Chronic Pancreatitis Pain When the Enzymes Are Normal: Why the Gland Goes Quiet and the Pain Does Not

What this video covers

• Why chronic pancreatitis pain is a nerve problem as much as a gland problem
• Where the celiac plexus sits, and why most pancreatic nociceptive traffic passes through it — and why blocking it still does not help everyone
• How the block is performed under fluoroscopic or CT guidance in a pain clinic, and under endoscopic ultrasound in a GI suite
• What the published evidence actually shows for the endoscopic ultrasound-guided version: pain relief in roughly half of patients at first, but only about one in five still improved at twelve weeks and about one in thirty at six months
• The honest risks: transient diarrhea, low blood pressure, and a short post-procedure pain flare after a steroid block — and the higher, rarely serious risks of alcohol neurolysis, including bleeding and rare spinal cord injury
• Where celiac plexus neurolysis fits for pancreatic cancer pain, and how it differs from a block
• MEDICAL DISCLAIMER: This content is for educational purposes only and is not medical advice. It does not substitute for professional diagnosis or treatment. Always consult a licensed healthcare provider regarding your condition. Viewing this video does not establish a doctor-patient relationship.

It sits below the breastbone and bores through to your back. You lean forward over your knees because that is the only posture that helps. Eating provokes it, so you eat less, and the weight comes off. There have been admissions this year — fluids, nothing by mouth, an opioid pump, discharge — and each one ended the same way. Then one night the lipase comes back normal while you are still gripping the rail of the bed, and the conversation in the room changes. This article explains why pancreatic pain can continue after the gland itself has gone quiet, where that pain signal actually travels, and what a celiac plexus block can and cannot do about it.

Repeated inflammation changes two different things

The first change is the one everybody already knows about, because it is the one imaging shows. Fibrosis — scar tissue — replaces working pancreatic tissue. The duct scars and narrows. Pressure builds behind the narrowing. That is the structural story, and it is real.

The second change is neural, and it is the one that goes unmentioned. Sensory nerves inside the gland enlarge. Immune cells infiltrate the nerve sheath. Axons sprout into inflamed tissue. The nerve stops being a passive wire reporting on the gland and becomes an independent generator of signal, while the spinal cord and brain raise the gain on everything arriving from that region.

The 2017 international consensus guidelines on pain in chronic pancreatitis, from Drewes and colleagues in Pancreatology, state it directly: pain here can relate to recurrent or chronic inflammation, to local complications, or to neurogenic mechanisms with corresponding changes in the nervous system. (Established — international consensus guideline.) Three mechanisms. Most patients arriving at a pain clinic have been treated for exactly one of them.

That is why the gland can burn itself out — fibrose, calcify, and go quiet on every study you own — while the pain continues. It has relocated into the nervous system.

Why it bores through to your back, and why eating sets it off

Pancreatic pain does not travel primarily with the vagus nerve. The vagus carries other traffic from this gland. The pain fibers run with sympathetic afferents into the celiac plexus — a dense retroperitoneal nerve network sitting around the aorta at roughly the twelfth thoracic and first lumbar vertebral levels — and then back along the greater, lesser, and least splanchnic nerves to the thoracic dorsal root ganglia.

That anatomy explains the felt experience. The plexus sits deep and behind, in front of the spine rather than under the skin, which is why the pain is reported as boring straight through to the back rather than as a surface ache. It is a visceral signal, and visceral signals are characteristically poorly localized — you can point at a region, not a spot. And because eating is the stimulus that asks the gland to work, meals provoke it, which is how food avoidance and weight loss get built into the illness itself.

It also explains why leaning forward over your knees is the posture patients discover on their own, and why an enzyme panel drawn during a flare can be completely unremarkable. Enzyme levels report on acute inflammation. They do not report on a remodeled nerve.

What the standard approach misses

None of this is a criticism of emergency care, and nothing here says the medications are worthless. Fluids, bowel rest, and analgesia are the right answers to an acute attack, and symptom-control drugs genuinely reduce suffering. What they do not do is address a pain generator that has moved into the nervous system.

