adeline

405090201
NAUSEA AND VOMITING
 Pathophysiology
• Vomiting Center (VC)- located in dorsal
portion of the lateral reticular formation in
the medulla
– coordinates the respiratory, GI and abdominal
muscles
– vomiting can be induced by electrical stimulus
of the VC
– the final common pathway that mediates
vomiting from all causes
Physiology (nausea, retching, vomiting)
 Nausea- awareness of urge to vomit
 loss of gastric tone and peristalsis with contraction of
duodenum and reflux of intestinal contents into
stomach
 can be accompanied by perspiration, salivation,
tachycardia, anorexia, headache
 Autonomic response
 Retching - consists of rhythmic, labored,
spasmodic movements, involving the
diaphragm, chest wall, and abdominal muscles
Physiology (nausea, retching, vomiting)
 Retching - usually precedes or alternates with
bouts of vomiting
 Vomiting (emesis) - forceful expulsion of
gastrointestinal (GI) contents through the
mouth.
 Diaphragm descends, abdominal muscles contract,
and gastric cardia open.
 Coordinated by somatic nervous system
 All 3 can occur together or independently
 Pathophysiology
 Vomiting can also be induced by stimulation
of the chemoreceptor trigger zone (CTZ), the
GI tract, and the vestibular apparatus
 CTZ- located in area postrema on the floor of
the fourth ventricle
 accessible to blood and cerebrospinal fluid (CSF)
 may not be as important to vomiting induction as
previously felt
 Pathophysiology
 CTZ- important in N&V, however
 when CTZ is surgically ablated can still have vomiting in
response to certain toxins
 Some feel that GI tract may be important initiator of
emesis as well
 Multiple neurotransmitters involved in N&V
 Dopamine, opiate, serotonin, acetylcholine, histamine
found in CTZ (see table 8-2)
 Dopamine and serotonin found in GI tract as well
 N&V associated w/distension or GI tract dysfunction-
responds best to metoclopramide
 Pathophysiology
 Input to Vomiting Center (VC) also occurs from
higher cortical centers
 e.g. patient experiences N&V in response to terror,
also, in cancer patients who have conditioned
response and have emesis even at sight of hospital
 Disturbance in vestibular function -> stimulate
cranial nerve VIII -> stimulates the VC.
 e.g. motion sickness- main neurotransmitters involved
- acetylcholine and histamine (dopamine and serotonin
not involved)
 Acute Vomiting
• Neonate/ Infant • Child/ adolescents
– With fever – With fever (but
• Sepsis, meningitis, otherwise well)
UTI • Gastroenteritis, esp
• Tonsillitis, otitis if also have
media, diarrhoea
gastroenteritis – With lethargy/ altered
– If no signs sepsis mental status
• Pyloric stenosis/ • Neurologic
outlet obstruction • Metabolic
• Metabolic • Endocrine
• Neurologic • Drugs, toxins,
• Endocrine alcohol
 Recurrent Vomiting
• Infants • Older child/
– GIT – feed Adolescent
intolerance – GIT
– Renal – Chronic sinusitis
– Metabolic – lethargy, – Drug intoxication
poor feeding, failure – Migraine
to thrive, seizures,
– Bulimia
abnormal tone
– Pregnancy
– Neurologic – raised
pressure –
meningitis, tumour,
hydrocephalus
 Pharmacotherapy
 First - In order to determine treatment,
 get history to determine the cause, onset and duration,
precipitating factors, recent ingestion (medication, food,
liquids), medical conditions
 e.g. acute onset of emesis in pt with large ingestion of
alcohol, may not need antiemetic tx at all
 mild to moderate N&V for <48hrs in absence of more
severe symptoms -> monitor hydration status ->OTC
products may help (e.g. carbohydrate solution-emetrol,
calmX, nausetrol) or pepto-bismo
 Pharmacotherapy
• N&V accompanied by more serious signs,
require more intervention
– blood in vomitus, abdominal pain or distension,
fever, severe headache, recent trauma, diabetes
DIFFERENTIAL DIAGNOSE
Clinical features differentiating GER and GERD in infants
and children
GER
Regurgitation with normal weight gain
No signs or symptoms of esophagitis
No significant respiratory symptoms
No neurobehavioral symptoms
GERD
Regurgitation with poor weight gain
Persistent irritability; pain in infants
Lower chest pain, dysphagia,
pyrosis/heartburn in children
Hematemesis & iron def anemia
Apnea & cyanosis in infants
Wheezing
Aspiration or recurrent pneumonia
Chronic cough
Stridor
Neck tilling in infants
 Common presenting symptoms of GER /
GERD
Infants and young Older children and
children Adolescents
Recurrent vomiting Regurgitation
Poor weight gain Heartburn & retrosternal
Irritability chest pain
Dysphagia Dysphagia
Asthma Asthma / chronic cough
Recurrent pneumonia Reccurent pneumonia
Upper airway symptoms Anemia & hematemesis
Apnea
 Gastroesophageal Reflux Disease
• Gastroesophageal Reflux (GER)
– Reflux of gastric contents into esophagus
– Normal physiologic process
– 50% of infants 0-3 months of age
– 25% of infants 3-6 months of age
– 5% of infants 10-12 months of age
– 20% of pH probe reflux episodes are visible reflux
– Result of Transient LES relaxations
 Gastroesophageal Reflux Disease
• Symptoms • Symptoms
– Weight loss or poor – Feeding refusal
weight gain – Apnea
– Irritability – Wheezing or stridor
– Frequent regurgitation – Hoarseness
– Heartburn or Chest pain – Cough
