NUTRITION IN

GASTROINTESTINAL DISEASES

PART-1
Upper Gastrointestinal diseases

dr. Ni Nyoman Sri Yuliani, Sp. GK

Clinical Nutrition Specialist-UPR
 WHY TALKING ABOUT GUT???

– The small bowel is where digestion and absorption of nutrients

occurs
– The intestinal microenvironment has an important influence on
the pathophysiology of many different diseases
– Diets don’t treat diseases, they treat patients
Upper Gastrointestinal diseases

– Gastroesophageal reflux & esophagitis

– Gastritis and peptic ulcers
– Gastric carcinoma
– Gastric surgery
– Dumping syndrome
– Typhoid fever
 Gastroesophageal Reflux
and Esophagitis
– GERD : episodes of reflux overwhelm esophageal protective
mechanisms result in symptoms heartburn ( a burning
sensation in esophagus, or inflammation with erotion)

– Manifestation : pharyngeal irritation , frequent throat clearing,

hoarseness, asmathic symptoms, heartburn , substernal pain
 Esophagitis
– Prolong acid exposure  esophagitis
(inflammation of the esophagus),
erotions, ulceration, scarring, stricture
and dysphagia

– Influence the health of mucosal barier

and gastric emptying

– Impair the ability to consume adequate

diet, interfere with sleep, work, social
event
MNT
– Medical management :
 Proton pump inhibitors
 Histamine-2 receptor antagonists
 Antacids
 Prokinetic agents

– Behavioral modification
Avoid :
 Eating within 3-4 hours of retiring
 Lying down after meals
 Tight-fitting garments
 Cigarette smoking
 GASTRITIS & PEPTIC ULCERS
– Result when infection, chemical or neural abn disrupt mucosal integrity of the
stomach
– Common cause : Helicobacter pylori (gram-negative bacteria)
– H.pylori induce inflammation from innate & systemic immune response
– other form of gastritis :
 Chronic use of ASPIRIN or NSAIDs, steroids, alcohol, erosive substances,
tobacco, etc
 Manifest : nausea, vomiting, malaise, anorexia, hemorrhage and epigastric pain
 Prolong gastritis : atrophy and loss of stomach parietal cells, loss of secretion of
HCl (achlorhydria) and intrinsic factor (pernicious anemia)
 Chronic reduction of gastric secretion of HCl reduce absorption of nutrients :
B12, calcium, and nonheme iron increase incidence of bone fracture,
intestinal infection (front barrier to microbial invasion)
 PEPTIC ULCERS

– Typically show more than one of the mechanism

– Primary causes : H. Pylori infection, gastritis, aspirin, NSAIDs,
corticosteroid and severe illnes
– Involve two major regions : gastric and duodenal ulcers
– Similar sign : dyspepsia and gastritis, abdominal pain
– Anorexia,weight loss, nausea and vomiting and heartburn more often
in gastric ulcers
– Ulcers can perforate into the peritoneal cavity or penetrate into other
organs (pancreas), or erode an artery and cause massive hemorrage
GASTRIC vs DUODENAL ULCERS
– PATHOPHYSIOLOGY :
GASTRIC ULCERS DUODENAL ULCERS

