UGIB secondary to Esophageal Varices

Case Presentation
Internal Medicine
8/5/2021

1. Good day, doctors. I’m Marianne Lorenzo, a post-graduate intern.

2. To start with, the cliche goes that drinking too much can harm one’s health. Alcohol consumption is associated
with a variety of short- and long-term health risks such as accidents and violence that over time, excessive use
can lead to the development of chronic diseases. So, will you still booze it up until you ooze?

3. These are my objectives

4. This is the case of a 26/M, single, from Solsona, Ilocos Norte, affiliated to Roman Catholic admitted for the 2 nd
time in our institution last May 28, 2021. The informant is the patient with 90% reliability.

5. With a chief complaint of hematemesis

6. For the history of present illness, patient is a diagnosed case of Liver Cirrhosis Child Pugh C last March 2021.
Given take home medications such as Omeprazole 40mg/tab OD, Propranol 20 mg BID, BCAA 1 sachet OD and
Lactulose 30cc ODHS and advised alcohol cessation. Ideally for EGD but procedures were on hold that time due
to OR lockdown. Still advised for EGD but was undecided until lost to follow-up.

7. During interim, patient was uncompliant to medications and still involves in alcohol drinking spree sessions with
friends consuming ~1/2 bottle of gin (5-6 oz of gin) 2-3x/week. He had icteric sclera and denies episodes of
melena, hematemesis, abdominal pain, seizures and tremors.

8. 6 days PTA, had binge drinking with his friends.

9. 2 days PTA, had nausea, dizziness, generalized body weakness and insomnia. Stopped drinking alcohol.
Denies melena, hematemesis, abdominal pain, seizures and tremors.

10. 1 day PTA, still with above symptoms, now with noted episodes of retching and eventually vomiting of coffee-
ground emesis 4x ~ 50-100cc per bouts. No consult done nor medications taken.

11. Few hours PTA, still with episodes of retching and eventually 1 episode of coffee-ground vomitus ~50 cc
accompanied with progressing generalized body weakness, easy fatigability and dizziness. No melena,
abdominal pain, seizure, tremors, change in sensorium. This prompted consult and was subsequently admitted.

12. For the review of systems, pertinents are

GENERAL: (-) fever, (-) anorexia, (-) dizziness, (+)weight loss (5 kg in 3 months or 9%)
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, (-) 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: (-) abnormal bleeding, (-) bruising, (+) pallor

13. For the Past Medical History

 He was diagnosed of Chronic Alcohol Liver Disease (October 2020) where he had several OPD
consults, advised alcohol cessation but still noncompliant.
 On March 2021, he was admitted with a final diagnosis of Hypovolemeic Shock resolved secondary to
Upper Gastointestinal Bleeding probably secondary to bleeding esophageal varices vs portal
gastropathy secondary to Liver Cirrhosis Child Pugh C Secondary to Chronic Alcoholic Liver Disease;
Acute Kidney Injury - resolved.- with series of blood transfusions
 Denies presence of hypertension, DM, asthma, blood dyscrasias and malignancies.
 No surgeries, no allergies noted, no recent vaccinations

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14. For the Family History, with noted history of HTN on the maternal side
 Denies presence of (-) DM, (-) Asthma, (-) PTB, (-) Liver Dses, (-) Kidney Dses, (-) Malignancy

15. Personal and Social History

 He is a high school graduate.
 Currently a construction worker
 He is a smoker for 5 pack years (stopped in 2020)
 Alcohol beverage drinker consuming 1/2-1 (5-10 oz) bottle of gin everyday for 10 years now
 Denies use of illicit drugs, IV drug injections
 Sexual History: Denies having in a relationship, denies sexual activity

16. For the 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 per 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

17. Breast: No gynecomastia

 THORAX AND LUNGS: No chest wall deformity, with tattoo on upper anterior chest 10x5 cm (+) 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
 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, brownish fecal
material on tactating finger
 EXTREMITIES: Full and equal pulses. Pale nail beds. No clubbing. No thenar atrophy, CRT <2secs.
(-) edema

***Percuss the left lower anterior chest wall roughly from the border of cardiac dullness at the 6th rib to the anterior axillary line and down to the
costal margin, an area termed Traube’s space. As you percuss along the routes, note the lateral extent of tympany. If tympany is prominent,
especially laterally, splenomegaly is not likely.

