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References: Video Lecture ppt + recording (Sept 2020)

Note: Iba yung flow of discussion ni doc ngayon
compared to PARBS. Kayo na po bahala to supplement. This trans
will be purely lecture based.
USE AT YOUR OWN RISK

List of topics Based on Video Lecture

Fig1. Patient presents with Acute Diarrhea with general features of
I. Common Etiologic Agent Causing Acute Diarrhea the stools: Mucoid, Bloody, Loose. Common organisms to consider
II. Common Disorders in Upper GIT are Enteroinvasive and Enteroadherent:
 Cleft Lip/ Cleft Palate o Shigella
 Ankyloglossia/ Tongue tie o EIEC
o EPEC
 Anencephaly/ Microcephaly
o Salmonella
 Esophageal Atresia and TEF
o E. Histolytica
 Congenital Esophageal Web and Stenosis
 Foreign bodies How will these organisms cause diarrhea?
 Caustic Ingestion  Shigella, EIEC/Enteroinvasive E.coli and E. histolytica are
 Hypertrophic Pyloric Stenosis Enteroinvasive, they cause damage to the epithelial cells.

 EPEC/ Enteropathogenic E.coli is an Enteroadherent, adhere

DIARRHEA:
to the enterocytes, do not produce enterotoxin, do not cause
-Has been and still is a common cause of morbidity mortality of any
damage to the enterocytes. Rather, they disrupt and blunt the
young child.
microvilli of the bowels
-In general, diarrhea is caused by Infectious and Non-Infectious
causes.
 Salmonella is Enteroinvasive with penetration of lamina
propria and systemic spread. It sets up an inflammatory
Infectious Non-infectious (less common) process in the intestines.
 Virus  secondary to lactose
 Bacteria intolerance (either primary Shigella
 Parasites or secondary) There are 4 types of Shigella
 Fungus  other carbohydrate  S. dysenteriae: classic agent of invasiveness and causes
 Extra-intestinal infections intolerance most severe dysentery
(UTI and URTI)  overfeeding  S.flexneri: most commonly encountered
 Pseudomembranous  drug-induced (antibiotic  S.boydii: least encountered
enterocolitis use)  S.sonnei
 food allergy (most
common: cow’s milk) The presentation of the diarrhea is dependent on the interaction of
 Poisons the enteric pathogen with the intestinal mucosa.
 inflammatory bowel disease
Clinical Manifestations:
Case 1: Shigella EIEC EPEC Salmonella E.
10 month old infant brought to you because of water stools a day Histolytica
prior to consult. The abnormal bowel movement was noted to High fever Afebrile Afebrile Afebrile
occur 4 times. (very high
can have
Important features:
convulsion) Shigella
 age of the patient (different organisms will be affecting
Odorless like but Fishy Rotten Egg Very foul
younger age group compared with the older children)
milder
 watery stools (you cannot never make a diagnosis of diarrhea, Tenesmus
without the stools being watery or very loose) Convulsion
 occurring 4 times in 24 hours (expected in patients with
Sporadic; Sporadic Endemic
diarrhea)
affects
 acute: duration is 1 day
others

Is diarrhea a diagnosis? No.

Diarrhea
It is essentially a clinical manifestation of altered GI function in
digestion, absorption or secretion leading to excessive loss of fluid
and electrolytes

ACUTE DIARRHEA: Sudden onset of excessively loose/watery

stools which lasts less than 14 days, more than 3 times in 24 hours

If more than 14 days: it is either chronic or persistent, depending on

what is the cause of that diarrhea
Fig2. Patient presents with Acute Diarrhea with general features: Fig3. Patient presents with Acute Diarrhea with general features:
Minimal or no mucus, no blood, it is watery and copious. No mucus or blood, explosive; after taking lactose containing
Common organisms to consider are Viruses (such as Rotavirus and formula. The common cause is Lactose intolerance, usually
others) and organisms that causes Secretory type of diarrhea accompanies acute infectious diarrhea, probably viral, acidic
(ETEC and V. cholera) stool and perianal dermatitis secondary to acidic stools and
frequency of the bowel movement.
How will these organisms cause diarrhea?
 Viruses have a selective infection and damage to the upper Lactose intolerance
villus tip cell of the small intestine. In effect, they decrease The signs and symptoms are due to the failure of intestine to
the absorption of salt and water. They also decrease hydrolyze Lactose leading to bacterial degradation and acid
disaccharide activities leading to malabsorption of complex fermentation of the substrate Lactose and consequent acidic
carbohydrates like Lactose. stool because of the pH.
 Rotavirus: Most common virus that causes diarrhea
among infants. Patients <1-2 years old Other signs and symptoms:
 Other virus that cause diarrhea:  Bloating: patient feels the abdomen is filled with air
o Parvovirus  Abdominal cramps: patients cry because of increase
o Astrovirus accumulation of gas into the abdomen
o Enterovirus
o Adenovirus
o Norovirus
o Norwalk virus Mechanism of Diarrhea
o Sapovirus

