- •O. L. Sytnik, V. V. Leonov, V. Ju. Petrenko surgery. Emergency abdominal surgery
- •Contents
- •Introduction
- •Chapter 1 Acute appendicitis
- •Clinical diagnostics of acute appendicitis
- •Special examinations
- •Differential diagnosis of acute appendicitis
- •Treatment of acute appendicitis
- •Complications of acute appendicitis
- •Chapter 2 Acute cholecystitis
- •Clinical diagnostic of acute cholecystitis
- •Special examinations
- •Investigations in acute cholecystitis
- •Differential diagnosis of acute cholecystitis
- •Treatment of acute cholecystitis
- •Chapter 3 Acute pancreatitis
- •Aetiology
- •Pathophysiology
- •Classifications Savelyev V. S. (1983)
- •Atlanta classification, Beger h. G., 1991
- •Clinical diagnostic of acute pancreatitis
- •Special examinations
- •Imaging studies
- •Treatment of acute pancreatitis
- •Surgical care
- •Operations
- •Chapter 4 Perforated peptic ulcer
- •Aetiology
- •1. Predisposing factor: progressive destruction of stomach or duodenal wall.
- •Classifications
- •Clinical manifestations
- •Diagnosis programmer
- •Treatment of perforated peptic ulcer
- •Various types of vagotomy
- •Chapter 5 Peptic ulcer acute haemorrhage
- •Pathophysiology
- •Classifications
- •History
- •Clinical manifistation
- •Differential diagnosis
- •Diagnosis program
- •Imaging studies
- •Policy and choice of treatment method
- •Operations for bleeding gastric ulcers
- •Chapter 6 Bowel obstruction
- •A small-bowel obstruction (sbo)
- •Frequency
- •Pathophysiology
- •History
- •Physical examination
- •Special examinations
- •Imaging studies
- •Treatment
- •Prognosis
- •A large-bowel obstruction (lbo)
- •History
- •Clinical diagnostics
- •Special examinations
- •Imaging studies
- •Procedures
- •Medical Care
- •Surgical Care
- •Further оutpatient сare
- •Prognosis
- •Pathophysiology
- •Imaging studies
- •Chapter 7 Acute peritonitis
- •Relevant anatomy
- •Functions of peritoneum
- •Classifications
- •Pathophysiology
- •Clinical diagnostic of acute peritonitis
- •Special examinations
- •Imaging studies
- •Medical therapy
- •Intraoperative details
- •Classification
- •Abdominal Wall Anatomy
- •Clinical signs
- •Inguinal Herniorrhaphy.
- •Inguinal Herniorrhaphy. Alloplastic Repair
- •Femoral Herniorrhaphy.
- •Umbilical and Paraumbilical hernia
- •Postoperative Hernia
- •Postoperative complications
- •Tests for control Chapter 1. Acute appendicitis
- •Standards of answers
- •Chapter 2. Acute cholecystitis
- •Standards of answers
- •Chapter 3. Acute pancreatitis
- •Standards of answers
- •Chapter 4. Perforated peptic ulcer
- •Standards of answers
- •Chapter 5. Peptic ulcer acute haemorrhage
- •Standards of answers
- •Chapter 6. Bowel obstruction
- •Standards of answers
- •Chapter 7. Acute peritonitis
- •Standards of answers
- •Chapter 8. Hernias of abdominal wall
- •Standards of answers
- •Situational problem tasks
- •Standards of answers
- •Standards of answers
- •Standards of answers
- •Standards of answers
- •Standards of answers
- •Standards of answers
- •Standards of answers
- •References Obligatory literature
- •Faculty literature
- •Appendix a Algorithm of acute appendicitis diagnostic
- •Appendix b Algorithm of diagnosis and treatment of appendicular mass and abscess
- •Appendix c Algorithm of acute cholecystitis treatment
- •Appendix d Algorithm of diagnosis and treatment of acute pancreatitis
- •Appendix e Algorithm of diagnosis and treatment of perforated ulcer
- •Appendix f Algorithm of diagnosis and treatment of bleeding ulcer
- •Appendix g Algorithm of diagnosis and treatment of bowel obstruction
- •Appendix h Pathogenesis of acute peritonitis
- •Appendix k Algorithm of hernias treatment
- •Appendix l Algorithm of treatment of the strangulated hernia
- •Subject index
Chapter 3 Acute pancreatitis
The pancreas is a gland located in the upper, posterior abdomen and is responsible for insulin production and the manufacture and secretion of digestive enzymes leading to carbohydrate, fat, and protein metabolism. Approximately 80% of the gross weight of the pancreas supports exocrine function, while the remaining 20% is involved with endocrine function.
