1

SURGERY 3B Non-bilious (i.e. vomiting of milk)

PEDIATRIC SURGERY o Medical vomiting
Dr. Leandro L. Resurreccion III o Non-surgical
o Most common cause of medical or non-surgical
Pediatric Surgery
vomiting:
5 years General Surgery
Gastroenteritis
2-3 years Pediatric Surgery
Gastroesophageal Reflux
4 Training Program Centers in the Philippines
o Long list of differentials. At the bottom the list is:
3-4 Pediatric Surgeons per year are produced Pyloric stenosis
60 Pediatric Surgeons currently in the country not very common
50% practicing in the province Most (99%) are non-surgical causes of
vomiting
ABDOMINAL PAIN
May not be always surgical
PHYSICAL EXAMINATION
o 80% of the referrals are non-surgical Very difficult especially a crying child
Try to come up with an accurate diagnosis to convince o Reassure not only the patient, but also the
the parents to consent the procedure parents
Common things are more common Optimize the environment:
o Think first of the more common rather than the o Heat up the room, establish good relationship
rarest condition It is difficult to examine in a very cold
or very hot room
TWO CONCERNS
o Do not rush
1. AS A SURGEON
The patient should feel at ease with
o Give an accurate diagnosis to the parents
you.
Attentive ear
o If necessary, examine the patient on mothers
A keen look
lap
Thorough Physical Examination
Imaging modalities INSPECTION
To support impression Observe the patient
2. AS PARENTS o Bouncy child = normal
o Is the operation necessary? o Wheeling = sign of obstruction
o Is it timely? o Quiet child, lying still = maybe peritonitis
Do we need to do it now? Observe the abdomen
Can we postpone it? o There are causes of obstruction without
o Will it correct the ailment which was indicated? abdominal distention
o If my child will be operated, will it cure the o Very globular = pneumoperitoneum, bowel
problem? perforation
o Distended abdomen with a scar = post-
Two Most Common Causes of Acute Abdominal Pain in
Children: operative adhesion
Acute Appendicitis
PALPATION
Intussusception
Touch the unaffected areas first
APPROACH TO PATIENT Ask to point with 1 finger where the pain is worst
1. FROM SYMPTOM TO DIAGNOSIS Put your warm hands gently on the childs abdomen
Whats Happening Here? Palpate with flat, full hands
2. EVALUATION Feel the temperature, guarding, rigidity, mass, etc.
The Balancing Act Observe facial expression
3. PREPARATION
Dress Me Slowly. Im in a Hurry Napoleon DIRECT RECTAL EXAMINATION
4. NOTE SELECTED CASES FOR ACUTE ABDOMEN As medical students, master this technique
Common Things Are More Common Explain the procedure
o In older children
VOMITING o Reassure
First Question: What is the color of vomitus? Well-lubricate the finger
Dictum: Any greenish vomiting should be considered o Wear gloves
abnormal unless proven otherwise o Warm lubricant
o High chance that it is pathologic Ball of finger should touch the anus first; rub gently
o High chance that it is surgical

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Tell the patient to relax by straining continuously, while INCIDENCE
slowly inserting the finger then slowly bend Majority are idiopathic
Done in all patients with abdominal pain Between 5-9 months of life
o 90% are within this age group
INTUSSUSCEPTION >50% occur in 1 y/o
One of the more common causes of abdominal pain in 10-20% occur in >2 y/o
children
M: F ratio is 3:2
Telescoping of one segment of the GIT into another
segment PATHOGENESIS
o Usually smaller to larger caliber segment Marked hypertrophy of the lymphoid tissue
Ileum to colon o When you open up old patients with
intussusception, you will see several enlarged
CAUSES
mesenteric lymph nodes which may have
IDIOPATHIC OR PRIMARY been the cause of obstruction.
o Unknown exact cause
Occur in the wake of Upper Respiratory Tract Infections
o Most common in children (18-25%)
(URTI) or Acute Gastric Enteritis (AGE)
o Age-specific cause of obstruction
o Viral Infection
NON-IDIOPATHIC OR SECONDARY o Incidence is thick before winter season or few
o Tumor, Polyps, Meckels Diverticulum, or months before the rainy season
Abnormal Lymph Node o Many patients with idiopathic intussusception
have previous history of hyperperistalsis (AGE)
ANATOMIC TYPES
which was caused by a virus
A study was done correlating
intussusception and this virus-related
disease which revealed no correlation;
thus, we cannot say that all
intussusceptions are caused by a
virus.
Adenovirus/rotavirus also implicated
Different calibre of lumens
o Cannot explain other causes of intussusception
2-12% with anatomic lead points

