Pancreatic Stones and Calcifications: What Does It Mean?

Pancreatic stones and calcifications are most often a manifestation of chronic pancreatitis: hard concretions and focal/diffuse calcium deposits form in the main pancreatic duct, its branches, or in the pancreatic parenchyma. They mechanically obstruct pancreatic secretion flow, sustain intrapancreatic hypertension and inflammation, leading to pain and exocrine and endocrine insufficiency. A significant proportion of patients have multiple, radiopaque concretions, most often in the head and body of the pancreas. [1]

Western guidelines consider endoscopic therapy and/or extracorporeal shock wave lithotripsy as first-line options for symptomatic patients with the "obstructive" phenotype of chronic pancreatitis—in the presence of stones/strictures of the main duct and dilation distal to the obstruction. Surgery is a priority in cases of endoscopic failure, recurrent pain, or complex anatomy (e.g., extended strictures, large stone clusters). The development of pancreatoscopy with contact lithotripsy (electrohydraulic/laser) has expanded the options for stones resistant to standard tactics. [2]

It is important to distinguish "calcifications" as a radiographic feature (pinpoint/diffuse dense foci) from "stones" as a clinically significant cause of duct obstruction. Calcifications are typical of chronic pancreatitis, but also occur in other conditions (e.g., some cystic neoplasms), requiring correlation with clinical, laboratory, and imaging findings. In certain regions (such as the tropics), calcific pancreatitis is often associated with genetic factors and has an onset at a young age. [3]

The goal of treatment is not a "sterile" stone-free image, but rather sustained pain control, prevention of pancreatitis recurrence, and preservation of pancreatic function. Therefore, not only duct clearance is assessed but also clinical dynamics: reduction in attacks, analgesic requirements, weight stabilization, improvement in steatorrhea and glycemia. Decisions are made multidisciplinary (gastroenterologist, endoscopist, surgeon, radiologist, nutritionist, and, if necessary, a geneticist). [4]

Code according to ICD-10 and ICD-11

ICD-10 does not have a separate code for "pancreatic stone"; it is classified under the heading "other diseases of the pancreas." For calcifications/calculi, K86.89 "Other specified diseases of the pancreas" is used, which explicitly includes "pancreatic calculus" and "calcification of pancreas." For chronic pancreatitis, K86.0 (alcohol-induced) or K86.1 (other chronic pancreatitis) are used, with accompanying codes for exocrine insufficiency or diabetes. [5]

In ICD-11, chronic pancreatitis is defined in block DC32, where the subcategory DC32.0 "Calcific pancreatitis" is explicitly identified. This allows for more precise coding of the phenotype with stones/calcifications and the addition of post-coordination information on etiology (alcohol, hereditary forms), stage, and complications. For statistical and routing purposes, it is better to also reflect the phenotype of main duct obstruction, as it determines the choice of endoscopic/surgical approach. [6]

Table 1. Coding examples

Situation	ICD-10	ICD-11
Calcifying pancreatitis (non-alcoholic)	K86.1 ± K86.89 (calcifications/stones)	DC32.0 (Calcific pancreatitis)
Alcohol-induced chronic kidney disease with stones	K86.0 ± K86.89	DC32.3 + post-coordination "calcific"
Isolated calcification/stones unspecified	K86.89	DC32.Y (other HP) or DC32.0 according to visualization data
Exocrine pancreatic insufficiency	K86.81 (add.)	post-coordination of "exocrine pancreatic insufficiency"

Epidemiology

Calcifications are considered a highly specific sign of chronic pancreatitis and, according to observational data, are found in 30-60% of patients, more often in alcohol-associated cases (up to 40-60%, in older series - up to 90%). Frequency varies depending on diagnostic criteria, disease duration, and the availability of high-quality imaging. [7]

In tropical regions (e.g., southern India), "tropical" calcific pancreatitis has historically been described with a high prevalence: estimates range from 98 to 126 per 100,000 population, with onset at a young age, large ductal stones, and a high incidence of diabetes. Today, the spectrum of etiologic factors in Asia is changing, but the "calcific" phenotype is still more common than in the West. [8]

Some analyses emphasize that calcifications are not equivalent to a diagnosis of chronic pancreatitis in 100% of cases. They are also found in some neoplastic processes (for example, malignant intraperitoneal neoplasms), but in the vast majority of cases they remain a marker of chronic inflammation. This requires clinical and radiological correlation, especially in atypical cases. [9]

Table 2. Epidemiological landmarks

Indicator	Grade
Calcifications in patients with chronic pancreatitis	≈30-60% (higher in alcoholic chronic pancreatitis)
"Tropical" calcifying HP (south India)	≈98-126 per 100,000
Age of onset in "tropical" chronic pancreatitis	More often young people
Comment	Calcifications are also possible in non-CP (rare)