Occur anywhere in the gaster First few cm of the duodenal bulb (below
Most along the lesser curvatura pylorus)
Associated w/ gastritis, inflammatory
involvement of parietal cells (acid prod.),
athropy of acid and pepsin prod.cells in
advancing age
Relativity low acid output Increased acid scretion (nocturnal acid
secretion)
Anthral hypomotility, gastric stasis, increased
duodenal reflux
Hemorrhage and mortality are higher than
duodenal ulcers
MNT – Gastritis  impaired intrinsic factor and decreased vit B12 malabsorption
– Low acid state  reduced absorption of iron and calcium
– Eradication of H.pylori
– Protein  temporarily buffer gastric secretion, but also stimulate secretion :
gastrin, acid and pepsin
– Orange juice  pH 3,2 – 3,6, soft drink : pH 2,8 – 3,5
– Acidic food from fruit juice and soft drink not likely causes peptic ulcers
– Alcohol  large amount can cause superficial mucosal damage and worsen
peptic ulcers
– Coffee and caffeine stimulate acid secretion
– Spices ( chili, cayenne, black peppers)  increase acid secretion, erosion,
inflammation of the mucosal lining and altered GI permeability or motility
– Probiotics  eradicated H.pylori
– Omega3 dan 6  anti inflammatory, cryptoprotective of the GI mucosa
 GASTRIC CARCINOMA
– Slow manifest, frequently overlooked until it is too late
for a cure
– Clinical symptoms : loss of appetite, loss of BW,
abdominal pain, nausea, vomiting, anemia and abdominal
mass
– Studies :
– (Lynch et al 2005) other factors may increase the risk :
chronic infect. H.pylori, smoking, intake highly salted,
pickled foods or inadequate micronutrients
– Lead to malnutrition cause of excessive blood and protein
losses
– Surgery : partial or total resection of the gaster
(gastrectomy) malnutrition
MNT
– Determined by the location of the cancer, nature function and stage
– Gastrectomy : difficulties w nutrition after surgery
– Inoperable cancer : diet is adjusted to the patients tolerances, preferences and
comfort.
– Advanced stage : if unable to tolerate oral feeding, consider to alternate route such as
gastric or intestinal feeding tube, or PN
 GASTRIC SURGERY
INDICATIONS :
– Ulcer diasease,
– Malignancy, Jojuoum

Afferen! loop
– Weight loss Billroth I Billrolh LI Partial gastric resection
gaslroduodenostomy gastroJeju™>Stomy
(bariatric) Los$ ou,,_,g than s.qu.1no. such aa stoolorrhoo.
Wllh Billroth II. waoght I06s. dumping. Smell poucti
11<>1iwtmg.
ana ollen with tho Bill101ti
mon, '>ae1ertOI II
oYerg,owtn.
p,ocedwe Chen "'1h Blliro.:h I.
oocur

Enlargement ol Jejunum
pylorlo spNncter

Vagolomy Pyloroplesty Roux·en·Y procedure

Depending on uie el<lenl ot lne Duodenal reflux often
vas,o1omy,HCI-Ion is loflows 1his suigery,
reclue&d, and gastric emptying
lti slowed. Dumping syndrome
orton lolows this surgery.
nGURE 28-4 C:1,saic surgtC'JI procedures,
Post gastrectomy MNT

– Understanding the anatomy

after surgery ERAS, gastrectomy consensus
– Nutrition complications after
gastric surgery  varied nasogastrik/
Pre-operation Post operation :
– Complications nasojejunal
- Routine - 1st day should give
decompression
 Obstruction artificial nutrition
- NGT is nt
nutrition  not - diet given gradually
 Dumping syndrome routinely used
recommended according to
 Diarrhea in gaster
- Severe patients tolerance
surgery
 Weight loss malnutrition 
recovery
optimalization
– Inadequate food intake protocols
oral or enteral
related to :
nutrition
 Early satiety
 Symptoms of dumping
 malabsorption
DUMPING SYNDROME

1. Early DS : 10-30 minutes after meal

2. Late DS : 2-3 hours after meal
Basic guidelines for Dumping
Syndrome
– Small, more frequent meal
– Limited fluids during meals, wait for 30 minutes after meals
– Fewer simple sugars
– More complex carbohydrates
– More soluble fiber
– Chew food thoroughly and eat slowly
 TYPHOID FEVER

– Systemic infection caused by S. Typhii

– Infects roughly 21,6 million people each year
– Mortality : 216.000 – 600.000 people each year, highest in patients suffering from
malnutrition.
– 62% occuring in Asia
– Clinically characterized by typical continous fever for 3-4weeks, relatively
bradycardia, with involvement of intestinal lympoid tissue, RES & gall bladder
– Complications: ileum perforation, septic shock, death
– General therapy: maintenance adequate hydration, antypiretic, approprite nutrition
– Spesific therapy : antimicrobial
 MNT- TYPHOID FEVER
High- calorie, high-protein diet  prevent weight loss

