A case to anchor the episodeA patient with chest pain and intermittent dysphagia. Cardiac workup is negative. Manometry shows a normal IRP, 30% of swallows with a distal latency of 3.8 seconds, and a normal DCI on the rest. What is the diagnosis, and what is the first treatment move? The normal-IRP side of the Chicago algorithm covers everything that is not achalasia or EGJOO. The sphincter relaxes; the question shifts to what the body is doing. Distal esophageal spasm is a timing problem (premature contraction). Hypercontractile esophagus is a vigor problem (DCI above 8000). Ineffective motility and absent contractility sit at the failed end. Scleroderma is the one disorder that breaks the rule, presenting as absent contractility plus a hypotensive LES that lets reflux through. And EGJOO is the elevated-IRP-with-preserved-peristalsis bucket that v4.0 made harder to call on purpose, because v3.0 was overcalling it. Topics coveredIRP as the sorter: elevated IRP routes to achalasia or EGJOO; normal IRP opens the body branchDistal esophageal spasm: ≥20% premature swallows (DL under 4.5s) on a normal IRP, in a symptomatic patientHypercontractile (jackhammer) esophagus: ≥20% of swallows with DCI above 8000, in a symptomatic patientWhy distal latency captures spasm and contraction front velocity does not: deglutitive inhibition vs raw wave speedSpasm treatment ladder: address contributors first (opioids, GERD, EoE), then calcium channel blockers, nitrates, sildenafil, peppermint oil, neuromodulatorsType 3 achalasia vs spasm: same body pattern, different IRP, and POEM vs medical therapy followsScleroderma esophagus: absent contractility plus hypotensive LES as a dual hit; Nissen contraindicated, partial wrap or no wrapIneffective esophageal motility (IEM): more than 70% ineffective or at least 50% failed swallows; surgical implications for fundoplication planningEGJ outflow obstruction: v4.0 requires both supine and upright IRP elevation, intrabolus pressurization, symptoms, and a confirmatory testFLIP distensibility index below 2.0 mm²/mmHg or maximum diameter below 12 mm confirms reduced EGJ openingOpioid-induced esophageal dysfunction: mimics type 3 achalasia, EGJOO, and spasm; reverses with taper before any therapy Key decisionsType 3 achalasia and distal esophageal spasm share the body pattern; the IRP separates them. The therapy follows: tailored myotomy for type 3, medical ladder for spasmDistal latency under 4.5 seconds identifies spasm; DCI above 8000 identifies jackhammer. Both require symptoms before they become a clinical diagnosisSevere IEM and absent contractility separate at 70% vs 100% failed swallows; absent contractility plus hypotensive LES is the scleroderma fingerprintEGJOO requires confirmatory imaging, FLIP or timed barium, before invasive intervention. v4.0 deliberately raised the barAny tracing that mimics type 3 achalasia in an opioid-using patient triggers an opioid taper and a repeat manometry before any procedureScleroderma esophagus contraindicates a full 360-degree Nissen; partial wrap or no wrap is the rule because the dysmotility cannot overcome a tight wrap Related episodesesophageal-motility/ep-1 For the full chapter with MCQs, tables, and primary-guideline references, visit www.boardpearls.com.Questions or feedback: [email protected]. (00:00) - Opening: IRP sorts everything (02:00) - Spasm and jackhammer share preserved relaxation (05:00) - Distal latency and why CFV was retired (08:30) - Spasm clinical picture and workup (11:30) - Spasm treatment ladder (16:00) - Hypercontractile esophagus and the symptom rule (19:30) - Scleroderma esophagus and the partial-wrap rule (23:00) - Ineffective and absent contractility (26:00) - EGJOO and the v4.0 bar (30:00) - FLIP and timed barium as the rescue (33:00) - Synthesis and what's next

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“What did the council decide on item 42?” — answered with the speaker and the moment.