Gastro-esophageal reflux disease (GERD)

Condition characterized by reflux of gastric acid content into the esophagus.

Pathophysiology: Following factors play important roles:
1. Lower esophageal sphincter (LES) dysfunction 3. Hiatus hernia
2. Irritant effect of refluxed acid 4. Delayed esophageal emptying.
Clinical features:
1. Heartburn: Typically aggravates on: Lying flat after meals After alcohol ingestion.
2. A bitter/ sour test in the mouth due to regurgitation of gastric contents.
3. Atypical/ extra-esophageal manifestation:
a. Chronic cough
b. Chronic laryngitis
c. Hoarseness of voce
d. Non-cardiac chest pain.
Investigation
1. Upper GI endoscopy:
Typically shows: reflux esophagitis.
2. Esophageal manometry with pH estimation.
Treatment
1. Lifestyle modification:
I. Stay upright for approx. half an hour after each meal
II. To raise the head end of the bed during night
2. Medications:H2 blockers/ PPI.
Complication: Barrett’s esophagus.
Barrett’s esophagus
It is condition where esophageal squamous epithelium is replaced by metaplastic columnar epithelium.
Risk factor:
Long standing GERD
Clinical features: Barrett’s itself is usually asymptomatic
Symptoms of GERD: Present.
Investigation
1. Upper GI endoscopy:
Shows orange, velvety gastric type epithelium in the esophagus
2. Confirmation of diagnosis by mucosal biopsy.
Treatment
1. Medications to treat GERD
2. Endoscopic surveillance:

*Resection of metaplastic mucosal nodule is done by snare resection to prevent submucosal invasion.
Complication: Esophageal adenocarcinoma.
 Peptic ulcer disease
Breech in the continuity of gastric +/ duodenal mucosa.
Risk factors:
1. Chronic H.pylori infection:
In duodenal ulcer, initial H.pylori infection typically occurs at the junction of body and antrum.
• Chronic H.pylori infection ↑Gastrin production ↑HCl secretion Small islands of metaplastic changes in
the duodenum Duodenitis Ulcer
• In Gastric ulcer:
Initial infection typically in the body of stomach Mucosal inflammation and damage Destruction of HCl
producing cells Inflammation overwhelms gastric mucosal protection Ulcer
2. Drugs:NSAIDs/ Steroids
3. Stress ulcer: Can occur in any critically ill patients.
4. Malignant ulcer
Clinical features
Abdominal Pain:
• Typically occurs in epigastrium
• Variable duration
• Often occurs periodically
• Nature: Dull aching pain
• Aggravating and relieving factors: Type Aggravating factor Relieving factor
• Radiation to the back should raise Gastric ulcer After food intake Empty stomach
the suspicion of: Duodenal ulcer Empty stomach Food/ meal
a. Perforation
b. Pancreatitis.
Associated symptoms:
a. Heartburn/ indigestion
b. Loss of appetite: Often patient is afraid of eating
c. Hunger pain
d. Nocturnal pain (in duodenal ulcer)
e. Water brush: Regurgitation of bitter/ sour contents with sudden salivation
f. Features usually absent in benign ulcer:
I. Significant vomiting
II. Unintentional weight loss.
Bleed- Hematemesis ± Melena……Bleeding may be overt or occult
There may be no obvious blood loss or blood loss may be massive enough to make the patient’s hemodynamics unstable
In hematemesis, the color of blood may be fresh/ altered depending upon the time elapsed between bleeding and
vomiting. PR examination reveals melena in stool.
Investigations
A.Blood:
1. Hb, TC, DC, CRP:
2. If no bleeding but iron deficiency anemia is suspected: Serum iron studies:Iron/Ferritin/Transferrin saturation
3. Renal function: Na+ K+ Urea Creatinine
4. Lipase ± Amylase: To rule out acute pancreatitis
5. Clotting profile: Platelet count, BT, CT, PT, aPTT, INR
B.Faecal occult blood test (FOBT)
C.Upper GI endoscopy: a. Confirms presence of ulcer b. Biopsy confirms histopathological diagnosis.
D.Diagnosis of H.pylori infection:
a. Endoscopically: Rapid urease test
b. Non-endoscopically: 1. Urea breath test 2. H.pylori fecal antigen 3. Blood serology
Treatment

Peptic ulcer disease with significant GI bleed

Short term treatment
A. Admit if ongoing bleeding or significant bleeding
Airway: To be protected particularly if there is risk of aspiration
B. Breathing: Oxygen
Bowel rest: Nil by mouth till bleeding is under control, nasogastric suction
C. Circulation:
I. One wide bore cannula in each hand
II. IV fluid resuscitation: Ringer lactate/ Normal saline
III. Blood transfusion.
D. Drugs:Infusion of PPI: Pantoprazole for at least 48 hours
E. Endoscopy:
I. Urgent endoscopy with rapid urease test to confirm the diagnosis as well as endoscopic interventions
II. Endoscopic therapy to achieve hemostasis: can be broadly categorized into
• Injection therapy: solutions of diluted epinephrine
• Thermal coagulation
Long term treatment (for bleeders as well as non-bleeders)
A. H.pylori +Ve

B. H.pylori –Ve: H2 blocker/ PPI for at least 4-8 weeks: Long term maintenance therapy for high risk patients
 Gastropathy/ Gastritis
Damage to the mucosal epithelium of the stomach which may/ may not be accompanied by inflammation if mucosa
(gastritis).
Types:

Clinical features:
• H/O intake of offending drugs/ alcohol may be present
• Epigastric pain
• Heartburn
• GI bleeding: Hematemesis ± Melena (if present at all, usually insignificant in amount).
Investigation:
Upper GI endoscopy with rapid urease test + Biopsy
Treatment:
1. Prevention:
I. H2 blocker/ PPI
II. Sucralfate.
2. Established cases:
I. Acute period: IV PPI infusion
II. Long term treatment: H2 blocker/ PPI
III. H.pylori eradication.

Acute Pancreatitis
Acute inflammation of pancreas.
Causes:
1. Alcoholic pancreatitis
2. Biliary tract disease: Gall Bladder stone: Usually due to a slipped/ passed stone causing acute inflammation of
pancreas. (Many cases of so called idiopathic acute pancreatitis are thought to be caused by microlithiasis)
3. ↑↑Calcium
4. Cystic Fibrosis
5. Dyslipidemia: Hypertriglyceridemia and/or Chylomicronemia
6. Drugs induced- Asparginase/Azathioprine/Valproate
7. ERCP- complication of ERCP
 Signs and symptoms: 1. Due to Pancreatitis itself 2. Due to complications, IF any
System Symptoms Signs
Abdomen Onset: Sudden/Rapidly developing Abdominal distension
Site: Epigastrium Reduced bowel sound
Character: Deep seated/dull/burning pain- Signs of peritonitis
may be excruciating Ascites may be present
Radiation: Towards the back Epigastric Lump- Pseudocyst/Pancreatic Phlegmon
Aggravates on: Supine position/Postpradnial Gullen’s test: Bluish discoloration around umbilicus due
Partly relieved by: Stooping forwards with to extravasation of blood.
trunk flexed and knee drawn up Grey-Turner’s sign: Greenish yellow discoloration over
Associated with the flanks due to tissue metabolism of bilirubin.
Severe nausea ± retching ± vomiting

Features due to Complications- may be develop rapidly within few hrs - days
Breathing ARDS: SOB Tachypnoea; ↓SpO2; Bilateral crepitations

Circulation Altered sensorium BP: Hypotension

Dry skin/mucous membrane CRT- prolonged
Decreased Urine output Extremity:Tachycardia/ Weak pulse

Dermal Erythematous skin lesion due to

subcutaneous fat necrosis.
Eye Eye: Jaundice may be present Icterus may be present
Mechanism: Inflammation of the head of
pancreas may lead to CBD obstruction.
Fever

Ranson criteria/ score

A predictive score which can reasonably predict prognosis/ development of complication(s) in an acute pancreatitis.
On admission Within first 48 hours
1. Age >55 years 1. Arterial PO2 < 60 mm Hg. 4.Ca++ <8 mg/dL
2. Blood 2. ↑ BUN value by > 5 mg/dL 5.Drop in hematocrit: >10%
a.WBC > 160000/cu.mm (BUN/2.8) = Urea 6.Estimated fluid deficit >6L
b.Blood glucose >200 mg/dl 3. Base deficit >4 mEq/L
c.SGOT(AST) >250 IU/L
d.Serum LDH >350 IU/L
Presence of >3 of the above predicts a complicated course

Investigations
1. To confirm the diagnosis of acute pancreatitis 2. To detect risk factors and complications of acute pancreatitis

1. Blood:
A.Hb, TC, DC CRP
Hb: ↓ in hemorrhagic pancreatitis
TC, DC, CRP: ↑inflammation or intra-abdominal infection- Necrotizing pancreatitis, Peri pancreatic abscess
B.Renal function: Na+/ K+/ Urea/Creatinine (To look for any dehydration)
C.Liver function: Bilirubin: ↑ AST, ALT, GGT, ALP: Mild ↑.
D.Pancreatic enzymes: Amylase or Lipase levels at least 3 times above the reference range are considered diagnostic of acute
pancreatitis.
However, there are other Intra as well as Extra-abdominal causes of elevation of serum amylase. Lipase has a slightly
longer half-life, so it’s MORE useful if there is a delay between the onset of pain and the time the patient seeks medical
attention. Elevated lipase levels are more specific for pancreas than elevated amylase levels. Lipase levels remain high for
12 days. In patients with chronic pancreatitis (usually caused by alcohol abuse), lipase levels may be elevated in the
presence of a normal serum amylase level.
The level of serum amylase or lipase does not indicate whether the disease is mild, moderate, or severe

E.Arterial blood gas (ABG): To look for: Metabolic acidosis/ ↓pO2.