 ETEC and Cholera are both Enteroadherent to the mucosal 1. Osmotic factor
epithelium with production of Enterotoxin, they also bind with  Ingestion of a poorly absorbed solute (patients with
the tips and crypts of the small intestine villi. Lactose intolerance)
 Fermented in the colon
V. cholera  Production of SCFA/ Small chain fatty acids
It usually activates the Adenyly cyclase in the cell membrane  Increased osmotic solute load
leading to increase cAMP/Cyclic Adenosine Monophosphate,  Lesser volume than secretory diarrhea
therefore increases Chloride secretion but inhibits Sodium  Stops with fasting
absorption.  Example: ingestion of lactulose, sorbitol etc.
Lactose with lactase deficiency
ETEC/Enterotoxigenic E. coli
It activates Guanylate cyclase and increases GMP/Guanosine 2. Secretory factor
monophosphate, inhibiting Sodium absorption but no effect on  Often caused by secretagogue
Chloride secretion.  Builds to a receptor on the bowel epithelium
 Stimulating intracellular accumulation of cAMP
Clinical Manifestations:  Accumulation of free bile acid, hydroxy fatty acid cause
the colonic mucosa to secrete through this mechanisms
also
Rotavirus Others ETEC V. Cholera  Example: Cholera toxin, ileal resection, IBD
Low grade Low to moderate Afebrile Afebrile
fever fever 3. Diminished anatomic or functional surface area
Unpleasant Unpleasant odor Strongly Fishy + rice  Short bowel syndrome (can be congenital or secondary to
odor fecal washing a resection)
o Congenital
Starts with Respiratory Acute,
 Congenital short bowel syndrome
vomiting infections severe
 Multiple Atresia
(Elicit if there (cough/colds) dehydration
 Gastroschisis
is vomiting (persistence
prior to loss of fluid o Acquired
passage of both orally  Necrotizing Enterocolitis
stool) and anally)  Hirschsprung
Epidemic Epidemic Sporadic Epidemic  Volvulus
Travelers  Trauma
Diarrhea  Crohn’s disease
(most
common  Celiac Disease
cause)  Mucosal disease like rotavirus enteritis

4. Altered Motility
 Hypermotility brought about the presence of thyroid
hormones, prostaglandins and serotonin
 Hypomotility as in malnutrition and idiopathic pseudo-
obstruction

5. Mucosal invasion
 Inflammation, decreased colonic reabsorption, increased
motility
 Salmonella, Shigella, Amebiasis, etc
 Refer to picture
1st picture 2nd picture 3rd and 4th picture