CLINICAL MANIFESTATIONS
Sudden episodic crampy abdominal pain in a
previously well baby MOST IMPORTANT
o Sudden onset of abdominal pain manifested as
The intussusceptum insinuates into the intussuscepien screaming, drawing up of legs, pallor, sweating
Intussusceptum = the one that goes in and vomiting (non-bilious)
Intussuscepien = the outside the outer layer o Sweating and Pallor because of pain
o Reflex type of vomiting due to pulling and
ILEOCOLIC dragging of intestines
o most common (prototype) o After several episodes of vomiting, the patient
o Ileum insinuates into the colon involving the becomes dehydrated, fatigue and lethargic
appendix as well Well and hungry in between
ILEOILEAL May progress to bilious vomiting
o Second most common Currant Jelly Stools
o may progress to ileocolic o Bloody mucoid stools
COLOCOLIC with NO fecal material
o Sloughing of mucosa of
JEJUNOJEJUNAL the intussusceptions
o Seen in post-operative patients o Not actually bright red.
Initial surgery is not related to Its more of mucoid.
intussusception (e.g. surgery d/t acute The color is more of reddish or brownish.
appendicitis, epidemic problem) Dance sign
o Rare A sausage-shaped mass can be palpated at the
upper abdomen with an empty right lower quadrant
More advanced stage of the disease process
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DIAGNOSTIC MODALITY Disease process is >48 hours
History and Physical Exam Very low chance of success
o Clinical Manifestations rate
o Rectal Examination Febrile
You can feel the head of the The cause is outside
intussusception dehydration.
If bright red in color = necrotic Peritoneal signs
Late sign of intussusception Tenderness (direct and
Abdominal X-ray rebound)
o Non-specific Frank intestinal obstruction
Barium or Air Enema Massive abdominal
o Coiled spring sign distention
Produced by insinuation of barium o Done under double set-up
between the intussusceptum and Prepare the patient as if youre going
intussuscepien to operate on that particular patient
o Both Diagnostic or Therapeutic It is not without complications.
o Done under pressure
You may perforate the bowel.
Principle: You try to push the
intussusceptum out of the
intussuscepien
o Success rate:
Early cases: 75-80%
If you diagnose early, 80% is
non-surgical.
Late cases: 40-50%
Delayed referral
Majority of patients are
Ultrasound
o Pseudokidney or Bean-shaped Sign diagnosed previously with
Intussusception is still active Amoebiasis because of the
blood in the stool
Operative Management
o Manual reduction
o Resection or End-to-End Anastomosis (EEA)
o Appendectomy
90% of pediatric surgeons remove the
appendix in young children
o Tire or Doughnut Sign To avoid diagnostic dilemma
Intussusception is recently 10% do not remove it
spontaneously reduced May still be part of the
immune system of the patient
If already outside the age-specific causes of obstruction,
then it is already SECONDARY
o Peutz-Jeghers Syndrome
Pigmentations, hamarthromas
Small chance to become malignant
Multiple polyps in the small intenstine
Dont attempt to remove all the polyps.
You can only resect the segment that
CT Scan
causes the problem at that moment.
TREATMENT You may end up with small bowel if
Resuscitation you resect these segments.
o To correct dehydration and metabolic o Polyp or Meckels diverticulum
derangement Resect if seen
Non-operative management: Barium or Air reduction Recurrence rate: 3-5%
o All patients with suspected intussusception o Whether surgical or non-surgical
should undergo Barium/Air reduction EXCEPT:

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CONGENITAL DIAPHRAGMATIC HERNIA Three conditions that are persistently present in Bochdalek
Bochdalek hernia Hernia:
o most common type 1. Malrotation
o sometimes synonymous with CDH Abnormal rotation and fixation in the GIT
Morgagni hernia because all the intestines will preferentially go
to the thoracic cavity
BOCHDALEK HERNIA 2. Pulmonary hypoplasia
INCIDENCE & EPIDEMIOLOGY
1:5000 live births
Etiology is unknown
o Theories:
Maldevelopment of the diaphragm
Causes herniation of the
intestines into the thoracic
cavity Control Lung Hypoplasia,
The space occupying lesion bronchi-rarification

prevents the lung to The degree of hypoplasia dictates the survival

developing into pulmonary of CDH-Bochdalek Hernia
hypoplasia The more severe the hypoplasia, the lesser
More accepted theory chance of survival of the patient
Primary pulmonary problem The main airways (bronchi) are not the only
The lung did not develop ones affected, but also the number of
preventing the diaphragm to respiratory units (no. of alveoli decreases)
develop
Associated with Trisomy 18, 21, 23 and other anomalies
o Occurs during First Trimester of Pregnancy
where all organs are developing
o If there is a defect in one developing organ, then
there is a higher chance that will involve the
other organ.
o Cardiac problems and chromosomal anomalies
30% are stillborn The terminal respiratory unit of the lung.
o Reflects the severity of the problem Normally, there is vascular, muscular, partially
80% are on the left side muscular and non-muscular layer. The problem
in Bochdalek Hernia is there is hypertrophy of
the muscles around the respiratory arterioles.
Very thick hypertrophic muscles are very
sensitive to metabolic acidosis. If theres slight
metabolic acidosis or hypoplasia, then there is
spasm of these muscles, preventing blood from
passing through the arteriole. Even if the patient
is breathing, blood cannot pass so there will be
no oxygenation. Then, it becomes a cycle.

If you have the defect, the intestines will herniate through the
defect. Almost all of the viscera will go to the thoracic cavity and
this will serve as a space occupying lesion pushing the
mediastinum towards inside and impinging the developing lung
causing pulmonary hypoplasia. Since there is deviation of the
mediastinum towards the opposite side, it will also impinge the
opposite developing lung to some degree. You may have bilateral
hypoplasia, but more on the affected side.

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3. Patent Ductus Arteriosus (PDA) TREATMENT
During early period, beneficial for the patient Prenatal Care
If you have Bochdalek Hernia, the fetal o Screening
circulation is maintained which will help the o Counseling
survival of the patient o Fetal Intervention
Came about because of the very poor
DIAGNOSIS results of patients
Prenatal Ultrasound If diagnosed prenatally, they repair the
Amniocentesis defect laparoscopically
o Decrease Sphingomyelin-Lecithin ratio The survival of patients was similar to
o Chromosomal analysis the ordinary treatment.
o Reduced MS-AFP Abandoned
Preoperative Care
CLINICAL PRESENTATION o Resuscitation
Respiratory Distress o Control of Pulmonary Hypertension
o 90% will present with respiratory distress Not easy
o 5-10% will have delayed presentation Control aggressively
(Honeymoon Period) Postoperative Care
Present with respiratory distress later Ventilation Strategies
on o Aggressive
Better prognosis o Gentilation
Scaphoid Abdomen Gentle ventilation
o All the intestines will be in the thoracic cavity Tolerate tachypnea
Asymmetrical funnel chest Better than the classic type of
o Only one side of the thoracic cavity is involved ventilation
o Confirmed by: o High frequency oscillatory ventilation (HFOV)
Chest X-ray o Extracorporeal Membrane Oxygenation
Contrast X-ray (ECMO)
Heart-lung machine that will take over
the circulatory system of the patient
Not all centers have this machine

This is an X-ray of a patient with a suspected Bochdalek Hernia

and you can see that all the intestines are in the thoracic cavity.
When we say Bochdalek Hernia, the defect is
POSTEROLATERAL (posterior and lateral). Even on X-rays, you
can determine the location of the defect.

Once the patient is stable enough for surgery. The easiest part of
the perioperative management is doing SURGERY

Here, an AP view. You can see the intestines going to the chest
from the lateral side and on lateral view, you can see the intestines
coming from the abdomen through a posterior defect. So, it is a
POSTEROLATERAL defect. You also note that the abdomen that
it is devoid of air. The mediastinum is also shifted compressing the
developing lung.