F.Ca level: Hypercalcemia is a risk factor of acute pancreatitis
Acute pancreatitis leads to hypocalcaemia (by saponification of fat)
G.Fasting lipid profile
2. Chest X Ray: To look for: ARDS/Pleural effusion.
3. USG abdomen: 4. CECT abdomen:
To look for: To look particularly for:
✓ Inflammation of pancreas ✓ Necrotizing pancreatitis
✓ Gallbladder stone ✓ Peripancreatic abscess
✓ CBD dilatation ✓ Pancreatic pseudocyst
✓ Ascites
5. Aspiration of ascitic and pleural fluid: Show elevated levels of amylase and lipase.

Treatment

Supportive treatment
A. Absolute bed rest till condition stabilizes
B. Breathing: Ventilator- for ARDS
B. Bowel rest:
• Nil by mouth initially till clinical/radiological improvement starts
• Ryle’s tube suction (if required)
• Gradual introduction of enteral feeding
• If required: Total Parenteral Nutrition
C. Maintain circulation:
• IV fluid : amount + rate + duration depends on clinical status- Bolus +/- maintenance

D. Drugs (Supportive):
• Analgesic-antispasmodic: • Antibiotics (particularly if intra-abdominal
Drotaverine infection is suspected): Imipenem-Silastin.
Opioids: Tramadol/ Pethidine • Antifungal (if intra-abdominal fungal infection)
Avoid morphine as it constricts sphincter of OD • Anti-ulcer drugs: To avoid stress ulcer: PPI.
D. Diet: Gradual introduction of normal diet: Initially clear liquid; then fat free liquid; then fat free (semi)solid
D. DVT prophylaxis

Interventional treatment
A. Percutaneous drainage (paracentesis) of peripancreatic abscess/ infected pseudocyst
B. ascites/ pleural effusion- rarely significant in amount requiring drainage
Surgical treatment
A. Necrosectomy/ debridement in necrotizing pancreatitis
B. Early cholecystectomy in case of gallstone pancreatitis.
 Complications of acute pancreatitis- ‘’PANCREAS’’
Organ Complications
involved
Pancreatic Necrosis Peripancreatic abscess
Hemorrhage Chronic pancreatitis
Pancreatic pseudocyst (sterile/ infected)
Abdomen 1. Ascites
2. Paralytic ileus
3. Peritonitis
Neurological Encephalopathy
Circulatory Circulatory shock/ collapse
Respiratory 1. ARDS
2. Pleural effusion- It results from leakage of pancreatic fluid through small pores in the
diaphragm into the pleural cavity

Eye Purtscher’s retinopathy (Sudden blindness due to vaso-occlusive and Hemorrhagic vasculopathy)
AKI Acute tubular necrosis (ATN) leading to AKI
Skin Subcutaneous fat necrosis

Hyperamylasemia
1. Abdominal causes:
✓ Acute/ chronic pancreatitis
✓ Perforation: Bowel/ peptic
✓ Bowel infarction
✓ Acute cholecystitis
✓ Ectopic pregnancy (ruptured)
2. Non-abdominal causes:
✓ Salivary gland diseases: Mumps/ Sialolithiasis (stone)/ tumor
✓ Bronchogenic carcinoma
✓ Ovarian carcinoma
 Malabsorption syndrome
A group of disorders characterized by impaired absorption of different food particles and nutrients.
Examples/Causes/Types:
1. Bacterial overgrowth syndrome 4. Crohn’s Disease
2. Short bowel syndrome (post-resection): 5. Dietary Intolerance: Lactose Intolerance/
Terminal ileum/Extensive small intestinal resection 6. Enteropathy: Protein losing enteropathy
3. Celiac disease
Mechanism of clinical manifestations and clinical features:
1. Due to Malabsoption of different nutrients
2. Unique features of the underlying disease
Substances malabsorbed/deficient Clinical features
A Albumin Swelling (anasarca)
Fat Steatorrhoea
Flatulence
B Bile acids Vitamin A Night blindness
Vitamin D Osteomalacia/Osteoporosis- Bone pain/deformity/fracture
Vitamin E CNS manifestations
Vitamin K Coagulopathy
Vitamin B12 Anemia ± Neurological complications
C Ca++ Tetany- spontaneous muscle spasm/Paresthesia (perioral)
Diet (Protein + Carbohydrate + Fat) Weight loss/Weakness/Wasting
D Vitamin D Proximal myopathy/Musculoskeletal pain/Bony deformity
E Electrolytes Sodium Encephalopathy
Potassium Muscle atony- Constipation/Faltulence
F Fe++ Iron deficiency anemia
Fluid Watery diarrhea

Investigations: To look for evidence of malabsorption & to detect its consequences

Blood:
1.Hb, TC, DC, CRP, MCV
Hb: ↓ (in Iron deficiency/ vitamin B12 deficiency) MCV: ↓/↑ (may be Dimorphic film).
2.Iron studies:Serum Iron/Serum Ferritin/ Serum Transferrin saturation
3. Biochemistry:Na+/K+/Ca++/Mg++/Urea creatinine
Clotting profile
Serum vitamin B12 level + Folate level+ Vit D3 level
Serum albumin
4.Tests to confirm Malabsorption:
Fecal fat content: ↑
D-Xylose test
5.Tests to confirm the underlying disease
Intestinal mucosal biopsy: Often confirm the diagnosis in some of the cases.
Treatment:
1.General treatment
1. Nutritional support- Dieatary +/- fluid replenishment
2. Supplementation of vitamins and minerals
2.Specific treatment- depends on the underlying disease
 Inflammatory bowel disease (IBD)
It is a condition characterized by widespread inflammatory damage to different parts of small and large intestine.
The pattern of inflammation and subsequent clinical features lead to 2 distinct clinical entities:
1. Crohn’s disease 2. Ulcerative colitis.

Crohn’s disease
Characterized by relapsing and remitting segmental/ patchy inflammation of intestine.
Sites (according to descending order of frequency):
1. Terminal ileum and proximal ascending colon: Ileocolitis
2. Terminal ileum: Ileitis
3. Large gut: Colitis- however, involvement of sigmoid colon and rectum is extremely rare and this variety is
usually associated with perianal manifestations.
/

Clinical features:
Mechanism of clinical manifestations: Manifestations can be chronic/rapid/acute on chronic- they may come back after a
quiscent stage when the disease flares up

Extra-intestinal features
manmanifestations
Clinical features of ileocolitis:
1. Due to chronic inflammation:
1. Pain abdomen: Often in right iliac fossa 4. RIF-tenderness / mass may be present
2. Diarrhea Usually watery, rarely bloody (matted intestine + lymph nodes + mesentery)
3. Fever, loss of appetite and weight loss 5. F/O Malabsorption syndro
2. Due to intestinal obstruction (fibrostenotic occlusion of intestine): Acute/Subacute
1. Abdominal pain 4. Distension
2. Borborygmi/Bloating 5. Emesis (Vomiting)
3. Constipation 6. Feces/Flatus

3. Due to fistulisation:
1. Enterocolic fistula: Malabsorption 3. Enterovaginal fistula: Feculent per-vaginal discharge
2. Enterovesicle fistula: Feculent urine 4. Enteromesenteric fistula: Intra-abdominal abscess

Clinical features of perianal disease:

1. Perianal fistula 3. Visible anal skin tag
2. Perianal abscess 4. Anal fissure
The disease classically relapses and remits.

Investigation
1.Blood: Hb, TC, DC, CRP/ESR- TC, DC, CRP, ESR: ↑ due to inflammation/ intra-abdominal infection
Hb: ↓ due to: Chronic inflammation/ Iron deficiency/ B12 deficiency
2.Renal function: Na+ K+ Urea Creatinine
3.If malabsorption is suspected: Albumin, Serum Ca++, Vitamin B12, Vitamin D, Iron studies.
4.Stool: Look for ova/ parasites/ cysts. Fecal Calprotectin level: High
5.Colonoscopy: shows mucosal inflammation/ ulceration with skip areas. Colonoscopic biopsy confirm the diagnosis.
6.Barium follow through: Shows any filling defect/anatomical deformity.It is done particularly when small bowel
involvement is suspected and colonoscopy is inconclusive.
7.Capsule endoscopy/enteroscopy: to visualize small gut
8.CECT abdomen: To visualize the internal structure for any obvious anatomical deviation.
Supportive treatment: ≥1 relevant if patient is very sick
1. Admit- if severe diarrhea/volume depletion IV fluid in severe diarrhoea
2. Bowel rest- NPM till clinically improved
3. Circulation- IV fluid in severe diarrhea- Bolus maintenance depending on the clinical scenario
4. Catheterisation- To monitor urine output- if required
5. Drugs:
Analgesic/Antispasmodic: Drotaverine/ Dicyclomine.
Antidiarrhoeal: Loperamide (May cause paralytic ileus)
Antibiotic- often given empirically
Specific treatment:
1. Aminosalicylate: To maintain remission- No longer the first line drug, can be used as adjunct with Steroid
Drugs: Mesalamine/Olsalazine/Balsalazide: No longer the first line drug, can be used as adjunct with Steroid
2. Corticosteroid: DOC in most CD patients to achieve remission
Systemic corticosteroids: Prednisolone/ Methylprednisolone
3. Immunomodulators: Used in moderate to severe disease- To induce + to maintain remission
Non biologics: Azathioprine/Methotrexate/Ciclosporine Biological agents: Infliximab/ Natalizumab
Surgery: In medically refractory cases/for complications- Ilectomy/Ileocolectomy

