Questions: Diagnosis and differential diagnosis, treatment of various clinical variants of chronic

pancreatitis, pancreatic cancer. Emergency care for acute pancreatitis.

DIFFERENTIAL DIAGNOSIS AND TREATMENT OF PANCREATIC
DISEASES
All diseases of the pancreas are divided into the following groups:
1) inflammatory diseases – acute and chronic pancreatitis.
2) pancreatic cysts;
3) pancreatic tumors.

Chronic pancreatitis (CP) is a chronic inflammatory disease of the pancreas characterized by the
development of diffuse or segmental fibrosis of the gland, and in the periods of exacerbation - its
edema and local necrosis. Long-term course of the disease leads to a violation of the external
secretory and endocrine functions of the pancreas. Numerous statistical data indicate an increase in
the incidence. Thus, in industrially developed countries, the number of patients with chronic
pancreatitis has increased 1.5-2 times over the past 20 years and amounted to 6.5% of all patients
with diseases of the digestive system. This increase is associated with an increase in alcohol
consumption and the incidence of gallstone disease.
Etiology and pathogenesis. As in acute pancreatitis, biliary-dependent and alcoholic forms account
for 70-80%. Biliary-dependent forms are most often associated with gallstone disease, especially
with small stones and the common bile duct, which, when they pass into the duodenum, increase
pressure in the wirsung duct (pancreatic duct) and lead to damage to the large duodenal duct. The
pathogenetic mechanism of chronic cholangiogenic pancreatitis is the difficulty of outflow of
pancreatic secretions. Alcoholism is an important cause of the development of CP, but in many cases
patients hide the fact of alcohol abuse from the doctor. Alcohol has a direct toxic effect on the
pancreatic parenchyma, increases the viscosity of pancreatic secretions and the content of proteins in
it, which leads to the formation of protein plugs in the small ducts of the gland. Protein umbilicals
clog the ducts and cause their structural damage, such as duct dilation and proliferation of their
epithelium, stretching of acinar tissue, and focal atrophy. Protein plugs, calcified, form calcifications.
Drug-induced pancreatitis develops more frequently. Among the drugs that most often damage the
pancreas. These include azathioprine, chlorthizide derivatives, estrogens, furosemide, and
tetracycline. Dysmetabolic forms are observed in hyperparathyroidism, hyperlipidemic syndrome
(familial hypercholesterolemia), hemochromatosis. The infectious origin of CP is likely if
pancreatitis is detected in the replicative phase of viral hepatitis B, when cytomegalovirus infection
and other viral infections are detected. Atherosclerotic abdominal ischemia and diabetic angiopathy
can also cause the development of chronic pancreatitis, especially in the elderly.

Clinical and morphological variants:

1. Interstitial edematous.
2. Parenchymal.
3. Fibro-sclerotic (indurative).
4. Hyperplastic (pseudotumorous).
5. Cystic.
Clinical picture. Manifestations of pancreatitis are largely determined by the clinical and
morphological variant and phase of the disease.
Interstitial edematous variant, sometimes called subacute, is characterized by a
relatively short history of Rare but significant exacerbations of the disease in the clinical and
laboratory picture resemble acute pancreatitis. Most patients have severe pain in the upper
abdomen, nausea, sometimes vomiting, which does not bring relief, palpation determines
pronounced soreness in the projection PJ. More than 90% of patients have a significant increase
in amylase activity in the blood serum and urine. At the height of the exacerbation, according to
ultrasound and CT, the size of the gland is usually moderately enlarged. Due to edema of the
gland and parapancreatic tissue, the contours of the organ are not learly formed: its structure is
heterogeneous. As the exacerbation subsides, the size of the pancreas becomes normal, and the
contours become clear. However, in contrast to acute pancreatitis, some of the morphological
changes are stable, for example, areas of moderate pancreatic compaction are preserved. Incases
of exacerbation, complaints are more often absent, although in some patients the use of fatty,
spicy food or alcohol causes moderate epigastric pain.
The parenchymal variant, also called recurrent, has alonger course (8-10 years). This
variant is characterized by alternating periods of exacerbation and remission. Clinical symptoms
in the acute period are less pronounced than in the interstitial-edematous variant; increased
amylase activity in the blood and urine is less frequent (in 70-80% of cases) and usually does
not reach high levels. More than half of the patients have symptoms of external secretory
pancreatic insufficiency: steatorrhea, polyphalia, and a tendency to diarrhea. According to
ultrasound and CT data, the size and contours of the gland are not significantly changed, the
structure is relatively uniform; there is a stable but uniform compaction of the organ. Changes in
the ductal system in most patients are not detected. During remission, some patients periodically
experience abdominal pain and dyspeptic symptoms.
The fibrosclerotic (indurative) variant usually has a long history. With diffuse lesion of
the gland, intense pain in the upper half of the abdomen is often observed, sometimes with
difficulty yielding to therapy. External secretory pancreatic insufficiency is observed in almost
all patients, and most of them require constant replacement therapy. Almost all patients have
asthenoneurotic syndrome: rapid exhaustion, low mood, sometimes depressive phenomena,
fixation on painful sensations. It is difficult for many patients to draw a clear line between
periods of exacerbation and remission of the disease. The amylase test in this variant is not very
informative; a moderate increase in amylase activity is observed only in half of the patients.
According to ultrasound and CT data, the size of the pancreas is either diffusely or locally
reduced, the parenchyma is in homogeneously compacted; the contours are clear, uneven;
calcifications are often detected. A number of patients show signs of dilatation of the pancreatic
ducts.
The hyperplastic (pseudotumorous) variant is relatively rare (approximately in 5% of
cases). In most patients, the disease lasts for a long time (more than 10 years). In the upper
abdomen, severe, persistent pain occurs. Many patients show clear signs of external secretory
pancreatic insufficiency. Insome cases, it is possible to feel a painful enlarged area of the gland,
similar to a tumor formation. Therapeutic measures often have little effect on the manifestations
of the disease. The amylase test is positive only in 50-60% of patients. Ultrasound and CT scans
reveal significantly enlarged areas of the gland. Its contours are not even in these areas. Often it
is possible to visualize the expansion of the pancreatic ducts. Differential diagnosis of this
variant with slow-growing pancreatic carcinoma is very difficult. To clarify the diagnosis, it is
necessary to perform repeated ultrasound and CT using a complete breast biopsy or dynamic
monitoring for at least 6-12 months.
Cystic changes of the pancreas are detected in 10-15% of patients with pancreatitis. The
formation of small (up to 15 mm in diameter) relatively stable cysts (more precisely,
pseudocysts, since they are not lined with epithelium) gives a certain originality to the course of
PC and allows it to be distinguished as a separate variant. The pain syndrome is more often
moderate, although in some patients during the formation of cysts, the pain reaches high
intensity. The amylase test is positive in almost 90% of patients, with hyperamylasuria