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Sometimes the defect is so big that we need to put on a MESH to Congenital
bridge the gap. o Non-development of the phrenic nerve
Acquired
o Injury to the phrenic nerve during a difficult
delivery
Paradoxical motion of the diaphragm
The manifestations depend on the severity.
o If the bulging is severe, the signs and symptoms
will be similar to Bochdalek Hernia
Treatment is surgery
o Plication
Plicate the weak part of the diaphragm

PROGNOSIS
Lung-to-Head Ratio (LHR)
o The volume of the lung compared to the head
of the patient
Stomach
o if the stomach will herniate to the chest, the
prognosis will be poorer
Liver
o if the liver will herniate to the chest, the ESOPHAGEAL ATRESIA/TRACHEOESOPHAGEAL FISTULA
prognosis will be poorer EMBRYOLOGY
Poorly understood
MORGAGNI HERNIA o Complex process
Retrosternal Defect
Airway & esophagus has a common progenitor
o ANTERIOR
22 days ventral diverticulum
Usually towards the Right side
34-36 days complete separation into 2 tubes
2-6% of congenital diaphragmatic defect
Discovered incidentally INCIDENCE/ETIOLOGY
o Discovered by X-ray 1:3000-4,500 live births
Treatment is surgical Slight male preponderance
o Elective Exact cause is not known
Milder form
Associated anomalies are common
o All patients are expected to survive
VACTERL
Incidence is ~20%
Vertebral: 20%
Anal: 12%
Cardiac: 20%
Renal: 16%
Limb:10%

ANATOMIC CLASSIFCATION

AP view: You see the defect almost in the midline, left or right but
more to the right. Lateral view: You see the herniation of the
bowels posterior to the sternum (retrosternal). So, its anterior
diaphragmatic defect. Sometimes the left lobe of the liver
herniates.
A. Proximal & distal (Isolated) esophageal atresia
EVENTRATION OF THE DIAPHRAGM B. Esophageal atresia with tracheoesophageal fistula
Weakness of one of the hemi-diaphragm between proximal segment of esophagus and trachea.
o Bulging of the diaphragm

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C. Esophageal atresia with tracheoesophageal fistula Anastomotic Stricture
between distal esophagus and trachea. Recurrent TEF
Most common (prototype) o recanalization
D. Esophageal atresia with fistula between both proximal Tracheomalacia
and distal ends of esophagus and trachea.
E. Tracheoesophageal fistula without esophageal atresia INTESTINAL OBSTRUCTION/VOMITING IN CHILDREN
(H-type fistula)
MALROTATION
CLINICAL MANIFESTATION Herniation
Excessive salivation/secretion Rotation
o Most common presentation Retraction
Choking or coughing on feeding Fixation
Abdominal distention
Chemical pneumonia
Tachypnea & hypoxia

DIAGNOSIS
History & Physical Examination
Inability to pass OGT
o For confirmation
Chest X-ray
o You will see coiled OGT
Contrast Studies

TREATMENT INCIDENCE
Preoperative resuscitation 1:6000
o Correct aspiration pneumonia before doing
Autopsy Studies: 0.5-1% of the general population
surgery o Asymptomatic > Symptomatic
Surgery 50-75%: 1st month of life
o Started as staged-procedure into one-stage
90%: 1st year
procedure
o Takes 7 hours Incidence of Associad Anomalies (by percent) with
Postoperative Care Malrotation
Intestinal atersia 5-26%
For Esophageal atresia w/ distal tracheoesophageal atresia: Imperforate anus 0-9%
Surgery Caradiac anomalies 7-13%
o Staged Procedure Duodenal web 1-2%
Gastrostomy Meckels diverticulum 1-4%
Ligation of Fistula Hernia 0-7%
Repair Trisomy 21 3-10%
o Primary repair Rare: esophageal atresia, biliary atresia, mesenteric cyst,
craniocynostosis, Hirschsprungs disease, intestinal duplication
For Isolated Esophageal atresia:
CLINICAL PRESENTATION
Primary repair not possible
o End-to-end anastomosis is not possible Related to duodenal obstruction &/or midgut volvulus
Bilious vomiting usual symptom
Esophageal replacement
o Irritability
Esophageal lengthening
Because of the Volvulus
For Tracheoesophageal fistula without esophageal atresia GI bleeding
Ligation of TEF through the neck o Abdominal wall erythema
Difficult to diagnose Late sign of Volvulus
o History & Physical Examination o Because of the ischemia in the midgut
o Cineradiography Upper abdominal fullness
o Paucity of bowel gas
COMPLICATIONS Less amount of gas in the abdoment
Anastomotic Leak o Newborn patient vomiting green without
Dysphagia abdominal distention, only upper abdominal
GER fullness, consider first malrotation