Ulcerative colitis
Characterized by relapsing and remitting inflammation of the colon which is continuous.
Common sites:
1.Sigmoid colon + rectum: Proctosigmoiditis 2.Left side of colon: Left sided colitis 3.Pancolitis
Clinical features: Manifestations can be chronic/rapid/acute on chronic- they may come back after a quiscent stage when
the disease flares up
Mechanism of clinical manifestations:
1. Due to chronic inflammation 2. Due to toxic megacolon 3. Extra-intestinal manifestations
1. Clinical features due to chronic inflammation:
1. Bloody/Non bloody diarrhoea 3. Abdo pain: LUQ/LLQ pain: continuous/ spasmodic
2. Hemodynamic instability ± Pallor 4. Constitutional: Fever, weight loss, loss of appetite
2. Clinical features due to toxic megacolon: Toxic megacolon, a potentially lethal condition, is a nonobstructive colonic
dilatation larger than 6cm with signs of systemic toxicity
1. Abdominal pain ± Distension 3. Sluggish bowel sound
2. Abdominal tenderness 4. Toxicity: Fever, tachycardia, flushing
Severity of UC-Helps to assess disease activity
Criteria Mild Moderate Severe
Number of stools/day <4 4-6 >6
Weight loss (% of body weight) None 1-10% >10%
Pulse < 90 90-100 >100
Fever None 99-100 ⁰F >100 ⁰F
Hematocrit (PCV) Normal 30-40% <30%
ESR <20 mm/hr 20-30 mm/hr >30 mm/hr
Albumin (gm/dL) Normal 3-3.5 <3
Clinical features due to extra-intestinal manifestations :….(SN)
Ocular: Uveitis + Episcleritis Liver: Primary sclerosing cholangitis (UC)
Lungs: Interstitial lung disease Kidney: Nephrolithiasis (more common in CD)
Heart: Non-infective endocarditis Skin:Erythema nodosum; Pyoderma gangrinosum.
Abdomen: Gall stone (more common in CD) Joints: Seronegative Spondyloarthropathy; Polyarthritis
Investigation
1. Blood: Hb, TC, DC, CRP/ESR- Hb: ↓ due to blood loss TC, DC, CRP, ESR: ↑ inflammation/ intra-abdominal infection
2. Renal function: Na+ K+ Urea Creatinine-To look for dehydration
3. Serum albumin level
4. Stool: Look for ovum/ parasite/ cyst/ Gram stain, culture and sensitivity Fecal Calprotectin- High
5. Straight X Ray abdomen: To look for toxic megacolon (diagnosed when colonic diameter is >6 cm.)
6. Sigmoidoscopy/ Colonoscopy: Will visualize inflamed, ulcerated mucosa and biopsy confirms the diagnosis
7. CECT abdomen: To look for any structural abnormality.
Treatment 1. Supportive treatment 2. Specific treatment 3. Surgical treatment
1. Supportive treatment- ≥1 relevant if patient is very sick
Admit if very sick
Bowel rest- nil by mouth till acute phase is over
Circulation -IV fluid – Bolus +/- Maintenance fluid depending on volume status
Blood transfusion- if required
Drugs: Antidiarrhoeal- Loperamide ( with caution, best avoided during active flare up!!)
Analgesic-antispasmodic: Drotaverine
Antibiotic (Particularly if toxic megacolon is suspected): Cefuroxime /Pip-Taz + Metronidazole
Emergency Rx for toxic megacolon:
1. Nil per mouth 4. Colonic decompression by: Flatus tube/ Colonoscopic
2. IV antibiotic- Pip-Taz + Metronidazole 5. Surgery- Partial Colectomy
3. IV Hydrocortisone
2. Specific treatment
1. ASA compounds: To achieve and to maintain remission
Usually 1st line therapy in mild disease: Mesalamine/ Osalazine/ Balsalazine: PO/PR preparation
2. Corticosteroids: To achieve remission in Moderate to severe ulcerative colitis
1. Prednisolone/Methylprednisolone: PO/IV 2. Hydrocortisone: Enema/ foam
3. Immunomodulators: To achieve and to maintain remsission- Moderate to severe ulcerative colitis
Non biologics: Cyclosporine Biological agents: Infliximab
3. Surgery: Surgery is done in medically refractory cases/ for complications- Partial/ hemicolectomy
Difference between Crohn’s disease and Ulcerative colitis
Points Crohn’s disease Ulcerative colitis
Pattern of inflammation Patchy Continuous
Site Ileocolitis, ileitis, colitis Proctosigmoiditis, left sided colitis, Pancolitis
Diarrhoea Not bloody Bloody
Malabsorption + -
Fistulisation + -
Perianal disease + -
Intestinal obstruction + -
Cholelithiasis + -
Nephrolithiasis + -
Toxic megacolon - +
Primary sclerosing cholangitis - +
 Irritable bowel syndrome (IBS)
Characterized by widespread GI manifestations in absence of any biochemical/ structural abnormality.
Pathogenesis: Usually the following 4 factors play important role:
1.Intestinal dysmotility 3.Enteric infection/ altered gut flora
2.Intestinal hypersensitivity to pain 4.Psychological factors
Clinical features:
1. Abdominal pain: Often lower abdominal- continuous/episodic-Typically associated with >1 of the following:
1. Relieved after defecation
2. Change in the form/ appearance/ consistency of stool (hard / semisolid/ liquid)
3. Change in stool frequency
(Rome Criteria of IBS: Recurrent abdominal pain or discomfort at least 3 days/month in the last 3 months associated
with two or more of the ABOVE)
2. Abdominal symptoms: 4. Absent symptoms:
1. Mucoid stool 1. Nocturnal diarrhea
2. Urgency/ frequency 2. Weight loss
3. Associated manifestations: 3. Per-rectal bleeding
1. Chest pain 4. Alternate constipation and diarrhoea
2. Palpitation
3. Pain at different sites of the body
4. Heartburn
Investigation IBS can be diagnosed from typical history, still organic diseases must be ruled out by investigations
1. Blood: Hb, TC, DC, CRP
2. Serum albumin, serum Ca++, iron studies (to rule out malabsorption)
3. Stool: OPC/ Gram stain/C.C. Faecal calprotectin: If ↑: indicates inflammatory diarrhea.
4. Colonoscopy: To rule out any structural lesion
Treatment
1. Appropriate dietary modification 6. Anti-depressants:
2. Antispasmodic: Drotaverine/Mebeverine Mechanism of action:
3. Anti-diarrheal: Loperamide a. Centrally acting pain inhibitors
4. Anti-constipation agent (Laxatives): b. Anti-cholinergic effect.
Magnesium salts/ Poly-ethylene-glycol Commonly used agents are:
5. Probiotics: Lactobacillus spore Amitriptyline/Imipramine/Fluoxetine/Paroxetine
7. Psychological counselling.
[ Blind loop syndrome/Bacterial Overgrowth Syndrome
Blind loop syndrome occurs when part of the small intestine forms a loop that food bypasses during digestion so food
particle cannot move normally through the GIT. Slowly moving food and waste products become a breeding ground for
bacteria. So it is also called Bacterial Overgrowth Syndrome.
(Bacterial overgrowth syndrome occurs when the normally low number of bacteria that inhabit the stomach, duodenum,
jejunum, and proximal ileum significantly increases or becomes overtaken by other pathogens)
Causes- ‘’Blind loops’’ from the following may result in bacterial overgrowth syndrome:
Side-to-side or end-to-side anastomoses Segmental dilatation of the ileum
Duodenal or jejunal diverticula Biliopancreatic diversion
C/F
Appetite loss Dyspepsia
Abdominal pain Evidence of deficiency of- Vitamin B12/ Folate/ Iron
Bloating Flatulence
Body weight loss Fatty stools (steatorrhea)
Diarrhoea
Investigaton: Abdominal x-ray/Abdominal CT scan/Contrast enema study
Treatment Medical- Antibiotic- Tetracycline/ Rifaximin Surgical- Repair of postoperative strictures and blind loops
 Celiac disease
Celiac disease (gluten-sensitive enteropathy), is a chronic disorder of the GIT that results in an inability to tolerate gliadin,
the alcohol-soluble fraction of gluten.
Gluten is a protein commonly found in wheat, rye, and barley. When patients with celiac disease ingest gliadin, an
immunologically mediated inflammatory response occurs that damages the mucosa of their intestines, resulting in
maldigestion and malabsorption of food nutrients.
Symptoms & Signs
Abdominal discomfort/pain
Anaemia
Bloating/Borborygmi
Bone- Osteoprosis
Body wt loss/weakness
Bleeding diathesis
Carpopedal spasm
Cheilosis and glossitis
Diarrhoea
Dermatitis herpetiformis- pruritic, papulovesicular
Edema
lesions involving the extensor surfaces of the extremities,
Endocrinopathy-
trunk
a.Amenorrhea
b.Delayed menarche
c.Impotence/Infertility
Flatulence
Investigations
1.Blood
Electrolytes and chemistries – Albumin, Urea, Creatinine, Na, K, Ca, Clotting profile
Hematologic tests – Hb, Iron study, Vit B12/Folate
Serology – IgA antibodies- Anti-tissue transglutaminase antibody (IgA TTG)
2.Stool examination –Increased Fat content due to Fat malabsorption
3.Endoscopy and biopsy- Duodenal biopsy- villous atrophy + Total mucosal hypoplasia
Management: Removal of gluten from the diet is essential
Whipple disease
Whipple disease is a systemic disease caused by a gram positive bacterium Tropheryma whippelii.
Manifestations are likely due to infiltration of various tissues by the organism.
1.GIT- Malabsorption- secondary to disruption of normal villous function due to infiltration of the lamina propria of the
small bowel.
2. Arthralgias 3.CVS 4.CNS
C/F
Abdominal discomfort/pain Anaemia
Arthralgia Bone- Osteoprosis
Bloating/Borborygmi Bleeding diathesis
Body wt loss/weakness Cheilosis and glossitis
Cachexia CNS
Carpopedal spasm a.Dementia
Diarrhoea b.Meningoencephalitis
Edema c.Ataxia/Involuntary movement
CVS- Valvular lesion
Investigations
1. Blood
Electrolytes and chemistries – Albumin, Urea, Creatinine, Na, K, Ca, Clotting profile
Hematologic tests – Hb, Iron study, Vit B12/Folate
2. Stool examination - Fat malabsorption
3. Endoscopy and biopsy- Small bowel biopsies show villi containing macrophages staining positive with periodic acid-
schiff (PAS)stain.
Treatment- Because of the tendency of whipple disease to relapse on short courses of antibiotics, most authorities suggest
a prolonged course (upto 1 y)- TMP/SZ or Penicillin or Chloramphenicol
 Liver
Overview
 Portal hypertension
Characterized by an elevated portal venous pressure (normal: 9-10 mm Hg).

