Кафедра хирургических

болезней

ACUTE
PANCREATITIS
 Clinical anatomy
●Pan – all , creas - meat (all of the meat). The
pancreas develops from three rudiments: two
ventral and one dorsal. At 4-5 weeks of fetal
development, there is already a close
relationship with duodenum and choledoch. Lies
behind the stomach at L1 - L2. Length 15-23 cm,
height - 3-6 cm, weight 70-150 g. Isolated head
with hook-shaped process, neck, body and tail.
●No clear capsule.
 ACUTE PANCREATITIS
●The incidence of acute pancreatitis (AP)
has increased during the past 20 years.
Most patients develop a mild and self-
limited course; however, 10% to 20% of
patients have a rapidly progressive
inflammatory response associated with
prolonged length of hospital stay and
significant morbidity and mortality.
Patients with mild pancreatitis have a
mortality rate of less than 1%, but in severe
pancreatitis, this increases up to 10% to
 ACUTE PANCREATITIS
●The most common cause of death in this
group of patients is multiorgan dysfunction
syndrome. Mortality in pancreatitis has a
bimodal distribution; in the first 2 weeks,
also known as the early phase, the
multiorgan dysfunction syndrome is the
final result of an intense inflammatory
cascade triggered initially by pancreatic
inflammation. Mortality after 2 weeks, also
known as the late period, is often caused
by septic complications.
 Definition
Acute pancreatitis is initially an aseptic
inflammation of the pancreas, in which it is
possible to damage the surrounding tissues
and distant organs, as well as systems.
THE MAIN COMPONENTS OF THE ACUTE
DESTRUCTIVE PANCREATITIS