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In older children:
o Chronic abdominal pain
postprandial vomiting
o GER
o Weight loss
o Failure to thrive
o Sometimes misdiagnosed as:
Chronic pancreatitis
Celiac syndrome
DIAGNOSIS
Prenatal Ultrasound
o See sonographic signs
Polyhydramnios, distended
duodenum
History & Physical Examination
Plain Abdominal X-ray
o To confirm suspicion
Upper GI Series (UGIS)
o Corkscrew appearance
o Birds beak appearance
Barium Enema
Ultrasonography/CT Scan
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INTESTINAL ATRESIA
Atresia complete obstruction; Stenosis - narrowing
Jejuno-ileal segment
Localized late intrauterine vascular insult
Ischemic necrosis of sterile bowel
o Postnatal intestine ischemia, gangrene,
necrosis, perforation (d/t presence of bacteria)
o
o Antenatal intestine ischemia, gangrene,
necrosis, no perforation
Resorption of the affected segment
o Ischemic bowel is still sterile (no bloating, no
such as gas formation, no perforation)
stomach or Usually an isolated anomaly
o d/t timing of the pathophysiology
TYPES

Type I
TREATMENT o no break in the continuity of the segments
Preoperative Resuscitation o presence of intraluminal web or diaphragm
o You only have 6-12 hours to untwist the midgut causing the obstruction
Surgery
o Ladds Procedure
o Appendectomy
To avoid diagnostic dilemma
Radiographic Malrotation
o Asymptomatic
o Talk to the parents or guardian that there is a Type II
risk of midgut volvulus o Break in the continuity of the segments
o Both segments are connected by fibrous cord

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Type IIIIa
o Separation with mesenteric defect

History & Physical Examination

Plain Abdominal X-ray
Type IIIb o To confirm your impression
o Mesenteric defect is bigger, more extensive o In malrotation, there is paucity of gas. In
and the distal segment is coiled around a intestinal atresia, you see multiple bowels that
retrograde artery or branch of the ileo-colic are distended. You see multiple gases in the
artery abdomen
o Apple peel or inverted Christmas tree
defect

Barium Enema
o Not required
o If requested, you will see an unused colon or
Type IV microcolon
o Multiple atresias

Clinical significance of classification: Management is the same but

differs in the prognosis. The lower type of atresia, the better the
TREATMENT
result. The higher the type, the poorer the result. The higher
the incidence of short bowel syndrome, the poorer the result Prenatal counseling
of atresias. o Financial aspect
Advise the parents that their unborn
CLINICAL MANIFESTATIONS child will be operated immediately after
Polyhydramnios birth.
Bilious Vomiting o Social aspect
Abdominal Distention Separate the mom from the newborn
o Site of obstruction is more distal than baby
malrotation Preoperative Resuscitation
o No abdominal distention in malrotation o Hydrate the patient well
Jaundice o Correct all electrolyte imbalance because of the
o Because of sepsis recurrent vomiting and dehydration
No meconium o Give antibiotics since the patient is septic.
o Majority of the patients will not pass meconium, Surgery
but some will do. It is not the usual meconium o Resection/End-to-End Anastomosis (EEA)
that is seen. It is more pale, small in amount, Postoperative Care
sometimes called Pigeon stools.

DIAGNOSIS
Prenatal Ultrasound
o Multiple distended bowel loops with thickened
interserosal spaces

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o Very important in high type atresias. You might TYPES
need to support them parenterally for a long
time after surgery.

