL ULTRASOUND
Findings:
Liver is enalrged with slightly increased parenchymal echogenecity and coarse
parenchymal echotexture. No focal mass lesion seen.
Intrahepatic and extrahepatic ducts are not dilated.
Gallbladder is normal in size and configuration with thickened wall.
Polyp is noted in the gallbladder, measuring approximately 0.50 cm.
Spleen is enlarged with normal parenchymal echopattern. No focal mass lesion seen.
Pancreas is unremarkable.
No paraaortic lymphadenopathy noted.
Kidneys are normal in size and parenchymal echogenecity. No pelvocaliectasia nor lithiasis
noted.
Urinary bladder is physiologically distended with smooth and not thickened wall.
No intravesical intense echo noted.
Prostate gland is normal in size with no calcifications within.

IMPRESSION:
Hepatosplenomegaly; Mild Fatty Liver
Cholecystitis; Gallbladder Polyp
Clinical correlation is advised to rule out probable liver cirrhosis
GLASGOW-BLATCHFORD SCORE

14 points:
High Risk GI bleed
that is likely to require
medical intervention
(eg. transfusion,
endoscopy)
 INDICATIONS OF ENDOSCOPY

1. Gastrointestinal bleeding:
• In patients with active or recent bleeding
• Anemia when the clinical situation suggests an
upper GI source or when colonoscopy is negative
2. In patients with suspected portal hypertension to
document or treat esophagogastric varices.

Harrison's Principles of Internal Medicine 20th edition

 ENDOSCOPIC FINDINGS
ESOPHAGUS:
CARDIA:
• Upper 1/3: Normal
• tightly hugging the scope
• Mid-Lower 1/3: 3 columns of large
upon retroflexed view. No
esophageal varices were seen at the
varix was noted.
mid-distal third of the esophagus

FUNDUS:
• Mosaic-like pattern of ANTRUM:
• Minute erosions were
the mucosa was noted at
the fundus and proximal seen
third of the cardiac body

PYLORUS, PYLORIC RING, DUODENUM BULB

AND DESCENDING DUODENUM
• Normal
Impression: Large Esophageal Varices; S/P EVL; Portal
Hypertensive Gastropathy; Gastric Erosion
3 columns of large
esophageal varices were
seen at the mid-distal third
of the esophagus

Mosaic-like pattern of
the mucosa was noted at
the fundus and proximal
third of the cardiac body
Harrison's Principles of Internal Medicine 20th edition
 FINAL DIAGNOSIS

Upper Gastrointestinal Bleeding secondary to (1)

Bleeding Esophageal Varices (2) Portal
Hypertensive Gastropathy secondary to Portal
Hypertension secondary to Liver Cirrhosis Child
Pugh C; Gastric Erosions
Anemia Secondary, corrected
S/P Esopagogastroduodenoscopy + Esopageal
Varices Ligation (5/31/2021)
 CASE
DISCUSSION
 LIVER
CIRRHOSIS
 Cirrhosis is an end result of
chronic liver injury leading to
fibrosis and nodular
Definition regeneration.

Harrison's Principles of Internal Medicine 20th edition

Harrison's Principles of Internal Medicine 20th edition
 ALCOHOLIC CIRRHOSIS
• Excessive chronic alcohol use can cause several different types of
chronic liver disease, including alcoholic fatty liver, alcoholic
hepatitis, and alcoholic cirrhosis
• Chronic alcohol use can produce fibrosis in the absence of
accompanying inflammation and/or necrosis. When fibrosis reaches
a certain degree, there is disruption of the normal liver architecture
and replacement of liver cells by regenerative nodules.

Harrison's Principles of Internal Medicine 20th edition

METABOLISM OF ETHANOL

https://www.researchgate.net/figure/Hepatic-metabolism-of-ethanol-MEOS-microsomal-ethanol-oxidizing-system_fig1_8658758
https://pubs.niaaa.nih.gov/publications/arh27-4/285-290.htm
Standard Drink

Drinking in moderation:
• 2 drinks or less in a day for men
• 1 drink or less in a day for women

Alcohol and public health. Center for Disease Control and Prevention (CDC)
Binge drinking Heavy drinking
• For women, 4 or more • For women, 8 or more drinks
drinks during a single per week.
occasion. • For men, 15 or more drinks
• For men, 5 or more drinks per week.
during a single occasion.
 MAJOR COMPLICATIONS OF CIRRHOSIS

Harrison's Principles of Internal Medicine 20th edition

 PORTAL HYPERTENSION
• elevation of the hepatic venous pressure gradient
(HVPG) to >5 mmHg.

