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A CASE OF GASTROPARESIS IN AN ADOLESCENT Laura Wozniak, MD K30 Monthly Meeting September 21, 2010

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A CASE OF GASTROPARESISIN AN ADOLESCENT

Laura Wozniak, MDK30 Monthly MeetingSeptember 21, 2010

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

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

99mTc-sulfur 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)

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 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!