occurring 2 times more often than hyperamylasemia. A prolonged increase in amylase activity
in the urine хаis typical for the formation of pseudocysts. Ultrasound and CT scans reveal a
moderately diffuse or locally enlarged pancreas. Along with liquid formations, there are
inclusions of high density up to calcification. Often, an extension of the ducts system is
detected. In half of cases, the disease occurs with frequent exacerbations. The effect of
conservative treatment у in most patients is positive.
With any variant of the course of chronic pancreatitis, complications may occur.
Violation of the outflow of bile is often short-term in the form of transient mechanical jaundice.
The formation of pseudocysts and abscesses is usually recorded с by ultrasound and CT.
Compression of the portal and splenic veins of the inflammately altered pancreas is rarely
detected. In fact, in severe forms of PH with a predominant lesion of the body and tail of the
gland, subhepatic forms of portal hypertension develop quite often. Pancreatogenic diabetes
mellitus is clinically manifested only in severe advanced зашедшем pancreatitis, usually
proceeds easily and инсулинотерапии does not require insulin therapy.
Treatment. An important prerequisite for successful treatment of pancreatitis is the
elimination of pathogenic factors. Thus, in alcoholic pancreatitis, the patient should completely
stop drinking alcohol; in bipolar-dependent pancreatitis, a cholecystectomy should be performed
as early as possible after the detection of calculous cholecystitis and, if necessary, surgery on the
biliary tract. Diet is the most important way to prevent pain and dyspeptic disorders. Patients are
very sensitive to all kinds of dietary disorders. It is recommended to eat within the limits of diet
No. 5 with a restriction of fats and taking into account the patient's intolerance to certain foods
and dishes. Food should be taken 4-5 times a day in a warm form. Avoid juicy and spicy dishes.
Pain management is the most urgent and difficult task. If the pain syndrome is
moderately pronounced, it is sufficient to prescribe a diet, anti - cholinergic drugs (atropine,
platyphylline, gastrocepin) and antispasmodic drugs (no-shpa, papaverine) inside to relieve pain.
Reducing the functional activity of the pancreas and reducing the intensity of pain contributes to
the use of antacids, and if necessary- H2-receptor blockers or flow pump blockers. With
persistent pain syndrome, cholinolytics and antispasmodics are administered subcutaneously or
intramuscularly. Prescribe injections of analgesics (analgin, baralgin) or narcotic drugs
(promedol, fentanyl). In the absence of an effect, which is usually observed in the indurative
and pseudotumorous variant of pancreatitis, radiation therapy (a single dose of 0.3-0.4 Gy) or
high-energy pulsed laser irradiation of the pancreatic region can be used in a very limited
number of cases. For a course of 4-6 irradiations.
External secretory pancreatic insufficiency is usually well compensated by taking
enzyme preparations. Use pancreatin or preparations mezim-forte 10 000, creon, pancitrate.
Especially effective are new enzymatic preparations in which small pancreatin granules are
coated with an anti-acid coating (pancitrate, creon). Drugs are prescribed depending on the
degree of enzymatic insufficiency, 1-3 tablets during each meal.
When the exacerbation subsides and in the intercostal period, physiotherapy is
prescribed. Hydrotherapy (coniferous, radon and pearl baths) is indicated. Ultrasound
techniques and magnetotherapy are used. The tolerance of thermal procedures is very
individual. In the interventional period, a rational, balanced diet is recommended with the
exclusion of refractory fats, cold fizzy drinks and fresh warm bread; if signs of external
secretory pancreatic insufficiency persist, you should continue taking enzymatic preparations.
Sanatorium-resort treatment is effective (Essentuki,Leznovodsk , etc.).
Surgical treatment is performed for persistent or frequently recurring diseases that are
resistant to conservative therapy; local complications that do not respond to conservative
therapy (pseudocysts, abscesses, duodenal stenosis, etc.); changes in протоках the pancreatic
ducts that prevent the outflow of pancreatic secretions; suspected на рак pancreatic cancer.
If false cysts occur, the affected part of the gland is removed, but more often-the cystostomy.
With stenosis of the large duodenal papilla and dilation of the Wirsung duct, endoscopic or
transduodenal papillotomy or longitudinal pancreatojejunostomy is performed, as well as
resection of the gland tail with the formation of a pancreatic intestinal anastomosis. With biliary
-dependent pancreatitis, the best option is to disconnect the bile duct and pancreatic duct. A
promising method is the occlusion of the pancreatic duct using filling fluids (silicone elastomer
SKTN-M, etc.).

