Acute pancreatitis in children

Introduction to acute pancreatitis in children Acute pancreatitis in children is relatively rare, and the onset of pancreatic juice spills into the interstitial cells of the pancreas and its surrounding tissues. It is now believed to be associated with viral infections, drugs, pancreatic duct obstruction, and certain systemic diseases or overeating. At least half of the cases are caused by mumps virus or blunt trauma of the upper abdomen, and 30% of cases still have no cause. The relevant data suggest that acute pancreatitis has a pathophysiological process of acute microcirculation. basic knowledge The proportion of illness: 3% Susceptible people: good for children Mode of infection: non-infectious Complications: pancreatic abscess, diffuse intravascular coagulation

Causes of acute pancreatitis in children

(1) Causes of the disease

The common causes of acute pancreatitis in children are viral infection, trauma, multi-system diseases and congenital malformations of the pancreaticobiliary system. 30% of the causes are unknown. The most important of these is viral infection.

Infection

Various infections such as bacteria or viruses secondary to other parts of the body.

(1) Viruses: such as acute mumps virus, rubella virus, measles virus, echovirus, coxsackie virus, hepatitis A and hepatitis B virus, cytomegalovirus, and the like. More common is pancreatitis caused by mumps virus.

(2) Bacterial infection: bacterial infections such as Salmonella cause pneumonia, bacillary dysentery, tonsillitis and other diseases, accompanied by acute pancreatitis, mostly caused by bacterial toxins. There are reports of typhoid fever complicated with acute pancreatitis in China.

(3) Mycoplasma infection: In addition, mycoplasma infection can also cause acute pancreatitis, and pancreatitis can be the first manifestation of mycoplasma infection.

(4) Parasitic infection: Ascending infection and obstruction caused by aphids and liver flukes. More common in Asia.

2. Digestive disorders

Upper gastrointestinal disease or malformation of the junction of the gallbladder and pancreas, bile reflux into the pancreas, causing pancreatitis.

Cause: Congenital pancreaticobiliary abnormalities cause poor pancreatic juice excretion or biliary ascariasis in the common channel, blocking the discharge of pancreatic juice. The most common obstructive cause in children is. Pancreatitis caused by biliary mites.

3. Systemic diseases

Systemic lupus erythematosus, allergic purpura and other systemic diseases, vasculitis involving the blood vessels of the pancreas and other organs, causing inflammation, necrosis, thrombosis of the blood vessel wall and necrotizing pancreatitis.

4. Trauma

Severe abdominal contusion causes the pancreatic duct to be easily injured and broken.

Pancreatic duct rupture, pancreatic juice spillover, plus blood supply disorders and infections can lead to acute hemorrhagic necrotizing pancreatitis.

5. Drugs and toxins

Such causes are rare in children.

Reason: Apply a large number of immunosuppressive drugs, adrenal hormones, morphine, etc.

6. Endocrine and metabolic diseases

Such causes are rare in children.

(1) Malnutrition: Low protein diet leads to pancreatic fibrosis, atrophy and stone formation.

(2) Hypercalcemia: It is caused by activation of trypsin, stimulation of pancreatic enzyme secretion, and formation of pancreatic duct stones.

(3) Hyperlipidemia: Triacylglycerol is acted upon by lipase to release free fatty acids, acting on the endothelium of small blood vessels of the pancreas, causing vascular damage and thrombosis, thereby causing acute pancreatitis.

(4) Diabetes: In children with type 1 diabetes and ketoacidosis, amylaseemia occurs due to increased salivary amylase. However, acute pancreatitis is rare.

(5) Metabolic diseases: such as lactateemia, propionic acidemia, glycogen accumulation syndrome type I, homologous cystine urine, and the like. Its pathogenesis is unknown.

7. Hereditary pancreatitis

It is an autosomal recessive hereditary disorder and is more common in white races.

It is characterized by typical acute pancreatitis in childhood, which is later converted to chronic recurrent episodes, which eventually lead to calcification, diabetes and steatorrhea in the pancreas.

(two) pathogenesis

The pathophysiology of acute pancreatitis is that the zymogen is prematurely activated into an active digestive enzyme in the pancreas, and at the same time, the secretion of pancreatic enzyme into the intestinal lumen is blocked.