Percussion by Castell’s method: percuss in the lowest Left intercostal space in the anterior
axillary line (usually the 8th or 9th IC space). This space should remain resonant during full inspiration. Dullness on full inspiration indicates
possible splenic enlargement (a positive Castell’s sign)

Percussion by Nixon’s method: Place the patient in Right lateral decubitus. Begin percussion midway along the Left costal margin. Proceed in a
line perpendicular to the Left costal margin. If the upper limit of dullness extends >8 cm above the Left costal margin, this indicates possible
splenomegaly

Palpation: begin palpation in the RLQ. Direct the patient's breathing by telling them when to take a deep breath and when to exhale. While
proceeding diagonally towards the Left Upper Quadrant (LUQ), try to palpate the spleen edge during each inspiratory phase

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18. Neuro Exam
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, gag
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

19. For the Salient features:

Subjective Objective
26/M Tachycardia
Liver cirrhosis Child Pugh C (March 2021) (+) palmar pallor
Binge alcohol beverage drinker (+) icteric sclera
(+) nausea, dizziness, generalized body (+) pale palpebral conjunctiva
weakness, insomia (+) spider angioma
Weight loss, palpitations (+) hepatomegaly (liverspan 14 cm MCL)
Retching Obliterated traube space
Hematemesis (-) palmar erythema, gynecomastia, caput
(-) Melena, abdominal pain, seizure, tremors, medusae, abdominal tenderness, fluid wave
change in sensorium shift, melena on examining finger, tremors,
asterixis

20. My primary working impression is

Upper Gastrointestinal Bleeding probably secondary to Mallory Weiss Tear vs Bleeding Esophageal Varices
secondary to Liver Cirrhosis secondary to Chronic Alcohol Liver Disease

21. For the approach to gastrointestinal bleeding

 Overt GIB: hematemesis, vomitus of red blood or “coffee-grounds” material; melena, black, tarry stool;
and/or hematochezia, passage of red or maroon blood from the rectum.
 Occult GIB: present with symptoms of blood loss or anemia such as lightheadedness, syncope, angina, or
dyspnea; or with iron-deficiency anemia or a positive fecal occult blood test on routine testing.

22. Site of bleeding

UGIB (esophagus, stomach, duodenum)
LGIB (colonic), small intestinal, or obscure GIB (if the source is unclear)
 Hematemesis indicates an UGIB source.
 Melena indicates blood has been present in the GI tract for ≥14 h, and as long as 3–5 days. The more
proximal the bleeding site, the more likely melena will occur.
 Hematochezia usually represents a lower GI source of bleeding, although an upper GI lesion may bleed
so briskly that blood transits the bowel before melena develops.
 When hematochezia is the presenting symptom of UGIB, it is associated with hemodynamic instability
and dropping hemoglobin.

23. With a chief complaint of hematemesis, upper GI bleeding is highly considered and these are my
differentials.
 Peptic ulcer disease
 Erosive disease
 Mallory-Weiss tear
 Esophageal varices
. . . and the best diagnostics that could rule out one from the other is thru endoscopy

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24. First is Peptic Ulcer Disease.
A peptic ulcer is defined as disruption of the mucosal integrity of the stomach and/or duodenum leading to a
local defect or excavation due to active inflammation
 I ruled it in due to the presence of Nausea and Vomiting of coffee-ground emesis and Tachycardia
 However, the classic presentation of PUD which is the burning, gnawing, aching epigastric pain
occur 90 mins-3hrs after meal/pain that awakens the patient from sleep in DU and precipitated by
food intake in GU is not present in the patient
 And denies use of NSAIDs
 Although endoscopy is the best diagnostics to rule out PUD, this is still less likely in our
differentials

25. Next is erosive disease.

 Erosions are endoscopically visualized breaks which are confined to the mucosa and do not cause
major bleeding due to the absence of arteries and veins in the mucosa
 The most important cause of gastric and duodenal erosions is NSAID use (~50%)
 Other potential causes: alcohol intake which is present in our patient, H. pylori infection and
stress-related mucosal injury

26. Next is Mallory-Weiss tear.

 is a linear mucosal rent near or across the gastroesophageal junction that may result to brisk
hemorrhage when the tear disrupts a submucosal arteriole
 The classic history is vomiting, retching, or coughing preceding hematemesis, especially in an
alcoholic patient.
 Bleeding usually abates spontaneously
 Endoscopy is the best method for diagnosis
 Hence, high likely