ACTUALLY
PANCREATITIS

PERITONITIS PARAPANCREATITIS
 Relevance of the problem
● The increase in the incidence rate (from 47 to 238
people per 1 million population per year) with a steady
trend towards growth and the proportion of severe
forms of AP.
● The overall case fatality rate from 4.5-15%, in
destructive forms of 24-60%
● In 73% of patients after pancreatic necrosis there is a
persistent disability.
● The peak incidence of patients with acute pancreatitis
falls on persons of active working age 30-50 years.
● The duration of inpatient treatment is on average 65
days.
 Etiology
● AP as an independent disease is polietiologic, but
monopatogenetic disease.
● Any reason that causes hypersecretion of pancreatic
juice and obstruction of its outflow with the
development of hypertension in the pancreatic ducts,
cast in the ducts of the cytotoxic and activation of
pancreatic enzymes substances, direct damage
pancreatitits, can lead to the development of AP.
 Etiology
● 1. Acute alcohol-alimentary pancreatitis– 55% .
● 2. Acute biliary pancreatitis (occurs due to bile reflux
in the pancreatic ducts in biliary hypertension, which
occurs, as a rule, due to cholelithiasis, sometimes –
from other causes: diverticula, papillitis, opisthorchiasis,
etc.)– 35%.
● 3. Acute traumatic pancreatitis (due to pancreatic
injury, including operating room or after ENDOSCOPIC
RETROGRADE CHOLANGIOPANCREATOGRAPHY ERCP)
-2 – 4 %.
 Etiology
4. Other etiological forms of causes: autoimmune
processes, vascular insufficiency, vasculitis,
medications (hydrochlorothiazide, steroid and non-
steroid hormones, mercaptopurine), infectious diseases
(viral mumps, hepatitis, cytomegalovirus), allergic
factors (varnishes, paints, smells of building materials,
anaphylactic shock), hormonal processes during
pregnancy and menopause, diseases of the nearby
organs (gastro, penetrating ulcer, tumors of the
hepatopancreatoduodenal region) – 6 – 8%.
●Gallstones and ethanol abuse account for
70% to 80% of AP cases.
●In pediatric patients, abdominal blunt
trauma and systemic diseases are the two
most common conditions that lead to
pancreatitis.
 Pathogenesis
● The combination of several triggering factors becomes the
impetus for the initial intraacinar activation of proteolytic
enzymes and pancreatic autolysis.
● Primary factors of aggression :
а) pancreatic enzymes: trypsin, chymotrypsin, cause
proteolysis of tissue proteins.
б) phospholipase destroys cell membranes.
в) lipase hydrolyses intracellular triglycerides to fatty acids and,
connecting with calcium, leads to lipolytic necrosis in the
pancreas, retroperitoneal tissue and mesentery of the small
and large intestine.
г) elastase destroys vessel walls and inter-tissue connective
tissue structures, which leads to necrosis.
● Active enzymes begins to act locally and goes beyond the
pancreas parenchyma, getting on the portal system in the liver,
lymphatic system in the circulating blood.
 Pathogenesis
● After entering the blood of pancreatic enzymes, the
kallikrein-kinin system is activated with the formation
and release of secondary aggression factors - free
kinins (bradykinin, histamine and serotonin).
● It is the activation of kinins that manifests itself as a
pain syndrome and leads to an increase in vascular
permeability with the formation of extensive tissue
edema, peritoneal exudation and thrombohemorrhagic
changes.
● Active phospholipase stimulates the production of
prostaglandins substances that enhance the secretory
activity of pancreas.
 Pathogenesis
●The factors of the aggression of the third order
is the importance of cytokines ( interleukin 1, 6
and 8, tumor necrosis factor, platelet-activating
factor, prostaglandins, thromboxane,
leukotrienes, nitric oxide), which is produced by
macrophages, mononuclear cells, neutrophils on
the background of microcirculatory disorders,
hypoxia.
 Pathogenesis
● Cytokines, enzymes, metabolites of different nature,
formed in the pancreas, adipose tissue, intestinal wall,
abdominal cavity increase the permeability of the
intestinal wall, there is a translocation of intestinal
flora, contribute to the flow of toxins into the portal and
systemic blood flow and lymphatic bed with the defeat
of target organs: liver, lungs, kidneys, heart, brain,
gastric and intestinal mucosa.
● Factors of aggression and organ dysfunction create a
syndrome of mutual aggravation.
 Atlanta Criteria for Acute
Pancreatitis
●In 1992, the International Symposium on
Acute Pancreatitis defined severe
pancreatitis as the presence of local
pancreatic complications (necrosis,
abscess, or pseudocyst) or any evidence of
organ failure. Severe pancreatitis is
diagnosed if there is any evidence of organ
failure or a local pancreatic complication.
 Atlanta Criteria for Acute
Pancreatitis
Systemic Complications
● Disseminated intravascular coagulation
(platelet count ≤100,000)
● Fibrinogen <1 g/liter
● Fibrin split products >80 μg/dL
● Metabolic disturbance (calcium level ≤7.5
mg/dL)
 Atlanta Criteria for Acute
Pancreatitis
Local Complications
●Necrosis
●Abscess
●Pseudocyst
Severe pancreatitis is defined by the
presence of any evidence of organ failure
or a local complication
 Atlanta Criteria for Acute
Pancreatitis
Organ Failure, as Defined by
● Shock (systolic blood pressure <90 mm
Hg)
●Pulmonary insufficiency (Pao2 <60 mm Hg)
●Renal failure (creatinine level >2 mg/dL
after fluid resuscitation)
●Gastrointestinal bleeding (>500 mL/24 hr)
● Acute pancreatitis
easy
heavy
● Sharp liquid formations
● Pancreatonecrosis
Sterile pancreatic necrosis
Infected pancreatic necrosis
Acute pseudocyst
Pancreatic abscess
 Classification of the Russian
society of surgeons– 2014г
● 1. Mild acute pancreatitis. Pancreonecrosis in this form of
acute pancreatitis is not formed (edematous pancreatitis) and
organ failure does not develop.
● 2. Acute pancreatitis of medium degree. It is characterized by
the presence of either one of the local manifestations of the
disease: peripancreatic infiltrate, pseudocyst, borderline
infected pancreonecrosis (abscess) - or/and the development
of common manifestations in the form of transient organ
failure (no more than 48 hours).
● 3. Severe acute pancreatitis. It is characterized by the presence
of either unlimited infected pancreonecrosis (purulent necrotic
parapancreatitis), or/and the development of persistent organ
failure (more than 48 hours).
 Phases of acute pancreatitis
● Edematous (interstitial) pancreatitis in frequency is
80-85% in the structure of the disease. It is
characterized by a mild severity of the disease and the
rare development of local complications or systemic
disorders, the phase course does not have.
● Necrotic pancreatitis (pancreonecrosis) occurs in
15-20% of patients, is always clinically manifested by
an average or severe degree of the disease, has a
phase course of the disease with two peaks of
mortality – early and late. After the early phase, which
usually lasts for the first two weeks, followed by a
second or later phase, which can be delayed for a
period of weeks to months.
 Phases of acute pancreatitis
● Phase I – early, in turn, is divided into two periods :
● - Phase IA is usually the first week of the disease.
During this period, there is the formation of necrosis
foci in the pancreatic parenchyma or the surrounding
tissue of various volumes and the development of
endotoxicosis. Endotoxicosis is manifested by light or
deep systemic disorders in the form of organ (multi-
organ) insufficiency. The maximum period of necrosis
formation in the pancreas is usually three days, after
this period it does not progress in the future. However,
in severe pancreatitis, the period of its formation is
much less (usually 24-36 hours).
 Phases of acute pancreatitis
IА phase,
In the abdominal cavity there is an accumulation of
enzymatic effusion (enzymatic peritonitis and
parapancreatitis), which is one of the sources of
endotoxicosis. The average severity of the disease is
manifested by transient dysfunction of individual
organs or systems. In severe forms of the disease in
the clinical picture may be dominated by the
phenomenon of organ (multi-organ) failure:
cardiovascular, respiratory, renal, hepatic, etc.
 Phases of acute pancreatitis
● I В phase, as a rule, the second week of the
disease. Is characterized by the body's reaction
to the formed foci of necrosis (as in pancreas
and parapancreatic tissue). Clinically prevalent
phenomenon resorptive fever, is formed
peripancreatic infiltration.
 Phases of acute pancreatitis
● Phase II – late, sequestration phase (usually begins
with the 3rd week of the disease, can last several
months). Sequesters in the pancreas and
retroperitoneal tissue usually begin to form from the
14th day of the onset of the disease. With the rejection
of large fragments of necrotic pancreatic tissue,
depressurization of its ductal system and the
formation of an internal pancreatic fistula can occur.
Two variants of this phase flow are possible
● · aseptic sequestration
● · septic sequestration - infected pancreonecrosis, which may
be limited (abscess) or undivided (purulent necrotic
parapancreatitis).
 symptoms
● Clinical manifestations depend on morphological form,
presence or absence of functional disorders and organic
complications.
Pain syndrome

● The initial manifestations of AP are characterized by severe

pain in the upper abdomen of a permanent nature with
irradiation in the back, shoulder blades, hypochondrium and
behind the sternum (encircling pain).