Reasons

The leading cause of the calcific phenotype is long-term chronic pancreatitis with ductal obstruction and protein plugs, which serve as a matrix for calcium carbonate deposition. In adults in the West, the alcohol-associated variant predominates; in some patients, smoking, metabolic, and dietary factors are significant. With prolonged progression, focal calcification becomes diffuse. [10]

Hereditary forms (PRSS1, SPINK1, CFTR, etc.) and "tropical" CP often occur with early and severe stone formation. Mechanisms include changes in the composition of the sap, disruption of protease inhibitors, secretion viscosity, and crystallization-modulating proteins. These cohorts have a higher risk of recurrent pain and early exocrine insufficiency. [11]

Stones can also form due to strictures/blockages of the main duct (consequences of pancreatitis, trauma, postoperative changes), and less commonly, due to cystic neoplasms, where thick secretions accumulate and salts precipitate. Therefore, with unilateral or "local" calcifications, it is important to exclude an alternative cause of obstruction. [12]

Risk factors

Modifiable factors include chronic alcohol consumption and smoking; their combination increases the risk of the calcifying phenotype and accelerates progression. Weight control and correction of deficiencies (including protein and micronutrients) are important in regions with nutritional deficiency. [13]

Non-modifiable factors include genetic predisposition (PRSS1, SPINK1, CFTR, CTRC, etc.) and place of residence (tropical zones with historically high prevalence). Patients from at-risk families are recommended genetic counseling and monitoring in centers with experience in the management of CP. [14]

Pathogenesis

Stone formation proceeds through the following stages: protein plugs in the ducts → calcium carbonate crystallization → calculus growth with fixation to the wall and obstruction. A persistent blockage maintains intrapancreatic hypertension, inflammation, and pain. The addition of strictures exacerbates the "vicious cycle." [15]

Parenchymal calcifications are a consequence of prolonged inflammation and necrosis; they correlate with the severity of structural damage and exocrine insufficiency. With prolonged progression, endocrine function is also impaired, leading to the development of "pancreatogenic" diabetes. [16]

Symptoms

The leading symptom is chronic or recurrent upper abdominal pain radiating to the back, intensifying after eating and drinking alcohol, and sometimes occurring at night. The pain is associated with ductal hypertension, inflammation of the nerve plexuses, and sometimes acute episodes caused by the migration of stone fragments. [17]

Steatorrhea (oily, shiny, difficult-to-flush stools), bloating, and weight loss are characteristic signs of exocrine insufficiency; over time, carbohydrate metabolism disorders develop. Complications include symptoms of common bile duct obstruction (obstructive jaundice), pseudocysts, and pancreatic fistulas. [18]

Table 3. Symptoms and mechanisms

Symptom	The most likely mechanism
Postprandial/night pain radiating to the back	Ductal hypertension, ductal plexus inflammation
Steatorrhea, weight loss	Exocrine insufficiency
Mechanical jaundice, itching	Compression/stricture of the terminal common bile duct
Recurrence of acute pain	Migration of fragments, transient obstruction

Classification, forms and stages

Based on their location, duct stones are divided into main duct stones (often radiopaque) and lateral branch stones; based on their structure, they can be single or multiple stones or conglomerates. Based on their clinical significance, they can be obstructive (with distal duct dilation) or non-obstructive (incidental finding/minimal symptoms). [19]

Most guidelines define "large" stones as stones >5 mm—these are less likely to be removed using standard ERCP techniques and require lithotripsy (ESWL/contact pancreatoscopy-guided lithotripsy). Size and density (radiolucent vs. radiodense) determine the choice of technique. [20]

Complications and consequences

Without treatment, pain, recurrent attacks of pancreatitis, progression of exocrine and endocrine insufficiency, and nutritional deficiencies persist. Ductal obstruction leads to the development of pseudocysts, strictures, pancreatic fistulas, and biliary obstruction. Some patients have an increased long-term risk of pancreatic cancer, especially with prolonged CP, although calcifications themselves are not a causative factor. [21]

When to see a doctor

Immediately - if there is a sharp increase in pain with vomiting and fever, signs of jaundice (yellowing of the sclera/skin, dark urine, light-colored stool), severe thirst and infrequent urination (dehydration). This may indicate an acute exacerbation, cholangitis, or complicated obstruction. [22]

Routine - for chronic postprandial pain, steatorrhea, progressive weight loss, fatty food intolerance, and the development of diabetes mellitus in a losing weight patient with upper abdominal pain. These symptoms require a targeted search for main duct obstruction and an assessment of glandular function. [23]

