bilious emesis 03.02.2012

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Morning ReportDevin Horton, R3

March 2, 2012

8/2/2019 Bilious Emesis 03.02.2012


HPI CC: Bilious emesis

13 yo female presents with bilious emesis and abdominaldistension.

Three days ago she began having stomach pain and had 5episodes of BRIGHT RED EMESIS!!

(however she reveals that she had just eaten a red slusheeand velvet cake).

Volume was about the size of a cereal bowl.

The following day she had bilious emesis x 1, andcontinued to have stomach pain.

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The day before admission she had 3 episodes ofbilious emesis.

On the day of admission she woke up crying because

of stomach pain and had another episode of biliousemesis.

She describes the pain as “pressure-like”, constant,and "all over".

She had a BM the day before that was not as soft astooth paste but not marbles and would not not furtherelaborate.

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In the ED In the ED she was tachycardia at 138 and was given

20cc/kg NS. Labs and imaging were done.

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PMH:

Anxiety disorder NOS with question of OCD

Multiple UTIs including: Klebsiela, enterococcus faecalis,citrobacter, VRE

Sigmoid volvulus at 6 mo

Surg: Right hemicolectomy with ileotransversecolostomy at 6 months.

Meds: none

Vacc: UTD

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NKDA

Fam: DM in grandfather, ovarian and uterine cancer ingrandmother. No family history of GI, congenital, or

childhood diseases.

Soc: 8th grader, likes school. Lives at home withparents and siblings. 3 cats and 1 dog. No recenttravel. No reptile or otherwise amphibious pets.

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Differential ??????????

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Isn’t this fun???

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Exam VS: AF, 110, 116/76, 16, 98% RA

Gen: No distress whatsoever, Has iPad in one hand and cellphone in other. Anderson in place. Pale.

HEENT: No lymphadenopathy, no OP exudate, MMM

CV: tachy, Regular rythym, no murmurs

Pulm: CTAB

ABD: Distended, no bowel sounds, tympanic.

Ex: no clubbing.

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Labs CBC: wbc: 9.5, hg 15.7, hct 45.3, plts 287, 5 bands, 71

neut, 16 lymph, 6 mono

CMP: na 142, k 3.3, cl 101, co2 26, bun 22, cr 0.76, ca9.6, prot 8.2, alb 4.9, tb 0.4, alt/ast 16/31

CRP: neg

UA: trace LE, neg nit, neg ketones>30wbc, 3+ bact, 0epi

Urine Micro: >100,000 klebsiella

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Imaging KUB: Stool. Chronically dilated segments containing a few

small air-fluid levels

KUB: Gaseous distention of upper abdominal bowel loopswith a paucity of bowel gas in the lower abdomen.

CT abd: MARKED GASTRIC DISTENTION.

MARKED SMALL BOWEL DISTENTION WITHOUTABNORMAL WALL THICKENING OR FREE FLUID. NOPNEUMATOSIS.

THESE FINDINGS ARE SUGGESTIVE OFSMALL BOWELOBSTRUCTION. NO TRANSITION POINT IS IDENTIFIED

NOT SUGGESTIVE OF SIGMOID VOLVULUS

NO FREE AIR IS IDENTIFIED.

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Contrast enema:

No obstructive lesion is seen.

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What I left out PMH: Chronic pseudoobstruction requiring multiple

hospitalizations. Chronic constipation.

Presumed bacterial overgrowth

History of TPN requirement

Meds: gent, nystatin, erythromycin, flagyl, daily golytely.

In the ED: 2L removed by anderson tube

This was two admissions.

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The Second Brain Communicates through the parasympathetic (vagus)

and sympathetic (prevertebral ganglia)

GI nervous system can act autonomously.

Has efferent neurons, afferent neurons, interneurons,capable of carrying reflexes and acting as integratingcenter in absence of CNS input.

90% of the bodies serotonin, 50% bodies DA”

Gangions Auerbach’s and Meissner’s Plexuses

Mechanical, chemical, bacteria, enzymes.

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Pseudobstruction Spectrum from Slow transit constipation to

Hirschsprungs, post viral gastroperesis, ogilvie’s

Chronic intestinal pseudo-obstruction: syndrome that suggests mechanical bowel obstruction in the

absence of an anatomic lesion

Segments of affected bowel appear dilated on radiography.

Problem with: 1. extrinsic nervous system (brain/spinalcord.) 2. Enteric NS, 3. Smooth muscle.

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Pathophysiology Myopathic vs. Neuropathic vs. Both

Neuropathic: DM, amyloidosis, paraneoplastic, neuronaldysplasia

Mutation in neural crest derived cells: Sox 10 gene:hypoganglionosis, aganglionosis (hirschsprung),Hyperganglionosis of inhibitory.

Reduced denity/abnormal interstitial cells of cajal(pacemaker cells)-slow transitconstipation/pseudoobstrucion

Gene mutation: Waardenbarg-shah

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Presents

Distension – 75 percent

Abdominal pain – 58 percent

Nausea – 49 percent Constipation – 48 percent

Heartburn/regurgitation – 46 percent

Fullness – 44 percent

Epigastric pain/burning – 34 percent Early satiety – 37 percent

Vomiting – 36 percent

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DX/TX Decreased motility -> distension -> stasis -> bacterial overgrowth -

> distension.

Imaging to r/o anatomical. Suspect: transit test or manometry

TX: Nutritional support

Antibiotics

Prokinetics

G tube: venting

59 pts for 4.6 years. 2.96 useless surgeries/pt before recognition.Need to recognize.

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THANKS Dr. Jackson

Netters

Uptodate Gastroenterology, 2000

Clinical Gastroenterology Hepat, 2005

bilious emesis 03.02.2012

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