A CASE OF GASTROPARESIS IN AN ADOLESCENT Laura Wozniak, MD K30 Monthly Meeting

Laura Wozniak, MD
K30 Monthly Meeting
September 21, 2010
A CASE OF GASTROPARESIS
IN AN ADOLESCENT
Chief Complaint
 12-year-old female with a 3-week history of
persistent nausea and vomiting
 Came to UCLA for a second opinion
HPI
 Developed acute onset of abdominal pain
 Initially diagnosed as “altitude sickness”
 Soon after developed “flu” symptoms
 Malaise, sore throat
 Treated with supportive care
 Nausea/vomiting persisted
 Prompted two admissions
Characteristics of Patient’s Emesis
 Nonbloody, nonbilious (usually clear)
 Approximately 7 times per 24-hour period
 Follows every meal and/or drink
 Also happens sporadically throughout the day
 Frequently wakes her up overnight
Associated Symptoms
 Intermittent epigastric pain
 Deep, “gnawing” right flank pain
 Different quality than previously
 Intermittent bifrontal headache
 10-15 pound weight loss
 Denied intentional vomiting/purging
 Review of systems otherwise negative
Pertinent History
 PMH: Congenital hip dysplasia
 PSH: None
 Family History: Non-contributory
 Social History:
 Intact family, A/B student
 Denied sex/illicit drugs
Physical Exam
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Weight 48kg (50-75%, down from 52kg)
T 97.9, HR 100, BP 117/66, RR 16
Gen: WD/WH adolescent, comfortable in bed
HEENT: Good dentition
Chest: RRR, no murmurs, CTAB
Abd: Normal BS, soft, ND, no HSM, no masses
 Epigastric tenderness with light palpation
 Diffuse tenderness with deep palpation (no
rebound/guarding)
 GU: Tanner 3, normal perianal exam, guaiac neg
 Neuro: CN 2-12 intact, 5/5 strength x4, 2+ DTRs,
normal heel-to-shin, normal gait
Summary
 12-year-old female with a 3-week history of
persistent nausea and vomiting
 Preceded by “flu” symptoms 1-month prior
 Progressively worsening, losing weight
 Exam notable for epigastric/nonspecific
tenderness
Differential Diagnosis
 Partial obstruction 2/2 adhesions
 Inflammatory bowel disease
 Hepatitis/Pancreatitis
 Pregnancy
 Ileus
 Dysmotility/gastroparesis
 Functional abdominal pain
 Hydronephrosis
 Increased ICP/central process
Labs
 BMP: 136/3.9/101/22/16/0.8
 Glucose: 76
 CBC: 6/13/40/249 (62%N, 31%L, 5%M)
 AST/ALT: 16/10
 T/D bili: 0.7/0.1
 Alk phos: 245
 Amylase: 11
 Lipase: 5
Labs
 ESR: 2
 CRP: <0.5
 Lactate: 5
 Hgb A1C: 5.3%
 Upreg: negative
 UA: 1.006, 1+ketones, o/w negative
Previous Work-Up
 Head CT and Brain MRI: unremarkable
 Neuro and Ophtho consults: unremarkable
 Upper GI: normal
 CT abdomen/pelvis: bilateral ovarian cysts,
otherwise negative
 EGD: mild erythema of distal esophagus, mild
gastritis, negative for H pylori
 Cortisol, ammonia, TFTs normal
Differential Diagnosis
 Partial obstruction 2/2 adhesions
 Inflammatory bowel disease
 Hepatitis/Pancreatitis
 Pregnancy
 Ileus
 Dysmotility/gastroparesis
 Functional abdominal pain
 Hydronephrosis
 Increased ICP/central process
Presumed Post-Viral Gastroparesis
 Admitted to Peds GI Service
 Bolused, started on MIVFs
 Zofran 4mg IV Q8 ATC
 Protonix 40mg po Qday
 Scheduled for gastric emptying study
Does this patient have gastroparesis?
How do we diagnose and treat her?
Stomach Anatomy
 Functionally divided into two regions
 Proximal: cardia, fundus and upper third of the
body
 Distal: rest of the body, antrum and pylorus
 Gastric motility results from
 Neuronal and hormonal controls
 Integration of inhibitory and stimulatory signals
Gastroparesis
 Impaired emptying of gastric contents into the
duodenum in the absence of a mechanical
obstruction
 May be due to neuropathic or myopathic
processes
 May be related to immaturity, congenital
abnormalities, or acquired conditions
Gastroparesis: Clinical Manifestations
 Nausea
 Vomiting
 Bloating
 Early satiety
 Abdominal pain
 82% of patients are women
 Mean age for onset is 34 years
Etiologies of Gastroparesis
 Medications: opioids, anticholingergics
 Metabolic: hypokalemia, acidosis, hypothyroidism
 Additional etiologies in pediatric patients: prematurity,
eosinophilic gastroenteropathy, CP, muscular dystrophy
Postviral Gastroparesis
 Associated with multiple viral agents
 Varicella zoster
 Herpes simplex
 Infectious mononucleosis (EBV or CMV)
 Acute gastroenteritis (Norwalk or Rotavirus)
 May also develop after nonspecific viral
symptoms (fever, myalgias, headaches)
Kebede et al, Dig Dis Sci, 1987.
