Abdominal pain Flashcards

1
Q

Case
General Data:
Our patient is J.C., a 18yr /F from Makati who was brought to the
OPD due to abdominal pain.

History of Present Illness
The patient presented with a 6-hour history of moderate pain in
the right upper abdomen that began after eating dinner and
radiates through to her back. This pain gradually increased before
becoming constant over the last few hours. She has had previous
episodes of similar pain since 1 month ago for which she has not
sought medical advice. She was only self-medicated with
omeprazole 20mg/cap OD and Buscopan which afforded
temporary relief.

Ancillary History
Past Medical History: No previous hospitalizations or surgery, (-
)no history of asthma ,
Family Medical History: (-) Family history of bronchial asthma or
malignancy, (+) family history of sickle cell disease, (+) family
history of DM and hypertension
Birth and Maternal History: Born FT to an 28 year old primigravid,
with no fetomaternal complications.
Immunization history: given BCG x 1 dose, OPV x 3 doses,
Hepatitis B x 2 doses, DPT x 3 doses , measles x 1 dose c/o the
local health center. No other immunizations were given.
Nutritional History: breastfed for 5 months , non-picky eater
Developmental History: sits with support at 8 yr old, walks with
support and one-word sentences at 1 yr old
HEADSSS: 1st year college student with average scholastic
performance, lives with parents and 1 sibling, no extracurricular
activities and prefers to stay at home, likes to cook at home,
denies illicit drug use/ smoking/ previous heterosexual
relationship, drives own car with seatbelt, no suicidal ideations

PHYSICAL EXAMINATION
General Survey
Awake, not in cardiorespiratory distress
Anthropometrics
Weight =79 kgs, height =160 cm, BMI = 30
Vital signs
BP 120/90 HR 92 bpm RR 32 bpm T 36.5C O2 sats (room air) =
100%
Skin
No rash, no jaundice
Head and Neck
Pink conjunctivae, anicteric sclerae, (-) nasal congestion, (-)
cervical lymphadenopathies
Chest and Lungs
Equal chest expansion, (-) retractions, (-)rales, (-) wheezes
Cardiac
Adynamic precordium, distinct heart sounds, normal rate and
regular rhythm, no murmurs
Abdomen
Normoactive bowel sounds, (+) tenderness to palpation in the
right upper quadrant , (-) guarding or rebound tenderness, (-)
hepatomegaly, intact Traube’s space
Extremities
Full and equal pulses, (-) edema/cyanosis/clubbing, CRT less than
2 sec

LABORATORY RESULT:
CBC
WBC 4 x109/L
RBC 3.1x109/L
Hgb 110 g/L
Hct 0.38%
MCV 85fL
MCH 25 pg
Platelets 350x109/L
Neut% 0.7
Lymph% 0.3
Mono% 0.0
Eo% 0.0
Baso% 0.0

Serum amylase: normal
Serum lipase: normal
Urinalysis: normal
Stool exam with FOBT: no ova or parasite seen, negative FOBT
Plain Abdominal xray: normal, no ileus
HBT UTZ: Normal liver, distended GB with reflective echo lodged
in its head measuring 1.8cm, wall not thickened, biliary tree not
dilated

A
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2
Q

(1) What is your primary working impression?

A

Primary Working Impression
* Cholesterol cholelithiasis

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3
Q

Basis for Diagnosis

A

(1) History
* 18/F
* (+) symptoms worsen with meals
* RUQ pain with radiation to the back
* (+) sedentary lifestyle
* Not relieved by PPI or antacids
* No vomiting, nausea or febrile episodes
(2) Physical Examination
* Obese with BMI 30
* (+) tenderness to palpation in the right
upper quadrant
* (-) guarding or rebound tenderness
* No hepatomegaly
* No jaundice, no fever

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4
Q

What are your differential diagnosis for this case?