Two failures follow from that gap.

The enzyme-normal trap. When the labs are quiet and the pain is not, the chart often stops asking why the patient hurts and starts asking what they want. A nerve problem gets recorded as a character problem. That is not a diagnosis. It is the absence of one.

The single-mechanism treatment plan. If a patient’s pain is neurogenic and the entire plan is aimed at inflammation, or at the duct, or at opioid dose alone, the plan can be well executed and still miss.

Before anyone advances a needle toward the aorta, though, the differential has to be finished — and this is where the honest gatekeeping happens:

• Abdominal wall nerve entrapment. Tensing the abdominal wall takes ten seconds: if the tenderness worsens, the source is more likely the wall than the viscera. That sign points; it does not prove. But a plexus block does nothing for it.
• Chronic mesenteric ischemia, suggested by strictly postprandial pain with food avoidance.
• Peptic disease, biliary obstruction, and malignancy, which must be excluded.
• Opioid-induced hyperalgesia — because sometimes the treatment has become the disease.

The sequence comes before the procedure

The guidelines place plexus interventions after the earlier steps, not instead of them. (Established — international consensus guideline.) In the Drewes consensus, that means abstinence from alcohol and smoking, which is strongly advised; pancreatic enzyme therapy and antioxidants, which may be helpful as initial treatment; a simple stepwise escalation of analgesic drugs; endoscopic treatment where there is ductal obstruction; and this line, which pain clinics rarely read aloud — surgery should be considered early, and after a maximum of five endoscopic interventions. Neurolytic interventions and neuromodulation are positioned last, for difficult patients.

Read that ordering carefully. If you have a dilated duct and a surgical option, that conversation belongs before a pain-procedure conversation, not after it.

Abstinence from alcohol and tobacco is the step with the most to give, and no trial has raced it head-to-head against a needle, so it will not be dressed up as though one had. It is also the one intervention a physician cannot perform for you.

Enzyme replacement has to be dosed adequately and taken with food, not an hour later. The guidelines use the word may about pain, and that word is worth keeping: enzymes reliably treat maldigestion and weight loss, while their effect on pain is inconsistent across trials. (Established for maldigestion; inconsistent for pain.) Do not start, stop, or change any medication without consulting your physician.

What a celiac plexus block actually is

Only when pain is refractory after those steps does the plexus become the target.

For a fluoroscopically guided block, you lie prone. Under live imaging the twelfth thoracic and first lumbar vertebral bodies are identified, a needle is walked off the lateral margin of the bone on each side, and advanced toward the target. Nothing therapeutic is injected until contrast confirms spread hugging the aorta on both projections, with no vascular uptake. Then local anesthetic, usually with a corticosteroid. Some centers perform the same block under CT, trading live imaging for soft-tissue detail. Gastroenterology reaches the identical plexus from the front, through the stomach wall, under endoscopic ultrasound — same target, different door.

Understand what the injection is doing: it interrupts a pathway temporarily. It does not repair the gland, and it does not remove the disease. Candidacy, procedural detail, and what the day itself involves are set out on the pancreatitis pain treatment page, and the technique is described further on the celiac plexus block page.

What the evidence actually shows — with the limits stated

This is the part of the conversation that usually goes missing.

The best pooled data are for the endoscopic version, and they are honest about the ceiling. In 2025, Machicado and colleagues pooled eleven studies and 729 patients in Pancreatology, all receiving endoscopic ultrasound-guided celiac plexus block for painful chronic pancreatitis. Overall efficacy was 53 percent (95% CI 39–67%). Mean duration of relief was 81 days (95% CI 30–217). Broken out over time: 52 percent improved at four weeks, 57 percent at eight weeks, 19 percent at twelve weeks, and 3 percent at twenty-six weeks. Adverse events occurred in 8 percent (95% CI 4–15%). The authors concluded that a sham-controlled clinical trial is still needed to establish analgesic efficacy. (Low-certainty for efficacy: pooled uncontrolled data, no sham comparison.)