Pancreatic cysts are wall-bound accumulations of fluid that form in the parenchyma of the
gland or in the surrounding tissues, which have the appearance of a sac-like tumor. Cystic
changes in the gland a requite common, but cysts are heterogeneous in their origin.
There are congenital cysts, retention cysts formed as a result of blockage of the ducts, parasitic
cysts, as well as inflammatory and traumatic cysts formed during tissue breakdown and are
pseudocysts, since they are not lined with epithelium. Cystic formations in the pancreas
(pancreas) can be manifestations of cystadenoma or cystadenocarcinoma.
 Congenital cysts should be considered as a malformation. Often, cysts in the pancreas
are combined with cystic lesions of the liver and kidneys.
Cystic fibrosis caused by cystic fibrosis is associated with the release of a viscous
secretion rich in glycoproteins, which clogs the pancreatic ducts. Of the parasitic cysts,
echinococcus is most common.
Pseudocysts have the appearance of cavities formed as a result of the breakdown of
gland tissue when it is damaged or autolysis as a result of inflammation.
Cystadenomas probably arise as a result of proliferation of the epithelium of small ducts,
since it is this epithelium that lines the cystadenoma walls, while cystadenocarcinoma develops
in malignant fasting.
Symptoms depend on the size, number, location, origin of cysts as well as their
relationship with neighboring organs. With small cysts, symptoms may be absent for a long
time, or with inflammatory pseudocysts, signs of pancreatitis are noted. In the case of an
enlarged cyst, there are constant dull or paroxysmal pains, which are more often associated
with a change in body position than with eating. When the cyst is located in the glandular head,
compression syndrome is observed (duodenal stenosis, mechanical jaundice). A cyst located in
the body and tail of the pancreas can compress the left ureter, portal vein, and other organs.
With secondary infection of the cyst, involvement of the biliary system in the process, fever,
leukocytosis, and jaundice are observed. Neoplastic cysts have all the signs of a malignant
tumor: infiltrative growth, a tendency to metastasis. An important objective symptom of a cyst
is the probing of the tumor. The pancreatic head cyst is palpable at the level of the navel, the
body and tail cyst - in the left hypochondrium. A benign cyst is palpated as a smooth, elastic
formation of a round or oval shape. A malignant cyst is usually irregular in shape, dense, with
an uneven surface.
With a decrease in the mass of the functioning parenchyma, signs of exocrine
(maldigestia syndrome) and endocrine (diabetes) insufficiency appear .
Diagnostics.The results of ultrasound examination (ultrasound) and computed
tomography (CT) are crucial in the diagnosis of pancreatic cysts. In these studies, even small
cavities are clearly visible. X-ray examination of the gastrointestinal tract allows you to clarify
the location of the cyst in relation to the stomach and colon (it can push these organs away).
Inflammatory and traumatic pseudocysts are characterized by prolonged hyperamylasemia and
hyperamylasuria. With an infected cyst, leukocytosis with a rod-shaped shift and an increase in
ESR are observed. A parasitic cyst is characterized by calcification of its capsule and positive
serological tests.
Treatment. For large pancreatic cysts, surgical treatment is performed: cystectomy or
partial resection of the pancreas (radial surgery), external drainage (application of an external
fistula), internal drainage (cisgastrostomy, cystoduodenostomy or cystojejunostomy).
In case of external secretory and endocrine pancreatic insufficiency replacement therapy
is performed
• control of vascular insufficiency (reopoliglyukin-400-500 ml intravenously, hydrocortisone-
250 mg intramuscularly or intravenously, prednisone -30-60 mg orally);
• correction of the water-electrolyte composition (500 ml of 0.9% sodium chloride solution, 500
ml of 5% glucose solution, 20 ml of panangin); liquid and electrolytes are administered under
the control of diuresis (the release of 50 ml of urine per hour indicates о compensation for the
volume of circulating blood).
After the clinical signs subside, treatment is continued for another 1-2 months according to the
principles of treatment of chronic pancreatitis (see chronic pancreatitis).