A
  1. Cholecystitis
    Rule in:
    -Abdominal pain RUQ
    rule out:
    -No fever
    -marked RUQ tenderness
    (Murphy’s sign)
    -leukocytosis. Some patients
    progress to sepsis if chronic
  2. Choledocholithiasis
    -abdominal pain RUQ
    Rule out: -Charcot’s triad of biliary
    pain, jaundice, and fever is absent
    -CBC usually shows
    leukocytosis
  3. Acute pancreatitis
    Rule in:
    - Persistent abdominal pain radiating to the back
    Rule out:
    -History includes nausea,
    vomiting, fever, respiratory distress
    -PE will show guarding,
    tenderness
    -With skin bruising (Cullen and Turner sign)
    elevated serum lipase and amylase
  4. Peptic ulcer
    -epigastric pain
    Rule out: -Worse on awakening or
    before meals
    -Relieved by antacids
  5. urolithiasis
    -abdominal pain
    Rule out:
    -Progressive, severe pain
    -Pain more common in flank to inguinal region
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5
Q

Less likely Dx

A

Less Likely DDX:
* Mittelshmerz
* constipation

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6
Q

(2) What is your plan of management for this patient?

A

a. Diagnostic Tests/Labs
* Clinical Diagnosis
* Gall bladder ultrasound
o Method of choice
* Plain abdominal radiograph- may reveal
opaque calculi, but radiolucent (cholesterol)
stones are not visualized
* Hepatobiliary scintigraphy - valuable
adjunct in that failure to visualize the
gallbladder provides evidence of
cholecystitis
* CBC – Normal
b. Management
b.1. Goals of Management:
Pharmacologic Management
* Pain control
* hydration
Non-pharmacologic management
* Surgical:
Laparoscopic cholecystectomy - routinely
performed in symptomatic infants and
children with cholelithiasis. Common bile
duct stones are unusual in children,
occurring in 2–6% of cases with
cholelithiasis, often in association with
obstructive jaundice and pancreatitis.
Operative cholangiography - should be done
at the time of surgery to detect
unsuspected common duct calculi
Endoscopic retrograde cholangiography
with extraction of common duct stones -
option before laparoscopic cholecystectomy
in older children and adolescents.
b.2. Anticipatory care
* Proper nutrition
* Adolescent vaccination
* Cardiometabolic risk for hypertension, DM

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7
Q

Common causes

A

0-2mos:
Serious –> NEC
Adhesions
Less serious– > Colic
Infant dyschezia

3-12mos:
serious–>Foreign body
Trauma
less serious–> Constipation
AGE
Viral illness
Dietary protein
allergy
UTI

1-5yo:
serious–>Appendicitis
FB
Intussusception
Trauma
less serious–>Constipation
AGE
Viral illness
Pharyngitis
UTI
PN

6-12yo:
serious–>Appendicitis
Adhesions
DKA
Trauma
IBD

less serious–> Constipation
AGE
Viral illness
Pharyngitis
UTI
PN

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8
Q

Differentials for RUQ pain

A

gastritis,PUD, cholecystitis, cholangitis, cholelithiasis, pneumonia, peritonitis

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9
Q

Differentials for epigastric pain

A

Hepatobiliary disorders
GERD, esophagitis, gastritis, PUD, pancreatitis

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10
Q

Differentials for LUQ pain

A

Gastrits, PUD, esophagitis, pneumonia, splenic infarction, hemorrhage, trauma

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11
Q

Differentials for periumbical pain

A

intussusception
appendicitis

peritonitis
intestinal parasitism
gastroenteritis

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12
Q

Differentials for RLQ

A

appendicitis
mesenteric adenitis
Meckel’s diverticulum
pyelonephritis, renal calculi
ureteropelvic junction
obstruction
ovarian torsion/cyst, abscess
PID

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13
Q

Differentials for hypogastric pain

A

cystitis
bladder anomalies
Sigmoid volvulus
PID

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14
Q

differentials for LLQ pain

A

pyelonephritis
renal calculi
Ureteropelvic junction obstruction
ovarian torsion cyst, abscess, PID