● The patient may lose consciousness from the intensity of the

pain. Pain in AP is not increased by coughing or deep breathing.
Severe pain syndrome without treatment lasts from several
hours to 2-3 days.
 symptoms
Vomiting
● Vomiting is repeated, very persistent and occurs after
each INTAKE of water or food and does not relieve the
patient's condition.
● Vomiting act even leads to increased pain – increased
pressure in the bile and pancreatic ducts, which
contributes to the progression of edema-destructive
process in the pancreas.
● Vomit initially contain food residues, and then only
mucus, bile. When joining erosive gastritis - vomiting
coffee grounds.
 symptoms
●Other mechanisms of vomiting: progressive
paresis of the intestine (5-7 days) and the
presence of high intestinal obstruction (8-12
days) at the expense of compression of 12
duodenal ulcer with infiltration of the head of the
pancreas. Feature of such vomiting in the
absence of preliminary nausea.
 symptoms
●Somewhat later in the upper abdomen appear
his swelling and pronounced tympanitis due to
paresis of the stomach and transverse colon.
For severe AP is characterized by the weakening
and complete disappearance of peristaltic
intestinal noise associated with dynamic
intestinal obstruction.
 symptoms
● At the very beginning of the disease, the pulse may
even be slow, and blood PRESSURE – increased. Only
then revealed tachycardia and hypotension. In severe
cases, AP very quickly develop the phenomenon of
cardiovascular, pulmonary, hepatic-renal and endocrine
insufficiency.
● At the beginning of the disease, the body temperature
is normal or reduced, subsequently increases and
remains subfebrile for a long time. A higher
temperature indicates the development of
complications of AP. Therefore, depending on the
characteristics of the current can be defined as a
complicated AP and uncomplicated.
 Psychotic disorders
● It develops due to brain intoxication – is considered a
typical symptom of AP. The predominant delirious
syndrome is a disorder of consciousness, disturbed
orientation in time and place. Sharp motor and speech
excitement, fear, anxiety, hallucinations. Recovery may
be simultaneous with somatic disorders, but may be
late. The severity of mental disorders does not always
correspond to the degree of destruction of the gland.
Compounded by the background, often the source of
cerebral and vascular insufficiency.
 Thrombohemorrhagic syndrome
● Causes: pancreatic enzyme evasion in the blood, deep
microcirculation disorders, hypoxia and acidosis, immune
aggression.
● Evident from the first hours. The essence scattered in a
hypercoagulable state and fibrinolizina. Aggravated by
disorders of microcirculation, inhibits the metabolism of cells.
Quickly, the stage of hypercoagulation passes into
consumption coagulopathy with the development of
thrombocytopenia. As a result, intravascular coagulation
inhibits hemostasis. In parallel, proteases, acting on the
proteins of the basal membrane of the vascular wall, increase
its permeability - common hemorrhages.
● Clinic of thrombohemorrhagic syndrome: increased thrombosis
of blood vessels at the puncture site, hemorrhage at the
puncture site due to the subsequent development of
consumption coagulopathy.
 Diagnosis
●The cornerstone of the diagnosis of AP is the
clinical findings plus an elevation of pancreatic
enzyme levels in the plasma. A threefold or
higher elevation of amylase and lipase levels
confirms the diagnosis. The serum half-life of
amylase is shorter than that of lipase. In
patients who do not present to the emergency
department within the first 24 to 48 hours after
the onset of symptoms, determination of lipase
levels is a more sensitive indicator to establish
the diagnosis.
 Diagnosis
●Lipase is also a more specific marker of AP
because serum amylase levels can be
elevated in a number of conditions, such as
peptic ulcer disease, mesenteric ischemia,
salpingitis, and macroamylasemia.
 Diagnosis
●Patients with AP are typically
hyperglycemic; they can also have
leukocytosis and abnormal elevation of
liver enzyme levels. The elevation of alanine
aminotransferase levels in the serum in the
context of AP confirmed by high pancreatic
enzyme levels has a positive predictive
value of 95% in the diagnosis of acute
biliary pancreatitis.
 Diagnostics
Diagnostic tasks :
1) diagnosis pancreatitis;

2) the detection of patients with severe

pancreatitis (destructive pancreatitis);

