1. Can severe acute pancreatitis be prevented?
Severe acute pancreatitis can be effectively prevented by doing the following (see the first question on the prevention and treatment of mild acute pancreatitis).
(1) Prevention by dietary management.
(2) prevention of task environmental adaptation.
(3) prevention of sleep quality adjustment.
(4) prevention of spiritual and psychological adjustment.
(5) prevention of drug application.
(6) standardized treatment, timely consultation and treatment according to the treatment norms.
2.What is severe acute pancreatitis?
Acute pancreatitis is called severe acute pancreatitis when there is abdominal pain with peritonitis, respiratory distress, hypotension, shock, renal insufficiency, disorders of water, electrolytes, acid-base balance, prolonged hyperthermia with pseudocyst or abdominal abscess formation, or even extensive necrosis of the pancreas.
3.What are the symptoms and manifestations of severe acute pancreatitis or what are the discomforts of the body?
(1) abdominal pain: often located in the upper abdomen, persistent, can spread to the whole abdomen, the nature of the pain is mostly distension, part of the colic. It is severe and often accompanied by symptoms of peritonitis. It lasts for a long time and conventional analgesic drugs are ineffective, requiring the use of opioids for analgesia.
(2) Abdominal distension: often accompanied by abdominal pain, along with the presence of anal cessation of defecation, severe abdominal distension can make breathing difficult, and sometimes gastrointestinal decompression and enemas are difficult to relieve.
(3) Vomiting: often occurs at the same time as abdominal pain and abdominal distension, vomit is basically the food entered before the onset of the disease, vomiting persists when intestinal paralysis occurs.
(4) Fever: high body temperature, often over 39 degrees, persistent, when the abdominal cavity infection occurs the body temperature can be sustained in the 40 degrees.
(5) Hypotension and shock: Hypotension or shock often occurs in severe acute pancreatitis, manifested as irritability, extreme thirst, pale, clammy skin, weak pulse, and decreased blood pressure. Very few patients shock can occur suddenly, and even sudden death. Shock is mainly caused by the following causes of insufficient effective circulating blood volume.
①Lack of blood volume due to massive leakage of blood and plasma.
② Loss of body fluids and electrolytes due to frequent vomiting.
(iii) Activation of pancreatic vasopressinogen and increased production of bradykinin in the blood, causing vasodilation and increased vascular permeability.
(iv) Complicated gastrointestinal bleeding.
(6) Water, electrolytes, acid-base balance and metabolic disorders: severe acute pancreatitis often has significant dehydration and metabolic acidosis, hypocalcemia can occur, blood calcium <2mmol/L, and often poor prognosis when blood calcium is consistently below 1.75mmol/L. Some severe pancreatitis elevated blood glucose, mostly temporary hyperglycemia, a few become permanent diabetes, occasionally diabetic ketoacidosis or hyperosmolar coma can occur.
(7) Acute respiratory distress syndrome: The main manifestations are sudden, progressive dyspnea, accelerated respiratory rate, cyanosis, irritability, sweating and other severe hypoxemia, which is difficult to correct with oxygen. Its occurrence is associated with inadequate pulmonary perfusion, decreased synthesis of lung surface active substances due to the breakdown of lecithin by phospholipase A, damage to alveolar capillary walls by free fatty acids, increased vasodilation and vascular permeability caused by bradykinin, and pulmonary microcirculatory embolism.
(8) Acute renal insufficiency: Patients with acute severe pancreatitis can be complicated by acute renal failure with high mortality. It manifests as oliguria, proteinuria, hematuria or tubular urine, progressive increase in blood urea nitrogen, and rapid progression to acute renal failure. The causes are mainly hypovolemia, shock and microcirculatory disorders leading to renal ischemia and hypoxia.
(9) Arrhythmia and cardiac failure: severe pancreatitis can cause pericardial effusion, arrhythmia and heart failure. Factors that cause circulatory failure include.
(i) insufficient blood volume and inadequate myocardial perfusion.
(ii) release of myocardial depressor factor (MDF) from the necrotic pancreas, which causes poor myocardial contraction.
(iii) Damage to the myocardium by activated pancreatic enzymes, which inhibit myocardial contraction and reduce beat volume.
(iv) In secondary infection or sepsis, toxins damage the myocardium.
(10) Gastrointestinal bleeding: upper gastrointestinal bleeding is often caused by gastric and duodenal mucosal erosion or stress ulcers, and a few are caused by portal hypertension due to splenic or portal vein embolism and rupture of esophageal varices. Lower gastrointestinal bleeding can be caused by pancreatic necrosis penetrating the transverse colon, and the prognosis is very poor.
(11) Skin changes: When pancreatic necrosis is severe, blood, pancreatic enzymes and necrotic tissue fluid penetrate into the abdominal wall through the fascia and muscle layer, grayish-purple skin (Grey-Turner sign) and cyanotic skin around the umbilicus (Cullen sign) can often be found under the skin on both sides of the abdomen.