1. Various trypsin is activated

The pathogenic factors can increase the secretion of pancreatic acinar cells, increase the pressure in the pancreatic duct, and cause the pancreatic duct and pancreatic acinus to rupture, the pancreatic juice overflows, and contact with the pancreatic parenchyma and extra-pancreatic tissue. At this time, trypsinogen in the pancreatic juice is in the acinar The cells are activated in advance as trypsin overflows into the cytosol and leaks through the basal membrane to the interstitial tissue, producing autodigestion, causing edema, hemorrhage or necrosis of the pancreatic tissue. At the same time, trypsin activates both the complement and kinin systems.

(1) Lipase causes peripancreatic fat necrosis, and damaged fat cells can produce harmful factors and more damage to peripheral acinar cells.

(2) Trypsin: activates various trypsins to make them active. In addition, chymotrypsin can cause tissue edema, hemorrhage and necrosis.

(3) Phospholipase A:

1 Hydrolyzed lecithin in acinar cells to produce free fatty acids (FFA) and lysolecithin. The lysolecithin can disintegrate the cell membrane, thereby releasing various digestive enzymes in the cells, causing pancreatic hemorrhage and necrosis and multiple organ damage. .

2 Activation leads to damage of the lysosomal membrane and release of lysosomal enzymes, further causing activation of trypsin and self-digestion.

(4) Elastic protease: The specific action is mainly to digest the elastic fiber, especially to dissolve the elastic fiber of the blood vessel wall, causing pancreatic blood vessel necrosis and rupture and bleeding.

(5) Thromboxane A2 (TXA2): causes blood supply disorders in pancreatic tissue, destruction of intracellular lysosomal membranes, and increase of intracellular calcium ions.

(6) kininase:

Upon activation by kininogen, it is converted to kininase. At the same time, the blood kininogen is decomposed into vasoactive substances, dilate blood vessels and increase capillary permeability, so that the effective circulating blood volume is reduced, resulting in blood pressure drop or shock;

Kinin is a pain-causing substance that produces severe visceral pain. At the same time, it causes histamine release and white blood cell agglomeration.

(7) Pancreatic kallikrein can catalyze the action of kininogen as bradykinin, which causes vasodilation, increased permeability of blood vessel walls, leukocyte exudation and pain.

(8) Lysosomal enzyme: Trypsinogen is activated in acinar cells. This is a key step in the digestion of pancreatic enzymes and hemorrhagic necrosis of pancreatic tissue.

In the case of acute pancreatitis, the secretion of antitrypsin is weakened, and the trypsin active complex is aggravated, causing damage to the body.

In addition: Oxygen free radicals can cause damage to macromolecules such as proteins, nucleic acids, lipids and polysaccharides, and increase the permeability of capillary wall in the pancreas. Pancreatic edema, hemorrhage, and tissue degeneration and necrosis increase, but do not affect enzyme activation.

2. Endotoxemia

The incidence is very high. It is caused by lipopolysaccharide in the cell wall of Gram-negative bacteria, which is mainly derived from the intestine, and is the main cause of multiple organ failure and death.

Its role is:

(1) Direct destruction of the lysosomal membrane in the cells of the mononuclear phagocytic system, causing cell damage.

(2) non-specifically binds to the cell membrane and interferes with the normal function of the cell membrane.

(3) damage to the mitochondrial structure, affecting the ATPase and oxidative phosphorylation coupling process, causing energy metabolism disorders.

(4) causing a series of pathological changes in the body, mainly affecting the vasomotor function, activating vasoactive substances, reducing platelets and leukocytes, lowering blood pressure, developing DIC and causing multiple organ failure.

(5) Change the immune function of the body.

3. Enzymatic toxic substances

It is a substance produced and secreted by the pancreas at the time of onset.

effect:

1 caused tissue edema, hemorrhage, and necrosis in the pancreas and pancreas.

2 and the toxins produced by necrotic tissue can be transported to the whole body via the lymphatic system and/or blood circulation, causing complications of the whole body organs and becoming the main cause of damage to the extra-pancreatic organs.