27-28. The last of the differentials is Esophageal varices

 Esophageal varices are dilated submucosal distal esophageal veins connecting the portal and
systemic circulations.
 It can be caused by Prehepatic, post hepatic and Intrahepatic. In the case of the patient, he is a
diagnosed case of liver cirrhosis, hence an intrahepatic cause.
 In a study, the prevalence is more common in males than in females. Fifty percent of patients with
esophageal varices will experience bleeding at some point.
 Hence, high like
 But still, endoscopy is the best method for diagnosis

29. Diagnostics were requested.

The initial CBC revealed normocytic normochromic anemia, with anisocytosis. Leukocytosis at 12.98 with
segmenters predominance and Thrombocytopenia at 119.
 The causes of anemia include acute or chronic gastrointestinal hemorrhage, and hypersplenism
secondary to portal hypertension.
 Splenomegaly, which is usually caused by portal hypertension in patients with chronic liver
disease, may lead to secondary hemolysis, an increase in plasma volume, macrocytosis and
megaloblastic anemia.
 Alcoholics often develop secondary malnutrition, a manifestation of which may be anemia caused
by folic acid deficiency.
 The pathogenesis of the thrombocytopenia is complex; it includes splenic pooling, and increased
destruction and impaired production of platelets

30. Patient was immediately transfused with a total of 3 units of PRBC. According to Harrisons, transfusion is
recommended when the hemoglobin drops below 7 g/dL, based on a large randomized trial showing this
restrictive transfusion strategy decreases rebleeding and death in acute UGIB compared with a transfusion
threshold of 9 g/dL. It is important to avoid overtransfusion in patients with suspected variceal bleeding and the
blood transfusion goals for variceal bleeding are to transfuse if the hemoglobin is <7 g/dL (70 g/L), as transfusion
can precipitate worsening of the bleeding. Transfusing patients with suspected variceal bleeding to a hemoglobin
>10 g/dL (100 g/L) should be avoided.
 Moreso, patients with UGIB should undergo stabilization and resuscitation before the initiation of
endoscopic therapy. After 3 units, hemoglobin level increased from 70 to 106. However, platelet count
decreased from 119 to 84 which could be due to dilutional effect of the transfusion.

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31. The Child-Pugh Score can be useful in the prognosis of patients with cirrhosis
Parameters involved are:
 The presence of encephalopathy and ascites, which are absent in our patient
 For the laboratories, total bilirubin, PT/INR and albumin are needed
 The patient had elevated total bilirubin, a decreased albumin and a prolonged INR.
 This sums up to a score of 10, interpreted as Class C with a life expectancy of 1-3 years

32. The MELD/Na score is a scoring system for accessing the severity of chronic liver disease using values as
serum bilirubin, serum creatinine, and the international normalized ratio and sodium to predict survival. Patient
had a score of 30, or a 27-32% estimated 90-day mortality.

33. This is the CXray of patient X taken at AP view. Trachea is at midline, no bony deformities. Good inspiratory
effort. No noted infiltrates. CT Ratio of 0.5 cm. No blunting of sulcus.

34. Whole Abdominal Ultrasound was also requested noting

 Liver is enalrged with slightly increased parenchymal echogenecity and coarse parenchymal
echotexture. No focal mass lesion seen.
 Splenomegaly, no ascites
 Cholecystitis; Gallbladder Polyp

35. The Glasgow-Blatchford bleeding score (GBS) is a screening tool to assess the likelihood that a person with
an acute upper gastrointestinal bleeding (UGIB) will need to have medical intervention such as a blood
transfusion or endoscopic intervention.
 Patient had a BUN of 38 mg/dl with equivalent score of 4
 Hemoglobin of 7 with an equivalent score of 6
 With systolic BP of 100mm/Hg with score of 1
 Heart rate of 137 with an equivalent of 1
 And for the other markers, patient has a liver disease with a score of 2
 Hence, the patient had a total score of 14 points interpreted as High Risk GI bleed that is
likely to require medical intervention (eg. transfusion, endoscopy)

36. So what are the indications of Endoscopy?

For the patient, since he presented an Upper Gastrointestinal bleeding, endoscopy is done
 In patients with active or recent bleeding
 Anemia when the clinical situation suggests an upper GI source or when colonoscopy is negative
 In patients with suspected portal hypertension to document or treat esophagogastric varices.

37. Endoscopy was done in our patient wherein the findings includes:
ESOPHAGUS:
 Upper 1/3: Normal
 Mid-Lower 1/3: 3 columns of large esophageal varices were seen at the mid-distal third of the
esophagus
FUNDUS:
 Mosaic-like pattern of the mucosa was noted at the fundus and proximal third of the cardiac body

CARDIA:
 Tightly hugging the scope upon retroflexed view. No varix was noted.