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15
Q

Most common cause of acute surgical condition in children

A

Appendicitis

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16
Q

Pathophysiology of appendicitis

A

Patho:
- Appendiceal luminal obstruction (secondary to
inspissated fecal material/LNE/parasites) –> inc
intraluminal P à inc bacterial proliferation, inc mucus
secretion, inc venous congestion, inc edema –>
ischemia of bowel wall –> gangrenous appendicitis –>
appendiceal perforation

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17
Q

Clinical manifestations of acute appendicitis

A

CM “PANT”
1. Pain, abdomen – usually 1st sx, vague, poorly localized,
colicky, periumbilical à after 12-24h, RLQ severe pain
exacerbated by movt
2. Anorexia – classic and consistent
3. Nausea, vomiting
4. T (fever) – LG
5. Malaise
6. Perforation – usually after 36-48h abdominal distention
7. Hyperactive à hypoactive BS
8. Localized abd tenderness – single most reliable finding
9. Dunphy signs – RLQ pain after coughing
10. Rovsing sign – referred rebound tenderness
11. Psoas sign – pain on active R thigh flexion/passive
extension of hip = retrocecal appendix
12. Obturator sign – abductor pain after internal rotation
of flexed thigh = pelvic appendicitis
13. Abdominal guarding
14. Rebound tenderness – red flag. Indication for surgical
consult. 50% Sn, 60% Sp
Mc Burney’s point – junction of lateral and middle 1/3 of line
joining ASIS and umbilicus

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18
Q

What are the diagnostics for acute appendicitis?

A

Dx
1. CBC – N/mildly elev with L shift (11-16K, PMN >7500,
elev WBC > 10K, 20K (perforated)
2. UA – few WBC, RBC, no bact. To r/o UTI
>5 wbc/hpf bacteriuria common after 48 hrs
3. Serum amyloid A protein
4. CT scan – gold standard; appendiceal diameter >6mm,periappendicial inflammation (fat streaking, phlegmon, fluid collection, extraluminal gas), appendiceal wall
thickness >1mm, adenopathy, abscess, non-filling of
appendiceal lumen, appendicolith
5. UTZ – appendiceal diameter >6cm, target sign with 5 concentric layers, distention/obstruction of lumen, high echogenicity surrounding the appendix, appendiceal wall thickness > 2mm, absence of appendiceal stasis, periappendiceal/ perivascular free fluid, appendicolith

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19
Q

Management of acute appendicitis

A

Mgt
1. Prompt appendectomy – within 23-24h
2. Abx: cefoxitin 80-100 mkd q6-8 IV – not perforated
If perforated: Piperacillin-Tazobactam 300-400 mkd IV q6/8
Ticarcillin/Clavulanate 200 mkd q6 IV
Ceftriaxone 50-75 mkd IV q12/24
Metronidazole 30 mkd IV/po q6
3. Non-operative treatment (NOT) – indicated for:
a. abdominal pain <48h
b. WBC <18,000/uL
c. normal CRP
d. No appendicolith on imaging
e. appendix diameter <1.1cm on imaging
f. not yet ruptured based on clinical findings
- in-px broad spectrum abx x 1-2d: Piperacillintazobactam,
ceftriaxone + metronidazole, ciprofloxacin
18-30 mkd q8 IV + metronidazole
Until there is resolution of sx and WBC is N
Followed by 7-10d of oral abx: co-amoxiclav 30-40 mkd q8-12, ciprofloxacin 20-40 mkd q12 + metronidazole 30 mkd q8
Complication
- MC: wound infection, intraabdominal abscess

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20
Q

Etiopathogenesis of intestinal obstruction

A

Etiopatho
- Accumulation of food, gas, and intestinal secretions proximal to the point of obstruction causes bowel distention
- Distention leads to dec intestinal absorption, inc fluid and electrolyte secretion, and isotonic intravascular depletion
- Intestinal contractions initially inc, then hypoactive BS persist
- Classified as:
o Intrinsic – atresia, stenosis, meconium ileus,
aganglionic megacolon
o Extrinsic – malrotation, constricting bands,
intra-abdominal hernias, duplications
- Atresia: complete obstruction of bowel lumen
- Stenosis: partial block of luminal contents

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21
Q

What are the clinical manifestations of intestinal obstruction?