(1) Heart changes:

a. Enzymatic substances directly damage the myocardium.

b. Insufficient circulation of blood.

c. Lymphocytes and mononuclear phagocytic cells infiltrate the myocardium.

d. Impaired cardiomyocytes release intracellular potassium ions, resulting in transient local hyperkalemia and affecting myocardial depolarization. An abnormal electrocardiogram appears, but blood potassium does not necessarily increase at this time.

e. Abdominal pain can cause coronary vasospasm, arrhythmia, etc. through vagus nerve reflex, and cardiogenic shock can occur.

f. Pancreatic enzyme enters the pericardium through the lymphatic system to cause epicardial fat necrosis, pericarditis or pericardial effusion.

g. Hypocalcemia occurs, affecting the conduction system of the myocardium.

(2) The mechanism of shock:

a. Intense abdominal pain.

b. Vomiting, intra-abdominal and retroperitoneal exudation and other factors can cause insufficient circulating blood volume.

c. Myocardium is damaged.

d. Massive bleeding in the pancreas, peripancreatic and gastrointestinal tract.

e. Infection poisoning.

(3). Mechanism of impaired respiratory function:

a. Tissue breakdown products (vasoactive kinins) cause damage to the capillary wall of the alveoli.

b. Phospholipase can reduce the amount of alveolar surfactant-active phospholipids, causing poor inflation of the alveoli and forming a state of atelectasis.

c. Abdominal pain, ascites, abdominal distension, etc. cause diaphragmatic movement limitation, exudation in the chest cavity, affecting the inflation and exchange of the lower alveoli.

d. Triacylglycerol decomposes to release a large amount of free fatty acids, which reduces lung compliance. Common pathological changes in the lungs are: opening of the arteriovenous short circuit in the lung, thereby destroying the capillaries of the alveolar membrane, and extravasation of the pulmonary blood vessels to form pulmonary interstitial and alveolar edema. Pulmonary interstitial edema, especially edema around the bronchioles, reduces lung ventilation and also affects or limits inflation. Severe edema can cause alveolar collapse and is difficult to reverse.

Prevention of acute pancreatitis in children

Mainly to actively prevent various causes of the disease.

(1) Prevent the occurrence of infectious diseases such as biliary tract mites, viral infections, sepsis, and mycoplasmal pneumonia.

(2) Prevent binge eating and malnutrition, so as to avoid gastrointestinal dysfunction, hinder the normal activity and emptying of the intestinal tract, hinder the normal drainage of bile and pancreatic juice, and cause pancreatitis.

(3) Avoid or eliminate biliary tract diseases: timely treatment of biliary stones and prevention of intestinal mites.

(4) to avoid upper abdominal damage, such as surgery? Endoscopic retrograde pancreatic ductography.

(5) Prevention and treatment of metabolic disorders such as hypercalcemia, hyperlipidemia, diabetes, and the like.

(6) Others: such as prevention and treatment of alcoholism, trauma, mood and drugs.

After 5 to 7 days of non-surgical treatment of acute pancreatitis, the symptoms disappear and gradually heal. Hemorrhagic and necrotic pancreatitis are serious and have a long course of disease. They may die due to shock and may form a localized abscess. After the pseudo-pancreatic cyst.

Pediatric acute pancreatitis complications Complications pancreatic abscess diffuse intravascular coagulation

1, early complications

Performance: water and electrolyte disorders, hypocalcemia and hand and foot spasms.

2, late complications

Mainly occurs in acute hemorrhagic necrotic pancreatitis.

Performance: pseudocyst formation, pancreatic abscess, can also leave chronic pancreatitis and diabetes.

(1) pseudocyst:

It usually forms 3 to 4 weeks after the disease, and is mostly located in the tail of the pancreas.

Cause: The pancreatic tissue is liquefied by trypsinization and the contents of the abscess are discharged from the pancreatic duct.

Performance: The wall of the capsule is necrotic, granulation and fibrous tissue without epithelial coverage.

The rupture or fissure of the wall is the main cause of pancreatic ascites.

(2) Pancreas abscess:

Usually 2 to 3 weeks after the onset of illness,

Causes: Pancreas and peripancreatic tissue necrosis followed by bacterial infection to form an abscess.

Performance: high fever does not retreat, persistent abdominal pain, upper abdomen can be licked and mass.

(3) Portal hypertension:

Symptoms such as segmental portal hypertension occur.

Cause: Pancreatic fibrosis or pseudocysts squeeze the splenic vein to form a thrombus.

