Chief of hospital surgeryChief of hospital surgery

Lection for students of 5 courseLection for students of 5 course

AcuteAcute ppancreatitisancreatitis.

Anatomy of pancreac.Anatomy of pancreac.

I — ventriculus; 2 — a. et v. gastrica sinistra; 3 — lien; 4 — lig. phrenicolienale; 5 — lig. gastrolienale; 6 — corpus pancreatis; 7 — cauda pancreatis; 8 — ния mesocolon transversum; 9 — flexura duodenojejunalis; 10 — caput pancreatis;

Anatomy of pancreac.Anatomy of pancreac.

1 — v. cava inferior; 2 — aorta abdominalis; 3 — truncus coeliacus; 4 — a. gastrica sinistra; 5 — a. lienalis; 6 — v. lienalis; 7 — v. mesenterica inferior; 8 — a. mesenterica superior; 9 — v. mesenterica superior; 10 — caput pancreatis; 11 — duodenum; 12 — a. gastroduodenalis; 13 — a. hepatica communis; 14 — a. hepatica propria; 15 — ductus choledochus; 16 — a. gastrica dextra; 17 — v. portae; 18 — ductus cysticus; 19 — ductus hepaticus communis.

Acute pancreatitisAcute pancreatitis

is a is a aseptic aseptic inflammatory process of inflammatory process of the pancreasthe pancreas, caused of autolysis in , caused of autolysis in consequence of pathology activation consequence of pathology activation of photolytic of photolytic enzymesenzymes

StatisticsStatistics

Acute PancreatitisAcute Pancreatitis is 15 - 20% part of all is 15 - 20% part of all acute surgical diseases organ to abdominal acute surgical diseases organ to abdominal cavity. On Ukraine frequency acute cavity. On Ukraine frequency acute pancreatitis forms from 10 before 40 on pancreatitis forms from 10 before 40 on 10000 populations. The General mortality 10000 populations. The General mortality under acute pancreatitis from 15-25%, to under acute pancreatitis from 15-25%, to 85%. 85%.

Risk Factors for Acute Risk Factors for Acute PancreatitisPancreatitis

Gallstones CholedocholithiasisGallstones Choledocholithiasis Chronic alcohol consumptionChronic alcohol consumption Congenital anomaliesCongenital anomalies Drug-induced hypertriglyceridemia (triglycerides greater than 1,000 mg Drug-induced hypertriglyceridemia (triglycerides greater than 1,000 mg

per dL [11.30 mmol per L])per dL [11.30 mmol per L]) Anatomic or functional disorders (e.g., pancreas divisum, sphincter of Anatomic or functional disorders (e.g., pancreas divisum, sphincter of

Oddi dysfunction)Autoimmune (e.g., systemic lupus erythematosus)Oddi dysfunction)Autoimmune (e.g., systemic lupus erythematosus) Hypercalcemia, hyperparathyroidismHypothermiaIdiopathicInfections Hypercalcemia, hyperparathyroidismHypothermiaIdiopathicInfections

(e.g., viral, bacterial, parasitic, fungal)(e.g., viral, bacterial, parasitic, fungal) Pancreatic or ampullary tumorsPancreatic or ampullary tumors Traumatic or postprocedure (e.g., endoscopic retrograde Traumatic or postprocedure (e.g., endoscopic retrograde

cholangiopancreatography or after abdominal surgery)cholangiopancreatography or after abdominal surgery) Vascular (e.g., vasculitis)Vascular (e.g., vasculitis)

Pathogenesis Pathogenesis Acute pancreatitis may occur when factors Acute pancreatitis may occur when factors

involved in maintaining cellular homeostasis involved in maintaining cellular homeostasis are out of balance. The initiating event may are out of balance. The initiating event may be anything that injures the acinar cell and be anything that injures the acinar cell and impairs the secretion of zymogen granules, impairs the secretion of zymogen granules, such as alcohol use, gallstones, and certain such as alcohol use, gallstones, and certain drugs. In addition, acute pancreatitis can drugs. In addition, acute pancreatitis can develop when ductal cell injury leads to develop when ductal cell injury leads to delayed or absent enzymatic secretion, delayed or absent enzymatic secretion, such as with the such as with the CFTRCFTR gene mutation. The gene mutation. The mechanisms by which alcohol or gallstones mechanisms by which alcohol or gallstones cause destruction to pancreatic acinar cells cause destruction to pancreatic acinar cells are not currently known. are not currently known.