The challenge is how to anastomose a very bulbous segment to a

very minute segment. The bulbous segment is usually resected. It
is hard because the muscles there are already stretched beyond
their contracting capacity. So, if you anatomose those ends Type C = there is an intraluminal web; fenestrated duodenal
together, they might not function together. You do some atresia
maneuvers more or less to approximate the calibers. CLINICAL MANIFESTATION
Polyhydramnios
Bilious vomiting
o 10%: Non-bilious
Upper abdominal fullness
Sepsis
45%: Prematures
25%: GI Anomalies
Another challenge is in multiple atresias. The segments are
already shortened. Dont discard small atretic segments. If you do DIAGNOSIS
multiple anastomoses. It is prone to anastomotic leak leak or Prenatal Ultrasound
strictures later on. What you usually do is you insert a silastic tube
intraluminally instead of doing anastomosis. After putting it, just
put 1 or 2 sutures and wait for 10-12 days then these packed
segments will auto-anastomose.

History & Physical Examination

Plain Abdominal X-ray
o Double Bubble Sign

The survival rate for Type 1 or Type 2 atresias is around 90%.

Whereas in the higher type of atresias, it depends on the length of
the bowel. Sometimes, you need to support them nutritionally
parenterally for a long time because of the short bowel segment.
In our locality, many of the patients will have some form of liver Upper GI Series (UGIS)
damage because parenteral nutrition somehow damages the liver.
o Especially if you have fenestrated type of
duodenal atresia
DUODENAL ATRESIA
EMBRYOLOGY
TREATMENT
3rd week = solid phase
Counseling
8th-10th week = coalescent of vacuoles
o Financial and social aspects
ETIOLOGY o Discuss the presence of associated anomalies
Failure of recanalization Preoperative Resuscitation
o 50% with associated anomalies Surgery
o 40% have Trisomy 21 o You cannot cut the distal segment because it
35%: Prematurity contains all the vital structures
25%: Other GI anomalies Postoperative Care
Results
PATHOLOGY o Generally, good
Majority are periampullary Complications
o Similar to malrotation o Anastomotic leak
Dilated stomach and duodenum o POA
With vomiting in utero o Functional obstruction
History of polyhydramnios Because you cannot excise the
distended obstruction, it may not
function properly

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Tapering Duodenoplasty
11
TRIAD
o Projectile non-bilious vomiting at 2-8 wol
o Visible gastric peristaltic wave
o Palpable pyloric olive

PYLORIC STENOSIS
INCIDENCE DIAGNOSIS
More common in Caucasians History & Physical Examination
o 1-3:1000 live births o Do not diagnose unless the mass is felt
4:1 male to female ratio Plain X-ray
Maternal History 19% boys, 7% girls Upper GI Series (UGIS)
Paternal History 5% boys, 2.5% girls o String Sign or Mushroom Sign
7% with associated anomalies