3, systemic complications

Acute hemorrhagic necrosis can occur with multiple organ dysfunction, such as adult respiratory distress syndrome (ARDS), arrhythmia or heart failure, thrombophlebitis and diffuse intravascular coagulation, sepsis, pneumonia, diabetes, renal failure, etc. The mortality rate is extremely high.

Acute pancreatitis symptoms in children Common symptoms Acute abdomen upper abdominal pain peritonitis jaundice nausea bloating edema dehydration umbilical cord skin blue purple spot inflammation

The main symptoms are upper abdominal pain, mostly persistent, and often accompanied by nausea, vomiting, vomit for food and stomach, duodenal secretion, severe cases in addition to acute severe illness, may have dehydration and early shock symptoms, And bloating due to intestinal paralysis, jaundice can occur at the end of the common bile duct due to edema of the head of the pancreas, but it is rare in children.

Mild edema cases have upper abdominal pressure (heart or slightly left side), which may be the only sign of the abdomen. In severe cases, except for abdominal distension, the abdomen has tenderness and muscle tension, and the heart is the most obvious. The skin of the umbilicus or waist is blue-purple, and the subcutaneous fat is decomposed by the spilled pancreatic juice and caused by capillary bleeding.

Pathological changes:

1. Edema-type pancreatitis accounts for about 80% to 90%. All or part of the pancreas is edematous, congested, and the volume is enlarged. The discharge of pancreatic juice is blocked, thus increasing the amylase in blood and urine.

2, hemorrhagic necrotic pancreatitis accounts for about 10% to 20%, the lesion is sharp, due to ischemia, hemorrhage or necrosis, the pancreas is dark red or purple-black, a large amount of exudate contains pancreatic juice into the abdominal cavity and cause diffuse peritonitis, which can occur Shock, even death, at this time the digestive pancreatic juice oozes out, acts on the fat-rich omentum, mesentery, etc., causing extensive fat necrosis, decomposing fat into glycerol and fatty acids, which in turn absorbs calcium in the blood. Calcification, blood calcium can be significantly reduced and the phenomenon of hand and foot spasm occurs.

When the parenchyma is inflamed, islet cells are also damaged, affecting glucose metabolism, so it can be complicated by diabetes.

Examination of acute pancreatitis in children

Laboratory inspection

Blood routine examination

(1) The hematocrit was increased before a large amount of infusion was performed.

(2) White blood cell count and neutrophil classification increased, and nuclear left shift phenomenon may occur.

2. Amylase assay

Blood and urine amylase are seen to increase. Often the main diagnostic basis, but not the determining factor

(1) Note:

1) The degree of amylase increase is often not proportional to the severity of inflammation.

2) Elevated serum amylase is not necessarily caused by acute pancreatitis. Normal serum pancreatase does not rule out acute pancreatitis.

Non-pancreatic causes of hyperamylasemia in children:

1 mixed or unexplained: head trauma, burns, renal failure, postoperative, macro amylase.

2 pancreatic amylase: biliary obstruction, duodenal ulcer perforation, intestinal obstruction, mesenteric ischemia or infarction, acute appendicitis, peritonitis.

3 salivary amylase:

Salivary glands: trauma, surgery, anorexia nervosa, mumps, salivary tube obstruction, diabetic ketoacidosis, bulimia.

Ovary: cyst, malignant lesion, malignant tumor.

3) Urine amylase is not as accurate as serum amylase.

4) The amylase in the ascites and ascites can be significantly increased, but it needs to be differentiated from pleural effusion and ascites caused by digestive tract perforation.

3. Electrolyte and acid-base balance determination

(1) Hypocalcemia: The normal value of blood calcium measurement is 2.25~2.75mmo1/L (9~11mg/dl), and 1.87mmol/L (7.5mg/dl) can cause hand and foot sputum.

Hypocalcemia usually occurs 2 to 3 days after onset, and also occurs 5 to 8 days after onset, which lasts for about 2 weeks.

The level of hypocalcemia is related to the severity of pancreatitis, blood calcium continues to decline, and the prognosis is poor.

Precautions:

Hypercalcemia caused by pancreatitis, there will be elevated blood calcium.

In children with normal blood calcium during the attack, hypercalcemia should be checked during the recovery period.