A
  1. Classic – nausea and vomiting, abdominal distention, obstipation
  2. High obstruction – large volume, frequent, bilous emesis, intermittent pain in epigastrium or periumbilical area, relieved by vomiting
  3. Low obstruction – moderate/marked distention with emesis that is progressively feculent, diffuse pain over entire abdomen
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22
Q

Diagnostics for intestinal obstruction

A

Radiograph
*Essential xray views in intestinal obstruction:
1. Plain supine/upright/decubitus xrays
2. cross-table lateral view: distended bowel above the obstruction with fluid level and gas in the distended loops

*Abdominal xray findings in obstruction:
1. poor gas distribution or gasless
2. smooth bowel walls like sausage
3. preferential dilatation of the bowel proximal to the obstruction
4. many dilated air fluid levels in a given loop at the different heights (candy cane)
5. dilated loops in “stepladder” fashion

*Pneumoperitoneum may be seen in perforation (free air in the subphrenic area or over the liver in the left lateral decubitus position)
*ground-glass appearance in the RLQ with trapped air bubbles seen in meconium ileus

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23
Q

Management of intestinal obstruction

A

Mgt
1. Fluid resuscitation
2. NGT decompression
3. Cultures, abx
4. Surgery – for strangulation
5. Conservative measures for adhesions or strictures
6. Water soluble contrast enemas – for malrotation, meconium
ileus/plug, intussusception (dx and tx)

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24
Q

What is Intussusception?

A
  • Portion of alimentary tract is telescoped into an
    adjacent segment
  • MC cause of intestinal obstruction 3mos-6yo (some 5mos to 3yrs), M>F
  • MC abdominal emergency <2yo

Patho
- Untreated intussusception –> infarction –> perforation –>peritonitis –>death
- Upper portion of bowel (intussusceptum) invaginatesinto lower part (intussuscipiens) dragging itsmesentery along with it into the
enveloping loop
- Mesentery constricts and obstructs venous return
- Intussusceptum engorges leading to edema and
bleeding from the mucosa
- Idiopathic (90%), adenovirus
- Lead point: Meckel’s diverticulum, swollen peyer’s
patches, polyp
- Ileocolic (MC), cecocolic, ileoileal

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25
Q

What are the clinical manifestations?

A

CM
1. Usually preceded by hx of infection
2. Triad: pain, palpable sausage-shaped abdominal mass (RUQ),
bloody/currant jelly stool
3. Severe paroxysmal colicky pain with straining effort, recurs
at freq intervals
4. Comfortable and playing child in between paroxysms of
pain, becoming progressively lethargic
5. Child usually has straining efforts with legs and knees flexed
and loud crying
6. Vomiting (early phase), later becomes bilous vomiting
7. Lethargy
4. Sausage-shaped mass RUQ or epigastrium
5. If not reduced, a shock-like state, with fever and peritonitis
6. Currant jelly stool (60%)
7. DRE: bloody mucus

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26
Q

What are the diagnostics for Intussusception?

A
  1. Abdominal UTZ – screening 98-100% sn, 98% sp.
    - Doughnut or target lesion (transverse view)
    - Tubular mass (longitudinal view)
  2. Pneumatic or contrast enema – dx and tx.
    - Coiled spring sign: thin rim of barium trapped around the invaginating part within the intussuscipiens
  3. Plain abd XR: vague and nonspecific. A density in the area of intussusception
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27
Q

Management of Intussusception

A

Mgt:
1. Reduction of acute intussusceptions ASAP
2. Hydrostatic reduction after under fluoroscopy/UTZ (if no signs of shock, peritoneal irritation, or intestinal
perforation)
3. Pneumatic/air reduction
4. Surgical reduction – if with refractory shock, bowel necrosis or perforation, peritonitis, multiple
recurrences
5. 4-10% can have spontaneous reduction
6. Recurrence rate 10%, post reduction 2-5%, postresection 0%.