Causes/Types:
1. Pre-hepatic causes:
1. Portal vein thrombosis 2. Septic thrombus of portal vein
3. Splenic vein thrombosis 4. Ca head of pancreas.
2. Intra-hepatic cause: Cirrhosis
3. Post-hepatic cause:
1. Hepatic vein thrombosis (Budd Chiari syndrome)
2. IVC obstruction:
a. Cancer (Ex: RCC)
b. Clot (rare)
3. Long standing systemic venous congestion- RHF
4. Constrictive pericarditis

Pathophysiological basis of Clinical features of Portal Hypertension

Pathophysiological changes Relevant clinical features
Elevated portal venous hydrostatic pressure A Ascites
Opening up of portocaval collaterals B Bleeding varices GI bleeding/ (at gastro-esophageal junction)
C Collaterals- Venous prominence at superficial abdominal wall
with direction of filling “away from the umbilicus”
(Caput medusae - visible collaterals surrounding umbilicus)
Portal venous congestion → Splenic venous C Congestive splenomegaly
congestion
D Disease- f/o underlying disease responsible for P. Htn
Toxic products of digestion bypass the liver E Brain: Encephalopathy- Portocaval/ hepatic encephalopathy
and reaches systemic circulation through
collateral circulation F Lung: Fetor hepaticus
Splanchnic (GI) congestion G Congestive gastropathy
Pathophysiological changes and features of the underlying disease

Clinical features
A AscitesAbdominal swelling
B Bleeding varices:HematemesisMelena (Black semisolid stool)
It may progress into hemodynamic instability.
C Caput medusae (collateral at periumbilical region) and superficial abdominal venous prominence:
Direction of filling is away from umbilicus.
Congestive splenomegaly
D Features of the underlying disease
E Portosystemic encephalopathy
F Fetor hepaticus (sweetish/ ammoniacal smell in the breath of the patient due to presence of mercaptan)
G Gastropathy (causing non-specific abdominal symptoms)
H Hypersplenism (peripheral destruction of blood cells due to hyperactive reticuloendothelial [RE] cells of
spleen)
Investigation:
a. Blood: TC, DC (Pancytopenia due to hypersplenism)
1. FBC+ ESR/CRP 3. Coagulation profile: PT, aPTT, INR.
Hb: ↓ (due to GI bleed) 4. LFT: Bilirubin, Albumin, transaminase
2. Renal function: Na+/ K+ / Urea/ Creatinine
b. USG upper abdomen:
Shows portal venous diameter which can roughly a. May show splenomegaly
predict hypertension i b. Show any cirrhotic changes
Detect ascites
c. Upper GI endoscopy: To look for any varices
d. Other relevant investigations to assess the underlying cause.

Treatment:
Supportive: Definitive:
Treatment of:
1. Ascites
2. GI bleed
3. Encephalopathy
4. Gastropathy

Complications:
1. Ascites 4. Encephalopathy
2. GI bleed 5. Gastropathy
3. Congestive splenomegaly 6. Hypersplenism

Hepatocellular failure
Types and causes
Acute hepatocellular failure:
Chronic hepatocellular failure:
Causes are:
Alcohol
Acetaminophen (Paracetamol) overdose
Non-alcoholic steatohepatitis
Acute viral hepatitis (HAV, HBV; HEV in pregnancy)
Budd Chiari Syndrome
Autoimmune hepatitis
Biliary cirrhosis (Primary/ Secondary)
Budd Chiari syndrome
Chronic hepatitis (HCV, HBV)
Cardiogenic shock (Shock liver)
Cryptogenic cirrhosis.
Drug induced liver injury
Deposition:
Exogenous toxin (Amanita phalloides, Aflatoxin)
Fulminant • Cu: Wilson
(Hepatic encephalopathy occurs within 8 weeks of onset of • Fe: Hemochromatosis
symptoms) Glycogen storage diseases
Sub-fulminant Indian childhood cirrhosis
(Hepatic encephalopathy occurs within 8-26 weeks of onset of
symptoms)
Pathophysiology of hepatocellular failure
• Derangement of synthetic function of liver
• Derangement of metabolic function
• Problem in detoxification
• Derangement of hormone metabolism
• Derangement of synthesis and metabolism of certain vasoconstrictor and vasodilator
• Derangement of carbohydrate metabolism
Ascites/Anasarca- Abdominal swelling Shifting Hepatopulmonary
dullness Oedema Hyperestrogenemia in hepatocellular failure
Bilirubinemia- Icterus It occurs in chronic hepatocellular failure due to
Coagulopathy- Asymptomatic OR Spontaneous derangement of testosterone metabolism, leading to:
bleeding- Superficial and/or Deep 1. Testicular atrophy
Disease- depends on the disease 2. Loss of secondary sexual characters (sparse
pubic and axillary hair)
Encephalopathy 3. Gynecomastia
A. Altered sensorium
4. Spider nevus/ angioma
B. Behavioral change (Indifference to others,
childish behavior)
C. Confusion, coma
D. Delirium, disturbed sleep rhythm (reversal of
sleep-wake cycle), disturbed mood
E. Features of cerebral edema (due to ↑ICT)
F. Flapping tremor
G. ↓GCS.
Fetor hepaticus
Glycemic
Hepato renal
Investigations
1. Blood: Hb, TC, DC, CRP/ESR
2. Renal function: Na+ K+ Urea Creatinine
3. LFT:
a. Bilirubin: Direct, indirect
b. Liver enzymes: AST, ALT, GGT (signifies hepatocyte inflammation); ALP (signifies intrahepatic cholestasis)
c. Serum albumin, globulin, total protein
d. Coagulation profile: PT, INR (Extrinsic), aPTT (intrinsic).
4. Other relevant blood tests that diagnose the underlying cause of hepatocellular failure
5. USG abdomen:
It can predict the underlying cause of hepatocellular failure, ascites etc.
Treatment of Hepatocellular failure
1. Supportive:
Treatment of:
a. Ascites d. Encephalopathy
b. Bleeding diathesis e. Hepato-pulmonary/ hepato-renal syndrome
c. Underlying disease

2. Definitive: Liver transplantation.

Hyperestrogenemia in hepatocellular failure
It occurs in chronic hepatocellular failure due to derangement of testosterone metabolism, leading to:
5. Testicular atrophy
6. Loss of secondary sexual characters (sparse pubic and axillary hair)
7. Gynecomastia
8. Spider nevus/ angioma
 Portocaval collaterals
Anastomotic vessels which open up between portal and systemic circulation in a patient of portal hypertension.
Effects:
Beneficial Harmful
Reduction of portal hypertension Rupture of collateral at gastro-esophageal region, leading to GI bleed
Toxic nitrogenous products bypass the liver & enter systemic circulation,
Portosystemic encephalopathy
Fetor hepaticus.
Sites:
1. Gastro-esophageal region (Varices) 4. Anal canal
2. Superficial abdominal wall 5. Retro-peritoneum.
3. Falciform ligament

Clinical features:
1. GI bleed: 2. Visible collaterals:
✓ Hematemesis Superficial abdominal venous prominence ±
✓ Melena Caput
✓ Hemodynamic instability Direction of filling: Away from the umbilicus.
✓ Black tarry stool. 3. Portosystemic shunting through collaterals:
✓ Portosystemic encephalopathy
✓ Fetor hepaticus.
Investigations: Same as portal hypertension
Treatment:

Immediate treatment
A.Airway:
Must be protected, particularly if there is risk of aspiration
If required: Oropharyngeal suction.
B.Breathing: Oxygen
C.Circulation:
1 wide bore cannula in each hand
IV fluid resuscitation (Preferred fluid of choice: Normal saline)
In case of severe bleeding: Blood transfusion (maintain a Hb level of 7-9 gm %)
Treat any co-existing coagulopathy (platelet, vitamin K, fresh frozen plasma).
D.Drugs:
Reduction of bleeding by splanchnic (and also systemic) vasoconstriction:
VasopressinTerlipressinGlypressin.Safer and selective splanchnic vasoconstrictors (with fewer side effects):
Somatostatin/Octreotide.
IV antibiotic therapy in all patients (to reduce the risk of potentially life-threatening infections).
Definitive treatment
E.Endoscopy:
Endoscopy confirms the presence of varices and subsequently they can be treated endoscopically by the 2
following techniques, the mechanism of both of which is stoppage of bleeding by variceal thrombosis:
▪ Variceal ligation (banding)
▪ Injection sclerotherapy:
Intra and para-variceal administration of sclerosing agents:
o Ethanolamine oleate/ Sodium tetradecyl sulfate.
F.Failure of endoscopy/ not feasible:
Balloon tamponade on varices by Sengstaken-Blackmore tube (SSBT): It is a last resort and highly effective in
controlling variceal bleeding; but it is associated with significant complications (high incidence of re-bleeding and
aspiration pneumonia after removal of the tube).
F.Future bleeding prevention (Prophylaxis of first episode of bleeding for non-bleeding varices
• Endoscopy- Surveillance Eradication of varices
• Medical prophylaxis- Nonselective β blocker: Propranolol
(Propranolol reduces portal pressure by causing splanchnic vasoconstriction and reducing cardiac output)
• Transjugular intrahepatic portosystemic shunting (TIPS)
• Liver transplantation.