(2) Other:

Often metabolic acidosis, respiratory acidosis, and mixed acid-base balance disorders, and hypokalemia.

In patients with fulminant pancreatitis complicated with renal failure, elevated serum potassium may occur.

Occasionally serum magnesium is reduced.

4. Amylase and creatinine clearance ratio

The normal ratio is 1% to 4%, and >6% indicates acute pancreatitis.

The formula is: urinary amylase / serum amylase × serum creatinine / urine creatinine × 100%

5. Coagulation mechanism

When disseminated intravascular coagulation (DIC) occurs, various coagulation tests are abnormal.

Very severe cases may have positive DIC index, platelet count is significantly lower than normal, prothrombin time (PT) is prolonged, Fbg is less than 2g/L, fibrinolytic index such as 3P test positive and blood clot dissolution time is shortened, etc. . Thrombin time (TT) is prolonged by more than 3 s, or plasma euglobulin lysis time (ELT) is shortened (<70rain).

6. Determination of serum metebumin (MHA)

Non-specific, intra-abdominal hemorrhage caused by any cause, the hemoglobin released by red blood cell destruction is converted into hemoglobin by fatty acid and elastase. The hemoglobin binds to albumin to form positive iron albumin.

In the case of hemorrhagic necrotic pancreatitis, serum tiboalbumin often appears 12 h after onset, while edematous pancreatitis is negative.

7. Serum lipase assay

It can be seen that serum lipase is increased. Because of the intestinal obstruction, ulcer perforation, common bile duct stones, acute cholecystitis and other blood lipase can also be elevated, so more than 3 times more specific.

The normal value is 0.5 to 1 U (comfort). It begins to increase after 24 hours of onset and lasts for 8 to 14 days. Patients who are late for treatment after onset have diagnostic significance and are of little value for early diagnosis.

8. Blood biochemical examination

Severe cases may have elevated blood sugar and urine sugar. Examination of urine creatinine, urea nitrogen, C-reactive protein, blood gas analysis, 2'-microglobulin, liver function, etc. can reflect the severity of pancreatitis.

9. abdominal puncture

In severe cases, there are peritonitis. If there is more peritoneal exudate, abdominal puncture can be performed. According to the nature of peritoneal exudate (blood, mixed with fat necrosis) and amylase determination is helpful for diagnosis.

Film degree exam

1.B type ultrasound examination

It is valuable for the diagnosis of edematous pancreatitis and late pancreatic cysts, and for the diagnosis of pancreatitis with biliary stones and biliary obstruction.

(1) edema-type acute pancreatitis: the pancreas is obviously diffusely enlarged, there is exudate around the pancreas, the pancreatic margin is regular, clear, uniform and low echo;

(2) Hemorrhagic necrosis: The pancreas is severely swollen, with irregular edges, blurred edges, uneven, irregular strong echoes and mixed echoes.

(3) concurrent pseudocyst: cystic mass borders smooth round or oval anechoic area, mostly outside the contour of the pancreas, the echo of the posterior wall is enhanced, and the boundary with the pancreas is unclear.

In addition, the patient's pancreas is unclear due to the influence of intestinal gas, and it cannot be detected.

2. X-ray inspection

The performance of the examination is not a specific manifestation of pancreatitis, so the abdominal plain film lacks specificity.

which performed:

The transverse colon is obviously inflated, and the duodenum or small intestine is paralyzed.

If there is ascites, it is smoky on the plane, the boundary of the psoas muscle is blurred or disappears, the gas bubbles are deformed, the distance between the stomach and the colon is increased, or the colon is cut. But these are not.

3. Computerized tomography (CT)

When the diagnosis of B-mode ultrasound is uncertain, it has certain value for judging whether the pancreas has necrosis and necrosis. However, more than 20% of patients with acute pancreatitis have normal CT results, so CT can not rule out the diagnosis of pancreatitis.

CT can show the presence of injury, diffuse pancreatic enlargement, pancreatic mass, abscess, and hemorrhagic pancreatitis.

Edema-type acute pancreatitis: diffuse enlargement of the pancreas and low CT value; hemorrhage can cause local high density; necrosis can show a distinct low-density translucent area.