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28
Q

What is malrotation?

A

MALROTATION
- Incomplete rotation of the intestine during fetal
development which is completed by 3 mos AOG
- MC: failure of the cecum to move into the RLQ
- Majority present within the 1st YOL
Embryology:
- Early fetal life: midgut attach to yolk sac and loops
outward
- 10th week: bowel reenters abdomen, rotates counterclockwise
until cecum reaches RLQ
- Incomplete rotation:
o Cecum near RUQ
o Duodenum in front of mesenteric artery
o Extremely narrow mesenteric root
o Susceptible to volvulus
o Abnormal mesenteric attachments (Ladd
bands) –> partial obstruction

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29
Q

What are the clinical manifestations of malrotation?

A

CM
1. Sx of acute or chronic obstruction
2. Bilious vomiting – 60% neonates, 40% infants/children.
MC sx.
3. Gut ischemia – pain, tenderness, bloody emesis and stools due to volvulus. Surgical emergency.
4. Suspect in patients with vomiting and fussiness or
abdominal pain

30
Q

What are the diagnostics for malrotation?

A

Dx
1. Abdominal xray with barium contrast: obstruction;
Double-bubble sign
2. UTZ – malrotation
3. UGIS – gold standard.
- Bird’s beak appearance of duodenum as it encounters the volvulated loop
- Absent c-loop of duodenum
- Right-sided jejunum
- Follow-through/contrast enema: high-sided cecum
- Corkscrew sign: distal duodenum and proximal
jejunum do not cross the midline and instead take an inferior direction (loop twists on a small bowel
mesentery)

31
Q

Management of malrotation

A

Ladd’s procedure – surgery. For any px with a
significant rotational abN regardless of age

32
Q

What is volvulus?

A
  • Life-threatening.
  • Twisting of a loop of intestine around its mesenteric attachment site which may occur at various parts of the GIT
  • MC: sigmoid and cecum
  • Small bowels twist around the superior mesenteric
    artery leading to vascular compromise of the bowel
  • Longitudinal: gastrohepatic, gastrosplenic, gastrocolic
  • Transverse: gastrophrenic, retroperitoneal attachment of duodenum
  • Organo-axial volvulus – along the longitudinal axis
  • Mesentero-axial volvulus – along the transverse axis
  • Combined volvulus (both)
33
Q

Triad of volvulus

A

Triad “SIR”
a. Sudden onset of severe epigastric pain
b. Inability to pass a tube into the stomach
c. Retching with emesis

34
Q

What are the diagnostics for volvulus?

A

Dx
1. Abdominal XR – findings:
a. Dilated stomach
b. Inverted U sign (distended sigmoid colon)
c. Coffee bean sign – midline crease
corresponding to the mesenteric root in a
greatly distended sigmoid
2. UGIS – gold standard. Partial duodenal obstruction.
Dilation of the stomach and proximal duodenum with a small amount of distal bowel gas.

35
Q

Management of volvulus

A

Mgt
1. Derotation and decompression by barium enema or with rectal tube, sigmoidoscope, colonoscope if with no signs of bowel ischemia or perforation
2. Laparoscopic derotation or laparotomy + bowel
resection

36
Q

What is mesenteric adenitis?