In acute pancreatitis there are not only symptoms of acute inflammation in the pancreas are present. There are the signs of haemorrhages and necrotic processes, which are caused by autodigestion of tissues by pancreatic enzymes. Secondary infection and multiorgan system failure may be associated with autodigestion process.
The overall mortality rate of patients with acute pancreatitis is 10–15%. In patients with severe disease (necrosis and/or organ failure), the mortality rate is approximately 30%.
Anatomy of hepato-pancreato-duodenal region is demonstrated at fig. 14.
Figure 14 – Anatomy of hepato-pancreato-duodenal region
Aetiology
Bile and digestive – pancreatic reflux.
Obstruction and hypertension of biliary and pancreatic ducts.
Blood supply disturbance of pancreas.
Allergic and toxic process.
Peptic ulcer disease.
Injuries.
A number of factors are capable of initiating acute pancreatitis although their mechanism of action is not known. Alcoholism and biliary tract disease are the processes most commonly associated with pancreatitis: together they account for 80% of acute cases.
The most common cause of acute pancreatitis is gallstones passing into the bile duct and temporarily lodging at Oddi’s sphincter. The risk of a stone causing pancreatitis is inversely proportional to its size.
Alcohol. Most commonly, the disease develops in patients whose alcohol ingestion is habitual over 5–15 years. Alcoholics are usually admitted with an acute exacerbation of chronic pancreatitis.
Acute pancreatitis may be the first manifestation of a tumor causing pancreatic duct obstruction: pancreatic carcinoma should be considered in non-alcoholic patients in whom no biliary disease is identified.
Infectious agents which have been implicated as a course of pancreatitis include mumps virus, coxsackie virus, Mycoplasma and parasites.
Many drugs are capable of causing acute pancreatitis: these include thiazide diuretics, 6-mercaptopurine, azathioprine, oestrogens, frusemide, methyldopa, sulphonamides, tetracycline, pentamidine, enalapril, and procainamide.
Patients with types I and V hypertriglyceridaemia frequently suffer from pancreatitis, usually associated with extremely high levels of serum triglycerides. However, hypertriglyceridaemia can also be the result rather than the cause of pancreatitis.
Postoperative pancreatitis can be fatal and is often due to iatrogenic pancreatic trauma. Pancreatitis following cardiopulmonary bypass is being recognized with increasing frequency. The majority of cases are mild or even subclinical, but evidence of severe pancreatitis is found in 25% of patients who die following cardiac surgery.
Abdominal trauma causes an elevation of amylase and lipase levels in 17% of cases and clinical pancreatitis in 5% of cases. Pancreatic injury occurs more often in penetrating injuries (e.g., from knives, bullets) than in blunt abdominal trauma (e.g., from steering wheels, horses, bicycles). Blunt injury may crush the gland across the spine, leading to a ductal injury in that location.
Toxins. Exposure to organophosphate insecticide can cause acute pancreatitis. In Trinidad, the sting of the scorpion Tityus trinitatis is the most common cause of acute pancreatitis.
Hypercalcemia cause can lead to acute pancreatitis. Causes include hyperparathyroidism, excessive doses of vitamin D, familial hypocalciuric hypercalcemia and total parenteral nutrition.
Developmental abnormalities of the pancreas. Two developmental abnormalities are associated with pancreatitis: anomaly of pancreatic ducts and annular pancreas.
Oddi’s sphincter dysfunction can lead to acute pancreatitis by causing increased pancreatic ductal pressures.