– Hematemesis – Abnormal Neck
– Dysphagia posturing (Sandifer
syndrome) often
confused with seizures
 Gastroesophageal Reflux Disease
• Findings • Associations
– Esophagitis – Reactive airway disease
– Esophageal stricture – Recurrent stridor
– Barrett’s esophagus – Chronic cough
– Laryngitis – Recurrent pneumonia
– Hypoproteinemia – ALTE
– Anemia – SIDS
 Gastroesophageal Reflux Disease
• Diagnosis
– History and physical
• No studies comparing H&P to diagnostic tests.
• Two pediatric studies – no relationship between
symptoms and the presence of esophagitis
• Still recognized by all as the first line in diagnosis
 Gastroesophageal Reflux Disease
• Barium Swallow
– Useful to detect anatomic abnormalities
– Not sensitive (31-86%), not specific (21-83%)
when compared to pH probe monitoring
– Not physiologic
– Snapshot of time (High false positive, false
negative)
 Gastroesophageal Reflux Disease
• Scintigraphy
– Technetium-labeled formula or food
– Stomach, esophagus, lungs scanned
– Good for gastric emptying, aspiration
– Scan for 1 hour, then 24 hours later
– Sensitivity 15% to 59%, specificity 83% to 100%
when compared to pH probe monitoring
– Role in diagnosis of GERD is unclear
 Gastroesophageal Reflux Disease
• Endoscopy and biopsy
– Can identify esophagitis, stricture, Barrett’s
esophagus, Crohn’s disease, webs, infectious
esophagitis
– 40% of normal appearing biopsy sites show signs
of esophagitis
– Eosinophils and neutrophils not present in
esophageal epithelium of children, and their
presence suggests inflammation.
 Gastroesophageal Reflux Disease
• Esophageal pH Monitoring
– Transnasal placement of electrode into distal
esophagus, +/- proximal esophagus, +/- above the
UES
– Acid reflux episode pH <4 for 15-30 seconds
– 12-24 hour studies recommended
 Gastroesophageal Reflux Disease
Esophageal pH Monitoring
 Normal reflux in 0-11 month old children
○ 31 reflux episode +/- 21, 73 upper limit
○ Reflux greater than 5 minutes 9.7 infants, 6.8 children,
3.2 in adults
○ Reflux index (% time spent below pH of 4) 11.7% in
infants, 5.4% in children, 6% in adults
○ Symptom index > 0.5 abnormal (Number of symptoms
with reflux/number of reflux episodes)
 Gastroesophageal Reflux Disease
• Esophageal pH Monitoring
– 60% of patients with poorly controlled asthma
have abnormal pH probe studies
– Correlate well with esophageal biopsies
– Considered gold standard
– Unclear whether proximal and distal probes more
effective than one distal probe
 Gastroesophageal Reflux Disease
• Prone vs. Supine
– Several studies have shown increased incidence of
SIDS with prone position (Relative risk 13.9,
4.4/1000 vs. 0.1/1000)
– Prone positioning postprandial period while
awake
– Prone positioning when child with life threatening
complications of GERD
– Otherwise, supine positioning
 Gastroesophageal Reflux Disease
• Medical treatment
– H2 receptor blockers
• Numerous studies in adults showing superiority over
placebo
• Several studies in children showing superior
improvement of pathology over placebo
• Side effects include rash, dizziness, nausea, vomiting,
blood dyscrasias
• No clear superior agent in class
 Gastroesophageal Reflux Disease
• Proton pump inhibitors
– Best if given ½ hour prior to breakfast, ½ hour before
evening meal
– Takes several days for a steady state acid suppression
– One study showed similar efficacy of omeprazole and high
dose ranitidine in children
– One study showed increased efficacy of omeprazole over
ranitidine in severe esophagitis
– Prevacid FDA approved for 1 -17 years old
 Gastroesophageal Reflux Disease
• Antacids
– Neutralize gastric acid
– Magnesium hydroxide and aluminum hydroxide as
effective as cimetidine in treatment of esophagitis
– High doses lead to near toxic aluminum levels
– Not recommended for treatment over 2 weeks
 Gastroesophageal Reflux Disease
• Prokinetic Therapy
– Increase LES pressure, no effect on transient
relaxations
– Double blind single drug studies for cisapride,
metoclopramide, bethanecol, and domperidone
have been done, with cisapride the only agent
better than placebo
– Cisapride off market due to potential cardiac
arrhythmias. Available only for severe cases
 Gastroesophageal Reflux Disease
• Surface agents
– Sodium alginate - forms surface gel that decreases
reflux and protects mucosa. Conflicting results
from studies, not available in US
– Sucralfate - adheres to peptic lesions. One study
available states as effective as cimetidine for
treatment of esophagitis. Aluminum
compound…toxicity
 Gastroesophageal Reflux Disease
• Surgical Options
– Nissen fundoplication +/- pyloroplasty
– Success rates from 57%-92% reported
– Complications from 2.2%-45%
• Breakdown of wrap, small bowel obstruction, infection,
atelectasis, pneumonia, perforation, esophageal
obstruction
– No difference in laproscopic vs. open except in
length of stay
 Gastroesophageal Reflux Disease
• Surgical
– Consider when maximal medical therapy fails
– Should be combined with G-tube when aspiration
a concern
– Most effective treatment
– Highest risk
GI Bleeding
http://www.wrongdiagnosis.com/bookimages/10/5248.png
 Sources of Bleeding in Patients Hospitalized for Upper GI
Bleeding in Years 2000–2002

