4yo Male Abd Pain x 1wk

8/9/2019 4yo Male Abd Pain x 1wk

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Problem RoundsMay 18, 2006

Almost 4 year old male

with abdominal pain for 1 week


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CC: abdominal pain x 1 week

HPI: Almost 4 year old Hispanic male was in usual state

of health until one week prior to admission when he

began to have abdominal pain. Patient began on 4/30/06

to complain of diffuse abdominal pain, greatest

immediately after eating. Patients abdomen also was

noted to swell and become taut. Mom would note relief

from pain after the patient had a bowel movement butcontinued swelling. No fever, vomiting, or diarrhea.

Patient was having regular bowel movements (1/day,

brown, soft, NB but decreased in caliber-pinky size). No

history of constipation. No change in diet. No other sickcontacts or other family members with similar symptoms.

No recent URI or sore throat symptoms.

instructed parents to bring patient to WCH PER due to

abnormalities in his labs.


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HPI Continued: Six days PTA, mom took patient to local clinic

as patient had an episode of vomiting (NB/NB, looked like food,

small amt) and continued abdominal pain. He had begun to have

decrease appetite and only wanted to lay down due to pain andabdominal swelling. New symptom was the onset of headache

with abdominal pain. At the clinic, a hemacue was checked as

well as urine and mom was told everything was normal and the

abdominal pain was due to gas. The patient continued to haveabdominal pain and swelling now drinking only milk and

orange juice with some fruit. Patient had another similar

episode of vomiting the following day and at noon on day of

admission.

Four days PTA, patients eyes became swollen and he was barely

able to open his eyes for 4 days, resolving one day PT coming to

the ER. No warmth or redness of the eyes, discharge or tearing,

and no itchiness.


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HPI Continued: On day of admission, mom brought

patient to Outside Hospital due increased abdominal

pain, abdominal swelling and now swelling of BLE and R

cheek. Patient developed bilateral lower extremities

(describes as the top of his feet) swelling 2 days PTA and

had stopped walking at home- now spending the entire

day laying on the couch or bed. No redness, warmth or

color change associated with the swelling. On morning ofadmission mom states patient awoke with swelling of his

right cheek and that both cheeks look red. Swelling does

not appear to be painful to the patient but mom notes he

would intermittently touch his right cheek- puzzled.At Outside Hospital, mom states blood and urine were

obtained and then the ER physician instructed parents to

bring patient to WCH PER due to abnormalities in his

labs.


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Take a moment

to consider your differential diagnosis


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ROS:

General: no fevers, no night sweats, no chills, no observed

weight loss

Neuro: + headache with abdominal pain

CVS: no chest pain

Pulm: no SOB or WOB, + dry intermittent cough 1-2

days PTA

Abd: no diarrhea, normal BM 1/day, + vomiting x 3Renal/GU: no dysuria, hematuria, polyuria

Derm: no rash or bruising

PMD: a clinic, no regular PMD


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Birth Hx: FT, NSVD at Outside Hospital, +PNC, no

complications with pregnancy or labor. Spent one day in

the hospital, birth weight 9 lbs, 6 oz.

PMHx: none

PSurgHx: none

Hospitalizations: none

All: NKDA

Meds: Tylenol PRN headache/abdominal pain- giventwice

Diet: Well balance diet. Fast food once/3 weeks. + candy-

lollipops and chocolate.

24oz of milk per day, 16 oz juice, some water. No

vitamins


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FH: mom- 24, father 25, mom works at fast food

restaurant, father works as a plumber. There are two

children- patient 31/2 year old male and 2 year old sister.

No family history of asthma, DM, cancer, HTN, CAD,

MI/strokes, GI, kidney or rheumatologic disease

SH: Lives with parents in 2 bedroom house.

No pets, alcohol, tobacco, drugs, violence, guns.

Patient in preschool- no known illnesses/outbreaks,enjoys school, likes to sing his ABCs.

No sick contacts. No recent travel or foreign visitors, no

exotic foods.

DevHx: walk at 8 months, first words mama at 10

months. Bilingual, speech fully understandable. Dress

himself, rides a tricycle with helmet.


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Admission PE:

Temp 97.8F BP 93/61 HR 105 RR 20 Pain 0/10

Wt 22kg (>95th%) Ht- 109 cm (>95th%) BMI- 18.5 (>95th%)

Gen: well-developed, well-nourished male, smiling, cooperative, NAD

HEENT: NCAT, PERRL, EOM intact, sclera clear, no periorbital edema, TMclear bilateral, nares turbinates non-erythematous, + dried discharge, no

polyps, MMM, good dentition, no oral/mucosal lesions, OP clear, tonsils 2+ no

exudates, no erythema, neck supple, FROM, no palpable thyroid, + facial

symmetry, fullness to R lower cheek, redness to both cheeks, NT

Lymph: no LAD- cervical, posterior, axillary or inguinalCV: RRR, normal S1 and S2, no m/r/g