3) the definition of infection of pancreatic

necrosis.
 Physical examination
● Objective data in the examination of the patient in the
first hours of the disease are scarce. Attention is drawn
to the change in skin color (pallor, cyanosis, jaundice.
For patients with AP characterized by mild and
percussion pain in the upper abdomen by the
projection of the pancreas. The defense of the muscles
of the anterior abdominal wall is not pronounced
sharply. In the early period of AP can be caught
localized in the upper abdomen Schetkin-Blumberg
symptom.
 Physical examination
●Cyanotic spots on the skin of the abdomen and
limbs (symptom of Mondor), petechiae around
the navel, on the gluteal areas due to damage to
peripheral vessels (symptom of Grunwald).
●Patients are afraid of palpation - Mondor.
“Rubber” abdomen due to the isolated swelling
of the transverse colon.
 Characteristic symptoms of acute
pancreatitis
●– the symptom of Mayo-Robson is pain in the
hypochondrium, more often in the right, as well
as on the posterior surface of the abdomen in
the left rib-vertebral corner;
●– the symptom of Voskresensky is the absence
of pulsation of the abdominal aorta above the
navel as a result of compression of its
edematous pancreas;
●–the symptom of Kurte is transverse tenderness
and resistance 6-7 cm above the umbilicus,
corresponding to the projection of the pancreas.
 Laboratory research
●Leukocytosis
●Lymphopenia
●Anemia
●Dysproteinemia
●Hypocalcemia
●Activity of pancreatic enzymes (amylase,
diastase)
 Imaging Studies
●Although simple abdominal radiographs
are not useful for diagnosis of pancreatitis,
they can help rule out other conditions,
such as perforated ulcer disease.
Nonspecific findings in patients with AP
include air-fluid levels suggestive of ileus,
cutoff colon sign as a result of colonic
spasm at the splenic flexure, and widening
of the duodenal C loop caused by severe
pancreatic head edema.
Reactive pleural effusion with
pancreatitis
 Imaging Studies
●The usefulness of ultrasound for diagnosis of
pancreatitis is limited by intra-abdominal fat and
increased intestinal gas as a result of the ileus.
Nevertheless, this test should always be ordered
in patients with AP because of its high
sensitivity (95%) in diagnosing gallstones.
Combined elevations of liver transaminase and
pancreatic enzyme levels and the presence of
gallstones on ultrasound have an even higher
sensitivity (97%) and specificity (100%) for
diagnosing acute biliary pancreatitis.
 Ultrasound diagnostics
● Ultrasonography remains a screening method for
assessing the condition of the pancreas , biliary
system, abdominal and pleural cavities in acute
pancreatitis. Ultrasound allows to diagnose acute
pancreatitis in 40-86% of cases, but it does not always
help to reliably verify the form of acute pancreatitis,
characterize the state of retroperitoneal tissue. The
attraction of methods of measurement of
hemodynamic parameters in the visceral vessels, the
density of the pancreas and retroperitoneal fat allows
to improve the specificity, sensitivity and accuracy of
ultrasonography in the pancreatic necrosis.
Ultrasound symptoms of edematous
pancreatitis
● Indirect symptoms
diffuse enlargement of the pancreas

● Direct symptoms
focal hypoechoic area in the parenchyma
 ACUTE INTERSTITIAL PANCREATITIS
1 variant – 32-35%

The acoustic density of the The acoustic density of the

pancreas is sharply pancreas is sharply reduced
reduced, the size is
increased, the pancreatic
duct is expanded
Ultrasound symptoms of destructive
pancreatitis
● Indirect symptoms
– diffuse enlargement of the pancreas
– effusion into the lesser SAC
– effusion in the retroperitoneal space
– effusion in the abdomen
● Direct symptoms
– focal hypoechoic area in the
parenchyma
 TRANSFORMATION OF FOCI OF
DESTRUCTION
48 to 72 hours from onset

Large anechogenic site of Large anechogenic site of

destruction of the body of the destruction along the posterior
pancreas surface of the tail of the
pancreas (p).
 TRANSFORMATION OF FOCI OF
DESTRUCTION
48 to 72 hours from onset

Transformation of a large Large hypoallergenic area of

hyperechogenic site of destruction in the area of the
destruction of the body and tail tail of the pancreas and
of the pancreas (p) into pancreatic fluid accumulation
anechogenic foci and the
development of inflammation
ENZYMATIC PERITONITIS
Enzymatic transformation of
parapancreatitis
 PANCREATOGENIC INFILTRATION

Infiltration in omental bag Large infiltrate in the

(lesser sac) mesogastrium on the right
 TRANSFORMATION OF THE
PANCREATOGENIC INFILTRATE

Transformation of the infiltrate along Transformation of the infiltrate in the

the descending colon with the root of the mesentery of the small
appearance of a liquid component intestine
 ACUTE PANCREATIC FLUID

Pancreatic accumulation of Pancreatic accumulation of

fluid in the body of the pancreas fluid in the area of the tail of the
pancreas, communicating with
the left pleural cavity
 PANCREATIC ABSCESS

The abscess formation of large Pancreatogenic infiltration. The

infiltration of the left epigastrium presence of gas bubbles in the
infiltrate
 NECROTIC PARAPANCREATITIS

The spread of parapancreatic The spread of parapancreatic

infiltrate in the left half of the infiltrate in the right half of the
abdominal cavity abdominal cavity
 Laparoscopy
● Laparoscopy it is a necessary diagnostic and treatment
method. However, the method does not always allow to
directly examine the pancreas, retroperitoneal tissue,
to assess the scale and nature of the lesion of the
pancreas and retroperitoneal space. Technique of
video laparoscopy allows to perform a decompression
operation on the gall bladder, formed through
necrosectomy omentopancreatobursostoma and
dynamic laparoscopy and sanitation of the abdominal
cavity in pancreatogenic peritonitis.
Indications for laparoscopy

1. Peritoneal syndrome and/or

ULTRASONIC signs of free liquid in
abdominal cavity
2. Differential diagnostics with other
acute surgical diseases of the
abdominal organs
 Tasks of laparoscopy
1. Diagnostics