Sources of Bleeding Proportion of Patients, %

Ulcers 31-59
Varices 7-20
Mallory-Weiss tears 4-8
Gastroduodenal erosions 2-7
Erosive Esophagitis 1-13
Neoplasm 2-7
Vascular ectasia 0-6
No Source indentified 8-14
 HEMATEMESIS
• Definition
Hematemesis is vomiting of gross blood. It is diagnostic of
bleeding from any site proximal to the ligament of Treitz.

• Source o Hematemesis
* Esophagus : Esophagitis, ulcer, Mallory-Weiss tear,
Esophageal varices
* Stomach : Gastric ulcer, Prepyloric ulcer , Pyloric
channel ulcer, Gastric erosions, Gastritis,
Varices , Portal-hypertensive
gastropathy, Gastric cancer , Polyp
,Dieulafoy lesion
* Duodenum : Ulcer, Duodenitis, Aortoenteric fistula,
Pancreatic pseudocyst, Postsphincterotomy
Hematemesis

Hereditary telangiectasia

http://www.wrongdiagnosis.com/bookimages/4/fig100b.jpg
 MELENA
• Definition
The passage of dark black, liquid, tarry, metallic-
smelling stools

• Melenic stools usually indicate bleeding proximal to

the right side of the colon

• It usually indicates that hemorrhage has remained

for at least 14 hour in the GI tract.

• The more proximal the bleeding site, the more likely

melena will occur.
 MELENA
Sources of melena
• All causes of upper gastrointestinal bleeding
• Jejunum and ileum: (Meckel's diverticulum,
angiodysplasia, Chron's disease, tumors,
bowel infarction).
• Colon: right sided tumors, angiodysplasia,
inflammatory bowel disease.
 Hematocezia
• Definition
The passage of bright red stools.

• Indicate a bleeding from the rectum & anus,

however 50% are due to proximal lesions
(mainly in the colon) that are profuse enough
that they avoid remaining in the gut for 8hrs &
are not expressed as blood intermixed with
stools.
http://www.wrongdiagnosis.com/bookimages/14/4791.1.png
 GI Bleeding

– Occult GI bleeding
Blood in the stool in the absence of overt
bleeding

–Symptoms of blood loss or anemia

(e.g., lightheadedness or shortness of
breath)
 Peptic Ulcer
• Definition
An excoriation area of gastric mucosal or
intestine.