ANTRUM:
 Minute erosions were seen

PYLORUS, PYLORIC RING, DUODENUM BULB AND DESCENDING DUODENUM

 Normal

The impression was: Large Esophageal Varices; S/P EVL; Portal Hypertensive Gastropathy; Gastric Erosion

38. So this is the view of the patient’s endoscopy. Sorry doctors, the result was printed in black and white :)

39. So this is an algorithm in the diagnosis and management of patient with upper gastrointestinal bleeding based on
endoscopic findings.
 Ideally, upper endoscopy should be performed within 24 h in most patients with UGIB. Patients at
higher risk (e.g., hemodynamic instability or cirrhosis) may benefit from more urgent endoscopy
within 12 h. However, as per protocol in our institution, all patients undergoing endoscopic
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 procedures are required to have a negative RT-PCR result. He was given a proton-pump inhibitor:
omeprazole 80mg IV bolus then as infusion drip of Omeprazole 40 mg for 5 hrs to complete for 72
hours. He also had 3 units PRBC for blood transfusion. He underwent EGD on his 4 th HD.
 Based on the endoscopic findings, the patient had esophageal varices noting 3 columns of large
esophageal varices were seen at the mid-distal third of the esophagus
 Hence, endoscopic ligation was done.
 Ocreotide was not given.
 He was then advised to have a clear liquid diet for 2 days.
 Regular oral feeding may cause postprandial hyperemia of mesenteric circulation which, in turn, may lead
to variceal rupture as a result of an increase of portal pressure.
 May dislodge the variceal bands, thus leading to early rebleeding.
 Dysphagia to solid food has been reported to occur in the initial few days post-EVL
 After 2 days, he was then discharged, stable.
Also, presence of minute erosions were seen on the antrum. So patient has gastric erosion.
40. Hence, the final diagnosis was :
 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 + Endoscopic Variceal Ligation (5/31/2021)

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41-42. For my case discussion, I will be focusing on liver cirrhosis and portal hypertension as one of its complications.

43. Cirrhosis is an end result of chronic liver injury leading to fibrosis and nodular regeneration.

44. This table shows the causes of cirrhosis, and alcohol is true to the patient

45. Alcohol cirrhosis is the 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.

46.
Ethanol is mainly absorbed by the small intestine and, to a lesser degree, through the stomach. Gastric alcohol
dehydrogenase (ADH) initiates alcohol metabolism.
Three enzyme systems account for metabolism of alcohol in the liver. These include cytosolic ADH, the microsomal
ethanol oxidizing system (MEOS), and peroxisomal catalase.
The majority of ethanol oxidation occurs via ADH to form acetaldehyde, which is a highly reactive molecule that may
have multiple effects. Ultimately, acetaldehyde is metabolized to acetate by aldehyde dehydrogenase (ALDH).
Intake of ethanol increases intracellular accumulation of triglycerides by increasing fatty acid uptake and by reducing
fatty acid oxidation and lipoprotein secretion.

47.
Oxidative damage to hepatocyte membranes occurs due to the formation of reactive oxygen species; acetaldehyde is
a highly reactive molecule that combines with proteins to form protein-acetaldehyde adducts. These adducts may
interfere with specific enzyme activities, including microtubular formation and hepatic protein trafficking. With
acetaldehyde-mediated hepatocyte damage, certain reactive oxygen species can result in Kupffer cell activation. As a
result, profibrogenic cytokines are produced that initiate and perpetuate stellate cell activation, with the resultant
production of excess collagen and extracellular matrix. Connective tissue appears in both periportal and pericentral
zones and eventually connects portal triads with central veins forming regenerative nodules. Hepatocyte loss occurs,
and with increased collagen production and deposition, together with continuing hepatocyte destruction, the liver
contracts and shrinks in size. This process generally takes from years to decades to occur and requires repeated
insults.

48. What is a standard drink?

A standard drink contains 0.6 ounces (14.0 grams or 1.2 tablespoons) of pure alcohol. Generally, this amount of pure
alcohol is found in
 12-ounces of beer (5% alcohol content).
 8-ounces of malt liquor (7% alcohol content).
 5-ounces of wine (12% alcohol content).
 1.5-ounces of 80-proof (40% alcohol content) distilled spirits or liquor (e.g., gin, rum, vodka, whiskey).

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49. Binge drinking, is defined as consuming
For women, 4 or more drinks during a single occasion.
For men, 5 or more drinks during a single occasion.

Heavy drinking is defined as consuming

For women, 8 or more drinks per week.
For men, 15 or more drinks per week.