Pancreatic cancer is a malignant tumor that develops mainly from the epithelium of small and minute
pancreatic ducts. Factors predisposing to the development of pancreatic cancer include smoking (the
incidence of pancreatic carcinoma in smokers is 2-2.5 times higher), chronic pancreatitis, and
diabetes mellitus (the probability of developing pancreatic cancer doubles). The risk of developing
cancer is increased by exposure to certain chemicals (such as naphthaolamine), eating high-fat foods,
and alcoholism. The question of the association of excessive coffee consumption with a possible risk
of cancer is discussed.
Classification of pancreatic cancer by stages:
Stage I - the tumor diameter does not exceed 3 cm, there are no metastases.
II stage – a tumor larger than 3 cm, but not extending beyond the organ, there may be
single metastases in nearby regional lymph nodes;
III stage – infiltrative growth of the tumor in the surrounding tissue, metastases of the
tumor in regional lymph nodes;
IV stage – there are distant metastases. In addition, it is customary to divide cancer by
localization: cancer of the head of the pancreas (60-65%), cancer of the body and tail of the
pancreas (30-35%), isolated cancer of the tail of the pancreas (up to 5%).
Clinical picture. Weight loss, abdominal pain, anorexia and jaundice are classic symptoms
of the disease. Nausea, weakness, fatigue, vomiting, diarrhea and pain in the spine are also quite
common. Weight loss increases rapidly, the patient loses more than 25% of the original body
weight, and this is not always explained only by anorexia. Pain is observed in 7-90% of patients;
with pancreatic head involvement, pain is more often localized in the epigastric region or in the
upper right quadrant of the abdomen, with tail involvement-in the left hypochondrium. Pain can
be blunt, burning, drilling, and often radiate to the back. A sharp increase in pain may indicate
the growth of the tumor in the retroperitoneal nerve plexus.
Jaundice occurs in 80-90% of patients with a pancreatic head tumor and in 10-40% of
patients with lesions of the body and tail. Jaundice increases rapidly and is accompanied by
itching of the skin. Many patients have neuropsychiatric disorders, insomnia, anxiety, anger,
agitation, a feeling of near death, suicidal intentions. Feel the seal in the depth of the abdominal
cavity, which sometimes transmits aortic pulsation, usually succeeds only with advanced,
inoperable cancer, more often with its localization in the body and tail of the gland. Although
the gallbladder is always enlarged in the presence of jaundice, it can be palpated in 15-40% of
cases (Courvoisier's symptom); thrombophlebitis is observed in 10% of patients with pancreatic
cancer, and migrating thrombophlebitis in some cases may be the first sign of the disease.
Diagnostics. Correct assessment of the clinical picture is of great importance in the
diagnosis of pancreatic cancer. Suspicious signs of pancreatic cancer are:
• age over 50 years.
• unexplained weight loss;
• persistent pain in the upper abdomen, especially with negative results of the gastrointestinal
tract study;
• unexplained pain in the spine;
• relapses of acute pancreatitis that occur without obvious causes:
• signs of exocrine pancreatic insufficiency that appear without obvious reasons;
• sudden development of diabetes mellitus without aggravating circumstances (obesity, family
predisposition to diabetes);
• rapid development of mechanical jaundice without a previous pronounced pain syndrome;
• migrating thrombophlebitis.
Diagnosis of pancreatic cancer is based on the results of instrumental studies
(ultrasound, CT, EPCG). Ultrasound can detect tumors in the head and body of the pancreas
larger than 2 cm in 70-90% of patients. Smaller tumors, as well as pancreatic tail tumors, are
more difficult to recognize. Based on CT results, the correct diagnosis of pancreatic cancer can
be established in 80% of patients, in 5-10% of cases of proven carcinoma, CT reveals only a
diffuse enlargement of the gland, rather resembling pancreatitis. CT has some advantage over
ultrasound, as it allows you to better visualize the pelvis and tail of the pancreas, as well as
adjacent organs. EPCG reveals narrowing, deviation or obstruction of the main or large
pancreatic ducts in 75-80% of patients, although in some cases the sechanges are determined
earlier than it is possible to detect signs of a tumor using ultrasound and CT. To verify the
diagnosis, if necessary, a targeted biopsy can be performed under the control of ultrasound or
CT. Laboratory biochemical blood tests can only clarify the nature of jaundice (obturation,
parenchymal, hemolytic). The amylase test has no significant significance in pancreatic cancer;
 a moderate increase in amylase in the blood and urine is observed only in 10-20% of patients.
Enzyme-linked immunosorbent assay of tumor markers has expanded the possibilities for
diagnosing pancreatic cancer. The indicators of carbo-hydrate antigen (Ca-19-9) and cancer -
embryonic antigen (CEA) can be used to assess not only the presence of pancreatic cancer, but
also the possibility of tumor metastases. The level of Ca-19-9 is increased 10-20 times in 80-
90% of patients with pancreatic cancer; a sharp increase in the level of Ca-19-9 or a
simultaneous increase in the level of Ca-19-9 and CEA indicates the presence of tumor
metastases. A decrease in tumor markers after radiological surgery indicates a favorable
outcome.
Treatment. Until now, pancreatic surgery is rarely performed. Total pancreatoduodenal
resection leads to the development of fatal diabetes, so this operation is not performed. Usually,
a partial pancreatoduodinal resection is performed with the application of a pancreatic-intestinal
anastomosis. In cancer of the head of the pancreas, resection of the head and part of the body of
the gland is performed, in cancer of the body and tail-resection of the body and tail of the
pancreas together with splenectomy. According to the literature, the proportion of radical
operations does not exceed 18%, postoperative mortality is 10-70%, depending on the selection
of patients and the surgeon's experience. The 5-year survival rate is not higher than 15%.
Chemotherapy with fluororacil (total dose for a course of 4-5 g) gives a temporary effect only in
15-20% of patients; chemotherapy (5-fluorouracil, cyclophosphamide, methotrexate,
vincristine) – in 20-30% of patients.

