Jamilah Alsaidan, Msc. The three consecutive phases of emesis are: Emesis NauseaRetchingVomiting.
Bilious Emesis 03.02.2012
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Transcript of Bilious Emesis 03.02.2012
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Morning ReportDevin Horton, R3
March 2, 2012
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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