Increased intrahepatic resistance to Increased splanchnic blood

the passage of blood flow through flow secondary to vasodilation
the liver due to cirrhosis and within
regenerative nodules the splanchnic vascular bed

Harrison's Principles of Internal Medicine 20th edition

 PORTAL HYPERTENSION

GASTROESOPHAGEAL
VARICES ASCITES HYPERSPLENISM

PORTAL
HYPERTENSIVE
GASTROPATHY

Harrison's Principles of Internal Medicine 20th edition

 PORTAL HYPERTENSION ESOPHAGEAL VARICES

3 factors that help identify patients who are at high risk

of bleeding are varices that are:
• large in size;
• appearance of red wale signs, cherryred spots, or
fibrin plug;
• severity of liver disease (CTP classes B and C)

Harrison's Principles of Internal Medicine 20th edition

PORTAL HYPERTENSION ESOPHAGEAL VARICES

columns of large esophageal

varices were seen starting at
the mid distal 3rd of the
esophagus
 PORTAL HYPERTENSION ESOPHAGEAL VARICES

TREATMENT
prevention of rebleeding once there has been
Primary prophylaxis an initial
variceal hemorrhage

• routine screening by
endoscopy of all patients
with cirrhosis
• nonselective beta
blockade or by variceal
• band ligation

Harrison's Principles of Internal Medicine 20th edition

The European Association for the Study of the Liver. EASL Clinical Practice Guidelines for the management of patients with decompensated cirrhosis. J Hepatol (2018)
 PORTAL HYPERTENSIVE
PORTAL HYPERTENSION GASTROPATHY

• occurs as a complication of portal hypertension

• can occur together with esophageal varices
• involves the lining of the stomach in which the gastric mucosa becomes
congested with dilated and distended capillaries.
• MC in the fundus
• Endoscopic findings:
• gastric mucosa becomes reddened and edematous with a
superimposed mosaic pattern
• Severe form: mucosa becomes friable and bleeds easily on contact

• MC clinical manifestation: chronic anemia

• Management: NSBB and iron supplementation and/or blood transfusion

Harrison's Principles of Internal Medicine 20th edition

 PORTAL HYPERTENSION SPLENOMEGALY

• Congestive splenomegaly is common in patients with portal

hypertension.
• Clinical features: enlarged spleen on physical examination
and the development of thrombocytopenia and leukopenia
• Hypersplenism with the development of thrombocytopenia is a
common feature of patients with cirrhosis and is usually the
first indication of portal hypertension.

Harrison's Principles of Internal Medicine 20th edition

 PORTAL HYPERTENSION ASCITES

• accumulation of fluid within the peritoneal cavity

Harrison's Principles of Internal Medicine 20th edition

 PORTAL HYPERTENSION ASCITES

• accumulation of fluid within the peritoneal cavity

• Clinical features: increase in abdominal girth that is often
accompanied by the development of peripheral edema
• Patients usually have at least 1–2 L of fluid in the abdomen
before they are aware that there is an increase
• PE: bulging flanks, may have a fluid wave, or may have the
presence of shifting dullness

Harrison's Principles of Internal Medicine 20th edition

 Risk Factors:
• Infections (Hepatitis)
• Autoimmune (AIH, PBC,PSC)
•
•
Toxin (Ethanol)
Metabolic (NAFLD)
CIRRHOSIS
• Genetic (Hereditary hemochromatosis, Wilson Disease)

↑ portal inflow due to Death of hepatocytes, inflammatory destruction of normal hepatic architecture to scarring
systemic vasodilation and fibrosis

Portal Hypertension Fluid exudes

↑ splanchnic from plasma in
circulation the capillaries
Blood backs up into splanchnic Ascites
collateral venous system vasodilation
arterial ↑ vasodilators
underfilling
Esophageal Portal Splenomegaly
Varices Hypertensive
Gastropathy Thrombocytopenia
↑Trapping of
blood cells
As variceal pressure Anemia
3 units PRBC transfusion Feso4 + Folic acid tablet
↑ vessels swell
Tachycardia supplemetation

↑ vessel size Blood loss from Hypotension Esophagogastroduodenoscopy Nonselective Beta-Blocker:

↓wall thickness circulation (EGD) Propranolol 10 mg TID
Death • Large Esophageal Varices;
↑ vessel Upper GI bleed
tension Omeprazole
Blood oxidized Melena • Gastric Erosion Rebamipide
Variceal rupture and vomited or Hematemesis
passed through GI Esophageal Varices Ligation
 Risk Factors:
• Infections (Hepatitis)
• Autoimmune (AIH, PBC,PSC)
•
•
Toxin (Ethanol)
Metabolic (NAFLD)
CIRRHOSIS
• Genetic (Hereditary hemochromatosis, Wilson Disease)

Death of hepatocytes, inflammatory destruction of normal hepatic architecture to scarring

and fibrosis

↓ liver function

Low albumin ↓oncotic pressure in Fluid exudes from plasma in

synthesis systemic capillaries the capillaries into interstitial
Edema
tissues
Encephalopathy
Liver unable to Toxins (NH3+)
remove toxins build up, cross (degeneration of
from the body BBB neurological functions,
confusion, asterixis) • Branched-chain
amino acid
↓conjugation of bilirubin
Jaundice supplement
↓secretion of of conjugated bilirubin •
Icteric sclera Lactulose
↓drainage of conjugated bilirubin
 REFERENCES

● Bischoff, Stephan, et. al. (2020). ESPEN practical guideline: Clinical nutrition in liver
disease.
● The European Association for the Study of the Liver. EASL Clinical Practice Guidelines
for the management of patients with decompensated cirrhosis. J Hepatol (2018)
● Harrison's Principle of Internal Medicine 20th edition
● Laine, Loren (2021). ACG Clinical Guideline: Upper Gastrointestinal and Ulcer Bleeding
● Shetyy, Akshay et. al (2019). The Gastroenterologist’s Guide to Preventive Management of
Compensated CirrhosisGastroenterology & Hepatology Volume 15, Issue 8
 THANK YOU!
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