COMMON GIT MANIFESTATIONS Combination of

Incomplete Cleft lip Complete Cleft lip Complete Cleft Lip
 Anorexia (loss of appetite, nonspecific) and Cleft Palate
 Dysphagia (difficulty in swallowing) **odynophagia (painful)
 Regurgitation (normal initially, then become abnormal)
o Infant reflex/regurgitation: peaks about 4 months of
simple cleft lip that more complicated combination of cleft
life, 88% are resolved by 12 months, nearly all of
only affects cleft lip because it lip and palate,
them will resolve at about 2 years of age
vermilion border, separates the skin, complete
o Tagalog “lumulungad”/ expelling gastric contents
varies from a small mucosa, muscle, (separation of skin,
effortless
notch at the tooth and the bone. muscle, mucosa,
 Vomiting (elimination of gastric content with effort, never
vermilion border bone)
normal)
o Mechanical
o Obstructive: Pyloric Stenosis, FEEDING PROBLEM
intussusceptions, atresia/stenosis  Cleft lip and palate have the same problem at birth. In order to
o Non-obstructive: GER, Ileus have an effecting sucking reflex, a negative intra-oral pressure
o Reflex is needed however patients with cleft lip/palate, may not do it
o GUT, CNS, Labyrinthe effectively due to the presence of the defect.
o Nonspecific
o Cyclic vomiting, eating disorder
CLEFT LIP
CRITERIA FOR CYCLIC VOMITING SYNDROME  Cause: Unknown cause
 (All of the criteria must be met)  Theory: failure of the medial nasal and maxillary processes to
 At least 5 attacks in any interval or a minimum of 3 join due to hypoplasia of the mesenchymal layer
attacks  More common than cleft palate
 Episodic attacks of intense nausea and vomiting lasting 1  More common on Males, left side
hour to 10 days and occuring at least 1 week apart  Common among Asians
 Stereotypical pattern and symptoms in the individual  Least common among Blacks
patient
 Vomiting during the attacks occur ≥4 times/hr for ≥ hr POSSIBLE CAUSES OF CLEFT LIP
 Return to baseline health between episodes  Maternal drug exposure (Phenytoin/ Corticosteroid)
 Not attributed to another disorder
 Part of a syndrome malformation complex
 Genetic factors
 Diarrhea  Incidence highest among ASIANS
 Constipation (difficulty of passing, hardened stools, frequency) **Important to counsel patients on next pregnancy
 Abdominal pain
CLOSURE OF THE CLEFT LIP
 Abdominal enlargement
 Age: 3 months
o Intestinal (cause is within the lumen of the bowel)  Requirements:
o Extraintestinal (outside the lumen of the bowel)  satisfactory weight gain
 Hematoma  No oral, respiratory and systemic infection
 Tumor masses
 GIT USUAL SEQUELAE OF CLEFT LIP
o 4th part of duodenum “Area of Ligament of Treitz”:  Malposition of the teeth
boundary between Upper and Lower GI)  displacement of maxillary arches
o Upper (1st manifestation: Vomiting)
o Lower (1st manifestation: Abdominal distention)
 GIT Bleeding CLEFT PALATE
o Upper (Melena/black)  Theory: Failure of the palatal shelves to fuse
o Lower (Hematochezia/red, fresh blood)
 Jaundice USUAL SEQUALAE OF CLEFT PALATE
 Recurrent otitis media leading to deafness

GOALS OF SURGERY FOR CLEFT PALATE

• Union of the cleft segments
 Important to consider what would prevent the patient from • Intelligible and pleasant speech
eating or sucking. • Reduction of nasal regurgitation
 Any disorders in the jaw, teeth, tongue, salivary glands or any • Avoidance of injury to the growing maxilla
in the buccal mucosa can prevent the patient to have
successful sucking/feeding activity. CLOSURE OF CLEFT PALATE
 Infection: most common cause of difficulty of sucking/  Patient is before 1 year to enhance speech development
swallowing (fungal infection, pharyngitis, stomatitis, glossitis
etc) TIMING OF CORRECTION
 Case to case basis, Depending on:
CLEFT LIP /CLEFT PALATE  Size
 Shape
 Degree of deformity

THE FOLLOWING WILL ALSO AFFECT THE DECISION WHEN TO

CORRECT
 Width of the cleft
 Adequacy of existing palatal segments
 Width of the oropharynx
 Neuromuscular function of soft palate and pharyngeal wall
 Associated malformation is more common on Cleft palate like
Chromosomal aberration and Holoprosencephaly. ESOPHAGEAL ATRESIA AND TEF

ANKYLOGLOSSIA/TONGUE-TIE

“FRENULUM LINGUAE”
 The thin tissue at the floor of the mouth connecting the dorsum
part of the tongue that prevents the patient’s tongue to be
protruded normally. Upon protrusion, tongue will not be
pointed rather it will be “heart shaped”

ANKYGLOSSIA Clinical types:

 It does not affect feeding A. Esophageal atresia with distal TEF 87%
 Sometimes it does interfere with speech: o Most common
o difficulty in pronouncing letter R o No continuity of esophagus
 Do you operate? YES AND NO o Atresia: failure to develop
o You may chose not to since some of the patients o Stenosis: there is development, but there is
when they grow old they will still be able to narrowing
pronounce letter R correctly o TEF/ Tracheoesophageal fistula: connection bet
 Surgery: just excise the tissue, very easy trachea and distal esophagus

B. Esophageal atresia without TEF 8%

ANENCEPHALY AND MICROCEPHALY
C. TEF without Esophageal atresia 4%
o Esophagus is normally continuous

D. Esophageal atresia with proximal TEF 0.5%

o least common, most complicated
o If you eat anything it goes to the lungs, there is
a connection of esophagus between the trachea

