Tag Archives: cyclic vomiting syndrome

Understanding Idiopathic Nausea

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A recent article describes a retrospective chart review of 45 children with chronic nausea and compares them to 49 children with chronic abdominal pain (J Pediatr 2014; 164: 1104-09).

Key findings:

  • While onset of symptoms was similar, the chronic nausea cohort presented at a median age of 15 years compared with 12 years for the pain cohort.
  • Comorbid conditions like anxiety, dizziness and fatigue were common in chronic nausea cohort.
  • Family history of migraines was note in 71% of nausea cohort compared with 22% in pain cohort
  • Extensive laboratory and imaging was much more frequent in nausea cohort.  With nausea cohort, 78% had abdominal ultrasound, 60% an upper GI, 58% brain imaging with either a CT scan or MRI, 38% gastric emptying, 31% abdominal CT or MRI, and 24% had HIDA.
  • Almost all endoscopies were normal (98% of chronic nausea group and 100% of pain cohort)
  • For nausea cohort treatment, tricyclic antidepressants showed a good response (=at least 50% symptom improvement) in 44% with a mean maximal dose of 50 mg. In contrast, with proton pump inhibitors, only 22% had some improvement (=at least 25% symptom improvement).  Similarly, ondansetron showed some improvement in 50% –though none had a “good response.”
  • Twelve patients (27%) of the nausea cohort met diagnostic criteria for cyclic vomiting syndrome (CVS) (with interepisode nausea) and another nine (20%) developed chronic nausea after ‘outgrowing’ CVS.
  • Postural (orthostatic) tachycardia syndrome (POTS) was noted in 16 of 45 in the nausea cohort based on an orthostatic screen (heart rate ≥30 beats/min during positional changes from 10 minutes in supine position to standing.

As the authors note, their study, conducted between 2006-2012, had numerous limitations, particularly the relative small size and retrospective nature.  In addition, the physician expertise in nausea/vomiting at Children’s Hospital of Wisconsin predisposes to a selection bias.

Take-home message: Nausea can be a severe symptom but is often difficult to manage. Extensive workup has a low yield in absence of other complaints or physical exam findings.

An AGA technical review on nausea and vomiting was published in 2001: GASTROENTEROLOGY 2001;120:263–286 

Related blog posts:

Disclaimer: These blog posts are for educational purposes only. Specific dosing of medications/diets (along with potential adverse effects) should be confirmed by prescribing physician/nutritionist.  This content is not a substitute for medical advice, diagnosis or treatment provided by a qualified healthcare provider. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a condition.

 

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NASPGHAN Postgraduate Course 2012

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Postgraduate course syllabus: naspghn.informz.net/

So far I’ve looked at the first few talks from the postgraduate course syllabus (see link above), including CVS slides by B Li.  Several good pointers are given.  For example, for abortive therapy, he recommends use of Zofran 0.3 mg/kg/dose.  Page 17 of course book details preventative measures.  Also, with regard to amitriptyline, he recommends starting at 0.3 mg/kg and titrating as needed up to 1-1.5 mg/kg/day.  Mitochondrial-type support often helpful as well (eg. CoQ10 10 mg/kg/day divided BID).

At the end of this lecture are a couple of questions –see how you do:

  1. Which NASPGHAN Consensus diagnostic criteria for CVS is the most specific?
    1. positive family history of migraine
    2. vomiting at least 4 times/hour at peak
    3. well between episodes of vomiting
    4. each attack resembles the others
    5. associated pallor and listlessness
  2. All of the potential mechanisms below have been implicated in CVS except:
    1. HPA axis activation
    2. migraine vascular changes
    3. autonomic nervous dysfunction
    4. mitochondrial dysfunction
    5. serotonin receptor polymorphisms

page22image7408 page22image7568

3. NASPGHAN recommended evaluation of a child with episodic vomiting:

  1. a. electrolytes, BUN, Cr
  1. electrolytes, BUN, Cr & UGI
  2. electrolytes, BUN, Cr, UGI & ultrasound
  3. electrolytes, BUN, Cr, UGI, ultrasound & endoscopy
  4. electrolytes, BUN, Cr, UGI, ultrasound, endoscopy & MRI
  1. Which is the best initial approach to the 11 year old child with CVS who has failed multiple medications and missed 4 weeks of school?
    1. consult psychology for anxiety and stressors
    2. redo all laboratory and radiographic testing
    3. consider induced sleep in the PICU
    4. hospitalize and observe teenager in episode
    5. add a second prophylactic medication
  2. Which statement best applies to the preventative approach to CVS?
    1. step‐wise increases in medicines are rarely required
    2. life style modifications are not recommended
    3. after anti‐migraine agents, anticonvulsants are used
    4. toddlers should receive propranolol first line
    5. topirimate does not cause cognitive dysfunction

    Answers: 1. d;2.e;3.b;4.a;5.c

Foreign body talk: if object >2cm or longer than 5 cm, may have difficulty passing.