Three limits belong immediately beside those numbers. First, that is a window, not a repair — the decay from 57 percent to 3 percent across eighteen weeks is the actual shape of the benefit. Second, the 81-day figure is a mean with a confidence interval running from 30 days to 217, which is too wide to plan a life around; it is not a duration anyone should be promised. Third, those figures belong to the endoscopic technique. They should not be quoted as though they described the fluoroscopic block performed in a pain clinic, and the duration of the fluoroscopic block has not been measured with the same care.

In pancreatic cancer the procedure is different, and so is the evidence. There the intervention is alcohol neurolysis, which destroys the plexus rather than interrupting it. The 2011 Cochrane review by Arcidiacono and colleagues pooled six randomized trials of the percutaneous approach in 358 participants. At four weeks the pain difference was −0.42 points on a 10-point scale (95% CI −0.70 to −0.13), and at eight weeks −0.44 (95% CI −0.89 to −0.01). Four tenths of a point is below what most patients would notice, and the review’s own authors called the statistical evidence for superiority of pain relief minimal. What was clearly different was opioid consumption, significantly lower in the neurolysis group, which the authors considered the more meaningful finding. (Consistent across the six pooled trials for the opioid-sparing effect; the authors’ own word for the pain-score difference is minimal.)

Risks, with the two procedures held apart

Risk belongs before consent, and the steroid block and the neurolytic procedure must not be blurred together.

After a steroid block, expect the possibility of transient diarrhea, a drop in blood pressure on standing, and a short flare of pain before any relief. In the pooled endoscopic series above, adverse events ran 8 percent.

Alcohol neurolysis carries a heavier and older set of numbers. Eisenberg, Carr, and Chalmers pooled 1,145 cancer patients receiving neurolytic celiac plexus block in their 1995 meta-analysis in Anesthesia and Analgesia: local pain in 96 percent, diarrhea in 44 percent, hypotension in 38 percent, with complications in 2 percent; the authors concluded severe adverse effects are uncommon. That paper does not report paraplegia at all, so the paraplegia figure comes from somewhere else. Davies, in a 1993 survey in the Journal of the Royal Society of Medicine covering 2,730 neurolytic blocks performed in England and Wales between 1986 and 1990, found four permanent paraplegias — roughly one per 683 blocks. Those are neurolysis figures from the 1990s, and in the Eisenberg data a cancer population. They do not describe the steroid block. That number is small. It is not zero.

Route hazards apply to any approach to this target, because the plexus sits against the aorta — which is exactly what the contrast run is for: intravascular injection and local anesthetic toxicity, retroperitoneal bleeding, injury to a kidney or a vessel, pneumothorax (uncommon but possible), and infection. If you take a blood thinner, that is planned around before a date is set, not on the table. Do not start, stop, or change any medication without consulting your physician.

A word on metabolic and adjunctive approaches — here, more restrictive

Other topics in this series discuss metabolic strategies. This one is deliberately more restrictive, not less.

A high-fat ketogenic approach is a poor fit for a gland that can no longer digest fat; it buys steatorrhea, not relief. Pro-resolving mediators and near-infrared light are investigational and untested in this condition — there is no controlled human outcome data in chronic pancreatitis. What matters nutritionally here is dull and specific: enzymes dosed correctly, fat-soluble vitamins checked, and calories sufficient to stop the weight loss. A hypothesis will not be dressed up as standard of care.

An honest picture of a good outcome

What follows is a composite — a picture assembled from many patients with this condition, not one person’s chart. It is a practice observation, not a trial result, and nothing in it should be read as an outcome you can expect.

An adult with calcific chronic pancreatitis on imaging. Six years of pain. Four admissions in eighteen months. An opioid regimen tripled without producing a good day.

The first eight weeks held no procedure at all. Enzyme dosing turned out to be wrong — roughly half the needed dose, taken after meals rather than with them. Corrected, the maldigestion and weight loss improved. How much of the pain change belonged to the enzymes cannot honestly be separated out. Tobacco was the hard part; there were two relapses before it held.