A
  • Nonspecific, self-limiting inflammation of mesenteric LNs
  • Usually mis-dx as acute appendicitis
  • “stomach flu”
  • Viral infection à LN inflammation in the mesentery
    (thin tissue that attaches to SI to the back of the
    abdominal wall)
37
Q

Clinical manifestations of mesenteric adenitis

A

CM “PaNT”
1. RLQ pain
2. Nausea, vomiting
3. T (Fever, LG)
4. Malaise, weight loss
5. Usually preceded by stomach flu/infection

38
Q

Diagnostics of mesenteric adenitis

A

Dx
1. UTZ of RLQ with graded compression – most
appropriate for <14 yo with fever, leukocytosis, with
presentation of atypical appendicitis. LN clustering the RLQ. Nodal hyperemia on sonogram.
2. CT scan – cluster of >3 LN (each measuring >5mm) is detected in the RLQ mesentery
3. Cbc – leukocytosis
4. Ua – r/o UTI

39
Q

Management of mesenteric adenitis

A

Mgt
1. Ibuprofen, paracetamol – for pain
Self-limiting

40
Q

MC surgical procedure performed in pedia surg

A

CH 346: INCARCERATED INGUINAL HERNIA

Sx usually 1st 6mos-1 yo
- Greatest risk of strangulation and incarceration (30-40%) @ 1yo
- 60% R, 10% B

41
Q

What is the pathophysiology of incarcerated inguinal hernia?

A

Patho
- 99% congenital indirect inguinal hernia – patent
processus vaginalis
- Direct inguinal hernia – muscular defect or weakness in the floor of the inguinal canal medial to the epigastric vessels

42
Q

clinical manifestations of incarcerated inguinal hernia

A

CM
1. Inguinal bulge/mass – hallmark; smooth, firm, emerges through the external inguinal ring aggravated by irritability, inc intra-abdominal P (crying, straining, coughing)
2. Incarcerated = colicky abd pain, vomiting
- Non-reducible mass in inguinal canal/scrotum/labia
- May contain SI, appendix, omentum, colon, ovary, FT
3. Strangulated IH – tightly constricted passage through inguinal canal –> contents ischemic/gangrenous

43
Q

What are the diagnostics?

A

Dx
1. UTZ – As the probe is moved inferiorly, the deep
inferior epigastric vessels pass from medial to lateral and superficial to deep toward their origin at the external iliac vessels. Keeping the image centered on the inferior epigastric vessels, a surrounding soft tissue bulge gradually becomes apparent deep and lateral to the posterior aspect of the rectus abdominis. This is the superior aspect of the inguinal canal.
2. Diagnostic laparoscopy
3. CT/MRI – demonstrate extracoelomic location of the bowel, bladder or female reprod organs

44
Q

What is the management?

A
  1. Herniorrhaphy – ideally w/in 6-12 mos old.
45
Q

What is cholecystitis?

A

CH 366: GALL BLADDER DISEASES (CHOLECYSTITIS,
CHOLELITHIASIS)
CHOLECYSTITIS

  • Uncommon in children
  • Usually caused by infection

Etiology:
- Streptococci (groups A and B), Salmonella, Leptospira, Ascaris, Giardia lamblia
- E.coli, Bacteroides fragilis, Klebsiella, Enterococcus,
Pseudomonas

46
Q

What is the pathophysiology?

A

Patho
- Obstruction of biliary outflow tract by a stone/
stricture/ kinking of the cystic duct/ intussusception of a polyp, GB torsion, LNE, or inspissate bile –> malfunction of mechanics of GB emptying –>
inflammation of GB

47
Q

What are the clinical manifestations of cholecystitis?

A

CM
1. RUQ or epigastric pain
2. Nausea, vomiting
3. Fever
4. Jaundice
5. RUQ guarding and tenderness

48
Q

What are the diagnostics?