Diagnostics

The first step is a laboratory examination and elimination of "masks": a complete blood count/biochemistry (bilirubin, alkaline phosphatase, transaminases), glucose, and, in case of pain, lipase/amylase (may be normal in chronic pancreatitis). For gland function, the clinical picture of steatorrhea, fecal elastase-1, and body weight are used as a guide; nutritional deficiencies are also calculated. [24]

The second step is visualization. At the initial stage, high-quality CT or MRI/MRCP is sufficient to evaluate the parenchyma, ductal system, strictures, pseudocysts, and exclude cancer. Calcifications are usually clearly visible on CT; MRCP better shows ducts and "blockages." EUS is especially useful in cases of "unclear" imaging and for planning interventions. [25]

The third step is diagnostic and therapeutic ERCP for symptomatic obstruction: pancreatography, removal of small stones, and dilation/stenting of strictures are performed. If large radiodense stones >5 mm in the head/body are visualized, extracorporeal shock wave lithotripsy (ESWL) is performed followed by ERCP extraction of fragments. Radiolucent or small stones ≤5 mm are more amenable to standard ERCP methods. [26]

The fourth step is that if ESWL/ERCP fails, pancreatoscopy with contact lithotripsy (electrohydraulic/laser) or surgical decompression (lateral pancreaticojejunostomy/Puestow procedure, resection for localized head disease) is considered. The choice is made at a consultation, taking into account the anatomy and experience of the center. [27]

Table 4. Diagnostic algorithm

Step	Target	Tools
1. Laboratory/Functional Assessment	Exclude cholestasis, assess exocrine/endocrine function	Biochemistry, fecal elastase-1, nutritional profile
2. Non-invasive visualization	Confirm stones/calcifications, strictures	CT (pancreatic protocol), MRI/MRCP, EUS
3. Therapeutic endoscopy	Removal of small stones, stents, preparation for ESWL	ERCP
4. Lithotripsy/pancreatoscopy	Fragmentation of large/resistant stones	ESWL → ERCP; contact lithotripsy under pancreatoscopy
5. Surgery	Long-term decompression	Bypass/resection operations

Differential diagnosis

Not every calcification is chronic pancreatitis. Calcifications have been described in some cystic neoplasms (e.g., intraperitoneal cystadenomas, mucinous cystadenomas), rare tumors, and even benign conditions. Therefore, in cases of "local" or "eccentric" calcification and atypical clinical features, it is important to rule out neoplasia (MRCP, EUS biopsy). [28]

Pancreatic stones are distinguished from gallbladder and common bile duct stones by the localization of pain, the absence of typical "biliary" colic, and other imaging findings. In recurrent pancreatitis in young patients, genetic forms and "tropical" CP should be considered: calcifications appear early, often large, in the main duct. [29]

Treatment

The first priority is pain control, nutritional support, and correction of exocrine/endocrine insufficiency. Pancreatic enzymes are prescribed with food (dose adjusted based on clinical steatorrhea and body weight), along with dietary recommendations emphasizing adequate protein intake and alcohol limitation. Pain management is gradual: from non-opioid agents to short-acting opioids; for refractory pain, EUS neurolysis of the celiac plexus is an option. These measures are combined with ductal decompression. [30]

ERCP is the basic tool for small (≤5 mm) stones and soft conglomerates, especially those with radiolucency: papillotomy, balloon/basket, and irrigation; for strictures, balloon dilation and temporary stenting with regular replacement. For multiple small stones, sequential sessions provide a "sanitary" effect, but recurrence is possible if the proximal block is not removed. Quality of imaging and operator experience are critical for success. [31]

ESWL is the first-line treatment for radiodense stones >5 mm in the head/body, especially with distal dilation of the main duct. Fragmentation to <3 mm is achieved in a single cycle, followed by ERCP evacuation of fragments and/or stenting. The procedure is minimally invasive and well-tolerated; transient pain, pancreatitis, and hematuria are possible. Pain control after ESWL is comparable to surgery in the short term in carefully selected patients. [32]

Pancreatoscopy with contact lithotripsy (electrohydraulic or laser) is indicated when ESWL is unavailable or has failed to fragment, as well as for occipital stones behind the stricture. This technology allows for the fragmentation of stones under direct vision and immediate evacuation of fragments. According to modern series, this method is safe and effective as an adjunct to ERCP/ESWL, increasing the rate of complete duct sanitation. [33]

In cases of dominant stricture of the main duct, its correction is important: sequential plastic stents or fully covered metal stents (depending on individual indications), with monitoring every 3-6 months. Untreated stricture is the main predictor of pain recurrence and recurrent stone formation. Simultaneous correction of stones and stricture ensures the best long-term outcome. [34]