2. Analysis of the severity of pancreatitis

3. Treatment
 Computer tomography
● Computer tomography it is the most sensitive method of
research (71-100%) in acute pancreatitis and its complications,
giving comprehensive information about the state of the
pancreas and retroperitoneal space, involvement in the process
of biliary tract, adjacent vascular structures and gastrointestinal
tract.
● Contrast CT (pancreatic angiography) it allows to diagnose the
presence of pancreatic necrosis with high accuracy, to assess
its scale and localization, to identify a variety of angiogenic
complications (pancreatic and parapancreatic vessels, the
formation of pseudoaneurysms, occlusion of the portal vein
branches).
●Contrast-enhanced computed tomography
(CT) is currently the best modality for
evaluation of the pancreas, especially if the
study is performed with a multidetector CT
scanner.
●The most valuable contrast phase in which
to evaluate the pancreatic parenchyma is
the portal venous phase (65 to 70 seconds
after injection of contrast material), which
allows evaluation of the viability of the
pancreatic parenchyma, amount of
peripancreatic inflammation, and presence
of intra-abdominal free air or fluid
collections.
●Noncontrast CT scanning may also be of
value in the setting of renal failure by
identifying fluid collections or extraluminal
air.
●Using imaging characteristics, Balthazar
and associates have established the CT
severity index. This index correlates CT
findings with the patient’s outcome.
 Computed Tomography Severity
Index (CTSI) for Acute Pancreatitis
●FEATURE POINTS
Pancreatic Inflammation
Normal pancreas 0
Focal or diffuse pancreatic enlargement 1
Intrinsic pancreatic alterations with
peripancreatic fat inflammatory changes
2 Single fluid collection or phlegmon
3 Two or more fluid collections or gas, in or
adjacent to the pancreas 4
 Computed Tomography Severity
Index (CTSI) for Acute Pancreatitis
●FEATURE POINTS
Pancreatic Necrosis
None 0
≤30% 2
30%-50% 4
>50% 6
 Computed Tomography Severity
Index (CTSI) for Acute Pancreatitis
●CTSI 0-3, mortality 3%, morbidity 8%; CTSI
4-6, mortality 6%, morbidity 35%; CTSI 7-10,
mortality 17%, morbidity 92%.
Parapancreatic necrotic phlegmon
Spread of phlegmon (right and left)
●Abdominal magnetic resonance imaging
(MRI) is also useful to evaluate the extent
of necrosis, inflammation, and presence of
free fluid. However, its cost and availability
and the fact that patients requiring imaging
are critically ill and need to be in intensive
care units limit its applicability in the acute
phase.
●Although magnetic resonance
cholangiopancreatography (MRCP) is not
indicated in the acute setting of AP, it has an
important role in the evaluation of patients with
unexplained or recurrent pancreatitis because it
allows complete visualization of the biliary and
pancreatic duct anatomy. In addition,
intravenous (IV) administration of secretin
increases pancreatic duct secretion, which
causes a transient distention of the pancreatic
duct.
 Endoscopic diagnosis
●Endoscopic retrograde cholangiography (ERCP)
and endoscopic papillotomy is indicated for
biliary pancreatitis with mechanical icterus and/
or cholangitis, taking into account the
visualization of the enlarged diameter of the
common bile duct according to ultrasound and
the inefficiency of complex conservative therapy
for 48 hours.
●In the setting of gallstone pancreatitis,
endoscopic ultrasound (EUS) may play an
important role in the evaluation of
persistent choledocholithiasis. Several
studies have shown that routine ERCP for
suspected gallstone pancreatitis reveals no
evidence of persistent obstruction in most
cases and may actually worsen symptoms
because of manipulation of the gland.
●EUS has been proven to be sensitive for
identifying choledocholithiasis; it allows
examination of the biliary tree and
pancreas with no risk of worsening of the
pancreatitis. In patients in whom persistent
choledocholithiasis is confirmed by EUS,
ERCP can be used selectively as a
therapeutic measure.
Performing endoscopic papillosphincterotomy
with wedged stone
 Differential diagnosis
● Differential diagnosis of AP at the prehospital stage is
carried out with the following diseases :
● – with the syndrome of acute inflammation (acute
appendicitis, cholecystitis, etc.);
● – with the syndrome perforation of a hollow organ in
the free abdominal cavity (perforated gastroduodenal
ulcer, perforation intestinal ulcers);
● – with the syndrome obstruction of the gastrointestinal
tract (ACUTE INTESTINAL OBSTRUCTION, gastric
volvulus, etc.);
● – with acute internal bleeding syndrome (ulcerative
gastroduodenal hemorrhages).
 Assessment of severity of acute
pancreatitis (AP)
To assess the severity of AP and prognosis of the disease, it is
possible to use a scale of criteria for primary rapid
assessment of the severity of acute pancreatitis . The most
important is the early detection of severe pancreatitis, the
results of treatment of which are largely due to the period of
its onset. The presence of at least two signs listed in the
school of rapid assessment, allows you to diagnose medium-
severe (severe) AP, which is subject to mandatory referral to
the intensive care unit. The remaining patients (mild AP) are
hospitalized in the surgical Department.
 Assessment of Severity of
Disease
●The earliest scoring system designed to
evaluate the severity of AP was introduced
by Ranson and colleagues in 1974. It
predicts the severity of the disease on the
basis of 11 parameters obtained at the
time of admission or 48 hours later. The
mortality rate of AP directly correlates with
the number of parameters that are positive.
 Assessment of Severity of
Disease
●Severe pancreatitis is diagnosed if three or more
of the Ranson criteria are fulfilled. The main
disadvantage is that it does not predict the
severity of disease at the time of the admission
because six parameters are assessed only after
48 hours of admission. The Ranson score has a
low positive predictive value (50%) and high
negative predictive value (90%). Therefore, it is
mainly used to rule out severe pancreatitis or to
predict the risk of mortality.
 Ranson Prognostic Criteria for
Non-Gallstone Pancreatitis
●At presentation
• Age >55 years
• Blood glucose level >200 mg/dL
• White blood cell count >16,000 cells/mm3
• Lactate dehydrogenase level >350 IU/liter
• Aspartate aminotransferase level >250 IU/
liter
 Ranson Prognostic Criteria for
Non-Gallstone Pancreatitis
●After 48 hours of admission
• Hematocrit: decrease >10%
• Serum calcium level <8 mg/dL
• Base deficit >4 mEq/L
• Blood urea nitrogen level: increase >5 mg/dL
• Fluid requirement >6 liters
• PaO2 <60 mm Hg
Ranson score ≥3 defines severe pancreatitis.
 Ranson Prognostic Criteria for
Gallstone Pancreatitis
●At presentation
• Age >70 years
• Blood glucose level >220 mg/dL
• White blood cell count >18,000 cells/mm3
• Lactate dehydrogenase level >400 IU/liter
• Aspartate aminotransferase level >250 IU/
liter
 Ranson Prognostic Criteria for
Gallstone Pancreatitis
●After 48 hours of admission
• Hematocrit*: decrease >10%
• Serum calcium level <8 mg/dL
• Base deficit >5 mEq/L
• Blood urea nitrogen level: increase >2 mg/dL
• Fluid requirement >4 liters
• PaO2: Not available
Ranson score ≥3 defines severe pancreatitis.
 Assessment of Severity of
Disease
●AP severity can also be addressed by the
Acute Physiology and Chronic Health
Evaluation (APACHE II) score. Based on the
patient’s age, previous health status, and
12 routine physiologic measurements,
APACHE II provides a general measure of
the severity of disease. An APACHE II score
of 8 or higher defines severe pancreatitis.
 Assessment of Severity of
Disease
●The main advantage is that it can be used
on admission and repeated at any time.
However, it is complex, not specific for AP,
and based on the patient’s age, which
easily upgrades the AP severity score.
APACHE II has a positive predictive value of
43% and a negative predictive value of 89%.
 Assessment of Severity of
Disease
●C-reactive protein (CRP) is an inflammatory
marker that peaks 48 to 72 hours after the
onset of pancreatitis and correlates with
the severity of the disease. A CRP level of
150 mg/mL or higher defines severe
pancreatitis.
 Assessment of Severity of
Disease
●The major limitation is that it cannot be used on
admission; the sensitivity of the assay
decreases if CRP levels are measured within 48
hours after the onset of symptoms. In addition
to CRP, a number of studies have shown other
biochemical markers (e.g., serum levels of
procalcitonin, IL-6, IL-1, elastase) that correlate
with the severity of the disease. However, their
main limitation is their cost, and they are not
widely available.
 Prognostic scale to assess the severity of acute pancreatitis