Treatment of non-acute pancreatitis

For the treatment of non-severe pancreatitis, it is sufficient to conduct a basic treatment complex:

- hunger,

- probing and aspiration of gastric contents,

- local hypothermia (cold on the stomach),

- analgesics,

- antispasmodics,

- infusion therapy in the amount of up to 40 ml per 1 kg of patient's body weight with forcing of diuresis
within 24-48 hours.

Basic therapy should be enhanced with anti-secretory and anti-enzyme therapy.

If there is no effect from basic therapy for 6 hours and at least one of the signs of severe pancreatitis is
present, severe pancreatitis should be detected and the patient should be transferred to the intensive care unit
(intensive care unit) and treated in accordance with severe acute pancreatitis.

Intensive therapy of severe pancreatitis

The main type of treatment is intensive conservative therapy. At the same time, the basic complex should be
supplemented with a specialized treatment complex, the effectiveness of which is maximum at an early start
of treatment (the first 12 hours from the onset of the disease). Surgical intervention in the form of
laparotomy is indicated for the development of surgical complications that cannot be eliminated by
endoscopic methods (destructive cholecystitis, gastrointestinal bleeding, acute intestinal obstruction).

Specialized treatment.

Anti-secretory therapy (optimal duration – the first three days of the disease):

- the drug of choice-sandostatin (octreotide) 100 mcg 3 times subcutaneously;

- reserve drugs- kvamatel (40 mg 2 times iv), 5-fluorouracil (5% - 5 ml iv).

Rheologically active therapy (heparin, reopoliglukin, refortan).

Compensation for plasma loss.

Correction of water-electrolyte and protein losses (in total, at least 40 ml of appropriate infusion agents per 1
kg of body weight; the ratio of colloidal and crystalloid solutions is 1: 4).

Histoprotection:

- anti-enzyme therapy (optimal duration-the first 5 days of the disease;

kontrikal – not less than 50,000 units, gordox – not less than 500,000 units in/in);

- antioxidant and antihypoxant therapy.

Detoxification:

- in severe acute pancreatitis, extracorporeal detoxification methods are indicated, of which the most
effective is serial therapeutic plasmapheresis (after BCC replenishment and in the absence of endotoxin
shock), followed by plasmosamination (1-3 sessions after 24-48 hours, the average volume of
plasmoexfusion is about 1 liter); each session of extracorporeal detoxification (in addition to
plasmapheresis) it should be accompanied by rehydration and correction of water-salt metabolism in the
mode of for ceddiuresis;

- the process of detoxification in severe acute pancreatitis can also be achieved by evacuation of toxic
exudates (peritoneal and retro-peritoneal) during laparoscopic (or laparocentesis), drainage of the abdominal
cavity and laparoscopic decompression of retroperitoneal tissue.

Antibiotic therapy (broad spectrum of action):

Cephalosporins of III-IV generations or fluoroquinolones of II-III generations in combination with

metronidazole.