ETIOLOGY/PATHOLOGY
Congenital or Acquired?
Gastric hyperacidity -> muscle spasm & hypertrophy
Abnormal pyloric innervation
Abnormal motility due to
decrease pacemaker cells
Marked muscle hypertrophy Ultrasound
-> partial/complete gastric o Target/Donut Sign
outlet obstruction o UTZ Diagnostic Criteria
Theory: Combination of 4 mm thickness
Congenital and Acquired 16 mm length
o They say that Caucasians have a pyloric
stenosis gene. If they are exposed to a TREATMENT
particular cows milk protein, there will be some Preoperative Resuscitation
type of allergic reaction. o Correct the electrolyte imbalance before
surgery
CONGENITAL VS ACQUIRED o Cl: 100, Serum CO2: <30, K: 4, HCO2: <26
Genetic Evidence Surgery
o Race o Pyloromyotomy
o Male Fredet-Ramstedt Procedure
o 1st born Postoperative Care
o ABO types Non-operative Management
Environmental Factors
o Method of feedings SERUM ELECTROLYTES
More common in breastfed patients Na K Cl HCO3
o Seasonal Gastric 60 5-15 120 0
o Exposure to Erythromycin Juice
o Transpyloric feedings Intestinal 140 15-20 155 40
Juice
CLINICAL MANIFESTATION Diarrhea 40 40 40 40
Projectile, non-bilious vomiting at 2-8 weeks of life Sweat 70 15 60 0
o Vomitus can be coffee-ground in appearance
Parental Fluids
but is never green. Fluids Cal/L Na K Cl HCO3
o Age group is very important D5W 170 0 0 0
Always hungry D10W 340 0 0 0
Hypochloremic Hypokalemic Alkalosis NSS 0 154 0 154
o Visible gastric peristaltic wave NSS 0 77 0 77
o Palpable Pyloric Tumor D5 170 34 0 34
NSS
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LRS 0 130 4 77 28 o Sibling of index patients; female = 360x, male =
Albumin 100 100- <120 130x
160 o The longer the disease, the higher the rate of
D50.3 170 51 0 51 familial incidence
NSS o Deletion of 10q11.2 & q21.2
D51MB 170 24 29 22 23
specific
NSS 0 154 0 154
NSS 0 77 0 77 o 13q22 with recessive susceptibility locus
Gastric 0 60 5-15 120 Error in endothelin B receptor gene
Juice (EDNRB) exon 4
LRS 0 130 4 77 28 o RET proto-oncogene, a transmembrane
D5 170 34 0 34 receptor
NSS Universal
Not specific
Pyloric stenosis entails different kind of IV fluids. Ideal fluid for Control of normal cell growth and
pyloric stenosis is half normal saline solution (0.45). But the only
development, enteric nervous system
available solution is 0.3.
MEN 2A & 2B
The treatment for pyloric stenosis is half the normal sodium,
plus potassium when the patient is already urinating. INCIDENCE
1:2000 live births, 70-80% are males
HIRSCHSPRUNGS DISEASE Familial predisposition
EMBRYOLOGY 25% with associated anomalies in familial cases
Neuroenteric cells migrate distally along the course of the Most are isolated in non-familial cases
vagus nerve Observed in all races but is less common in blacks
5th week AOG -> esophagus
7th week AOG -> midgut CLINICAL PRESENTATION
12th week AOG -> complete migration Most present with intestinal obstruction or
o Transmural migration constipation
Failure to pass meconium within the 1st 24h of life
Severity of constipation vary between patients
Explosive discharge of fluid stools & air on DRE
Enterocolitis
Complete obstruction at birth
Delayed passage of meconium followed by repeated
obstruction
Mild constipation followed by acute obstruction
Mild symptoms followed by enterocolitis
Mild chronic constipation

Mid-Transverse to Anus -> 4 weeks DIAGNOSIS

Diagnosis by elimination
PATHOPHYSIOLOGY
History & Physical Examination
Absence of ganglion cells
Radiography
o Meissners Plexus, Auerbachs Plexus, Henle
o Plain Abdominal X-ray
Loss of intrinsic enteric inhibitory nerves Non-specific
Short segment in 80-85% Will show distended intestinal loops
o Most common with some fecal retention
o Affects the recto-sigmoid area o Barium Enema
o Beyond the sigmoid is called long segment Will show the transition
Hirschsprungs zone
Total colonic aganglionosis Area between the ganglionic
o Involves the entire colon and aganglionic segment
o Incidence is 5 to 8% Funnel-shaped area
Will tell you what level of
ETIOLOGY
Hirschsprungs you are dealing
Exact etiology not known
with
Genetic Cause
Anorectal Manometry
o May affect more than one sibling

SURGERY 3B: PEDIATRIC SURGERY: DR. RESURRECCION (2016) PAUZKI

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Rectal Biopsy
o Only definitive diagnostic
o Not all chronically constipated patients are
subjected to biopsy

TREATMENT
Non-surgical
o NGT
o Colonic washout
Surgical
o 3 Stage procedure
o 2 Stage procedure
o 1 Stage (Primary) procedure
Open
Laparoscopic
Incisionless
o Pullthrough Procedure
Swenson, Soave, Scott-Boley,
Duhamel, Transanal (Incisionless)
Remove the aganglionic segment and
replace with a ganglionic segment
o Transanal Pullthrough (TAPT)
History & Physical Examination
Barium Enema
Rectal Biopsy
Admitted day before the surgery
Clear liquid diet (ORS)
Laxative / colonic washouts
IV antibiotics 1hour prior to surgery
Final colonic washout in the OR
Feed 6 hours postop
Shift IV antibiotics to oral
d/c on the 2nd-3rd POD
f/u 1 week postop
minimally invasive surgery
less physiological stress
technically easy & safe mobilization of
distal colon
no postoperative ileus
less postoperative pain
adhesion formation
Shorter hospital stay
Good cosmetic result

#MPP #JAPC

SURGERY 3B: PEDIATRIC SURGERY: DR. RESURRECCION (2016) PAUZKI