Pulm: CTA B/L, slightly decreased BS bilateral bases, dullness to percussion

BL bases, no w/r/r, no retractions

Abd: mildly distended, positive BS, NT, no visible fluid wave, no HSM, no

massesGU: Tanner 1 male, uncircumcised, testes down B/L, mild edema scrotum/fat

pad, NT

Ext: no c/c. No edema on B/L feet, no sacral edema, no other swelling of any

extremities. 2+ distal pulse. CR~ 2 seconds

Neuro: CN II-XII intact, strength 5/5, DTR 2+ bilaterally, normal gait

Skin: no petechiae/purpura, no ecchymoses, no rash, no jaundice or pallor


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ER course:

Arrived at 1316

Vitals: T- 97 (ax), BP 97/57, HR 119 RR 24

pain 0/10

Cc: abdominal pain x 1 week and mom notes increasing

abdominal girth

Was seen at OSH and referred with lab results:

albumin 1.3, radiology report of small ascites and BL smallpleural effusions, hemoconcentrated H/H, ua- trace protein

Abdominal girth measured: 65.4 cm


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ER PE:

Gen: asleep, arousable, smiling, in NAD

HEENT: NCAT, PERRL, EOM intact, no periorbital edema,

TM clear B/L, dried discharge noted on B/L nares, MMM, OP

clear, no exudates, neck supple, no LAD

Pulm: CTABL, decreased BS at bilateral bases, + dullness to

percussion at bases

CV: tachycardic, RR, no m/r/gAbd: soft, NT, slight distension, + hyperactive BS, no HSM

GU: Tanner I male, uncircumscribed, testes descended BL, slight

scrotal edema

Back: no deformities

Ext: no c/c/e, pulses 2+ cap refill


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ER Plan:

admission- fluid management

diagnosis-

abdominal pain

hypoalbuminemia

R/O nephrotic syndrome vs protein losing gastroenteropathy,

R/O spontaneous bacterial peritonitis

labs- CBC, TPN panel, PT/PTT, blood culture, C3/C4, urine dip,micro and culture, repeat CXR, KUB


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Admission Plan- spoke with Renal and GI Attendings

Neuro- monitor pain- abdominal, activity bed rest

CVS- HDS

Pulm- CXR, SORA, watch for S/S respiratory distress, O2 sat

Q4

FEN/GI- regular diet, no fluid restriction

Renal- strict I/O, maintain balance

ID- watch fever- SBP, f/u urine and blood culturesHeme- H/H hemoconcentrated- 3rd spacing

Labs:

total IgA, anti-endomysial IgA and anti-tranglutaminase IgA

upper GI w/contrast- increase gastric folds

CMV and h.pylori

Studies

CXR- reassess pleural effusions

KUB

Upper GI


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Take a moment



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Labs


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Labs Continued


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Labs Continued


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CXR: Expiratory film, Left pleural effusion,

interstitial prominence suggestive of interstitial edema


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KUB: nobg pattern


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Take a moment


U GI S


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Upper GI Scout

Film

U GI


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Upper GI

Continued

U GI


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Upper GI

Continued


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U GI


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Upper GI

Continued

U GI


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Upper GI

Continued


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Take a moment



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Hospital Course

5/9/06 HD#1

GI Consult: acute onset albumin with absence of proteinuria- most

likely protein losing enteropathy- infantile Menetriers disease(associated with CMV) Celiac less likely, onset of malrotation

possible.

UGI: thickened folds consistent with Menetriersdisease

Progress Note: appetite- jello, milk, UOP 1.5 cc/hr, started highprotein diet

5/10/06 HD#2

Progress Note: headache, + intermittent cough, PO- liquid, now

solids, nutrition teaching, started on zinc 1 mg/kg (due low alk phos),

UOP 1.2 cc/hr

Labs: alb- 1.6 (1.8)


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Hospital Course

5/11/06 HD#3

Progress Note: abd pain. FROC- abdominal girth and scrotum

size. Abdominal girth- 67 cm (65 cm) PE-2+ tibial edema, dullnessabdomen, distended, scrotal edema. Later oxygen sat 93-94%,

ordered CXR, started oxygen 0.5L- 98% sats. PE- crackles B/L.

Increased 1L then down 0.5L. Labs- alb- 1.5 (1.6)

5/12/06 HD#4GI Consult: PE ascites, scrotal edema, consider single trial albumin

(1gm/kg) and lasix (1 mg/kg). likely to only be transient benefit but

may be useful in improving mucosal function and subsequent

increase in protein absorption.

Progress Note: UOP 0.9 cc/hr, PE- distended, dullness, scrotal

edema, 1+ pitting edema sacral, continue oxygen, albumin/lasix

Resident On Call: abdominal girth- 70cm, comfortable, 96-98%

0.5L NC, pedal and scrotal edema

Labs: alb- 1.7 (1.5)


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Hospital Course

5/13/06 HD#5

Progress Note: UOP 4.2 cc/hr, decrease to 67 cm, frustrations

ID Consult: CMV positive, rec- gancicyclovir x 7days

Labs: alb- 2.0 (1.7)

5/14/06 HD#5

Progress Note: no pain/swelling, girth 65 cm, no scrotal edema, wean

to RA5/15/06 HD#6

Progress Note: appetite and activity, girth-66 cm, RA, cough, rales

on exam, UOP 3.4 cc/hr

Labs: alb- 2.2 (2.0)5/16/06 HD#7

Progress Note: Good enery, regular appetite, walking, girth 62 cm

Labs: alb- 2.4 (2.5)


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Menetriers Disease

Hyperplastic gastropathy is a rare condition characterized by

giant gastric folds associated with epithelial hyperplasia. Two

clinical syndromes have been identified: Mntriers disease anda variant of it referred to as hyperplastic, hypersecretory

gastropathy, and Zollinger-Ellison syndrome.

