A CASE OF GASTROPARESIS IN AN ADOLESCENT Laura Wozniak, MD K30 Monthly Meeting September 21, 2010
Welcome message from author
This document is posted to help you gain knowledge. Please leave a comment to let me know what you think about it! Share it to your friends and learn new things together.
Transcript
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!
Related Documents