(12) Jaundice: Jaundice can appear 1 to 2 days after the onset, often as temporary obstructive jaundice, mainly due to compression of the common bile duct by the enlarged head of the pancreas, which mostly subsides within a few days. If the jaundice persists and deepens, it is usually caused by embedded stones in the common bile duct or jugular abdomen. If jaundice appears after the second week of disease onset, it is most often due to complications of pancreatic abscess or cysts compressing the common bile duct. In a few patients, hepatocellular jaundice can be caused by complications of hepatocellular damage.
(13) Thoracoabdominal effusion: When pancreatic fluid and necrotic tissue infiltrate into the peritoneal cavity and mesentery, or enter the thoracic duct via the retroperitoneum, peritonitis and pleurisy are produced, resulting in thoracoabdominal effusion, which is mostly bloody or purple-brown in color, with abnormally high amylase content. Large amounts of pleural fluid can lead to respiratory distress, and large amounts of ascites can produce compression symptoms, aggravating respiratory distress and abdominal pain and distension.
(14) Pseudocysts: Most of them form 3-4 weeks after the onset of the disease and are accumulations of pancreatic fluid encapsulated by fibrous tissue or granulation tissue cyst walls. Large cysts can produce symptoms of compression and abdominal distension. A mass can often be palpated in the abdomen, and there is pressure pain. When the cyst wall ruptures or has fissures, the pancreatic fluid inside the cyst flows into the abdominal cavity, causing pancreatic-derived ascites.
(15) Infection: pancreatic and peripancreatic necrosis secondary to bacterial infection, which forms abscesses after 4-6 weeks of onset. The boundary of peripancreatic abscess is unclear, often located in front of the tail of the pancreatic body, but also at the back of the head, and may extend to the ascending and descending colon and the root of the small intestinal mesentery. In this case, the patient has high fever, persistently elevated white blood cell count, persistent abdominal pain and hyperamylasemia, and an epigastric mass may be palpated during abdominal examination. If the localized infection spreads to the whole body, sepsis develops. Gram-negative bacilli are predominant in the early stages, but mixed strains of infection may be present in later stages.
(16) Coagulation abnormalities: Patients with severe pancreatitis are often in a hypercoagulable state, which can lead to thrombosis and local circulatory disorders, and even develop into disseminated intravascular coagulation (DIC).
(17) Pancreatic encephalopathy: manifests as mental abnormalities, disorientation, mania with hallucinations and delusions, and abnormal changes in the EEG. Its occurrence is related to phospholipase A damage to brain cells, causing extensive demyelination changes.
(18) Multiple organ failure: Acute severe pancreatitis can occur simultaneously with multiple organ failure, such as acute respiratory distress syndrome, acute renal failure, circulatory failure, gastrointestinal bleeding, pancreatic encephalopathy, sepsis and DIC. In case of multiple organ failure, the death rate is extremely high.
4.What factors can cause severe acute pancreatitis?
The same causes as those that induce mild acute pancreatitis, but pancreatitis induced by biliary tract disease, heavy drinking and overeating, hyperlipidemia and diabetic ketosis can easily progress to acute severe pancreatitis.
5.Why does severe acute pancreatitis occur?
As with mild acute pancreatitis, the underlying cause is obstruction of the pancreatic ducts, resulting in poor drainage of pancreatic fluid, activation of pancreatic enzymes in the pancreatic tissue, and active pancreatic enzymes causing the pancreas to digest itself and inducing the inflammatory process. After the occurrence of severe acute pancreatitis, the pancreatic duct cannot be effectively recanalized, resulting in the persistence of a vicious cycle of pancreatic enzymes digesting the pancreas and surrounding tissues, which eventually causes multi-organ damage. Meanwhile, a variety of inflammatory cytokines such as platelet activating factor (PAF), tumour necrosis factor (TNF), interleukins 2, 6 and 8 (IL-2, IL-6, IL-8), etc., mediate local and systemic inflammatory responses in the pancreas as inflammatory mediators. Among them, PAF plays a key role in the development of systemic inflammatory response syndrome (SIRS).
6.How to diagnose severe acute pancreatitis? How to self-judge whether there is severe acute pancreatitis?
Because acute pancreatitis takes some time to damage other organs, the diagnosis of severe acute pancreatitis is often determined 48 hours after the onset of the disease. There are strict clinical diagnostic criteria, currently the commonly used diagnostic criteria are Ranson criteria and APACH II criteria, which require an experienced gastroenterologist to make an accurate judgment.
Usually, the occurrence of pancreatitis with persistent unremitting severe abdominal pain with peritonitis manifestations, uncorrectable hypotension and shock, electrolyte disturbance, persistent hyperthermia, early onset of respiratory distress and persistent oliguria often indicate the occurrence of severe acute pancreatitis.
7.Which diseases are easily confused with severe acute pancreatitis or which diseases need to be differentiated?
(1) peptic ulcer perforation: most of them have a history of peptic ulcer, sudden onset, severe abdominal pain, and abdominal muscle plate-like ankylosis, loss of hepatic turbinates, free gas under the diaphragm on X-ray abdominal plain film, moderate elevation of blood amylase, usually not more than 2 times the normal value.