Sigurdsson et al, J Ped, 1997.
Vassalo et al, Gastroenterology, 1991.
Postviral Gastroparesis
 Overall seems to have a better prognosis than
other forms of gastroparesis
 Case series of 11 children: All had symptom
resolution within 6-24 mos (mean 12.2 mos)
 Dysmotility thought to be due to damage to
the enteric neurons
 Inflammatory
 Immune-mediated
Kebede et al, Dig Dis Sci, 1987.
Sigurdsson et al, J Ped, 1997.
Vassalo et al, Gastroenterology, 1991.
Gastroparesis: Diagnosis
 Radioscintography or gastric emptying scan is
the gold standard
 Imaging or EGD usually required to exclude
mechanical obstruction or ulcer disease
 Note: Barium delays gastric emptying
 Antroduodenal motility or electrogastrography
is indicated if there is no identifiable
mechanism or disease
Gastric Emptying Scan
colloid is bound to a solid food
 Serial images are acquired with the patient in the
supine position for up to 4 hours
 Results are usually expressed as the gastric half
emptying time (T ½)

99mTc-sulfur
Dr. Martin Auerbach, UCLA
Electrogastrography
 Records gastric myoelectrical activity using cutaneous
electrodes placed over the stomach
 Measures slow wave activity
 Dominant frequency is 3cycles/minute
 Increases in amplitude with ingestions
Chang, J Gastroenterology and Hepatology, 2005.
Electrogastrography: Gastroparesis
 Dysrhythmias lead to incooordination
between gastric body and antrum
 Tachygastria (4-9cycles/minute)
 Bradygastria (<2cycles/minute)
 Impairment of the amplitude response
Gastroparesis: Management
 Nutritional
 Medical
 Prokinetics
 Antiemetics
 Endoscopic
 Injection of botulinum toxin
 Surgical
Dietary Recommendations
 Goal: Maintain adequate oral intake of fluids
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and nutrients
Rely on measures that either promote or do
not retard gastric emptying
Small, frequent low-fat meals consisting of
complex carbohydrates (starch based foods)
Reduction of solid food intake
Avoid indigestible fiber, gasiferous foods,
carbonated beverages
Pharmacologic Agents: Prokinetics
Hasler, Gastroenterol Clin N Am, 2007.
Pharmacologic Agents: Antiemetics
Hasler, Gastroenterol Clin N Am, 2007.
Success Rate of Conservative Therapy
 Improvement is seen in the overwhelming
majority of patients
 Up to 5% of patients are refractory, requiring
more aggressive management
Endoscopic Botulinum Injections
 Potent inhibitor of neuromuscular transmission
 Injection into the pylorus transiently reverses
pylorospasm and promotes pyloric relaxation
 Studies are inconsistent
 Improved response seen in:
 Females
 Younger patients (<50 years)
 Nondiabetic/nonpostsurgical etiology
Coleski, Dig Dis Sci, 2009.
Surgical Treatments
 Tube placement
 Venting gastrostomies may provide symptom relief
 Feeding jejunostomies may reduce hospitalizations
 Performed only as a last resort:
 Pyloroplasty (effective in diabetic gastroparesis)
 Partial gastrectomy (effective in postsurgical
gastroparesis)
 Reconstruction of a gastroenteric anastamosis
(rarely effective)
Hasler, Gastroenterol Clin N Am, 2007.
Gastric Electrical Stimulation
 High frequency gastric electrical stimulation
 Essentially paces the stomach
 Aims to reset a regular slow-wave rhythm
 Improves symptoms and nutritional status
Familoni, IEEE Trans Biomed Eng 2008.
Familoni, IEEE Trans Biomed Eng 2008.
Abell et al, Gastroenterology, 2003.
Back to the patient…
 Gastric emptying study showed borderline
delayed gastric emptying
 46% of tracer emptied at 90 minutes
Treatment Course
 Started on Erythromycin 240mg po TID
 Able to tolerate po’s
 Juice
 Yogurt
 Cheeseburger!
 Discharged home (to Montana)
Thanks for your attention!