FOOD TO BE TAKEN FOOD TO BE AVOIDED

 Hygiene food & serving  Roughage foods
 Soft food (easy digest)
 Strong flavor (onion, garlic)
 High biological value protein
 All spices (chilli, vinegar)
 Simple sugar content ( honey, candy, syrup)
 High fiber content
 Low fiber foods
 Butter, fried snacks, thick cream soup
 juice, soup, wtery foods
 Vegetables with soluble fiber  Food that cause gas : jakefruit, pineapple,
durian
 Fluids : at least 6-8 glass/day
 Diet lambung di RS
Diet Lambung I Diet Lambung II
1. Diberikan pada penderita Tifus 1. Fase akut sudah teratasi
Abdominalis berat. 2. Tifus Abdominalis dengan suhu
2. Makanan bentuk saring tubuh tinggi.
3. Makanan bentuk saring atau lunak
3. Diberikan setiap 3 jam selama 1-2
tergantung toleransi pasien
hari (pasien mudah bosan, rendah
kalori, vitamin dan mineral) 4. Diberikan tiap 3 jam

Diet lambung III Diet lambung IV

1. Tifus Abdominalis, suhu tubuh 1. Fase recovery
normal. 2. Makanan bentuk lunak atau biasa
2. Makanan bentuk lunak. 3. diberikan 6 kali sehari dalam porsi
3. Diberikan 6 kali sehari, porsi kecil. kecil
 Next to
PART 2 (LOWER GIT DISEASES)
dr. Ni Nyoman Sri Yuliani, Sp.GK
Clinical Nutrition Specialist - UPR
 Constipation
 Diverticular disease
 Inflammatory bowel diseases
 Irritable bowel syndrome
 Ileostomy and colonostomy
 Fistulae
  a difficult or infrequent passage of stool
 causes of constipation :

• Lack of exercise or mobility

Lifestyle • Ignoring the urge to defecate Chronic use • Oncology patients
• Inadequate fiber of opiates • Chronic pain

Dysmotility • hypothyroid Pelvic floor • pregnancy

disorders • Gastroparesis,Hirschprung’s disorder
disease, diabetes

Other GI • IBS, anal fissure, hemorrhoid

Neuro • Anorectal malformations, outlet
• Muscular dystropy disorders obstruction
muscular • Cerebral palsy,etc
disorders
 Adequate of dietary fiber (soluble and insoluble )
 Fiber increases :
 colonic fecal fluid,
 microbial mass ( 60-70 % of stool weight)
 Stool weight and frequency
 Rate of colonic transit
 Fiber soften stool and make easier to pass
 Diverticulosis : having saclike herniations (diverticula) in the colonic wall
 Pathophysiology

Combination of :
- Colonic
structure, Hard fecal
motilility,
genetics
- Lifelong low
Intra colonic
fiber intake
pressure

Herniation to
the weaker
segment of
the colon
 25 % diverticulosis develop diverticulitis
 Complications: range from painless- mild bleeding

 DIVERTICULITIS : inflammation, abscess formation, acute perforation, acute

bleeding, obstruction, & sepsis
 Modified diet or bowel rest  based on degree of illnes
 MNT :
 High fiber diet with adequate hydration  promotes soft, bulky stools
 HFD  bloating or gas  increase HFD gradually 2-3 weeks

 Avoid seeds, nuts, or skin of plant matter to prevent complications, but

evidance low
 Major form : Crohn’s disease and ulcerative colitis (UC)
 Rare disorders, 130 cases /100.000 persons for Crohn’s disease;
100/100.000persons for UC
 Geneti Unknown "irritant"
c
predispositi Viral? B;icterlal?
on ·\I
I ,j-,iiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiiii,!! Autoimmune?

