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       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     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!