E. Esophageal atresia with proximal and distal TEF 0.5%

o Least common
 Deformed newborn o Abnormal connection bet esophagus and
 Anencephaly: absence of brain tissue trachea, proximal and distal
 No brain function, baby cannot suck the amniotic fluid of the
mother, leading to Polyhydramnios. AF will go to the uterus.
ESOPHAGEAL ATRESIA AND TEF
 Most common congenital anomaly
 Cause: Unknown
**Majority of GI disorders are always of unknown cause
 Normal length of esophagus in the newborn: 8-10cm  ASSOCIATED FEATURES:
 Adults: 25cm  advanced maternal age
 By age: 2-3 y/o, the length of the esophagus will almost be the  obesity
same of that with the adult  low socioeconomic status
 tobacco smoking
 90% have TEF
Esophagus
 90% survival rates
 passage of food and liquid to the stomach
 50% nonsyndromic
 3 normal narrowings/strictures
 50% with associated anomalies VACTERL
o Cricopharyngeus
 Vertebral body defect
o Arch of aorta
 Anorectal anomaly
o Diaphragmatic area
 Cardiac defect
**Patient accidentally ingest foreign body, you have to
 TE tracheoesophageal
look first at the 3 areas
 Renal
 Limbs
A. Anatomical
1. Esophageal atresia and TEF
2. Congenital Esophageal webs and stenosis

B. Acquired
1. Caustic Ingestion/ Corrosive strictures
2. Foreign bodies

Case. A CXR of a Newborn, an insertion of tube was done. The tube

did not push through the stomach, it coiled back and the tip of the
tube went out through the mouth. Indicates something is wrong with
the esophagus: either atretic or stenotic
  If the manifestation of the patient is Respiratory, chances are
 Film shows the patient has gas in the stomach. Consider the foreign body impinges on the larynx or the membranous
Clinical type A, since it is most commonly encountered and in posterior tracheal wall. Manifested as
A there is a connection between the trachea and distal o Stridor
esophagus that causes gas in the stomach. o Wheezing
o Cyanosis
PRESENTING SYMPTOM OF ATRESIA: o Dyspnea
 frothing and bubbling of the mouth at birth
 Episodes of choking, coughing, cyanosis (3Cs of EVALUATION OF PATIENTS WITH HISTORY OF FOREIGN BODIES
aspiration)  PLAIN XRAY
 Respiratory distress o AP of the neck, chest and abdomen
 In Clinical type C (TEF without Esophageal atresia), these o Lateral view of neck, chest only
are patients who are discharged from the nursery
undetected because the esophagus is okay. The  ENDOSCOPY
manifestation will come later on weeks after and the o Failure to visualize the object with Plain film in a
patient will complain of chronic respiratory problem: symptomatic patient warrants an urgent endoscopy.
o recurrent pneumonia Endoscopy has to be done among patient ingested a
o refractory bronchospasm foreign body but not seen on plain film.