Mntriers disease is typically associated with protein-losing

gastropathy and with hypochlorhydria, whereas the hyperplastic,

hypersecretory variant is associated with increased or normalacid secretion and parietal and chief cell hyperplasia, with or

without excessive gastric protein loss.

Other more common conditions can also cause enlarged gastric

folds, including gastric neoplasm (lymphoma, carcinoma),granulomatous gastritides, gastric varices, infectious gastritis

(particularlyH. pyloriand CMV), and eosinophilicgastritis.

Resolution ofH. pylorihypertrophic lymphocytic gastritis with

antibiotics may result in reversal of excess protein loss.

Taken From Feldman: Sleisenger & Fordtran's Gastrointestinal and Liver Disease, 7th ed.


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Examples of Hyperplastic gastropathy with giant gastric folds

Mntriers disease

Zollinger-Ellison syndrome



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In one series, 31 patients with large gastric folds of

uncertain etiology underwent full-thickness gastric mucosal

biopsies. Six patients showed the features of Mntriers disease,

1 showed the features of hyperplastic, hypersecretorygastropathy, and 6 showed features of Zollinger-Ellison

syndrome.The remaining 18 (the majority) had peptic ulcer

disease. (Komorowski R, Caya J: Hyperplastic gastropathy clinicopathologic correlation. Am J Surg Pathol 15:577, 1991.)

The enlarged gastric folds in Mntriers disease are dueto foveolar cell hyperplasia, edema, and variable degrees of

inflammation. Patients may present with weight loss, epigastric

pain, vomiting, anorexia, dyspepsia, hematemesis, and positive

fecal occult blood tests. The mechanism responsible for the low

gastric acid secretion is unclear, but it could be related to

transforming growth factor- (TGF-) or its closely related

peptide, epidermal growth factor (EGF).



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Gastric resections from patients with Mntriers disease

typically show large polypoid gastric folds or large cerebriform

gastric folds with antral sparing.

Total gastrectomy specimen

in a patient with Mntriers disease

(right, body, with hyperplastic mucosa

and cerebriform rugal folds;

left, antrum, with relative sparing)



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In the absence of a gastrectomy, a full-thickness gastric mucosal

biopsy is required to adequately assess the gastric histology in

patients with hyperplastic gastropathy. The predominant

microscopic feature of Mntriers disease and hyperplastic,

hypersecretory gastropathy is foveolar hyperplasia with cystic

dilation.

The parietal and chief cells may be decreased and replaced by

mucous glands. Inflammation in hyperplastic gastropathies is

variable and may be absent.

Histology of

Mntriers disease

showing enlarged

folds with foveolar

hyperplasia, cysticallydilated glands, and

minimal gastritis



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Ideal treatment of hyperplastic gastropathy is unclear,

because the condition is rare and controlled trials are lacking.H.

pyloriinfection should be treated, if present, and the entire

syndrome may resolve. Symptoms may improve withantisecretory agents (histamine2 [H2 ] receptor antagonists,

anticholinergic agents, proton pump inhibitors), especially if the

patient has Zollinger-Ellison syndrome or normogastrinemic

hyperplastic, hypersecretory gastropathy. It has been suggestedthat H2 blockers and anticholinergics reduce gastric protein loss

by strengthening intercellular tight junctions. Some patients with

Mntriers disease have responded to corticosteroids,

octreotide, antifibrinolytic agents, or monoclonal antibody

against the EGF receptor. Partial or total gastric resection is

reserved for severe complications, such as refractory or

recurrent bleeding, obstruction, severe hypoproteinemia, or

cancer development.



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Eosinophilic gastroenteritis is a disease characterized by tissue

eosinophilia that can involve any layer or layers of the gut wall.

Kaijser is credited with the first description of eosinophilic gastroenteritis in

1937.

A definite diagnosis must fulfill the following criteria:

(1) the presence of GI symptoms

(2) eosinophilic infiltration of one or more areas of GI tract on biopsy

(3) absence of eosinophilic involvement of multiple organs outside GI tract

(4) absence of parasitic infestation.

Peripheral blood eosinophilia is absent in at least 20% of patients and should

not be considered a diagnostic criterion. Furthermore, food intolerance or

allergy is not required for the diagnosis, because many patients have no

objective evidence of these problems.

The disease is rare; although increasing numbers of cases have been reportedin the medical literature, the incidence is difficult to estimate, because some

patients are probably undiagnosed and surely unreported. Patients typically

present in the third through fifth decades of life, but the disease can affect any

age group. An equal gender distribution or a slight male preponderance has

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4yo Male Abd Pain x 1wk