Ascites
Accumulation of free fluid in the peritoneal cavity.
Causes of ascites:
1. Ascites with anasarca: 2. Ascites without anasarca:
a. CCF-Right heart failure a. Peritonitis (TB/ Malignancy)
b. Chronic kidney disease b. Acute pancreatitis
c. Constrictive pericarditisCirrhosis
c. Nephrotic syndrome
Clinical features:
Symptoms
Progressive abdominal swelling
Weight gain
Massive ascites--Abdominal discomfort and SOB may occur due to mechanical effect (uplifting of
Signs
1. Shifting dullness
2. Fluid thrill may be present
3. Puddle sign (insignificant)
4. Often signs of underlying disease will help to determine causes of ascites.
Causes of ascites in cirrhosis/ CLD

Initiating factor: Abnormal renal retention of Na+ and water. What starts this abnormality is not clear, however, there are
3 possible hypothesis:
A. Underfilling theory:
Portal hypertension/ splancnic sequestration of blood- Effective blood volume↓- Renal ischemia- Stimulation of RAS axis-
Na+ and water retention
B. Vasodilator theory: Nitric oxide (NO)- Splancnic vasodilation- Splancnic sequestration of blood- Effective blood
volume↓- Renal ischemia- Stimulation of RAS axis- Na+ and water retention
C. Overfilling theory: Abnormal salt and water retention- Overfilling of splancnic vascular bed- Initiation of ascites

Aggravating factor:
A. Non-compliance to drugs/ diet prescribed
B. Spontaneous bacterial peritonitis (SBP)
C. Development of hepatocellular CA
D. Tubercular peritonitis.
Investigation
1. Blood: Hb, TC, DC, CRP
2. Renal function: Na+ K+ Urea Creatinine
3. Liver function test
4. Urine analysis
5. CXR
6. ECG
7. USG
 8. Diagnostic peritoneal paracentesis:
I. Physical appearance:
• Turbid: SBP
• Hemorrhagic: TB/ Malignancy.
II. Biochemical properties:
• Serum ascitic albumin gradient (SAAG): >1.1 gm/dL: Suggestive of portal hypertension.
III. Cytological properties:
• WBC count:
✓ Neutrophilic leukocytosis: Suggestive of SBP
✓ Lymphocytic leukocytosis: Suggestive of TB/ Malignancy
• Atypical cells: Malignancy.
IV. Microbiological properties:
• Gram stain
• AFB staining + Mycobacterial culture.
V. Special tests:
• X-PERT TB/ RIF assay:
Detects M.tuberculosis genome + Rifampicin resistance (which is a very reliable indicator for MDR-
TB).
• Adenosine deaminase (ADA):
ADA levels may be high in tubercular ascites. However, it is a nonspecific marker and results should
be interpreted very cautiously.
9. Endoscopy:
If ascites is suspected to be due to cirrhosis/ portal hypertension, then look for GI varices (endoscopy).
10. Series of other tests may be required to diagnose the underlying cause.
Treatment of ascites
1. Diet (fluid and salt restriction)
2. Diuretic:
a. Spironolactone: It is a K+ sparing diuretic; having side effects of dehydration, hyponatremia, hyperkalemia
and painful gynecomastia.
b. Furosemide: It is a loop diuretic; having side effects of dehydration, hyponatremia and hypokalemia.
3. Daily (regular) monitoring of the following parameters:
a. Body weight c. Intake and output
b. Abdominal guts d. Renal function.
4. Drain (Therapeutic abdominal paracentesis):
Indication:
a. Significant ascites (symptomatic)
b. Ascites refractory to diuretics
c. If required, even 5-6 L fluid may be drained in a single sitting.
Note:
To prevent post-paracentesis circulatory disequilibrium, concomitant transfusion of IV albumin preparation was
practiced earlier. However, its role is doubtful.
5. Treat the underlying disease.
 Hepatic encephalopathy
It is a complex neuropsychiatric syndrome due to temporary cerebral dysfunction in a patient of hepatocellular failure
and/or portal hypertension.
Etiopathogenesis
Underlying defect:
1. Hepatocellular failure:
Toxic nitrogenous products and other toxins can’t get detoxified in the liver, so they reach systemic circulation
and then go to brain causing encephalopathy.
2. Portal hypertension:
Due to portosystemic collaterals, toxins bypass liver and reach systemic circulation and go to brain.
Ultimately these toxins; after reaching the brain cause cerebral dysfunction, leading to encephalopathy.
Toxins responsible for hepatic encephalopathy:
A. Ammonia
M. Mercaptan
M. Manganese
O. Octopamine
N. Benzodiazepine
I. Inhibitory neurotransmitters (GABA)
A. Fatty acids.
Aggravating/ precipitating factors:
1. Conditions which cause ↑ protein load:
▪ High dietary protein intake (especially animal protein)
▪ GI bleeding
▪ Uremia/ azotemia (pre-renal renal failure).
2. Conditions which cause ↑ ammonia production in intestine:
▪ Constipation
▪ Metabolic alkalosis (which may occur in hypokalemia caused by loop diuretics): Here conversion of NH3 to
NH4+ is hampered.
3. Hepatotoxins:
▪ Alcohol
▪ Sedatives.
4. Infection: Commonly SBP is responsible for it.
Clinical features
Symptoms
A. Altered sensorium
B. Behavioral change (Indifference to others, childish behavior)
C. Confusion, coma
D. Delirium, disturbed sleep rhythm (reversal of sleep-wake cycle), disturbed mood
E. Features of cerebral edema (due to ↑ICT)
F. Flapping tremor
G. ↓GCS.
Signs
1. Apraxia:
Inability to perform a voluntary skillful activity in spite of normal motor, sensory cerebellar and extrapyramidal
structures.
Constructional apraxia:
Inability to draw a 5 pointed star
When asked to join 20 numbered points by a line, the patient either takes very much time or unable to do it.
2. Jerks:
Usually normal, however in deep coma: hypo/a-reflexia may be seen.
3. Plantar:
 Normal, however in deep coma: plantar may be bilateral extensor/ absent.
Investigation
1. Blood: Hb, TC, DC, CRP/ESR 5. Arterial blood gas: To assess acid base
2. Renal function: Na+ K+ Urea Creatinine equilibrium
3. Liver function test 6. USG abdomen
4. Arterial NH3 level: ↑ (But it is a nonspecific 7. Upper GI endoscopy (to look for any varices)
marker) 8. Diagnostic ascitic fluid tap and analysis
9. CT head: Particularly if raised ICT is suspected/ the cause of encephalopathy is not clear.

Treatment
Airway:To be protected, if in deep coma.
Breathing: Oxygen and if required, ventilation. A. Avoid alcohol/ hepatotoxic drugs
Circulation: IV fluid B. Urgently treat any associated GI bleed
Regular capillary blood glucose monitoring C. Prevent/ treat constipation: Lactulose
Constipation:Prevention of constipation by: D. Dietary protein restriction
Lactulose (Per oral/ Per rectal)LactitolHigh bowel wash enemaRifaximine. E. Treat any electrolyte imbalance
Cerebral edema:Mannitol. F. Fluid: Maintain proper hydration
Diet: Dietary protein restriction. G. Gut cleansing agent (Rifaximine)
Cerebral edema:Mannitol. H. Prevent hypovolemia
Electrolyte imbalance: hypokalemia is promptly treated. I. Treat any associated infection
Fever (infection):
Any infection should be promptly treated by antibiotics.
GI bleed:It should be promptly treated.
Hypovolemia: Promptly treated.
Hepatotoxic drugs: To be avoided.

Role of lactulose in hepatic encephalopathy

1. Being a non-absorbable disaccharide, it gets metabolized in the gut, to form H+ which converts toxic NH3 to
nontoxic NH4+.
2. It directly acts on ammonia forming colonic flora and reduces their load.
3. It also acts as a laxative.

Spontaneous bacterial peritonitis (SBP)

It is primarily a bacterial infection of ascitic fluid, in absence of any intra-abdominal focus of infection.
Risk factors:
Any patient with ascites are at risk of SBP, however, chronic liver disease/ cirrhotic patients, particularly those with
ascitic fluid albumin level <1gm/dL are at greater risk as the fluid is often deficient in opsonins.
Pathogens: Organisms enter ascitic fluid either by translocation across the gut wall/ through intestinal lymphatics.
E.coliStreptococcus
Clinical features: Investigation:
1. Fever 1. Blood: CBC, ESR/ CRP, Blood culture sensitivity
2. Pain abdomen 2. Ascitic fluid tap
3. Aggravation of ascites 3. Ascitic fluid:
4. Hepatic encephalopathy may get precipitated a. Cell count (WBC count > 500/cu.mm.)
5. Tenderness ± signs of peritonitis are usually b. Gram stain + culture sensitivity.
absent.
Treatment: Treatment of SBP
Established case of SBP- 1⁰/2⁰ prevention in high risk patients-
IV Ceftriaxone ± Metronidazole Long term antibiotic prophylaxis with Ciprofloxacin/
• To be changed to proper oral form after few days Metronidazole
• Total duration of antibiotic therapy: 7-10 days Prescribe when ascitic fluid albumin level <1 gm/dL
•
 Hepatopulmonary syndrome (HPS)
It is a pulmonary complication of chronic liver disease characterized by widespread intrapulmonary vasodilation and
arterio-venous communication.
Pathogenesis:

Clinical features:
Symptom: Breathlessness/ shortness of breath
Signs
• Shortness of breath becomes more prominent when the patient is in standing position: Platypnea.
• Arterial oxygen saturation (SaO2) falls when the patient is in standing position: Orthodeoxia.
Investigation
1. Arterial blood gas (ABG)
2. Chest X Ray (CXR): To rule out focal lung lesion
3. ECG and Echocardiogram: To rule out any cardiac abnormality
4. Highly specialized test (expensive): Contrast echocardiogram with saline agitated microbubble: Injected bubbles appear
very quickly in the left atrium due to intrapulmonary shunting.
Treatment
1. Oxygen 2. Liver transplantation.