A

Dx
1. UTZ – enlarged, thick walled GB (>5mm), without
calculi, perocholecystic fluid, GB distention (>5cm),
sonographic Murphy sign
2. Elev alkaline phosphatase
3. Elev DB
4. CBC – PMN leukocytosis
5. Scintigraphy – nonvisualizing GB on HIDA scan

49
Q

Management of cholecystitis

A

Mgt
1. Bowel rest, IV hydration, correction of e’ abN,
analgesia, IV abx
2. Abx: Piperacillin-Tazobactam 300-400 mkd IV q6/8
Ampicillin/sulbactam 100-200 mkd IV q6
Meropenem 60 mkd q8 IV
Imipenem/cilastatin 60-100 mkd q6 IV – for severe lifethreatening
cases
3. Cholecystectomy – primary mode of tx

50
Q

Choledocholithiasis

A

CHOLELITHIASIS/ CHOLEDOCHOLITHIASIS
- Rare in children
- Predisposing factors: obesity, DM, PT, prolonged
fasting or rapid weight reduction, CF, hemolytic ds,
pregnancy, sepsis, cirrhosis
- >70% pigment-type, 15-20% cholesterol stones

51
Q

Pathophysiology of choledocholithiasis

A

Patho
- Bile is concentrated in the GB, it becomes
supersaturate then precipitate to form microscopic
crystals –> bile sludge –> crystals grow, aggregate, fuse to form microscopic stones (cholesterol/ calcium bilirubinate)
- Gallstone in the CBD = choledocholithiasis

52
Q

Clinical manifestations of choledocholithiasis?

A

CM
1. Recurrent abd pain, colicky, localized to RUQ – most
impt clinical fx
- pain may radiate to area below the R scapula
2. Intolerance for fatty foods
3. Fever

53
Q

What are the diagnostics?

A

Dx
1. UTZ – method of choice. Stones appear as echogenic foci in the GB that move freely with positional changes and cast an acoustic shadow.
2. Plain XR – may reveal opaque calculi, exclude other causes of abd pain (obstruction)
3. Hepatobiliary scintigraphy – highly accurate for cystic duct obstruction. Failure of HIDA to fill the GB, while flowing freely into the duodenum.
4. CBC – PMN leukocytosis if with cholecystitis
5. Elev LFT
6. Amylase, lipase – r/o pancreatitis
7. CT scan – more expensive, less sn than UTZ

54
Q

What is the management?

A

Mgt
1. Expectant management – if asx’c
2. Cholecystectomy – >2 cm gallstone, nonfunctional/
calcified GB
3. Operative cholangiography – to detect CBD calculi
4. Oral bile salt tx – ursodeoxycholic acid: for xray
negative cholesterol stones with N GB function
5. Extracorporeal shockwave lithotripsy – for noncalcified
cholesterol stones with N GB function

55
Q

most common pancreatic disorder in children

A

Acute pancreatitis

56
Q

What is the pathophysiology?

A

Patho
- Following an insult, trypsinogen is prematurely
activated to trypsin within the acinar cell, activating
either pancreatic proenzymes, leading to autodigestion
- Release of active proteases, hydrolases
- Inc release of cytokines and proinflamm mediators
- Common causes:
o Blunt abdominal injury
o Multisystemic disease (HUS, IBD)
o Biliary stones, microlithiasis
o Drugs (valproic acid, L-asparaginase, 6-
mercaptopurine, azathioprine)

57
Q

What are the clinical manifestations?

A

CM
1. Severe abdominal pain – epigastric/RUQ, steady
2. Child assuming antalgic position – hips, knees flexed,
sitting upright, lying on side
3. Distended abdomen
4. Persistent vomiting
5. Fever
6. Severe AP – life-threatening –> shock

58
Q

Diagnostics and management?

