NON CARDIAC CP
1. Definition: recurrent chest pain that is indistinguishable from cardiac pain after a reasonable workup.
2. GI disorder for chest pain is commonest cause, then cardiac and then chest wall.
3. NCCP is most common functional GI disorder. Incidence is same all over the world – around 25%
4. The incidence decreases as people get older and M=F. Except between 50-59, F>>M due to menopause?
5. Panic disorder is the commonest cause to drive patients to the ER for chest pain
6. Commonest cause of nCCP is reflux. Half of them will have abnormal pH studies but range of erosive esophagitis is 10-70%. But most patients will NOT have erosions in esophagus
7. Second most common cause after reflux is esophageal dysmotility 15-18%. But 70% of them will have normal motility
8. Nutcracker esophagus – high amplitude contraction with more than 180 mm pressure. It is most common motor disorder in NCCP pt. Nutcracker is caused by reflux, possibly.
9. Hypercontractile esophagus / jackhammer esophagus when index is more than 8000.
10. Chest pain of presumed esophageal origin / functional chest pain. Not burning, no reflux and no motility disorder. Symptoms present for 3 months.
11. Esophageal hypersensitivity is when non painful stimuli appears as painful stimuli
12. Lower esophagus is constantly exposed to reflux, then patients develop primary hyperalgesia. The proximal esophagus also develops hyperalgesia and is called secondary hyperalgesia. Eventually they develop chest wall hypersensitivity also from somatic nerves
13. How do you evaluate ? – Start with cardiac evaluation
14. Second step is PPI trial. Omeprazole 40 mg in AM and 20 mg in PM for 7 days to 14 days.
15. 24 hour pH off treatment with impedence measurement. If on treatment then use bravo
16. Role of EGD for NCCP:
17. Always compare psychological issues in all patients. Eg panic disorder, depression and anxiety
18. Treat motility with nitrates, ca channel blocker, sildenafil, botox injection, Surgery or POEM for NCCP.
19. Procardia 10-30 mg tid takes 3 weks to respond and response is not enduring.
20. Botox for NCCP works.
21. TCA, trazodone, selective serotonin antagonists, adenosine, pain modulators work for NCCP.
22. TCA work on NE, 5 HT, H1 receptors. Use low dose TCA.
23. TCA – start with 10 mg a day at bedtime. Good sleep is analgesic ! Weekly increase by 10 mg and target is 10-50 mg a day. May combine with SSRI. TCA – they do not cause mood altering at this dose
24. Venlafaxine 75 mg at bedtime. Citalopram 20 mg once a day is effective. Venlafaxine pt have problems falling asleep.
25. Zofran is a pain modulator; gabapentin also is a pain modulator.
26. Hypnotherapy gives a good response.
27. Johrei treatment – Similar to Reiki. It works too.
XXI. REFRACTORY GERD
1. Bariatric surgery causes secondary achalasia !
2. Sigmoid esophagus if more than 8 cm esophagus diameter
3. Refractory reflux : Symptoms that don’t respond to bid PPI for 12 weeks.
4. More common in females, and is in 32% -45% of patients
5. Non responders is around 3% and partial responders are 20%?
6. Most common breakthrough is at nighttime. More than 60% of them
7. Nighttime reflux drives barretts and esophageal adenoca
8. NERD: more acid, more likely they will respond
9. Erosive esophagitis: more acid, less likely they will respond
10. Mechanisms for refractory reflux: EoE, compliance, improper dosing time, psychological issues, bile reflux, IBS, gastroparesis, acid pocket. The most common cause is FUNCTIONAL REFLUX
11. Functional reflux: heartburn without acid reflux.
12. Usually esophageal hypersensitivity.
13. Acid pocket: an unbuffered acid pocket in the stomach. Partial responders have more proximal reflux events and increased sensitivity to balloon distension.