Abnorma Ulctre11¥e COlltlt

l
activation
of the mucosa!
immune uil:eratlon
response.
Secondary suo1v1n
c
systemi
mucosa
c (p.seudo-
respons ro"of ~l)OtyOS)
1
e haustra dlstOCl«ln

Inflammatory Respon~

Odllld\l" Lu tho, u.11~ur tho, >111dll d11llfur ldryo,

intestine with malabsorplion, ulceration, or stricture

• Diarrhea
• Weight Joss
• Poor growth
• Hyperhomocysteinemla
• Partial GI obstructions
Ulcerative versu Crohn's Disease
Colitis s Ulcerative Crohn's Disease
Presentation
Colltls Perianal disease, abdominal pain (65%), mass m
Bloody diarrhea abdomen
Gross Pathology Rectum always involved Rectum may not be involved
Moves connnuously, proximallyfrom Can occur anywhere along gastrointestinal tract
recrum Not continuous: "skip lesions"
Thin wall Thick wall Strictures
Few stnctures common Cobblestone
Diffuse ulceration appearance Granulomas
Histopathology o granulomas lvioreinfla1111nation
Low inflammanon Shallow ulcers
Deeper ulcers (hence named ulcerative) Fibrosis
Pseudopolyps
Abscesses 111 crypts
Extramtesnnal Marufestanons clerosmg cholangms Erythema nodoswn
Pyoderma gangrenosum Migratory polyarthritis Crohn's Disease
Gallstones
Complications _, Toxic megacolon l\Ialabsorption
Cancer Cancer
Ulcerative Colitis Strictures and fistulas are very rare "'rr1ctures or fistulas
Perianal disease
 Diet  enviromental factor trigger relapses of IBD
 Malnutrition
 Dietary lipid
 Food allergies, intolerance
 Sucrose intake, low intake fiber, red meat and alcohol, altered omega6/3 ratio
 Diet & spesific nutrients  supportive role in maintaining nutrition status,limiting exacerbation
 Energy requirement : not greatly increased (unless weight gain is desired)
 Protein : may incrased depends on the severity & stage of the disease
 Protein losses occur in inflamed and ulcerated intestinal mucosa to maintain positif nitrogen
balance : 1,3-1,5g/kgbw/day
 Vit: folate, B6 & B12, also mineral and trace elements (Zinc, potasium,and selenium)
 Probiotics
 Possible Intestinal Causes of the Irritable Bowel Syndrome Altered

C
colonic motility
Chronic or acute inflammation
lschemia
Alterations in ion channels
Sodium ,--. - Bloating and
Medications Type 2 chloride (CIC-2) Excess production of
intestinal gases distention
Trauma Guanylate cyclase C (GCC)
Chronic or acute infections (H2, CO,. CH,)
Food-mediated (e.g.,
Bacteria (e.g., spirochetes) fructans, gluten)
Viruses Mutated ion

I
Disaccha ridase deficiency
Changes in
Parasites gut flora

 According to criteria symptoms

Bile acid malabsorption

 Abdominal discomfort at least 3 [ Healthy gut flora J

days /month for at least 3 months,

include at least 2 of three feature Maintain Nourish Complete
pH epithelial digestion Recruitment
of mast and
dendritic cells
• •
1. Defecations discomfort channels
Normal ion ~i Release of inflammatory mediators

2. Altered frequency of stool

.
•~m
(histamine, tryptase, serotonin,
TNF-a, proteases, and interleukins)
.:P
~~ ,, Normal tight
~1
~

