Patient Medical Synopsis — Cleveland Clinic Consultation

Current Status

GI Diagnoses — Unified Through EDS

Severe GI Pain (eating + lifting/pushing)Active

Active — EDS enteric neuropathy and visceral hyperalgesia; pressure-triggered neurological pain response

Biliary Dyskinesia (low gallbladder EF)Noted

Functional finding — HIDA ejection fraction 28% (borderline low) with otherwise normal study; a scheduled gallbladder removal was declined on the operating surgeon's own advice given her systemic history. Treated as dysmotility, not a surgical target

Pancreatitis / Pancreatic DiseaseExcluded

Excluded — lipase low (17), fecal elastase normal (>800), and EUS, CT, and ultrasound all clean; pain is not pancreatic in origin

Condition	Status & EDS Connection
Severe GI Pain (eating + lifting/pushing)Active	Active — EDS enteric neuropathy and visceral hyperalgesia; pressure-triggered neurological pain response
Biliary Dyskinesia (low gallbladder EF)Noted	Functional finding — HIDA ejection fraction 28% (borderline low) with otherwise normal study; a scheduled gallbladder removal was declined on the operating surgeon's own advice given her systemic history. Treated as dysmotility, not a surgical target
Pancreatitis / Pancreatic DiseaseExcluded	Excluded — lipase low (17), fecal elastase normal (>800), and EUS, CT, and ultrasound all clean; pain is not pancreatic in origin

Completed GI Workup

The GI Investigation — What's Excluded, and the One Thing That Worked

Audrey's severe GI pain — triggered by eating and by lifting or pushing — has been worked up exhaustively across imaging, endoscopy, nuclear medicine, and labs. The structural, vascular, and pancreatic causes are excluded. One functional finding remains (stated honestly below), and one intervention worked. Together they point away from the organs and toward the nervous system. Please build on this workup; do not repeat it without new clinical justification.

Definitively Excluded — Please Don't Re-Order Without New Justification

Pancreatitis / pancreatic disease5 modalities — all negative

Lipase 17 (low) · fecal elastase-1 >800 (normal exocrine function) · EUS — pancreatic head, genu, body, tail and the entire main bile duct all clean (5/1/26) · CT abdomen & pelvis with contrast — "no acute findings" (5/1/26) · abdominal ultrasound — visualized pancreas within normal limits (9/26/25)

Celiac disease / mucosal enteropathyMucosa normal

EUS biopsies taken during the 5/1/26 block — duodenum with preserved villous architecture and no increase in intraepithelial lymphocytes (excludes celiac disease); stomach with only minimal chronic inactive gastritis, negative for intestinal metaplasia or dysplasia. Normal gut mucosa — no structural correlate for the pain.

MALS / celiac & SMA compression3 modalities — all negative

Dedicated MALS-protocol CT angiogram — "no evidence of MALS or compression of the celiac artery or SMA" (5/26/26) · mesenteric duplex — celiac, SMA, and IMA all 0–69%, none hemodynamically significant (4/29/26) · prior CT angiography — negative

Gastroparesis / delayed gastric emptyingNot delayed

4-hour gastric emptying scan (10/9/25) — retention at or below normal at every interval (1h 25%, 2h 7%, 3h 4%, 4h 2%). Emptying is normal-to-rapid — the opposite of gastroparesis — so there is no delayed-emptying basis for a feeding tube

SMA syndromeNegative

Dedicated imaging protocol — negative

Cause	Evidence	Verdict
Pancreatitis / pancreatic disease	Lipase 17 (low) · fecal elastase-1 >800 (normal exocrine function) · EUS — pancreatic head, genu, body, tail and the entire main bile duct all clean (5/1/26) · CT abdomen & pelvis with contrast — "no acute findings" (5/1/26) · abdominal ultrasound — visualized pancreas within normal limits (9/26/25)	5 modalities — all negative
Celiac disease / mucosal enteropathy	EUS biopsies taken during the 5/1/26 block — duodenum with preserved villous architecture and no increase in intraepithelial lymphocytes (excludes celiac disease); stomach with only minimal chronic inactive gastritis, negative for intestinal metaplasia or dysplasia. Normal gut mucosa — no structural correlate for the pain.	Mucosa normal
MALS / celiac & SMA compression	Dedicated MALS-protocol CT angiogram — "no evidence of MALS or compression of the celiac artery or SMA" (5/26/26) · mesenteric duplex — celiac, SMA, and IMA all 0–69%, none hemodynamically significant (4/29/26) · prior CT angiography — negative	3 modalities — all negative
Gastroparesis / delayed gastric emptying	4-hour gastric emptying scan (10/9/25) — retention at or below normal at every interval (1h 25%, 2h 7%, 3h 4%, 4h 2%). Emptying is normal-to-rapid — the opposite of gastroparesis — so there is no delayed-emptying basis for a feeding tube	Not delayed
SMA syndrome	Dedicated imaging protocol — negative	Negative

The One Functional Finding — Gallbladder, Stated Plainly

A HIDA scan (12/5/25) showed normal hepatic uptake, biliary excretion, and gallbladder visualization, but a low gallbladder ejection fraction of 28% (borderline; most labs flag below 35–38%). This is consistent with biliary dyskinesia — a functional motility finding, not structural disease.