PathogenesisPathogenesis

Once a cellular injury pattern has been initiated, cellular Once a cellular injury pattern has been initiated, cellular membrane trafficking becomes chaotic, with the following membrane trafficking becomes chaotic, with the following deleterious effects: (1) lysosomal and zymogen granule deleterious effects: (1) lysosomal and zymogen granule compartments fuse, enabling activation of trypsinogen to compartments fuse, enabling activation of trypsinogen to trypsin; (2) intracellular trypsin triggers the entire zymogen trypsin; (2) intracellular trypsin triggers the entire zymogen activation cascade; and (3) secretory vesicles are extruded activation cascade; and (3) secretory vesicles are extruded across the basolateral membrane into the interstitium, where across the basolateral membrane into the interstitium, where molecular fragments act as chemoattractants for molecular fragments act as chemoattractants for inflammatory cells. Activated neutrophils then exacerbate the inflammatory cells. Activated neutrophils then exacerbate the problem by releasing superoxide (the respiratory burst) or problem by releasing superoxide (the respiratory burst) or proteolytic enzymes (cathepsins B, D, and G; collagenase; proteolytic enzymes (cathepsins B, D, and G; collagenase; and elastase). Finally, macrophages release cytokines that and elastase). Finally, macrophages release cytokines that further mediate local (and, in severe cases, systemic) further mediate local (and, in severe cases, systemic) inflammatory responses. The early mediators defined to date inflammatory responses. The early mediators defined to date are tumor necrosis factor–alpha, interleukin-6, and are tumor necrosis factor–alpha, interleukin-6, and interleukin-8.interleukin-8.

PathogenesisPathogenesis

These mediators of inflammation cause an These mediators of inflammation cause an increase pancreatic vascular permeability, leading increase pancreatic vascular permeability, leading to hemorrhage, edema, and eventually pancreatic to hemorrhage, edema, and eventually pancreatic necrosis. As the mediators are excreted into the necrosis. As the mediators are excreted into the circulation, systemic complications can arise, such circulation, systemic complications can arise, such as bacteremia due to gut flora translocation, acute as bacteremia due to gut flora translocation, acute respiratory distress syndrome, pleural effusions, respiratory distress syndrome, pleural effusions, gastrointestinal hemorrhage, and renal failure. gastrointestinal hemorrhage, and renal failure. Eventually, the mediators of inflammation can Eventually, the mediators of inflammation can become so overwhelming to the body that become so overwhelming to the body that hemodynamic instability and death ensue.hemodynamic instability and death ensue.

SymptomsSymptoms Acute pancreatitis usually begins with pain in the upper abdomen that Acute pancreatitis usually begins with pain in the upper abdomen that

may last for a few days. The pain may be severe and may become may last for a few days. The pain may be severe and may become constant—just in the abdomen—or it may reach to the back and other constant—just in the abdomen—or it may reach to the back and other areas. It may be sudden and intense or begin as a mild pain that gets areas. It may be sudden and intense or begin as a mild pain that gets worse when food is eaten. Someone with acute pancreatitis often looks worse when food is eaten. Someone with acute pancreatitis often looks and feels very sick. Other symptoms may includeand feels very sick. Other symptoms may include

swollen and tender abdomen swollen and tender abdomen nausea nausea vomiting vomiting fever fever rapid pulse rapid pulse Severe cases may cause dehydration and low blood pressure. The Severe cases may cause dehydration and low blood pressure. The

heart, lungs, or kidneys may fail. If bleeding occurs in the pancreas, heart, lungs, or kidneys may fail. If bleeding occurs in the pancreas, shock and sometimes even death follow.shock and sometimes even death follow.