4. Chest X-ray examination

Acute pancreatitis often has pulmonary complications, often showing diaphragmatic elevation, limited movement, pleural reaction or effusion, patchy infiltration of the lung base or no shadow. Chest changes in acute pancreatitis are not specific.

5. Endoscopic retrograde cholangiopancreatography (ERCP)

ERCP is particularly useful for the diagnosis of recurrent pancreatitis with pancreatic duct abnormalities and pancreatic schizophrenia.

Indications: Pancreatitis remains unresolved 1 month after onset, pancreatic enzymes continue to rise, recurrent pancreatitis, family history of pancreatitis, pancreatitis after liver transplantation, and pancreatitis with fibrocystic changes.

Complications of ERCP in children: pain, intestinal paralysis, pancreatitis, cholangitis, fever, etc.

6. ECG examination

Severe cases may have manifestations of myocardial ischemia or injury.

Diagnosis and diagnosis of acute pancreatitis in children

diagnosis

1, clinical symptoms

Occurred in children over 4 years old, mainly for upper abdominal pain, nausea, vomiting and abdominal tenderness,

2, amylase determination

Often the main diagnostic basis, if measured by Somogyi colorimetry, normal children are below 64 units, while children with acute pancreatitis up to 500 can increase, serum amylase value can increase after 3 hours of onset And gradually rise, after 24 to 28 hours peak, then gradually decline, urinary amylase also changes, but the rise is slower after the onset, the time after the lesion is relieved is slower than serum amylase, and is affected by renal function and urine concentration. The effect is not as accurate as serum amylase, other related to acute abdomen such as intestinal perforation, intestinal obstruction, intestinal necrosis, amylase can also rise, rarely more than 300 to 500 units,

3, serum lipase determination

It starts to rise after 24 hours of onset, and lasts for a long time. It can be used as a diagnostic method for advanced patients. The normal value is 0.5~1U (comfort).

4, abdominal puncture

In severe cases, there are peritonitis, which is difficult to distinguish from peritonitis caused by other causes. If the pancreas is severely damaged, the serum amylase will not increase, which will cause more difficult diagnosis. At this time, if the peritoneal cavity is more, it is feasible to perform abdominal puncture. According to the nature of peritoneal exudate (blood, mixed with fat necrosis) and amylase determination is helpful for diagnosis,

5, B type ultrasonic inspection

The diagnosis of edematous pancreatitis and later stage pancreatic cysts is valuable. The former shows a marked increase in the pancreas and the latter shows a cystic mass connected to the pancreas.

Differential diagnosis

Acute pancreatitis should be identified with the following diseases:

First, acute perforation of peptic ulcer

There is a typical history of long-term ulcers, sudden onset, abdominal pain suddenly increased, and spread to the whole abdomen. Abdominal muscle tension occurred, liver dullness disappeared, X-ray fluoroscopy showed free gas under the armpit, and serum amylase increased slightly.

Second, myocardial infarction

Have a history of coronary heart disease. Abdominal pain suddenly occurred with nausea and vomiting. Serum myocardial enzymes are elevated. Blood and urine amylase are normal. The electrocardiogram shows an image of myocardial infarction.

Third, acute intestinal obstruction

In particular, high-stranded intestinal obstruction, abdominal pain is paroxysmal colic, abdominal distension, vomiting, and even shock. In the early stage, it can be accompanied by high-pitched bowel sounds, with sound of water and water, no venting, and visible intestinal type. The x-ray of the abdomen shows the level of the fluid and shows typical mechanical intestinal obstruction. Serum amylase is normal or slightly elevated.

Fourth, cholelithiasis and acute cholecystitis

There is often a history of biliary colic, the pain is in the right upper abdomen, often radiating to the right shoulder or back. Blood and urine amylase are slightly elevated. B-ultrasound and X-ray cholangiography can confirm the diagnosis.

Murphy sign positive: the left palm is placed flat on the lower right chest of the patient, and the thumb is pressed against the point of the lower rib cage. When the inflamed gallbladder moves down during the inhalation, the patient touches the thumb that is pressed hard, causing the inhalation to stop.

Five, acute gastroenteritis

Before the onset, there is often a history of unclean diet. The main symptoms are abdominal pain, vomiting and diarrhea, etc., which may be accompanied by hyperactivity of bowel sounds, normal blood and urine amylase.

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