Also a link to the meeting notes and abstracts:
naspghan.org/wmspage.cfm?parm1=723 …

NASPGHAN POSTGRADUATE COURSE Table of Contents

MODULE A: WHAT GOES IN, MUST COME OUT: CLINICAL GASTROINTESTINAL ISSUES

FROM PROPRANOLOL TO INDUCING COMA: CARING FOR A CHILD WITH INTRACTABLE CYCLIC VOMITING SYNDROME (CVS)………………………13 INCONTINENCE WITHOUT FECAL IMPACTION    …………………………….23 ELIMINATION DIETS: RISKS AND BENEFITS……………………………………..37

MODULE B: LIVER BEYOND VIRUS, METABOLIC, STORAGE, TUMORS

METABOLIC LIVER DISEASE: WORKING THROUGH THE MAZE ……………….51 UPDATE ON ALPHA‐1‐ANTITRYPSIN DEFICIENCY         ……………………………61 THERE IS A LIVER MASS ON THE ULTRASOUND: WHERE DO YOU GO FROM HERE? ….75

MODULE C: THE INFLAMED INTESTINE

GI INFLAMMATION, IMMUNE FUNCTION AND IBD          ………………………………87 MY STOMACH IS BUGGING ME!: THE MICROBIOME IN IRRITABLE BOWEL SYNDROME ……………………………………………………………………………………………101                                                                                                THE SORE BOTTOM: PERIANAL INFLAMMATORY BOWEL DISEASE         ……111 RESCUE ME FROM MY IBD: UPDATES ON INFLAMMATORY BOWEL DISEASE THERAPY ………………………………………………………………………………………………125

MODULE D: IMAGING AND ACCESSING THE TUBES

LOOKING DEEPLY INTO THE NOT SO SMALL INTESTINE ……………………………..137 PUTTING TUBES WITHIN TUBES: ENTERAL THERAPEUTIC ACCESS    ………….151 IMAGING THE PANCREATO‐BILIARY TREE                …………………………………….169 UPDATE ON CRITICAL FOREIGN BODY INGESTIONS  ………………………………….189

MODULE E: WHEN ALL ELSE FAILS: LIVER, INTESTINE AND POUCH

THE KID IS ON THE LIST: KEEPING COMPLICATIONS AT BAY FOR THE
NON‐TRANSPLANT HEPATOLOGIST ……………………………………………………201 TRICKS OF THE TRADE FOR INTESTINAL FAILURE ……………………………….213 GASTROINTESTINAL AND LIVER COMPLICATIONS OF BONE MARROW TRANSPLANT                                                                    …………………………225 POUCH DYSFUNCTION AND SURVEILLANCE: WHAT ARE MY OPTIONS? .235

Diet or drugs for cyclic vomiting syndrome

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Dietary modifications are frequently recommended for migraines.  Given the overlapping features between migraines and cyclic vomiting syndrome (CVS), dietary treatments for CVS have aimed at eliminating trigger foods.  Investigators from the UK describe a single center cohort of 21 children (2-16 years) were placed on a low-amine diet with instruction from a dietician (JPGN 2012; 54: 698-99).  16 (76%) of the children had a strong family history of migraines.  The diet was implemented for a ‘minimum of 6 to 8 weeks.’ 13 had a complete resolution of vomiting and 18 (86%) had at least a partial response.

Specific foods that were avoided included cheese, chocolate, citrus fruits, pork, peas, broad beans, shellfish, yeast extract, beef extract, gravies, caffeine, and alcohol.

This small study does not prove that a low-amine diet is effective.  In fact, most of the information on a low-amine diet is derived from alternative medicine sources (eg .  Low Amine Diet | www.integrative-medicine.com.au).  Nevertheless, it is likely that a subset of patients will benefit from avoidance of trigger foods.  How to identify potential culprits is unclear.

NASPGHAN Guidelines for CVS (JPGN 2008; 47: 379):

  • Diagnostic criteria: (90% will have idiopathic CVS)

1. at least 5 attacks or 3 over 6-month interval
2. episodic, last 1 hour to 10 days & at least a week apart
3. stereotypical pattern for individual patient
4. vomiting >4 times/hr for at least 1 hour
5. healthy in between & no other attributable problem

  • PROPHYLACTIC Measures:

Avoid triggers:
fasting, excessive excitement (eg. downplay big events), sleep deprivation
foods that trigger symptoms (?chocolate, cheese, caffeine, MSG)
excessive fatigue

Assure adequate carbohydrates
-provide sugar-containing drinks & extra snacks before exertion & bedtime

  • PROPHYLACTIC TREATMENT:

Less than 5 years:
1. cyproheptadine (0.25-0.5mg/kg/day divided bid)
2. propranolol 0.25-1/kg/day –often 10mg bid or tid
contraindications: asthma, diabetes, heart disease, depression
keep resting heart rate >60

5 years & older
1. amitriptyline (or nortriptyline -liquid formulation) start at 0.25mg/kg qhs and increase ’til 1mg/kg/dose
check EKG before and 10 days after peak dose
2. propranolol 0.25-1/kg/day –often 10 mg bid or tid
contraindications: asthma, diabetes, heart disease, depression
keep resting heart rate >60

Alternative prophylactic treatments:
1. phenobarbital 2mg/kg qhs
2. anticonvulsants: topiramate, valproid acid, gabapentin, levetiracetam -?consult neurology

Supplements:
L-carnitne 50-100mg/kg/day divided bid (max 1gm tid)
Co-enzyme Q10 10mg/kg/day divided bid (max 100mg tid)

  • SUPPORTIVE/ABORTIVE CARE

Fluids: D10NS w KCL @ 1.5 maintenance (or possibly D10 0.45NS -some children prone to hyponatremia); add TPN if no enteral intake for 3-5 days
Antiemetics:
1. ondansetron 0.3-0.4mg/kg/dose q4hours (max 20mg); alternative granisetron
Sedatives:
Benadryl 1mg/kg/dose q6hours
Ativan 0.05-0.1mg/kg/dose q6hours
Thorazine (chlorpromazine) 0.5-1mg/kg/dose q6hrs (with benadryl)
Analgesics:
Toradol 0.4-1mg/kg/dose q6hrs (max 30mg)
Narcotics (morphine)

May need to treat hyponatremia, hypertension, hematemesis (H2RAs & PPIs)

Also, can try Sumatriptan 20mg intranasally at onset of episode as potential abortive measure or other triptan

  • TYPICAL EVALUATION:

1. CMP, Amylase/lipase, UGI on all patients
2. If pain/hematemesis, check U/S of abd/pelvis, and EGD
3. If abnormal neuro features: (motor asymmetry, gait abnormality, severe altered mental status)
ammonia
lactate, serum amino acids, urine organic acids, plasma carnitine/acylcarnitine profiles, urine ketones
MRI brain
4. If precipitated by fasting/high protein meals, or intercurrent illness= neuro w/u w/o brain MRI.

  • ALARM symptoms:

1. pain & bilious emesis
2. attacks precipitated by intercurrent illness, fasting or high protein meals
3. progressive/worsening/chronic pattern
4. abnormalities on neuro exam

**Note to blog readers –I recommend that all drug dosing be reviewed for individual patients.  The recommended doses are based on my reading of the referenced material & transcription errors are possible.

Additional references:

  • -Clin Gastro & Hep 2007; 5: 44. Use of zonisamide or levetiracetam (used at Sz dosing in 20 adults); 75% response & 20% remission.
  • -J Pediatr 2002; 141: 724. Suggests initial treatment along with UGI as most cost-effective strategy. Extensive w/u in those with persistent sx.
  • -Am J Gastro 1999; 94: 2855. response to TCAs.
  • -J Pediatr 1999; 134: 567. 82% migraine-assoc or FHx. Better response to Rx
  • NASPGHAN 2003:  postgraduate course (B Li):80% response to elavil if fhx migraines.
    “There are no controlled randomized, double-blinded trials, only open label ones. In these studies, beta-blockade (Pfau Pediatrics 97:364,1996), cyproheptadine (Anderson Pediatrics 100:977, 1997), amitriptyline (Anderson), phenobarbital (Gokhale JPGN 25:64, 1997) and erythromycin (Vanderhoof JPGN 17:387, 1993) all have approximately 70% efficacy as prophylactic agents. In Dave Fleisher’s work, he has demonstrated a 70% effect of consultation alone without pharmacologic therapy. In other words, there appears to be a striking placebo effect in this disorder that should temper any interpretation of results. In addition, I believe CVS is a heterogeneous disorder that has multiple etiologies that could allow it to respond to multiple classes of agents.”

DDx:
Infection, IBD, addison’s, diabetes, renal dysfxn, metabolic errors/urea cycle d/o, FAO d/o, porphyria, CDG (glycosylation), pregnancy, ipecac/munchausen, PUDz, Giardia, pancreatitis, UPJ, malrotation/duplication, increased ICP/CNS Dz, Migraine-equivalent

Workup:

1. CBC, ESR, amylase, ammonia,UA, stool heme, chem 20, HCG
2. UGI
3. giardia ag, abd U/S & DPTA, EGD, urine organic acids, plasma amino acids, carnitine, lactate, pyruvate, sinus films, head CT/MRI, toxicology, delta-aminolevulic acid/ porphobilinogen (urine), beta-HCG, serum transferrin isoelectric focusing