● peritoneal syndrome;
● oliguria (less than 250 ml of urine in the last 12 hours);
● skin symptoms (redness of the face, cyanosis);
● systolic blood pressure less than 100 mm;
● encephalopathy;
● the hemoglobin level of more than 160 g/l;
● the number of leukocytes more than 14 х109/l;
● blood glucose level over 10 mmol/l;
● urea level above 12 mmol/l;
● metabolic disorders according to ECG;
● cherry or brown-black color of enzymatic exudate obtained by laparoscopy (laparocentesis);
● detection by laparoscopy common enzymatic parapancreatitis emerging in the retroperitoneal
space on the right and left;
● the presence of common fat necrosis, identified by laparoscopy;
● the absence of effect of the basic treatment.

ASSESSMENT
● If a particular patient has at least 5 signs from among the listed, then with 95% probability he
has a severe form of AP.
● If you have 2-4 symptom – AP of medium degree.
● If there is no sign or there is a maximum of one of them – a light (edematous) form of AP.
 Treatment
● Most patients suffer from the disease in mild to
moderate severity and usually recover. Pancreatic
necrosis is complicated by the 20-30% of cases.
● Drug prevention of pancreatic necrosis is not yet
possible. “The pancreas is an organ you can't rely on” -
Zollinger.
● Back in 1894, Korte suggested the priority of surgery in
the treatment of pancreatitis. But, perhaps, none of the
urgent disease was not so frequent shifts opposite
strategies of surgical treatment.
 Treatment
● Open classical interventions and swab drainage
inevitably lead to infection of the abdominal cavity and
retroperitoneal space with severe hospital infection. At
the same time, the area of infection as a result of
operations inevitably expands. As a result, the
detoxifying effect of the operation is quickly replaced
by the generalization of the infectious process. Further,
in the early period of the disease, the patient
experiences a state of endotoxic shock and is more
vulnerable to surgical aggression.
A single medical concept of pancreatic
necrosis is absent.
The thesis about the inexpediency of
early operations in the phase of
enzymatic shock or pancreatogenic
infiltrate in the absence of other
indications of an emergency nature
seems to be dominant
 Tactics of treatment
● An active conservative strategy with deferred operations is
used. Based on a powerful intensive therapy, including
detoxification, antibiotic therapy, treatment of intestinal
insufficiency syndrome for relief of translocation of intestinal
microflora, correction of insufficiency of organs and systems.
● Surgical treatment in this version of the strategy is maximally
delayed for a long period. This intensive care often avoids local
and systemic complications. On arrival, patients are treated
with intensive care.
 Directions of therapy of acute
pancreatitis
●Tactics and methods of complex treatment of
destructive pancreatitis are determined by the
category of severity of the patient's condition.
Complex treatment of the patient with
destructive pancreatitis is carried out only in the
intensive care unit.
●The main directions and methods of complex
therapy of destructive pancreatitis include
several sections.
 1. Intensive corrective therapy