50. These are the major complications of cirrhosis and this are true to my patient

51. Portal hypertension is caused by a combination of two simultaneously occurring hemodynamic processes: (1)
increased intrahepatic resistance to the passage of blood flow through the liver due to cirrhosis and regenerative
nodules, and (2) increased splanchnic blood flow secondary to vasodilation within the splanchnic vascular bed

52. The portal venous system normally drains blood from the stomach, intestines, spleen, pancreas, and gallbladder,
and the portal vein is formed by the confluence of the superior mesenteric and splenic veins. Deoxygenated blood
from the small bowel drains into the superior mesenteric vein along with blood from the head of the pancreas, the
ascending colon, and part of the transverse colon. Conversely, the splenic vein drains the spleen and the pancreas
and is joined by the inferior mesenteric vein, which brings blood from the transverse and descending colon as well as
from the superior two-thirds of the rectum. Thus, the portal vein normally receives blood from almost the entire GI
tract.

53. Portal hypertension is further divided into esophageal varices, portal hypertensive gastropathy, splenomegaly and ascites.

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57. Primary prophylaxis requires routine screening by endoscopy of all patients with cirrhosis. Once varices that are at ncreased
risk for bleeding are identified, primary prophylaxis can be achieved either through nonselective beta blockade or by variceal
band ligation.
In patients with cirrhosis who are screened for portal hypertension and are found to have large varices, it is recommended that
they receive either beta blockade or primary prophylaxis with EVL

Medical management: use of vasoconstricting agents (usually somatostatin or octreotide)

Octreotide, a direct splanchnic vasoconstrictor, is given at dosages of 50–100 μg/h by continuous infusion

NSBBs prevent variceal hemorrhage by decreasing portal pressure via β1 and β2 blockade. β1 blockade helps reduce cardiac
output, while β2 blockade leads to an unopposed a-adrenergic effect, thus indirectly causing splanchnic vasoconstriction.
Together, these effects reduce the portal blood inflow. Traditional NSBBs include propranolol and nadolol.

Antibiotic prophylaxis is recommended in cirrhotic

patients with acute GI bleeding because it reduces the incidence of infections and improves control of bleeding and survival.
Treatment should be initiated on presentation of bleeding and continued for up to seven days
Ceftriaxone (1 g/24 h) is the first choice in patients with decompensated cirrhosis, those already on quinolone prophylaxis, and
in hospital settings with high prevalence of quinolone-resistant bacterial infections.
Oral quinolones (norfloxacin 400 mg b.i.d) should be used in the remaining patients

59. EVL involves placing rubber bands around esophageal varices to obliterate them. Once EVL is pursued,
endoscopy or banding is repeated every 2 to 8 weeks. When obliteration is confirmed, repeat endoscopy should be performed in
3 to 6 months to assess for recurrence. If the result is negative, endoscopy should be repeated every 6 to 12 months

Nutrition
 Malnutrition is a predictor of morbidity and mortality and worsens as Child-Pugh status advances 50-90% prevalence of
malnutrition among cirrhotics
 Greater incidence of complications such as ascites, hepatorenal syndrome, hepatic encephalopathy, infections,
compromised respiratory function
 Associated with longer hospital stays

Caloric Requirement
25-35 kcal/kg/day without encephalopathy
35 kcal/kg/day with acute encephalopathy

Recommended protein intake 1-1.5g/kg/day

Carbohydrates should make up 45-65% of caloric intake
Frequent meals and snacks reduce hypoglycemic episodes
25-35% of calories from fat

Fluid intake 30-40mL/kg/day maintains fluid balance

Dilutional hyponatremia develops due to decreased renal blood flow and greater free water accumulation
Fluid restriction of 1.5L/day only if with ascites and hyponatremia <120mEq/L

Vitamins A, D, E, and K, zinc and selenium supplementation for all cirrhotics

Alcoholics need folate and thiamine supplements

Branched-Chain Amino Acids

Cirrhotics have lower concentrations of leucine, isoleucine, valine
Cirrhotics have a low ratio of branched-chain amino acids (BCAAs) to aromatic amino acids (AAAs)
AAAs increased due to impaired deamination

BCAA Supplementation
Reduces ammonia levels
Inhibits muscle proteolysis
Improves manifestations of recurrent hepatic encephalopathy
Heterogeneity in clinical trials in mode of administration and methods of assessing hepatic encephalopathy
Recommended by ESPEN because of increased albumin, and lower combined rates of decompensation and death