Why This Didn't Lead to Surgery — and Why That Matters

On the strength of that 28%, a gallbladder removal was scheduled — and it was technically within range to operate. The operating surgeon reviewed her full workup and cautioned that, given her medical history, the gallbladder was unlikely to be the "golden goose." On that advice, surgery was declined. A careful surgeon already chose restraint over a technically-qualifying number because the isolated finding did not fit her systemic picture. That judgment should inform every future procedural decision.

The One Thing That Worked — the Celiac Plexus Block

During the 5/1/26 EUS, a celiac plexus block was performed — and it resolved her pain and restored her ability to eat. She has had this block once. With every structural, vascular, and pancreatic cause excluded, the fact that chemically interrupting the autonomic nerve supply worked is the single most important data point in the workup: it localizes the problem to the nervous system, not the organs. This is the bridge to the clinical hypothesis below.

Primary Clinical Hypothesis

The Pain Is Neurological, Not Structural — EDS-Related Enteric Neuropathy & Visceral Hyperalgesia

This is not a diagnosis of exclusion. It is a specific, mechanistic explanation.

hEDS affects the connective tissue surrounding enteric nerves. The enteric nervous system — approximately 500 million neurons embedded in the gut wall — depends on that connective tissue for structural support and normal signaling. In hEDS, this architecture is abnormal, producing a hypersensitive and dysregulated pain signaling system. Pressure changes from eating or lifting trigger genuine neurological pain responses that have no structural correlate on imaging because the dysfunction is in the nerve signaling itself, not the organs.

The celiac plexus is the primary autonomic nerve cluster serving the abdominal organs. Chemically interrupting this pathway resolved her pain and restored her ability to eat. With all structural and vascular causes now ruled out, this block efficacy is strong confirmatory evidence that the pain originates in the autonomic/enteric nervous system — not in the organs themselves.

Why the Celiac Plexus Block Working Is Essentially Diagnostic

Why Pain Is Triggered by Both Eating AND Lifting

Both triggers share one mechanism: increased intra-abdominal pressure. Eating expands the stomach; lifting spikes pressure through core bracing. In visceral hyperalgesia, the enteric nervous system interprets any significant pressure change as a pain signal. This is not a digestion problem or a structural problem — it is a sensitized neurological response to pressure.

The PTSD → Autonomic → Enteric Nervous System Chain

PTSD (or PTSD-adjacent symptoms) chronically dysregulates the autonomic nervous system. The autonomic nervous system directly governs the enteric nervous system. In a patient with hEDS — where the enteric nervous system is already structurally vulnerable — chronic autonomic dysregulation creates compounding dysfunction. The gut pain and the trauma response are not separate problems. They are the same problem expressing simultaneously in two systems. Treating one without the other limits results for both.

Procedural Caution

Strong Caution: PEG-J Feeding Tube Recommendation

The specific recommendation was a PEG-J feeding tube — and it is not a settled GI plan. It surfaced as a conditional suggestion from Nutrition (6/16/26), to be considered *only if GI could not stabilize her*. As options narrowed, the GI team was prepared to proceed with the tube; the family pushed back and requested another celiac plexus block to buy more time before any procedural step. Repeating the one intervention that already restored her eating is the live alternative on the table.

Recommendation: Hold on PEG-J Placement

Do not proceed until the neurological treatment pathway has been fully pursued and the procedural risk in an hEDS patient with a history of multiple failed connective-tissue repairs has been formally assessed.

A history of repeated failed shoulder repairs (5 surgeries across both shoulders; the first three did not hold and required revision) demonstrates connective tissue fragility that materially elevates the risk and complexity of any abdominal procedure, including a PEG-J stoma that must heal and hold in fragile tissue
Her gastric emptying scan was normal-to-rapid, not delayed — she does not have gastroparesis, which removes the most common mechanical indication for a feeding tube
A PEG-J feeding tube is a management tool, not a treatment — it bypasses the problem without addressing the neurological cause
The celiac plexus block previously restored eating — demonstrating the pain mechanism is interruptible without surgery
A gallbladder removal was already scheduled on a technically-qualifying finding and declined on the operating surgeon's own advice — surgical restraint, not intervention, is the established posture in this patient
Ongoing therapeutic blocks, LDN, spinal cord stimulation, and the current treatment stack should be exhausted before surgical intervention
Long-term quality of life implications are significant for a 19-year-old patient

Action Items

GI Requests for Cleveland Clinic

Specialist Consults to Request

Neurogastroenterology — EDS-related visceral hyperalgesia and enteric neuropathy; specifically request this subspecialty, not general GI
Pain Management — celiac plexus block as ongoing therapy, spinal cord stimulation evaluation, LDN

Key Questions for Every Appointment

Given that a celiac plexus block resolved her pain and restored eating, what is the plan for repeated or sustained nerve block therapy?
Has EDS-related enteric neuropathy and visceral hyperalgesia been evaluated as the primary pain mechanism?
Given her history of multiple failed shoulder repairs, what is the formal procedural risk assessment for any abdominal procedure before a PEG-J feeding tube is considered?
Is duloxetine dose escalation to 120mg appropriate given partial or incomplete response at 60mg?
Is spinal cord stimulation an appropriate next step given the centrally mediated pain mechanism?