● А. Pain relief. Light complaints are removed by a

combination of antispasmodics with analgesics of
peripheral action. In case of insufficiency, analgesics of
Central action (tramal) are connected. In the third
stage, narcotic analgesics are prescribed. With
prolonged severe pain - peridural anesthesia.
● Introduced glucose novocaine mixture (25 ml of 2%
solution of novocaine in 400 ml of 5% glucose solution).
● Are of great importance procaine blockade.
 1. Intensive corrective therapy

B. Restoration of circulating blood volume.

At medium-heavy form enough 2-4 liters per day, with
heavy - 6-10 liters. In the latter case, it is important to
add 500-1000 ml of 5% albumin or plasma due to
significant loss of protein;
Infusion detoxification, elimination of hypovolemia
and dehydration (colloids + crystalloids 3000-4000 ml
per day) under the control of blood PRESSURE and
heart rate.
C. Therapy of cardiovascular disorders.
D. Respiratory therapy.
 2. Extracorporeal detoxification
methods
●Used: hemo - and limfosorbtsiya, hemo - and
plasmafiltration, plasmapheresis, and
enterosorption.
●However, currently, the algorithm of
extracorporeal and enteral detoxification is not
fully developed.
 3. Blockade of the secretory
function of the pancreas.
●Tried and tested methods of oppression of the
secretory function of the pancreas – cold,
hunger, peace.
●Local hypothermia, in addition to the cold
warmer (on the abdominal wall), gastric lavage
is carried out to eliminate the source of humoral
stimulation pancreas (water +4-+6°C for 2-4
hours 2 times a day).
 3. Blockade of the secretory
function of the pancreas.
● For this purpose, somatostatin/octreotide preparations are
used.

Octreotide is a synthetic analogue of

somatostatin, which is a derivative of the
natural hormone somatostatin and has
similar pharmacological effects, but much
longer duration of action
 4. Antibacterial prevention and therapy

●In mild pancreatitis, antibiotic prophylaxis was

not shown.
●The duration of antibiotic therapy in
pancreonecrosis is determined by the timing of
complete regression of symptoms of systemic
inflammatory reaction.
 5. Nutritional support in acute
pancreatitis
● Parenteral nutrition after 24 hours if long-term
treatment is expected.
● Appropriate and effective for pancreatic necrosis
conduct enteral nutrition in the early stages of the
disease through nationally probe mounted
endoscopically or during surgery. Enteral nutrition
begins gradually with low-fat food.
● In the case of the development of tolerance to enteral
nutrition (increase of levels of amylases and lipaemia,
persistent ileus, diarrhea, aspiration), patients with
pancreatic necrosis is shown holding only parenteral
nutrition.
 Other targets of conservative
therapy
●1. Spasm relief for removal of ductal
hypertension and vasoconstriction: nitroglycerin,
platyphylline.
●2. Antiemetic: dimetpramid, torecan,
metoclopramide (reglan), a permanent tube into
the stomach.
●3. Evacuation of gastric contents: a probe is
inserted into the stomach in severe forms with a
clear violation of motility.
 Other targets of conservative
therapy
●4. Stimulation of the intestine : the novocaine of
0.25% 100-200 ml + sorbitol 20% 100-200 ml.
 Surgical treatment
●Until 1985, patients were more likely to die from
toxic shock at an early stage of AP.
●Patients with limited and aseptic necrosis
should be treated conservatively (mortality is
twice less). The total percentage of pancreatic
necrosis infection is 40-60 %, which occurs
10-14 days after the onset of the disease.
 Early surgical interventions
● Early interventions are carried out in total or subtotal
infected necrosis. Next, the operations are performed
during the melting and sequestration period (7-10-14
days) - stage-by-stage necrsecvestrectomy.
● Both options provide detoxification. peritoneal
exudation in hemorrhagic pancreonecrosis gives a
maximum of intoxication in the first 4-6 hours and lasts
24-48 hours. After removal of peritoneal effusion
peritoneal exudation intensity decreases 10-12 times.
 Early surgical interventions
● Classical open access operations for edematous
pancreatitis should be considered an error due to
unavoidable infection of the gland.
● Modern technology - careful sparing necrectomy with
intraoperative and staged lavage followed by open
management and multiple sanation. The volume of
washing liquid in the first days after the operation is
24-48 liters. The criteria for the effectiveness of
washing can be the presence and level of enzymes and
microbiological analysis of the washing liquid.
 Operations after 10 days
● Interventions more than 10 days from the beginning
(including repeated). The goal is the timely removal of
dead tissues of the pancreas and retroperitoneal
tissue. There can be multiple interventions, since
necrotization in different parts of different time and
necrectomy in one go often not possible.
Indications for repeated interventions :
● 1) formation of pancreatic abscess;
● 2) arrosive bleeding;
● 3) clinic of ongoing peritonitis.
 Drainage operations
● Currently, three main methods of drainage operations
in pancreatic necrosis are used, which provide different
conditions for drainage of the retroperitoneal space
and the abdominal cavity, depending on the scale and
nature of the lesion of the pancreas, retroperitoneal
tissue and the abdominal cavity.