Portopulmonary hypertension
Pulmonary hypertension occurring as a consequence of CLD.
It occurs due to abnormal circulating level of Endothelin: a potent pulmonary vasoconstrictor.
Treatment:
1. Bosentan: Endothelin antagonist
2. Sildenafil: NO donor.

Hepatorenal syndrome
A state of renal dysfunction occurring as a consequence of CLD.
Diagnostic criteria:
1. Presence of azotemia: Creatinine↑
2. No pre-renal/ intrinsic renal causes of kidney dysfunction (Ex.: dehydration)
3. No improvement of renal function even after withholding diuretic therapy for 48 hours.
Pathogenesis:
• Due to CLD, there is impaired synthesis/ malabsorption of renal vasodilators, leading to intense renal
vasoconstriction; leading to reduced renal blood flow.
• There is altered hemodynamics but no structural damage to kidneys.
Clinical features:
1. Oliguria/ anuria
2. Symptoms and signs of volume overload
3. Features of uremic encephalopathy (due to accumulation of toxins in blood).
Investigations: Renal function test: Na+ K+ Urea Creatinine
• Urea creatinine: ↑
• Serum Na+: ↓ (Dilutional hyponatremia); Urinary Na+: ↓
• Serum K+: ↑.
Treatment:
1. Any other cause of renal dysfunction needs to be treated
2. Combination of medical agents: Midodrine/Vasopressin/ Terlipressin/Norepinephrine/Somatostatin/ Octreotide
 3. Liver transplantation
4. A special dialysis method which selectively albumin bound compound (experimental).

Coagulopathy
Cause:
Impaired synthesis of coagulation factors due to deranged hepatic function.
Clinical features:
1. Asymptomatic
2. Bleeding manifestation:
External: Gum bleeding, epistaxis, ecchymosis
Internal: Intracerebral hemorrhage, GI bleed, GU bleed.
• If blood loss is significant, patient may become hemodynamically unstable.
Investigation: Coagulation profile
1. BT/ CT/ Platelet count
2. PT, INR (Extrinsic pathway) ↑
3. aPTT (Intrinsic pathway) ↑
- Often only PT/INR is elevated in CLD as factor VII is the first factor to get depleted.
Treatment:
1. Fresh frozen plasma transfusion, only when there is active bleeding/ before invasive procedure
2. Although it is very commonly used, vitamin K has no role, unless coexistent vitamin K deficiency is suspected
3. Recombinant factor VIII concentrate.

Congestive splenomegaly
It is a common complication of portal hypertension where portal and splanchnic venous congestion leads to passive
congestion in the spleen and finally, splenomegaly.

Hypersplenism
It can occur in a patient with long standing portal hypertension and defined as the combined presence of the following:
1. Splenomegaly
2. Pancytopenia (which gets corrected after splenectomy)
3. Bone marrow hyperplasia.
Cause of pancytopenia:
Excessive splenic sequestration of peripheral blood cells due to overactivity of RE cells.

Congestive gastropathy
• Pathogenesis:

• Clinical features:
Patients are often asymptomatic; sometimes may present with nonspecific symptoms like epigastric discomfort ±
pain.
• Diagnosis:
Endoscopy shows gastric mucosal congestion and hyperemia.
 Acute viral hepatitis
Virus Incubation period Mode of transmission Acute Fulminant hepatic failure Chronic
(days) hepatitis hepatitis
HAV 15-45 Faeco-oral + + -
HBV 30-180 Sexual/Parenteral/Vertical + + ++
HCV 50-160 Sexual/Parenteral - - ++
HDV 30-180 Sexual/Parenteral + - -
HEV 15-60 Faeco-oral + + (in pregnancy) -

Viral markers
HAV: Anti-HAV antibody: IgM Anti HAV (acute) and IgG Anti HAV (acute or remote)
HBV:
HBsAg: In most cases, the first viral marker to appear
Appears very early during acute hepatitis and usually disappear within few months
If persists 6 months after an episode of acute hepatitis it signifies a carrier/ chronic hepatitis stage
Anti HBs
Appears after disappearance of HbsAg
Presence signifies immunity by vaccine/ a previous episode of acute hepatitis
Anti-HBc-antibody: It is of 2 types:
IgM: Rises during acute infectionIgG: Develops during acute period and persists indefinitely

HBeAg: Secretory form of core antigen. Appears during acute infection- marker of active viral replication. Therefore, its
presence suggests high infectivity. Usually disappears within few months of acute infection, if persists beyond 3 months,
it suggests a high possibility of chronic hepatitis.
Anti-HBe-antibody: Appears after disappearance of HbeAg

HBV-DNA: Highly sensitive marker of viral replication. Quantification of HBV-DNA denotes viral load and therefore is
monitored during initiation and monitoring of antiviral treatment response in chronic hepatitis

Viral markers S: E: B: C: E: S: C
HBsAg HBeAg HBV-DNA Anti-HBc (IgM) Anti-HBeS Anti-HBs Anti-HBc (IgG)

HCV:
Anti-HCV: Usually appears during acute period of infection. Although in substantial proportion of Hepatitis C patients
will have detectable Anti-HCV, a subpopulation of the patients will be Anti-HCV –ve.
HCV-RNA: Detectable during acute period of infection Signifies active viral replication
Quantification denotes viral load and is monitored during antiviral treatment.
HDV: It causes co/super-infection with HBV. The marker is HDV-RNA
HEV: Anti-HEV-antibody: It is of 2 types: IgM and IgG.

Clinical features of Acute viral hepatitis It goes through 3 stages

Pre-icteric stage (few days- Icteric stage (1-3 week): Recovery/ convalescent stage:
1week): Symptoms start to subside Symptoms and signs gradually
Nausea and vomiting Icterus disappears and patient normalizes.
Apathy/ distress for food Soft/ form tender hepatomegaly Examination may reveal RUQ pain
Right upper quadrant pain Mild splenomegaly and soft tender hepatomegaly
Fever/Arthralgia/Myalgia
.
Investigation
1.Blood: Viral Markers
Hb, TC, DC, CRP/ESR: Leukopenia may be seen a. Anti-HAV
Renal function test: Na+ K+ Urea Creatinine b. HbsAg
Liver function test: c. Anti-HCV
• Bilirubin (Unconjugated and conjugated): ↑↑ d. Anti HEV
• Transaminases: ALT, AST: ↑↑↑ (often >1000 2.USG abdomen
U/L) ALT typically > AST
• GGT/ ALP: ↑ (mild to moderate rise in level)
• Albumin: normal/ ↓
• PT, INR, aPTT: normal/ ↑
Low albumin level and coagulation abnormalities are warning signals of a possible impending hepatic failure
Treatment
A. Absolute bed rest: till transaminase level STARTS to come down/ patient becomes asymptomatic
B. Bowel clearance: Lactulose
C. Circulatory support by IV fluid if oral intake is inadequate. Usually dextrose containing fluid is given.
D. Diet: Normal palatable diet, restrict protein in case of encephalopathy.
Drugs: Avoid drugs which are hepatotoxic/ having hepatic metabolism.
E. Look for early signs of encephalopathy
F. Fulminant Hepatic failure
A. Admit, if required
Airway- to be secured if comatose, if required intubate
B. Breathing= O2/ ventilatory support, if in coma
Bed Sore prevention-if comatose- Regular change of position
Blood Biochemistry- monitor regularly- INR/Albumin/LFTs
C. Circulation- IV fluid
Catheterisation- to monitor urine output
D. Drugs Avoid hepatotoxic drugs N-Acetylcystiene
Bowel cleansers-Lactulose/Rifaximin- if encephalopathy
Diet- Nutritious diet orally/if comatose through Ryle’s tube- Protein restriction if encephalopathy
DVT prevention- Prophylactic Heparin/ DVT stocking
E. Encephalopathy- look for/prevent/treat if occurs
F. Failure of conservative Rx- consider Liver transplantation
Complications
1. Early: Fulminant hepatic failure
2. Late: 1. Cirrhosis 2. Chronic hepatitis 3. Hepatocellular carcinoma.
 Alcoholic liver disease
Risk factors:
1. Alcohol related: men > 40 g, particularly > 80 g/day for > 10 yrs (Women: Half of this amount)
2. Non-alcohol related: a. Malnutrition b. Gender: Females risk > than males c. Coexisting liver disease

Stages and clinical features:

Alcoholic fatty liver (steatosis): Alcoholic hepatitis: Alcoholic chronic liver disease/
Often asymptomatic RUQ pain cirrhosis:
Mild RUQ pain Loss of appetite Symptoms and signs of chronic
RUQ tenderness ± Hepatomegaly Nausea hepatocellular failure
Fever ± Symptoms and signs of portal
RUQ tenderness ± Hepatomegaly hypertension

Stigma of chronic alcohol excess:

1. Haptic facies: Wasted face with facial hollowing + muddy discolouration
2. Bilateral parotid swelling
3. Dupuytren’s contracture: Fibrotic thickening of palmar fascia leading to fixed flexion deformity and limited extension
of ring and little fingers
4. Hyperestrogenemic manifestations: More prominent than other causes of CLD
Investigation
1.Blood:
a.Hb, TC, DC, ESR/ CRP
• Hb: ↓ in case of GI bleed
• TC, DC: Leukocytosis in case of alcoholic hepatitis Cytopenia: Due to marrow toxic effect of alcohol
• ↑MCV: Due to coexisting folic acid deficiency
b.Renal function test: Na+ K+ Urea Creatinine: Urea-creatinine level may be ↓ due to low catabolic state.
c.Liver function test:
• Bilirubin: May be ↑
• ALT, AST: Mild to moderate ↑, usually don’t exceed 300 U/L, (due to alcohol induced inhibition of
pyridoxal phosphate, a coenzyme of all transaminases)
• GGT, ALP: Mild to moderate ↑ (markers of cholestasis)
• Albumin: Normal/ ↑
• PT, aPTT, INR: Normal/ ↑
2. USG abdomen: May show (depending on the stage) 4. Fibroscan
a. Fatty liver b. Hepatomegaly
b. Evidence of portal hypertension- Ascites/Splenomegaly
3. Upper GI endoscopy: To look for varices

Treatment of alcoholic liver disease

A. Abstinence: If required, drugs can be given to D. Drugs: Hepatotoxic drugs/ drugs with significant
control acute withdrawal symptoms: hepatic metabolism should be avoided in chronic
Chlordiazepoxide liver disease
Diazepam Acamprosate. Corticosteroid: Methyl-prednisolone/equivalent: for
B. Bowel clearance: Lactulose + 4 weeks If Maddrey's discriminant score >32
Vitamin B supplementation Pentoxifylline (TNF inhibitor): for 4 weeks
C. Circulatory support by dextrose containing IV fluid
 Non-alcoholic fatty liver disease (NAFLD)/ Non-alcoholic steatohepatitis (NASH)
Liver disease due to fatty infiltration with/ without accompanying inflammation in absence of alcohol abuse.
Risk factors:
• High BMI • Drugs (Corticosteroid/ Amiodarone)
• Diabetes • Endocrine (Cushing’s syndrome/ Polycystic
• Dyslipidemia ovarian syndrome)
Pathogenesis: The following factor play important role in NAFLD:
Insulin resistance: It ultimately leads to lipid peroxidation and oxidative damage to the liver
(In Alcoholic liver disease, 2 important factors are: toxic effect of acetaldehyde and toxic effect of TNF)
Clinical features:
1. Often asymptomatic: Detected incidentally 4. In advanced cases, chronic liver diseases or
2. RUQ discomfort ± Pain cirrhosis may occur
3. RUQ tenderness ± Hepatomegaly
Investigation
Blood: Liver function: Variably deranged
Hb, TC, DC, CRP a. Usually ALT> AST
Renal function: Na+ K+ Urea Creatinine b. In advanced cases progressing to fibrosis:
Fasting lipid profile AST > ALT
Blood glucose: Fasting and post-prandial
USG abdomen: Evidence of steatosis: fatty infiltration is seen (steatosis and steatohepatitis cannot be differentiated)
Upper GI endoscopy: If CLD is suspected
Treatment
Risk factor modification: Avoid alcohol/ Dietary modification
Lifestyle modification
Drug treatment Reduction of insulin resistance: Metformin
Drugs: Anti-hypertensive/Anti-diabetic/Anti- Antioxidants: Vitamin E
lipidemic/Anti-obesity. Treatment of chronic liver disease (if present).

Hemochromatosis
It is a disorder of iron metabolism characterized by excessive hepatic and extrahepatic iron deposition.
Pathogenesis:
HFE gene: It plays a vital role in sensing body iron stores. In mutations of this gene, there is ultimately excess intestinal
iron absorption.
Hepcidin: A key iron regulatory protein which is not synthetized properly. So, there is excessive hepatic iron deposition
which “spills over” into extrahepatic sites.
Clinical features:
H- Hepatic- Features of chronic liver disease Heart- Cardiomyopathy- Cardiac failure/ Conduction disturbances
A-Arthralgia/ Arthritis- Commonly affects MCP joints (particularly 2nd and 3rd)
E- Endocrinal glands- Pancreas- Diabetes; Pituitary- Hypogonadism
M- Melanin (brown) + excess iron deposition in skin- Slate grey/ Greyish brown- Bronzing of skin/ Bronze diabetes
Investigation
To diagnose organ defect: To confirm hemochromatosis:
Liver function: Nonspecific abnormality Iron study: Serum iron: ↑↑ Serum ferritin: ↑↑
Blood glucose: Fasting and post-prandial Liver biopsy with estimation of hepatic iron index
ECG; Echocardiogram Molecular testing: Detection of C282Y mutation
Treatment
 1. Supportive treatment: For organ complications
2. Treatment of iron deposition: 1. Regular phlebotomy 2. Iron chelators: Desferrioxamine: SC infusion.

Wilson’s disease (Hepatolenticular degeneration)

It is a disorder of copper metabolism characterized by excessive hepatic and extrahepatic copper deposition.
Risk factors: 2 important factors which lead to excessive hepatic copper deposition which spills over different extra-
hepatic sites are:
1. Excessive intestinal Cu++ absorption
2. Impaired hepatic Cu++ excretion
There is underlying defect in the key transporter protein ATP7B which is responsible for all of these.
Clinical features:
H- a. Acute hepatitis b. Fulminant hepatic failure c. Chronic liver disease
L- Lentiform nucleus Cu++ deposition- a. Parkinsonism b. Choreoathetoform movement c. Cerebellar degeneration
D- Descemet membrane Cu++ deposition-Brownish-yellow ring on limbus- Best seen by slit lamp= Kayser-fleischer ring
Investigation
To detect organ damage: To confirm the disease:
1. Liver function test 1. Serum Cu++: ↓
2. MRI brain 2. Ceruloplasmin: ↓
3. Urinary Cu++: ↑
4. Liver biopsy: It estimates hepatic Cu++ store
Treatment
1. Cu++ chelating agent: D-Penicillamine- If fails/ patient can't tolerate- Triamtene
2. Reduction of Cu++ absorption from intestine: Zinc
3. Treatment of chronic liver disease

Primary biliary cirrhosis (PBC)

Autoantibody mediated by inflammation and subsequent fibrotic obliteration of intrahepatic biliary canaliculi.
Pathogenesis: Antibodies against Pyruvate dehydrogenase complex of canalicular cell mitochondria (Anti-mitochondria
antiantibody) - Intrahepatic cholestasis - Canalicular inflammation and fibrosis - Eventually chronic liver disease
Clinical features:
P: Pigmentation (due to ↑melanin)
B: ↑Bile acid: Pruritus
C: Cholestasis Fat malabsorption- Steatorrhea/ Flatulence
Vit A, D, E, K malabsorption: A- Night blindness D-Musculoskeletal pain K- Coagulopathy
Conjugated hyperbilirubinemia- Icterus
Chronic liver disease
Clubbing
CholesterolHypercholesterolemia Xantholesma Xanthomata
Investigations:
1. Blood: PT, aPTT, INR: May be ↑ in vitamin K deficiency and
Hb, TC, DC, CRP chronic liver disease.
Renal function: Na+ K+ Urea Creatinine Detection of serum anti-mitochondrial antibody
Liver function test: 2. USG
Bilirubin: Conjugated hyperbilirubinemia 3. Upper GI endoscopy: If portal hypertension/CLD is
AST, ALT: Mild to moderate↑ suspected; to look for varices
Albumin: May be ↓ 4.Liver biopsy
Treatment:
1.Cholestasis: Ursodeoxycholic acid (UDCA): 3. Vitamin supplementation (parenteral, if required)
2. Pruritus: Cholestyramine (Bile acid binding agent) 4. Treatment of chronic liver disease.

Autoimmune hepatitis
Autoantibody mediated inflammation of liver which may lead to acute hepatitis as well as chronic liver disease.
Clinical features:
Age- young females
Association: Autoimmune disorders- Sjogren’s syndrome, autoimmune thyroiditis
Asymptomatic till they develop CLD
Amenorrhea
Hepatic- Acute hepatitis ± fulminant hepatic failure or Chronic Hepatitis
acute hepatitis like illness is triggered off by: a. Recent viral illness b. Drugs/ toxins c. Post-partum period
Investigations
1.Blood: Hb, TC, DC, CRP
Renal function: Na+ K+ Urea Creatinine
Liver function test: Variable abnormal: ALT, AST: May be very ↑Hyperglobulinemia
Autoantibodies: Type1: Anti-soluble liver antibody+ (ASLA); ANA+ Type 2 autoimmune hepatitis: Anti-liver kidney
microsomal antibody type 1 (ALKM1)
2.USG abdomen
Treatment
1. Acute hepatitis: Long term corticosteroid + Azathioprine OR Mycophenolate mofetil
2. Treatment of chronic liver disease

Amoebic liver abscess

Pathogenesis: Trophozoite of Entamoeba histolytica Organism enters by faeco-oral route Cyst/ vegetative form in the intestine
Trophozoite in the liver Abscess formation
Clinical features:
Constitutional symptoms: RUQ discomfort.
a. Fever On examination:
b. Loss of appetite 1. RUQ tenderness: On percussion, tenderness
c. Weight loss over right lower intercostal spaces noted
d. Anorexia 2. Hepatomegaly may be present.
e. Nausea
Investigation
Blood: Hb, TC, DC, ESR USG abdomen: Usually shows a single abscess
Liver function test: Nonspecifically mildly deranged
Complications: P1: Pleural empyema P2: Pericardial empyema P3: Peritonitis
Pyogenic liver abscess
Portal of entry:
1. Through portal vein: Pylephlebitis (infection of portal vein)
2. Through CBD: Ascending cholangitis
3. Through hepatic artery: Bacteremia.
Clinical features:
Constitutional symptoms: d. Drowsiness
a. Appetite lossHigh temperature e. Elevated temp
b. Body weakness; bodyache
c. Chill=/- rigor Focal/Local
RUQ discomfort
RUQ tenderness ± Hepatomegaly

Investigation
1. Blood: Hb, TC, DC, CRP 4. Liver function test: Variably abnormal
2. Renal function: Na+ K+ Urea Creatinine 5. USG: It shows multiple small abscesses.
3. Blood culture and sensitivity
Treatment Empirically IV Ceftriaxone + Metronidazole To be changed to appropriate oral forms once patient starts to
improveTotal duration: Approx. 3 weeks.