EARLY CLUES/HINTS OF EA TREATMENT

(Prior to onset of signs and symptoms)  Endoscopy
 Presence of Maternal polyhydramnios o Goals in endoscopy:
 Inability to pass NGT/OGT  Visualize the object and underlying mucosa
 Removal of the object
TREATMENT PRINCIPLES
 Maintain a patent airway  Removal of foreign object
 Prevent aspiration o If the object is disc button batteries: remove it, since
 Use of antibiotic to prevent Pneumonia button batteries can induce mucosal injury in less
 Positioning of the patient than one hour, and involve all layer of esophagus in
o Put the patient to prone position to minimize four hours
movement of gastric secretion to the distal TEF,
aspiration of gastric contents via distal TEF  Asymptomatic
causes more damaging Pneumonitis than o Asymptomatic agents, observe the patient for 24
aspiration of pharyngeal secretions from blind hours and anticipation of passage in the stomach,
upper pouch. wait for the pt to defecate and dissect the stool for
 Continuous esophageal suctioning has to be done to the foreign bodies
minimize aspiration from the upper blind pouch
 Surgical ligation of TEF and end to end anastomosis
o If the gap between the ends is >3 to 4 cm, use CAUSTIC INGESTION
gastric jejunal or colonic segments to interposed
that gap  Ingestion of caustic agents: Alkali and Acidic agents
 70% of ingestion of caustic agents: Alkali
CONGENITAL ESOPHAGEAL WEBS AND STENOSIS  Alkali are the agents commonly used in bathroom
o Kids drink more of this, commonly seen and
accessible, tasteless (ingested amount is more)
ESOPHAGEAL STENOSIS  Acid 20% because acid is bitter in taste
 Usually seen in the middle and distal 3rd of the esophagus  Usually seen 5 years old and below
 It appears months after birth with gradual onset of  Males usually drinks more caustic agents than females
 Dysphagia
 Vomiting
ALKALI INGESTION
 Regurgitation
 Leads to development of liquefaction necrosis and the lesion is
described to be severe and deep
ESOPHAGEAL WEB
 Web is almost seen as a transparent membrane across the
ACID INGESTION
esophagus
 Leads to coagulation necrosis and development of Eschar
 Usually seen upon introduction of solid in the diet
which is supposed to be a protective layer
 SIGNS AND SYMPTOMS
 Intermittent dysphagia
EARLY SIGNS AND SYMPTOMS
 Regurgitation
 Vomiting
 Aspiration
 Drooling
 Refusal to drink
FOREIGN BODIES  Oral burns
 Dysphagia
 Dyspnea
FOREIGN BODIES  Stridor
 80% of foreign body are seen within 6 months to 3 years of age  Hematemesis
 Most common foreign body: coins and small toys  Abdominal plain
 Usually lodges in the level of Cricopharyngeus/ UES, Aorta arch
and LES/GEJ ESOPHAGITIS
 Atleast 30 % of patient who ingest foreign bodies are  End result of ingestion, followed by necrosis and then
asymptomatic perforation then stricture formation for about 20%
 USUAL MANIFESTATION  Development of the stricture is the most difficult / challenging
 Choking complication to treat
 Gagging
 Coughing UPPER ENDOSCOPY
 Excessive salivation  Most sufficient means of rapid identification of tissue damage
 Dysphagia among symptomatic patients
 Food refusal
 Vomiting TREATMENT
 Pain either in the neck/ throat/ sternal notch  Water or milk (emergency)
 Bring the patient to the hospital
THE FOLLOWING SHOULD NOT BE DONE DIAGNOSTICS
 Neutralization • ULTRASOUND
o Because the heat produce by chemical reaction will o Sensitivity of 95%
further damage the mucosa o Pyloric Thickness 3-4mm
 Do not induce emesis o Pyloric Length 15-19mm
 Gastric lavage o Pyloric Diameter 10-14mm
 Steroids are not given in 1st degree burns, but given in
more advance caustic Esophagitis to reduce the risk of  CONTRAST STUDIES
strictures o String sign/ elongated pyloric channel
o Pyloric canal stenosis
FOR STRICTURES
 Dilatation TREATMENT
 Surgical resection  Correction of fluid acid base and electrolyte losses
 Endoscopically placed silicone stents  Surgical referral: Ramstedt pyloromyotomy
o Operative moratlity 0-0.5%

DIFFERENTIAL DIAGNOSIS
 Hiatal hernia
 Gastroesophageal reflux disorder/ GERD
HYPERTROPHIC PYLORIC STENOSIS  Inborn errors of metabolism
 Adrenal insufficiency
HYPERTROPHIC PYLORIC STENOSIS  Sepsis
 Hypertrophy of the muscle of the pylorus o easily r/o: sepsis 1st manifestion: refusal to feed
 More common in whites, less in blacks rare in Asians
 Etiology: unknown
 Not present at birth

FEATURES
 Males, especially first-borns are affected more than
females (Males are affected than females more than 6
times)
 Genetic predisposition
 Incidence is increased in infants with type B + O blood  Plain film: Distended abdomen, rest of abdomen has little
groups amount of gas. Pyloric portion is obstructed, so only large
 Full term newborn bubble which is stomach is seen.
ASSOCIATED FEATURES:
 Syndromes like Apert syndrome
 Use of Erythromycin in neonates within 1st 2 weeks of life
 Mothers treated with Macrolides during pregnancy and
breastfeeding
 Abnormal muscles innervations
 Elevated serum prostaglandins
 Infant hypergastrinemia

CLINICAL MANIFESTATIONS
 Non-bilious vomiting, progressive, post feeding
 Seen after 3 weeks of age, can be seen 1 week of age to 5
months
 After vomiting, the infant is hungry and wants to feed
again
 Progressive loss of fluid, Hydrogen ion and Chloride
leading to Hypochloremic Metabolic Alkalosis
o HPS is a classic example HMA
 Dehydration and electrolyte losses
 Jaundice
 Abdominal Mass
 Visible gastric peristaltic wave
 Failure to thrive
 Malnutrition

COEXIST WITH OTHER CLINICAL DIAGNOSIS

 Ictero pyloric syndrome jaundice secondary to unconjugated
hyperbilirubinemia
 Hiatal hernia
 PUD
 Congential Nephrotic syndrome

DIAGNOSIS
 PHYSICAL EXAM FINDINGS:
 poorly nourished/ emaciated/ dehydrated patient
 Examination of abdomen: firm, movable, 2 cm
length mass, hard, best palpated from the left side
of the patient, located above and right of the
umbilicus mid epigastric region beneath or below the WAG PO MASYADO MARUPOK! ARAL WELL!
liver edge Photo credits: medical memes

 Presence of visible gastric peristaltic wave that

progresses across the abdomen best felt, post feeding