Surgery is preferred in cases of endoscopic failure, frequent recurrence of pain, severe duct dilation over a long period, and complications. The classic Puestow procedure (lateral pancreaticojejunostomy) ensures drainage along the entire length of the dilated duct; in cases of localized disease of the head, resection-drainage procedures (Frey/Beger) are chosen for simultaneous decompression and removal of the inflamed "mass" of the head. In the long term, in some patients, surgery is superior to purely endoscopic pain control. [35]

The choice between "endoscopy → surgery if unsuccessful" and "early surgery" depends on the phenotype: in the case of clear obstruction by one or more large stones in the head/body, it is reasonable to begin with ESWL + ERCP; in the case of an extended stricture and a "chain" of stones, or severe duct dilation, the chances of success with early surgery are higher. The decision is made at a consultation, taking into account the center's experience and the patient's preferences. [36]

Steatorrhea control and nutritional support remain part of therapy regardless of intervention. Enzyme preparations reduce steatorrhea and gas formation, improve body weight, and indirectly reduce visceral hypersensitivity. In diabetes, an antiglycemic regimen must be adjusted, taking into account the tendency toward hypoglycemia in the pancreatogenic variant; in case of deficiencies, replacement of fat-soluble vitamins, micronutrients, and protein is necessary. [37]

Repeated interventions are not uncommon: stones may recur, stents require scheduled replacement, and pain requires a combined approach (medications and interventions). Protocol-based management with follow-up visits (usually every 3-6 months in the first year) and access to a multidisciplinary team reduces the risk of treatment failure. [38]

Table 5. Tactics depending on the characteristics of stones

Characteristic	Preferred tactics
≤5 mm, radiolucent	ERCP (papillotomy, basket/balloon)
>5 mm, radiodense, head/body	ESWL → ERCP-evacuation
ESWL-resistant, "occipital" stones	Pancratoscopy + contact lithotripsy
Concomitant long stricture of the MPD	Ductal surgery (Puestow/Frey/Beger) after/instead of endoscopy

Prevention

There is no complete primary prevention, but reducing alcohol consumption and stopping smoking slows progression, reduces pain, and reduces the risk of recurrent stone formation. Early correction of strictures and duct decompression reduces the likelihood of new stones. In regions with nutritional deficiencies, protein-energy status should be addressed. [39]

Patients with genetic forms require monitoring in specialized centers and early referral if pain/weight loss/steatorrhea worsens. Patient education (diet, taking enzymes with every meal, monitoring stool/weight, and warning signs of complications) significantly reduces hospitalizations. [40]

Forecast

The prognosis is determined by pain control and preservation of glandular function. Successful decompression (endoscopic, lithotripsy, surgical) consistently reduces pain and the frequency of exacerbations, and timely enzyme/nutrition support slows the progression of steatorrhea and cachexia. However, recurrence of stone formation is possible, especially with persistent stricture and ongoing exposure to risk factors. [41]

The long-term risk of pancreatic cancer in chronic pancreatitis is increased, but the absolute risk depends on the phenotype and duration; there is no routine screening for everyone, and indications are discussed in high-risk groups. A "second look" is important in cases of atypical dynamics and "discrepancy" between clinical and imaging findings. [42]

FAQ

1) Do calcifications always indicate chronic pancreatitis?
Almost always, yes; this is a highly specific sign, especially with a typical clinical picture. However, there are rare exceptions (some cystic neoplasms), so in cases of "local" calcification and atypical symptoms, clarification is required (MRCP, EUS biopsy). [43]

2) When to initiate active treatment of stones?
When there is pain, recurrent exacerbations, or signs of main duct obstruction (distal dilation, steatorrhea, progressive weight loss). In these cases, the first line is endoscopic therapy ± ESWL; if unsuccessful, pancreatoscopy or surgery. [44]

3) Which is better: endoscopy or surgery?
For isolated/limited stones in the head/body with duct dilation, ESWL + ERCP is most often used. With extended strictures and "chains" of stones throughout the gland, long-term pain control is often better after decompression surgery (Puestow/Frey). The decision is made at a consultation. [45]

4) Are enzymes needed if stones have been removed?
Yes, if there is steatorrhea, weight loss, or low fecal elastase-1. Enzymes improve digestion, reduce bloating/diarrhea, and help restore weight—regardless of the intervention performed. [46]

5) What is the size threshold for ESWL?
Most guidelines use a threshold of >5 mm for radiodense stones in the head/body: ESWL followed by ERCP evacuation is indicated. Small stones ≤5 mm are more often removed by standard ERCP. [47]