3. Change in form of the stool

IBS·Constipation (IBS C)
Food moves too
slowly
through the

 Three subtype of syndrome

bowel.
This stool
causes
is thot
afferent neurons and then

1. Diarrhea predominant
to dorsal root ganglia
hard to pass Upstream signaling to

2. Constipation predominant
Abdominal pain,
185-Diarrhea (IBS·D) diarrhea, or constipation
Food moves too

3. mixed
tquickly th bowel.
hrough
This causes watery
 MNT goals: adequate nutrient intake, modified diet for the spesific IBS pattern,
potential role of food for managements symptoms
 Diarrhea predominant IBS  Food may be poorly tolerated : fat, caffeine, lactose,
fructose, sorbitol & alcohol
 Constipation-predominant IBS recommendation foods: insoluble fiber (psylium,
wheat bran) & adequate fluid are recommended
 Food with fiber prebiotic food  maintain healthy microflora
 Probiotics  significant improvement in abdominal pain, bloating & distension
 Low FODMAPs diet  low in fermentable oligo-, di-, monosaccharides and polyols.
 FODMAPs poorly absorbed in small intestine, highly osmotic and rapidly
fermented by bacteria
 Entire colon, colon, rectum and anus must be removed
 Some cases, a temporary opening  healing distal parts of the intestinal tract
allow surgery
 Odorous food : legumes, onions, garlic, cabbage, eggs, fish.
 Persistent odor  poor stoma hygiene stoma complication (bacteria overgrowth
in the ileum)
 Normal output from ileum-colon : ± 750 -1500mL (intact GIT)
 Ileostomy : adaptation 1-2 weeks
 Depends on resektion, ileostomy
 ENTEROCUTANEOUS FISTULAE (ECF)

abnormal connection Retrospective studies

between intestinal  2373 laparotomy of
lumen and skin acute  1,5% ECF

75-85% iatrogenic, Mortalitality

others: surgical
40-60%
procedural & trauma
 Klasifikasi
THINK FRIENDS Gastrocutaneus
natomy
A
Enterocutaneus
colocutaneus
Iatrogenic malignancy
Etiology
Operation infection
percutaneus drain Crohn’s disease
Trauma Tuberculosis
Foreign body Actynomicosis
Low output (<200ml/day)
Physiology
Moderate output (200-500mL/day)
High output (>500 mL/day)
 CLINICAL MANIFESTATION & DIAGNOSIS

Clinical Assesment : Malabsor ption

Fluid Status symptoms:
Electrolyte diarrhea, dehydration,
Nutrition Status malnutrition
& BW↓
*The remaining length
of intestine (<100cm
malabsorption nutrient and Depends on type and
fluid)
*Citrulline test < 20 umol/L
length of intestine
 SBS
resection.
MEDICAL TREATMENT
PHASE II PHASE III
PHASE I
Definitive
Outcome
Anatomic
Identification&
Identification & Operation depends on :
stabilitation
assesment  Nutritional Status
 Loss of fluid and
- fluid, electrolyte
stabilitation, electrolyte
CT scan,
skin treatment, gastrointestinal  Fistulae site
sepsis contrast - Fistula Resection  sepsis
management radiogram.
and nutrition - goals: formation
- Volume and of intestinal
support content of fistula
continuity
- Priority : fluid & secretion,
electrolyte effective drainage
resusitation
 MNT - ECF
 Personalized based on underlying disease, age,
comorbid and response therapy

• Phase I : starting with TPN to repair catabolic status

• Phase IIa : main goal is to determine length of

functional intestine & feeding access
• At least 75cm small intestine to ensure EN
therapy.
 MNT – PHASE IIB :
DETERMINE EARLY NUTRITIONAL STATUS

 Harris Benedict, indirect calorimetric

 Energi : 20-30kcal/kgbw/day (start)
 Protein 1,5-2,5g/kgbw/day
 High output Fistula :
 1,5-2x calorie requirement
 zinc 2x RDA
 Vitamin C 5-10x RDA
MNT-PHASE III
 Enteral Nutrition (EN)
 Early enteral feeding rapid wound healing,
↓pneumonia and ↓ new fistula.
 Contraindication EN: gut discontinuity, short functional
gut, hard to get EN access, intolerance, high output
fistula.

 Parenteral Nutrition
 Depend on case severity
 High output and proximal fistula  TPN decrease GI secretion 30-50%
 Nowadays : PN and EN combination  good outcome
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