● – " Close "

● – " Open "
● – " Half-open "
 «Closed method»
● I. " Close " method draining operations include the active
drainage of the retroperitoneal tissue and peritoneal cavity in
terms of the anatomic integrity of the cavity of the stuffing bags
and abdominal cavity. This is achieved by implantation of
multichannel silicone drainage structures for the introduction
of antiseptic solutions fractionally or drip into the focus of
destruction (infection) with constant active aspiration. The
"closed" method of drainage involves repeated interventions
only "on demand". Control over the focus of destruction/
infection and drainage function is carried out according to the
results of ultrasound, CT, video optics, fistulography.
 «open» method
● II. The "open" method of drainage operations in pancreatic
necrosis involves performing programmable revisions and
sanations of the retroperitoneal space and has two main
options for technical solutions determined by the predominant
scale and nature of the lesion of the retroperitoneal space and
the abdominal cavity. This method includes :
● – pancreatoomentobursostomy - lumbotomy;
● – pancreatoomentobursostomy - laparostomy.
 «Half-open» метод
● III. " Half-open " the method of drainage in pancreatic necrosis
involves the installation of tubular multibranch drainage
structures in combination with Penrose drainage. Under these
conditions, the laparotomic wound is sutured in layers, and the
combined design of the drains is removed through a wide
counterperture in the lumbar-lateral parts of the abdomen
(lumbotomy).
● It should be particularly noted that the presented methods of
"closed" and "open" retroperitoneal drainage are not
competitive, since, subject to the methodology and reasonable
indications, they are designed to ensure adequate and complete
sanitation of all zones of necrotic destruction and
pancreatogenic infection.
 Late operations
● Performed with subsiding acute inflammatory
processes (not earlier than 2-3 weeks after the onset
of the disease): with subacute pseudocysts, scar
strictures of the pancreatic duct.
● False cysts, as a result of the development of
pancreatitis, can disappear on their own. Cysts can
first be punctured under ultrasound or CT. If, after
repeated punctures, the cyst is filled to a value of more
than 5-6 cm, catheterization is shown under the control
of ultrasound. At failure -operation is shown.
 Perspective of surgical treatment
● The prospect of surgical treatment of pancreatic
necrosis today is seen in the combination of intensive
treatment, starting from the first minutes of the
patient's treatment, and the use of minimally invasive
surgical technologies for the organization of effective
drainage of the destruction zone and purulent
inflammation of the gland, abdominal cavity and
retroperitoneal space. Re-sanitation of the abdominal
cavity and retroperitoneal space is useful. The latter is
the testing ground on which the purulent-necrotic
drama is played out, since the pancreas is a
retroperitoneal organ.
● “Obviously, the era of minimally invasive
interventions in pancreatic necrosis is
coming, but there is no sufficient evidence
base for their effectiveness – there are no
randomized studies”
The severity of the condition of patients in
dependencefrom the type of surgical
treatment Percutaneous sequestrectom

COMPENSATION

Minimally invasivedrainage
laparotomy
Sub-COMPENSATION

laparotomy

DECOMPENSATION

14-16 day 24-26 day

 Types of minimally invasive
treatment in the phase of purulent
complications
● Minilaparotomy with a set Mini
assistant
● ULTRASOUND-controlled puncture
drainage of the abscesses
● Endovideosurgical drainage of the
abscesses
 Surgical challenges in percutaneous
treatment of patients with pancreatic
necrosis and parapancreatitis common

● Adequate drainage and sanitation of all

lesions of retroperitoneal fiber
●Percutaneous extraction of necrotic tissues
Scheme of drainage of acute liquid
pancreatic accumulation
Fistulogram, appearance and overview radiograph
of patient E. (2 weeks from the beginning of
treatment)
Replacement of 10 mm drainage with
20 mm drainage
Variants of drainage of the affected parts
of retroperitoneal fiber
Extraction of sequesters by catheter with
end hole.

Puncture channel 15 mm
Removal of sequester by
special extractor
Hooks "Mini-assistant" routinely omental bag
In the packing bag wound up the finished clip
The finished clip removed the sequester
Washing of the omental bag with a
solution of hydrogen peroxide
Washing of the omental bag with antiseptic
solution
Appearance of postoperative wound after
minilaparotomy
Sequesters removed from the omental bag
 Result of treatment
●The results of treatment of acute pancreatitis
have stabilized in last years.
●In edematous forms of acute pancreatitis
outcomes and prognosis are favorable.
Mortality in sterile pancreatic necrosis ranges
from 10 to 15%, in infected pancreatic necrosis
ranges from 40-60% mainly due to purulent-
septic complications.
Mortality from acute pancreatitis

Infected pancreatic
necrosis

Sterile
pancreatic
necrosis
Late
Early

1 2 3 Weeks
The end