(2) Cholelithiasis and acute cholecystitis: there is often a history of colic attacks; the pain is mostly in the right upper abdomen, mostly with right shoulder involvement pain; jaundice is often present during attacks, Murphy’s sign is positive, there may be pressure pain, rebound pain and muscle tension in the right upper abdomen; blood and urine amylase may be mildly elevated; ultrasound and CT examination show signs of cholecystitis and gallstones. If the blood amylase exceeds 3 times the normal value, it indicates the combination of acute pancreatitis at the same time.
(3) Acute intestinal obstruction: paroxysmal abdominal cramps, mostly located around the umbilicus; accompanied by vomiting, abdominal distension, anal discharge and cessation of defecation; high-pitched bowel sounds, visible intestinal pattern; serum amylase may be mildly increased, X-ray plain film shows signs of intestinal obstruction such as air-fluid plane.
(4) Mesenteric vascular embolism: Most commonly seen in the elderly, patients with hyperlipidemia or heart disease; acute onset, severe abdominal pain, abdominal distension, fever, blood in stool, bloody ascites, shock and signs of peritoneal irritation; serum amylase may be mildly elevated, and mesenteric angiography may show signs of vascular obstruction.
(5) Angina pectoris or myocardial infarction: history of coronary artery disease; mostly presenting with episodes of pressure or pain in the precordial region. Individual patients may have pain in the upper abdomen, resembling acute pancreatitis; blood and urine amylase are normal, while ECG shows myocardial ischemia or myocardial infarction changes, and cardiac enzymes such as CPK, AST, LDH are elevated in myocardial infarction.
(6) Others: There are fashions that need to be differentiated from acute appendicitis, renal colic, splenic rupture, ectopic pregnancy rupture and diabetic ketoacidosis with acute abdominal pain, uremia, etc.
8.What tests can help to confirm the diagnosis of severe acute pancreatitis?
(1) Blood leukocytes: consistently exceed 20×109/L or more.
(2) Blood amylase and blood lipase continue to rise and not decrease.
(3) Blood calcium persistently decreases and cannot be corrected by timely and aggressive supplementation.
(4) Persistent elevation of serum bilirubin that does not decrease and persistent decrease in serum albumin level.
(5) Progressive deterioration of coagulation function.
(6) Abdominal CT indicates massive exudation and extensive necrosis around the pancreas, and pseudocyst or abscess formation is seen.
9.How to treat severe acute pancreatitis?
The treatment principles are the same as those for mild and severe acute pancreatitis, namely: to reduce pancreatic secretion of pancreatic juice, to prevent continuous pancreatic self-digestion, and to prevent and control the emergence of various complications.
The specific measures are basically the same as those for mild acute pancreatitis, but we should emphasize the monitoring of vital signs, early detection and timely management of various complications.
When jaundice occurs in biliary pancreatitis, endoscopic Oddi sphincterotomy should be performed early to perform biliary decompression and drainage and remove embedded gallstones, which can remove the cause of biliary acute pancreatitis and reduce the morbidity and mortality rate.
Once infected pancreatic necrosis is confirmed, necrosis removal surgery should be performed immediately. If the necrosis is not yet secondary to infection, it is advisable to continue medical treatment and close observation, depending on changes in the condition to decide whether to operate or not.
Surgical drainage or percutaneous percutaneous drainage can be chosen for pancreatic abscesses.
Pancreatic pseudocysts can be treated by surgery, percutaneous puncture drainage or endoscopic drainage.
If the diagnosis is unclear and perforation of abdominal organs or intestinal necrosis is suspected, a dissection will be performed.
10.What are the precautions in drug treatment and prevention of severe acute pancreatitis?
The drug treatment and prevention of severe acute pancreatitis is basically the same as that of mild acute pancreatitis, but the use of enteral and parenteral nutrition is emphasized. Since patients with severe acute pancreatitis cannot eat for a long period of time, and the body is in a highly catabolic state, nutritional support is very important. Total gastrointestinal nutrition (TPN) is used at the beginning of the disease, and timely supplementation of fresh plasma is emphasized. When the intestinal obstruction is lifted, it is early transition to enteral nutrition (EN) by jejunal intubation to maintain intestinal mucosal function and prevent pancreatic necrosis and infection caused by intestinal bacterial translocation. It is advisable to choose low-fat, amino acid-rich enteral nutrition, and to strictly control the infusion rate and infusion volume. If the patient’s body function cannot tolerate sufficient amount of enteral nutrition, combined use of enteral and parenteral nutrition is required.
11.What should be the dietary management in the prevention and treatment of severe acute pancreatitis?
(1) Avoid high-fat diet.
(2) Avoid eating too much at once.
(3) Avoid alcohol abuse, and patients with biliary tract disease should completely abstain from alcohol.
During treatment, when abdominal pain is completely relieved, abdominal pressure disappears, and bowel sounds return to normal, you can start with fat-free fluids, and then gradually resume a normal diet, and the recovery process should be gradual, avoiding rapidly starting to eat foods with high fat content.