A

Dx
1. Serum TB, DB, IB – plot TB in Bhutani chart
2. Transcutaneous bilirubin – linearly correlated with serum levels, used for screening
3. Blood type, Rh status of mother and infant – mom O, non-O infant. Cord blood can be sent for routine BT of NB
4. (+)Direct Coombs test – detects Ab bound to RBC
surface
5. CBC and PBS – r/o anemia.
6. (+)Reticulocytosis – NV 0.5-2.5%
Mgt: as above

59
Q

What is RH incompatibility and give the pathophysiology

A

Patho
- Caused by transplacental passage of maternal Ab vs paternal RBC Ag of the infant à causing inc RBC
destruction
- Rh(-) woman + Rh(+) man conceive 1st Rh(+) child >
cells from Rh(+)fetus enter woman’s bloodstream
making her sensitized –> Rh Ab form vs Rh(+) blood
cells
- In the next pregnancy: maternal Ab attack fetal Rh(+) RBC
-The severity of RHI increases with successive
pregnancies

60
Q

What are the clinical manifestations of RH incompatibility?

A

CM
1. Mild anemia (15%) to severe
2. Hepatosplenomegaly
3. Hydrops fetalis – excessive abN fluid in >2 fetal
compartments (skin, lungs, heart, placenta,
peritoneum, AF)
4. CHF – edema, ascites
5. DIC – petechiae, purpura, dec plt
6. Jaundice at 1st DOL

61
Q

What are the diagnostics of RH incompatibility?

A

Dx
1. Antenatal Dx:
a. Maternal IgG titer @12-16wks, 28-32 wks,
36 wks – titer >1:16 is (+)
b. UTZ with doppler
2. Postnatal Dx: same as ABO incompatibility

62
Q

Management?

A

Mgt
1. DVET of group O Rh(-) leukoreduced and irradiated
FWB cross-matched vs. maternal serum
- Severe hemolysis: Cord blood Hgb <10mg/dL, DB
>5mg/dL
2. IVIG

63
Q

How do we prevent RH incompatibility?

A

Prevention
1. RhoGAM 300ug within 72h of delivery of Rh(+) infant then per subsequent pregnancy at 28-32 wks and at birth

64
Q

What is G6PD deficiency?

A
  • X-linked deficiency, spontaneous missense mutation
  • M>F, usually Greeks, southern Italian, Jews, Filipinos, S. Chinese, African American, Thais
  • MC inherited enzymatic disorder (1 in 61 children in PH)
65
Q

insert table of precipitants of hemolysis

A
66
Q

What is the pathophysiology?

A

Pathophysio
- Genetic defect in RBC Glucose-6-phosphate
dehydrogenase deficiency
o Lack of this enzyme causes hemolytic
anemia when exposed to oxidative stress
- G6PD enzyme important in pentose phosphate
pathway which provides reduced NADPH to keep
glutathione in reduced form as an antioxidant.
- Therefore, G6PD deficiency leads to oxidant stress to RBCs –> hemolysis

67
Q

Safe drugs in therapeutic doses

A
  • Pct, ASA, VitC, chloramphenicol, ciprofloxacin,
    diphenhydramine, isoniazid, phenytoin, quinidine, vit.K
68
Q

what are the clinical manifestations?

A

CM
1. Asymptomatic unless triggered by precipitants
2. Acute hemolytic anemia (AHA) – MC, classic Sx
- Triad of hemolytic anemia:
o Pallor/anemia
o Jaundice
o splenomegaly
3. Jaundice –> kernicterus
4. Episodic hemolytic anemia (chronic nonspherocytic)
- Hemolysis 24-48h after ingestion of oxidative
substance
5. Hemoglobinuria

69
Q

Diagnostics

A

Dx:
1. CBC – anemia, dec Hct, mod elev WBC, granulocyte
predominance, N/inc/dec plt
2. NBS – for screening
3. G6PD assay – confirmatory test
4. PBS – Heinz bodies, anisopoikilocytosis, bite cells,
normocytic, normochromic
5. Reticulocyte count elev

70
Q

Management of G6PD deficiency

A

Mgt
1. Avoidance of precipitants
2. Acute hemolytic episode
a. ID and remove the culprit agent
b. Hydration and Blood transfusion for severe
anemia
o Indications for BT:
§ <7g/dL – ASAP
§ <9g/dL with hemoglobinuria
§ >9g/dl but persistent hemoglobinuria

71
Q
A