Hepatocellular carcinoma (HCC)

It is a primary malignancy of liver.
Risk factors:Chronic hepatitis (HBV and HCV)Cirrhosis of any etiology.
Clinical features:
Constitutional: 1. Patient may/ may not be aware of chronic
Weight loss hepatitis
Loss of appetite 2. Icterus, Hepatomegaly: +Ve, Evidences of CLD
Fever may be present.
Sudden deterioration of a previously stable cirrhotic
patientEx.: Worsening of ascites
Investigation
Blood: Hb, TC, DC, ESR Value of >200 U/L is quite specific for HCC. But
Hb% may rise in a tumor producing erythropoietin it is not sensitive.
Leukocytosis is common due to underlying Mild to moderate increase in value is not
inflammatory condition. specific.
Renal function: Na+ K+ Urea Creatinine 1. USG abdomen: Visualizes the lesion
Liver function test: 2. CECT/ MRI
Non-specifically abnormal But ALP and bilirubin may 3. Biopsy of the lesion:
rise significantly. Carries risk of massive bleeding as it is a highly
Serum AFP (α-fetoprotein): Significantly high vascular tumor.
Treatment
• Surgery- Tumor resection/ Liver transplantation
• Chemotherapy- Transarterial chemoembolization/ Transarterial chemoinfusion/ Infusion of ethanol
• Interventional radiotherapy- Palliative treatment for the bridge therapy for liver transpalanatti

Budd Chiari syndrome

Thrombosis of the hepatic vein
Causes:
1. Hypercoagulable state/ disorders: ✓ Factor 5 Leyden.
✓ Anti-phospholipid antibody syndrome 2. Idiopathic
✓ Nephrotic syndrome 3. Tumor occlusion/ invasion:
✓ Protein C/ protein S/ antithrombin 3 Common tumors responsible: RCC, HCC.
deficiency
Clinical features:
1. Sudden RUQ pain 3. Patient may develop fulminant hepatic failure
2. Tender soft hepatomegaly 4. Ascites.
Investigation
1. USG abdomen with Doppler study
2. CECT abdomen
3. Coagulation studies
Treatment: Anticoagulation
 Wernicke Korsakoff Syndrome
It is a neurodegenerative complication of vitamin B1 deficiency, most commonly seen in chronic alcohol abusers.
Pathogenesis:
Degeneration of different areas of brain: mammillary body/ thalamus/ median temporal lobe/ cerebellum. Chronic alcohol
abuse interferes with absorption and metabolism of thiamine, often leading to severe thiamine deficiency.
Clinical features:WKS has two components: 1. Wernicke’s encephalopathy 2.Korsakoff psychosis

Wernicke’s encephalopathy: Usually these symptoms are reversible with thiamine replacement therapy
1. Ataxia
2. External ophthalmoplegia: Commonly lateral rectus palsy + Nystagmus
3. Psychiatric disturbances:
Behavior/ personality disturbances/ dementia.
Korsakoff’s psychosis: Irreversible
1. Amnesia:It may be of 2 types:
a. Anterograde amnesia: Inability to create new memories + impaired recent memory + no remote memory loss
b. Retrograde amnesia: Remote memory loss + new memory intact
2. Confabulation: Incorrect memory to which the patient holds onto/ on the basis of which patient may act
3. Patient may have features of Wernicke’s encephalopathy
Investigation 1. CT/ MRI of brain 2. Vitamin B1 estimation
Treatment
1. Prevention: In chronic alcoholic- must receive high dose thiamine
In patients with H/O significant alcohol abuse, if requires high dose dextrose containing fluid, must receive high dose thiamine before/ at least
along with the fluid. (glucose oxidation is a thiamine consuming process and therefore, may unmask any underlying deficiency and may
precipitate Wernicke Korsakoff syndrome)
2. Established cases: High dose thiamine replacement.

Ranson’s criteria/ score

A predictive score which can reasonably predict prognosis/ development of complication(s) in an acute pancreatitis.
On admission Within first 48 hours
3. Age >55 years 4. Arterial PO2 < 60 mm Hg. Ca++ <8 mg/dL
4. WBC count > 60000/cu.mm 5. ↑ BUN value by > 5 mg/dL Drop in hematocrit: >10%
5. Blood glucose >200 mg/dl (BUN/2.8) = Urea Estimated fluid deficit >6L
6. AST >250 U/L 6. Base deficit >4 mEq/L
7. Serum LDH >350 U/L
Presence of ≥3 of the above Presence of ≥1 of the above predicts worst prognosis.
predicts a complicated course.

Child-Pugh Score for chronic liver disease/ cirrhosis

Criteria 1 2 3
Ascites None Medically controlled Poorly controlled
Encephalopathy None Medically controlled Poorly controlled
Albumin (gm/dL) >3.5 2.8-3.5 <2.8
Bilirubin (mg/dL) <2 2-3 >3
↑PT (sec.) 1-3 4-6 >6

Total score 5-6 7-9 10-15

Prognosis Good Bad Worse
 Cirrhosis: A comprehensive review for long case discussion
It is a condition characterized:
• Clinically by: Hepatocellular failure + Portal hypertension
• Histopathologically by: Hepatic fibrosis + Necrosis + Regenerative nodules (pseudo-lobules) + Architectural
destruction of liver.
Causes:
A-Alcoholic cirrhosis/ Laennec's cirrhosis Chronic hepatitis (B and C): Micronodular
Non-alcoholic fatty liver disease (NAFLD) Cryptogenic cirrhosis
Alpha1 antitrypsin deficiency Deposition of copper: Wilson’s disease
Autoimmune hepatitis Glycogen storage disease
Biliary cirrhosis (primary and secondary) Hemochromatosis
Indian childhood cirrhosis.
Clinical features:
Features of portal hypertension Features of hepatocellular failure
• Ascites • Hepatic encephalopathy
• Variceal bleed • Icterus
• Splenomegaly • Fetor hepaticus
• Portosystemic encephalopathy • Ascites
• Superficial venous prominence (direction • Edema
of filling is away from umbilicus) • Miscellaneous*

*Miscellaneous points to be looked for • Dupuytren’s contracture

(Hyperestrogenemic features): Points suspicious for primary biliary cirrhosis (PBC):
• Spider nevus • Clubbing (although it may be present in any
• Gynecomastia cirrhotic patient)
• Palmar erythema • Pigmentation and scratch marks on skin
• Sparse facial/ axillary/ pubic hair Points suspicious for Wilson’s disease:
• Testicular atrophy • Kayser–Fleischer ring
• Flapping tremor • Involuntary movements
Points to be looked for specific underlying etiology: Palpation of liver:
• Bilateral parotid swelling • May be palpable (left lobe): Due to its firm
• Hepatic facies: Muddy discoloration with consistency
hollowing of face due to wasting of temporalis • Hepatic span often reduced
and masseter muscles
Investigations
Preliminary investigations:
Blood:
Hb, TC, DC, CRP Renal function: Na+ K+ Urea Creatinine
Hb: ↓ in GI bleed Urea creatinine: ↑ Hepatorenal syndrome
Pancytopenia: In alcohol induced marrow toxicity/ ↑ long term diuretic use
hypersplenism Na/K: Diuretics/ Dilutional hyponatremia
TC, DC, CRP: ↑ in SBP K+↑: Aldosterone antagonist
 K+↓: Loop diuretics AST/ALT >1 is suggestive of alcoholic liver disease
GGT, ALP: ↑ is suggestive of intrahepatic cholestasis
Liver function test: PT, aPTT, INR: ↑ is suggestive of synthetic function
Bilirubin: ↑, but significant hyperbilirubinemia occurs failure
only in end stage liver disease Arterial NH3 level: ↑ in encephalopathy.
AST, ALT: ↑, but often <300 U/L
Chest X Ray:To look for any effusion
USG abdomen: Detects liver size, texture; ascites, portal vein diameter, splenomegaly
Upper GI endoscopy: To look for any varices
Diagnostic ascitic fluid aspiration:
✓ Serum ascitic fluid gradient >1.1. gm/dL
✓ WBC count >500/μL with PMN fraction >50% is suggestive of SBP.

Treatment of chronic liver disease

1. Treatment of complications: ✓ Prevention: β-blocker/ nitrate.
A. Ascites: C. Coagulopathy:
✓ Dietary Na+ and water restriction Treat by fresh frozen plasma in case of
✓ Diuretics (Loop diuretics/ K+ sparing active bleeding.
diuretics) E. Encephalopathy:
✓ Daily body weight monitoring A. Avoid alcohol/ hepatotoxic drugs
✓ Daily intake-output chart B. Urgently treat any associated GI bleed
✓ Drainage: therapeutic ascitic fluid C. Prevent/ treat constipation
aspiration D. Dietary protein restriction
E. Treat any electrolyte imbalance
B. Bleeding varices: F. Fluid: Maintain proper hydration
✓ Circulation maintenance (IV fluid + G. Gut cleansing agent (Rifaximine)
blood transfusion) H. Prevent hypovolemia
✓ Drugs (Vasopressin) I. Treat any associated infection
✓ Endoscopy (Endoscopic rubber band
ligation/ sclerotherapy)