The first fluoroscopic block produced two days of worse pain, then relief that was real and incomplete — enough to finish a meal, sleep flat, and begin tapering. It held into the third month. That number deserves caution: in the pooled endoscopic data only about one in five is still better at twelve weeks, and the fluoroscopic block’s duration has not been carefully measured. Hear it as one plausible course, not a figure to plan around. A second block did roughly the same; no published evidence supports predicting what a third would do.

What changed was the ratio — fewer emergency visits, a lower dose, weight regained. That is not a cure. The disease is still there. What was bought was function, and enough quiet for the slow work no needle will do. Again: this is a practice observation, not a trial result. Individual results vary.

Frequently asked questions

Key takeaways

• Chronic pancreatitis pain has three possible sources — inflammation, local complications, and neurogenic change in the nervous system — and most patients have been treated for only one.
• Pancreatic pain fibers travel with sympathetic afferents through the celiac plexus in front of the aorta, which is why the pain bores through to the back, worsens with eating, and can persist after the gland goes quiet.
• A celiac plexus block interrupts that pathway temporarily. Pooled endoscopic ultrasound-guided data show roughly 53 percent efficacy and a mean 81 days of relief — with a confidence interval on that mean running from 30 to 217 days, 19 percent still improved at twelve weeks, and no sham-controlled trial yet performed.
• Alcohol and tobacco abstinence, adequate enzyme dosing, stepwise analgesia, and decompression of an obstructed duct come first; guidelines also say surgery should be considered early.
• Normal enzymes with continuing pain is not evidence that nothing is wrong — it is a reason to look at the nerve, not at the patient’s character.

Medically reviewed by Dr. Gurpreet Singh Padda, MD, MBA, MHP — Board Certified in Anesthesiology, Pain Medicine, Interventional Pain Management, Addiction Medicine, and Obesity Medicine. Last reviewed July 2026.

This article is educational and is not a substitute for evaluation, diagnosis, or treatment by a physician. Individual results vary. Do not start, stop, or change any medication without consulting your physician. To have your abdominal pain properly evaluated before any procedure is scheduled, call (314) 481-5000 or text (314) 886-5902.

References

1. Machicado JD, Tanner S, Adoor D, Chalhoub JM, Plann-Curley B, Lee UJ, Bang JY, Varadarajulu S, Wilcox CM; US Pancreatic Disease Study Group. Endoscopic ultrasound-guided celiac plexus block for painful chronic pancreatitis: A systematic review and meta-analysis. Pancreatology. 2025 Sep;25(6):860-867. PMID 40813224101016202508006. PubMed
2. Drewes AM, Bouwense SAW, Campbell CM, Ceyhan GO, Delhaye M, Demir IE, Garg PK, van Goor H, Halloran C, Isaji S, Neoptolemos JP, Olesen SS, Palermo T, Pasricha PJ, Sheel A, Shimosegawa T, Szigethy E, Whitcomb DC, Yadav D; Working group for the International (IAP-APA-JPS-EPC) Consensus Guidelines for Chronic Pancreatitis. Guidelines for the understanding and management of pain in chronic pancreatitis. Pancreatology. 2017 Sep-Oct;17(5):720-731. PMID 28734722101016201707006. PubMed
3. Arcidiacono PG, Calori G, Carrara S, McNicol ED, Testoni PA. Celiac plexus block for pancreatic cancer pain in adults. Cochrane Database Syst Rev. 2011 Mar 16;2011(3):CD007519. PMID 214129031010021465185800751926464722. PubMed
4. Eisenberg E, Carr DB, Chalmers TC. Neurolytic celiac plexus block for treatment of cancer pain: a meta-analysis. Anesth Analg. 1995 Feb;80(2):290-295. PMID 78181151010970000053919950200000015. PubMed
5. Davies DD. Incidence of major complications of neurolytic coeliac plexus block. J R Soc Med. 1993 May;86(5):264-266. PMID 85057481011770141076893086005071294001. PubMed

Dr. Gurpreet Singh Padda, MD, MBA, MHP