• Etiology
* Increase secretion of HCL
* H. pylori
* NSAID
 EPIDEMIOLOGY
• 6 – 15 % of the western population
• 4 millions of patients ( new & recurrent )
have a peptic ulcer per year
• 12%  men & 10%  women
• 15.000 mortality per year, occured
because of complicated peptic ulcer.
 Classification
• Encompasses both gastric and duodenal ulcers
 Risk Factors
• Hereditary ( increase parietal cell number )
• Smoking
• Hipercalcemia
• Blood group O (antigens may bind H.pylori)
 CLINICAL FEATURES
• Duodenal Ulcer
* Burning epigastric pain 90 min to 3 hr after meals
* Often Nocturnal
* Relieved by food

• Gastric Ulcer
*burning epigastric pain made worse by or unrelated to
food
* Anorexia
* Food aversion
* Weight loss ( in 40% )
 COMPLICATIONS
• GI bleeding
• Perforation
• Obstruction
• Penetration causing acute pancreatitis
• Intractability
Summary of potential mechanisms by which H. pylori may lead
to gastric secretory abnormalities

H. pylori
Natural history of H. pylori infection
Schematic representation of the steps involved in synthesis of
prostaglandin E2 (PGE2) and prostacyclin (PGI2)
Mechanisms by which NSAIDs may induce mucosal injury.
 Diagnostic
• Endoscopy
 Esophageal varises
• Bleeding esophageal varices occur when veins
in the walls of the lower part of the esophagus
and sometimes the upper part of the stomach
are wider than normal (dilated).
 Epidemilogy
• Varices develop in 90% of cirrhotic patients
and are most often associated with alcoholic
cirrhosis.
• Hepatic schistosomiasis is the second most
common cause of variceal bleeding.
• Bleeding from esophageal varices is associated
with a mortality rate of at least 20% at 6
weeks, although bleeding ceases
spontaneously in up to 40% of patients
 Etiology
• Bleeding varices are a life-threatening
complication of increased blood pressure in
the portal vein caused by liver disease (portal
hypertension).
• Increased pressure causes the veins to balloon
outward. The vessels may break open
(rupture). Any cause of chronic liver disease
can cause bleeding varices.
 Pathofisiology
Obstuction of portal
venous flow
dilated tortuous
Elevated portal venous vessels called
thence into the azygos veins, varices
pressure (>10 mmHg )
and eventually into the
systemic circulation
Development of
increased
colateral circulation
pressure in the
esophageal plexus

Diverting the obstructed blood flow into the plexus of

to the systemic veins esophageal mucosal and
(portosystemic collaterals ) submucosal veins
Esophageal
varices
Increases capillary pressure in blood flow is diverted
organs drained by the through the coronary veins
obstructed veins. of the stomach
http://www.njsurgery.com/html/Anatomy%20Lessons/esophageal%20varices.JPG
 Sign & Symptoms
• Black, tarry stools
• Bloody stools
• Light-headedness
• Paleness
• Symptoms of chronic liver disease (such as cirrhosis)
• Vomiting blood
• Lowblood pressure
• Rapid heart rate
• Signs of chronic liver disease or cirrhosis
 Diagnostic
• Esophagogastroduodenoscopy ( EGD)
• Tube through the nose into the stomach (nasogastric tube) to
look for signs of bleeding
• X-Ray
 Treatment
• The goal of treatment :
Stop acute bleeding as soon as possible, and treat varices with
medicines and medical procedures.

Note: The combination of band ligation and sclerotherapy is not routinely used
except when the bleeding is too extensive for a vessel to be identified for banding. In
such cases, sclerotherapy can be carried out in order to control the bleeding and
clear the field sufficiently for banding to be done afterward.
Sengstaken-Blakemore tube

• For ruptured esophageal-

varices.
• There were two balloons, the
bigger ballon sat in the stomach
and the smaller balloon in the
esophagus to put direct
pressure on the varices.
• The end of the tube had an
aspiration port as well as the
ballon inflation ports, the
esophageal ballon was inflated
with the aid of a manometer ,
specify how much pressure to
have in the esophagus.
Once acute bleeding has been stopped, several treatments are
available:

• Beta blockers, such as propranolol and nadolol, are used to

reduce the risk of bleeding.
• A catheter
Placed through a vein across the liver where it connects the
portal blood vessels to the regular veins in the body, and
decreases pressure in the portal vein system (transjugular
intrahepatic portosystemic shunt, TIPS, procedure).
• Octreotide and vasopressin  used to decrease portal blood
flow and slow bleeding.
• Patients with bleeding varices from liver disease may need a
liver transplant.
 Mallory-Weiss Tears
• Mallory-Weiss syndrome is characterized by
upper gastrointestinal bleeding secondary to
longitudinal mucosal lacerations at the
gastroesophageal junction or gastric cardia.
 Etiology
• Continuing emesis
• Strong Cough
Virulence Factors of Helicobacter
gastritis
 Definition
• Gastritis is a term used to describe a group of conditions with
one thing in common: inflammation of the lining of your
stomach. The inflammation of gastritis is often the result of
infection with the same bacterium that causes most stomach
ulcers. However, other factors — such as traumatic injury,
regular use of certain pain relievers or drinking too much
alcohol — also can contribute to gastritis.
• Gastritis may occur suddenly (acute gastritis) or it can occur
slowly over time (chronic gastritis). In some cases, gastritis can
lead to ulcers and an increased risk of stomach cancer. For
most people, however, gastritis isn't serious and improves
quickly with treatment.
 Symptoms
• A gnawing or burning ache or pain (indigestion) in your upper abdomen
that may become either worse or better with eating
• Nausea
• Vomiting
• Loss of appetite
• Belching or bloating
• A feeling of fullness in your upper abdomen after eating
• Weight loss
• Acute gastritis occurs suddenly and is more likely to cause nausea and
burning pain or discomfort in your upper abdomen. Chronic gastritis
develops gradually and is more likely to cause a dull pain and a feeling of
fullness or loss of appetite after a few bites of food. For many people,
though, chronic gastritis causes no signs or symptoms at all.
• Occasionally, gastritis may cause stomach bleeding, although it's rarely
severe. But be aware that bleeding in your stomach that causes you to
vomit blood or pass black, tarry stools requires immediate medical care.
 etiology
• Bacterial infection.
• Regular use of pain relievers.
• Excessive alcohol use.
• Stress.
• Bile reflux disease.
• Autoimune disease. including Hashimoto's
disease, Addison's disease and type 1 diabetes.
Autoimmune gastritis can also be associated with
vitamin B-12 deficiency.
• Other diseases and conditions.
 Risk factors
• H. pylori infection.
• Regular use of aspirin or other NSAIDs
• Older age.
 complications
• Left untreated, gastritis may lead to stomach
ulcers and stomach bleeding. Some forms of
chronic gastritis may increase your risk of
stomach cancer, especially if you have
extensive thinning of the stomach lining and
changes in the lining's cells.
 Test and dX
• Blood tests.
• Breath test..
• Stool tests.
• Upper gastrointestinal
• Upper gastrointestinal X-ray.
 treatment
• Medications to treat stomach acid
Stomach acid irritates inflamed tissue in your stomach,
causing pain and further inflammation. That's why, for
most types of gastritis, treatment involves taking drugs to
reduce or neutralize stomach acid, such as:
• Antacids.
• Acid blockers.
• Medications to shut down acid 'pumps.'
• Medications to treat H. pylori
• Practice good eating habits. Just as important as what you eat is the manner in which you eat. Eat
moderate portions, eat at regular times and relax while you eat.
• Maintain a healthy weight. Digestive problems can occur no matter what your weight. But
heartburn, bloating and constipation tend to be more common in people who are overweight.
Maintaining a healthy weight can often help prevent or reduce these symptoms.
• Get plenty of exercise. Aerobic exercise that increases your breathing and heart rate also stimulates
the activity of intestinal muscles, helping to move food waste through your intestines more quickly.
It's best to aim for at least 30 minutes of aerobic activity most days of the week. Check with your
doctor before you begin an exercise program.
• Manage stress. Stress increases your risk of heart attack and stroke, dampens your immune system,
and can trigger or aggravate skin problems. It also increases stomach acid production and slows
digestion. Because stress is unavoidable for most people, the key is to learn to handle it effectively
— a task that's made easier by a nutritious diet, adequate rest, regular exercise and healthy ways to
relax. If you have trouble relaxing, consider taking up meditation or studying yoga or tai chi. These
disciplines can help focus your mind, calm your anxieties and reduce physical tension. In addition,
therapeutic massage may loosen taut muscles and calm frazzled nerves.
 preventive
• Eat smart.
• Limit or avoid alcohol.
• Don't smoke.
• Switch pain relievers.
• Follow your doctor's recommendations.
 References
1. Contran, Kumar, Collins. Robbins Pathologic Basis of Disease. 6th edition.
Saunders company
2. Rubin, Ravael. Rubin’s Phatology clinicopathologic foundation of
Medicine. 5th edition. Philadelphia
3. Buku Ajar Ilmu Penyakit Dalam, edisi 3, jil. 1, Balai Penerbit FKUI: Jakarta,
2001.
4. Litien,scott C. Mayo Clinic Family Heath Book. 5th edition. 2009. Jakarta :
Gramedia.
5. http://digestive.niddk.nih.gov/ddiseases/pubs/cvs/index.htm
6. http://www.nlm.nih.gov/medlineplus/ency/article/003118.htm
7. http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1411788&blobt
ype=pdf