Main clinic syndromesMain clinic syndromes

Pain-syndromePain-syndrome Dyspepsia Dyspepsia Intoxication Intoxication Mechanical jaundice Mechanical jaundice Disturbance of hemodynamic Disturbance of hemodynamic Paralytic of bowel Paralytic of bowel

PhysicalPhysical examination examination

The following physical examination findings vary with the The following physical examination findings vary with the severity of the disease.severity of the disease.– Fever (76%) and tachycardia (65%) are common abnormal vital Fever (76%) and tachycardia (65%) are common abnormal vital

signs.signs.– Abdominal tenderness, muscular guarding (68%), and distension Abdominal tenderness, muscular guarding (68%), and distension

(65%) are observed in most patients. Bowel sounds are often (65%) are observed in most patients. Bowel sounds are often hypoactive due to gastric and transverse colonic ileus. Guarding hypoactive due to gastric and transverse colonic ileus. Guarding tends to be more pronounced in the upper abdomen.tends to be more pronounced in the upper abdomen.

– A minority of patients exhibit jaundice (28%).A minority of patients exhibit jaundice (28%).– Some patients experience dyspnea (10%), which may be caused Some patients experience dyspnea (10%), which may be caused

by irritation of the diaphragm (resulting from inflammation), pleural by irritation of the diaphragm (resulting from inflammation), pleural effusion, or a more serious condition, such as acute respiratory effusion, or a more serious condition, such as acute respiratory distress syndrome.distress syndrome.

– In severe cases, hemodynamic instability is evident (10%) and In severe cases, hemodynamic instability is evident (10%) and hematemesis or melena sometimes develops (5%). In addition, hematemesis or melena sometimes develops (5%). In addition, patients with severe acute pancreatitis are often pale, diaphoretic, patients with severe acute pancreatitis are often pale, diaphoretic, and listless.and listless.

PhysicalPhysical examination examination

A few uncommon physical findings are associated with A few uncommon physical findings are associated with severe necrotizing pancreatitis.severe necrotizing pancreatitis.– The Cullen sign is a bluish discoloration around the umbilicus The Cullen sign is a bluish discoloration around the umbilicus

resulting from hemoperitoneum.resulting from hemoperitoneum.– The Grey-Turner sign is a reddish-brown discoloration along the The Grey-Turner sign is a reddish-brown discoloration along the

flanks resulting from retroperitoneal blood dissecting along tissue flanks resulting from retroperitoneal blood dissecting along tissue planes. More commonly, patients may have a ruddy erythema in planes. More commonly, patients may have a ruddy erythema in the flanks secondary to extravasated pancreatic exudate.the flanks secondary to extravasated pancreatic exudate.

– Erythematous skin nodules may result from focal subcutaneous fat Erythematous skin nodules may result from focal subcutaneous fat necrosis. These are usually not more than 1 cm in size and are necrosis. These are usually not more than 1 cm in size and are typically located on extensor skin surfaces. In addition, polyarthritis typically located on extensor skin surfaces. In addition, polyarthritis is occasionally seen.is occasionally seen.

ComplicationsComplications

Acute pancreatitis can cause breathing problems. Many Acute pancreatitis can cause breathing problems. Many people develop hypoxia, which means that cells and people develop hypoxia, which means that cells and tissues are not receiving enough oxygen. Doctors treat tissues are not receiving enough oxygen. Doctors treat hypoxia by giving oxygen through a face mask. Despite hypoxia by giving oxygen through a face mask. Despite receiving oxygen, some people still experience lung failure receiving oxygen, some people still experience lung failure and require a ventilator.and require a ventilator.

Sometimes a person cannot stop vomiting and needs to Sometimes a person cannot stop vomiting and needs to have a tube placed in the stomach to remove fluid and air. have a tube placed in the stomach to remove fluid and air. In mild cases, a person may not eat for 3 or 4 days and In mild cases, a person may not eat for 3 or 4 days and instead may receive fluids and pain relievers through an instead may receive fluids and pain relievers through an intravenous line.intravenous line.

DiagnosticDiagnostic

Abdominal ultrasonographyAbdominal ultrasonography Contrast-enhanced computed tomographyContrast-enhanced computed tomography Endoscopic ultrasonographyEndoscopic ultrasonography Laparoscopy Laparoscopy Magnetic resonance Magnetic resonance

cholangiopancreatographycholangiopancreatography CContrast-enhanced computed tomography ontrast-enhanced computed tomography

DiagnosticDiagnostic

Abdominal ultrasonographyAbdominal ultrasonography– This is the most useful initial test in determining This is the most useful initial test in determining

the etiology of pancreatitis and is the technique the etiology of pancreatitis and is the technique of choice for detecting gallstones.of choice for detecting gallstones.