14. Proximal reflux: have liquid and gas and usually refractory
15. Dilated intercellular space in NERD with resistant to PPI is abnormal
16. Value of upper endoscopy: indicated if PPI bid fails after 4-8 weeks.
17. Role of pH in failed PPI bid patients: only 7% will have abnormal results
18. Mucosal impedance is done through scope: This uses dilated interstitial space. If dilated space, then reflux.
19. pH plus impedance: On treatment. Is best. High probability for gerd, do it on treatment. If low probability of gerd then do Bravo off treatment.
20. First step in management of refractory is: compliance. Most patients take it only on demand 70%. Moreover, PPI is taken incorrectly. Take it 30 min before meals.
21. Dose splitting of PPI is more effective or switch to another PPI. Dexilant once a day works in 88% of patients on bid PPI
22. Baclofen reduces TLESR. 10 mg q hs and can increase to 20 tid. Has neurological side effects
23. Stretta: is effective in 20% cases
24. Esophyx TIF: good success.
25. Antireflux surgery in refractory reflux. Useful in large HH, severe erosive esophagitis and regurgitation
26. LINX reflux management: Effective in partial responders. Study from NEJM.
27. Functional reflux: follow the tegaserod, TCA, SSRI, etc
28. Melatonin in functional reflux is effective also.
29. Hypnotherapy helps in functional reflux.
30. Acupuncture plus PPI bid helps.
Surveillance how good is it. Depends on how long Barretts is If more than 9 cm only 10% did it right.
Bx the funny looking things first!
Prague Classification – C and M. CIrcumferential and M maximum
If dysplasia noted, take bx every 1 cm.
Progression is 0.1% per year not 0.5% as previously thought
HGD risk of progression is 19% to cancer
LGD 10.3 progress to HGD and 3% go to cancer
If there is consensus for LGD progression is 13.4%. So confirm with 2 pathologist
Confocal endoscopy – — — USE it. (Probe based) Improves sensitivity from 34% to 45 percent to 75% (regular to NBI to confocal)
RFA AT end of it, looks like searing a steak at the end.
RFA, eliminates intestinal metaplasia but it is NOT 100%. Failure usually in patients with large HH
Progression to cancer reduced to 1%. HOWEVER, surveillance MUST CONTINUE INSPITE OF RFA. Recurrence of Barretts after RFA is 13%
Liquid nitrogen spray cryotherapy is another option – Must put in orogastric tube to suction out air that is used for cryo. Similar to RFA.
DO NOT DO RFA if patient has NODULAR BARRETTS
Stage 1a esophageal adenoca manage endoscopically
Pneumonia from increased bacterial colonization and from direct immunosuppression from PPI? Actually, CAP more likely in first 30 days. Moderately increased CAP from drug. Increased risk of CAP is true for both H2 blocker and PPI within first 2 days is highest. This might be a protopathic bias. Similar protopathic bias for PPI and colorectal cancer!!
PPI and osteoporosis – Osteoclastic PPI inhibition, Ca absorption, gastrin may induce parathyroid hyperplasia, PPI induced B 12 insufficiency. Low B 12 causes decreased bone formation. This might be more confounding meaning co morbidities that gives it the appearance than reality. 2008 study showed there is no increase risk of hip fracture. Long term and high risk may be associated with increased risk. Risk increase in high risk patients mostly FDA labelled PPI as possible increased risk fracture
Avoid long term, high dose PPI. Set treatment goals, dose reduction, on-demand therapy. Bone density screening or monitoring is NOT indicated
Encourage use of Ca/Vitamin D
Esophageal AdenoCa deaths are still increasing (2013 data)
Visible columnar metaplasia – 46% of them have intestinal metaplasia. If no dysplasia risk is 0.31%. If low grade dysplasia, risk is 1.45% per year. 36% of them had NO intestinal metaplasia. They still had .06% per year even if no dysplasia. 18% of the bx was indeterminate
LGD second look by pathologist only 75% thought LGD was true.
RFA develop strictures 8%, bleeding and hospitalization is 1.6%
RFA is not proven to decrease cancer rate or need for surveillance
Barrett’s Esophagus :
Whats new in GERD and motility
Newer Techniques for Barrett’s Ablation