– In the setting of acute pancreatitis, sensitivity is In the setting of acute pancreatitis, sensitivity is reduced to 70-80%. In addition, the ability to reduced to 70-80%. In addition, the ability to identify choledocholithiasis is limited.identify choledocholithiasis is limited.

– Ultrasonography cannot measure the severity of Ultrasonography cannot measure the severity of disease.disease.

DiagnosticDiagnostic Abdominal CT scanningAbdominal CT scanning

– This is generally not indicated for patients with This is generally not indicated for patients with mild pancreatitis unless a pancreatic tumor is mild pancreatitis unless a pancreatic tumor is suspected (usually in elderly patients).suspected (usually in elderly patients).

CT scanning is always indicated in patients with CT scanning is always indicated in patients with severe acute pancreatitis and is the imaging study severe acute pancreatitis and is the imaging study of choice for assessing complications. Scans are of choice for assessing complications. Scans are seldom needed within the first 72 hours after seldom needed within the first 72 hours after symptom onset unless the diagnosis is uncertain, symptom onset unless the diagnosis is uncertain, because inflammatory changes are often not because inflammatory changes are often not radiographically present until this timeradiographically present until this time

DiagnosticDiagnostic Endoscopic ultrasonographyEndoscopic ultrasonography

– Endoscopic ultrasonography (EUS) is an endoscopic Endoscopic ultrasonography (EUS) is an endoscopic procedure that allows a high-frequency ultrasound procedure that allows a high-frequency ultrasound transducer to be inserted into the gastrointestinal transducer to be inserted into the gastrointestinal tract to visualize the pancreas and the biliary tract. tract to visualize the pancreas and the biliary tract. This study allows a more detailed image to be This study allows a more detailed image to be obtained than with transcutaneous ultrasonography obtained than with transcutaneous ultrasonography because the high-frequency transducer can be because the high-frequency transducer can be introduced directly adjacent to the pancreas. introduced directly adjacent to the pancreas.

– EUS is often helpful in evaluating the cause of severe EUS is often helpful in evaluating the cause of severe pancreatitis, particularly microlithiasis and biliary pancreatitis, particularly microlithiasis and biliary sludge, and can help identify periampullary lesions sludge, and can help identify periampullary lesions better than other imaging modalities. better than other imaging modalities.

– Its principal role in the evaluation of acute Its principal role in the evaluation of acute pancreatitis is the detection of microlithiasis and pancreatitis is the detection of microlithiasis and periampullary lesions not easily revealed by other periampullary lesions not easily revealed by other methods.methods.

TreatmentTreatment

The treatment of acute The treatment of acute pancreatitis pancreatitis conservativeconservative Operative treatment if patients have Operative treatment if patients have

ccomplicationsomplications

Conservative treatmentConservative treatment The fight with painThe fight with pain Correcting hemodynamic.Correcting hemodynamic. The Inhibitor of function of pancreas The Inhibitor of function of pancreas The preventive maintenance to festering The preventive maintenance to festering

infectioninfection Inactivation of pancreatic enzymes in blood Inactivation of pancreatic enzymes in blood Correcting of the metabolismCorrecting of the metabolism Detoxic therapyDetoxic therapy Identical protein-energy ensuring the organismIdentical protein-energy ensuring the organism

Antioxid therapyAntioxid therapy

Introduce to Introduce to operative treatmentoperative treatment

non effective non effective conservative treatment 2-3 conservative treatment 2-3 days days

septic cseptic complicationsomplications

peritonitis peritonitis increase of intoxication increase of intoxication increase of mechanical jaundice.increase of mechanical jaundice.

Methods of operationMethods of operation

Abdominization of pancreasAbdominization of pancreas MarsoopylyzationMarsoopylyzation Drainage Drainage Correction of mechanical jaundice Correction of mechanical jaundice Treatment of peritonitis Treatment of peritonitis

Operative treatmentOperative treatment

Abdominization of pancreasAbdominization of pancreas

ComplicationsComplications

Acute cyst of pancreas Acute cyst of pancreas Fistools of pancreas Fistools of pancreas Abscess and flegmons retroperitoneum Abscess and flegmons retroperitoneum Perforation of cavity organsPerforation of cavity organs Arosive Arosive bleeding bleeding Abscess of omentum bags Abscess of omentum bags Trombosis of vessels Trombosis of vessels