Acute ascaris pancreatitis

　　Acute ascaris pancreatitis is a series of chemical pancreatitis of the pancreas caused by the obstruction of bile and pancreatic juice due to the entry of ascaris into the Vater's ampulla or pancreatic duct. Clinically, it is common to have acute edematous pancreatitis, and some patients may develop into hemorrhagic necrotic pancreatitis.

　　Acute ascaris pancreatitis is classified into local complications, systemic complications, multiple organ failure, chronic pancreatitis, and diabetes. Local complications are manifested as pancreatic abscess or cyst, with the former appearing more than 2-3 weeks into the course of the disease, presenting with high fever, abdominal pain, toxic symptoms, and an upper abdominal mass; the cyst usually forms more than 3-4 weeks into the course, which can compress adjacent tissues and cause corresponding symptoms. Systemic complications are often sepsis or dual infection (fungal infection) and gastrointestinal bleeding. Multiple organ failure can manifest as organ failure of the kidney, heart, and other organs, and also diffuse intravascular coagulation and adult respiratory distress syndrome.

　　Acute pancreatitis caused by ascaris can manifest as abdominal pain, nausea, vomiting, abdominal distension, hypotension, and other symptoms, and its specific clinical manifestations are described as follows.

　　One, Symptoms

　　1, Abdominal pain Almost all patients have abdominal pain, most often in the upper abdomen, which often radiates to the lumbar and back, accompanied by nausea, vomiting, and pain that can be described as piercing or colicky, and may persist for hours or even days. Nausea, vomiting, changes in position, and general antispasmodic gastrointestinal drugs cannot relieve the symptoms of abdominal pain. Coughing and deep breathing can worsen abdominal pain.

　　2, Nausea, vomiting, and abdominal distension It usually appears after onset, manifested as vomiting of stomach contents and bile, sometimes with vomiting of ascaris, and most patients have symptoms of abdominal distension, even paralytic ileus.

　　3, Fever Patients usually have moderate to high fever, lasting for 3 to 5 days. If the patient's body temperature persists for more than a week or gradually increases with an elevated white blood cell count, one should be vigilant for secondary infection, such as pancreatic abscess or biliary tract infection.

　　4, Hypotension or shock Mainly seen in hemorrhagic and necrotic pancreatitis, a few patients may suddenly develop it, or it may gradually appear after other complications. The main cause is insufficient effective blood volume. Bradykinin causes peripheral vascular dilation, and myocardial depressant factor is released from pancreatic necrosis, with concurrent infection or gastrointestinal bleeding.

　　5, Water, electrolyte, and acid-base balance disorders Patients may develop metabolic alkalosis due to frequent vomiting, with varying degrees of dehydration. Severe patients may develop significant dehydration and metabolic acidosis, accompanied by decreased blood potassium, calcium, and magnesium levels.

　　6, Other Severe patients may develop acute respiratory failure or adult respiratory distress syndrome, and other organ failure may also occur, such as renal and cardiac failure. Some patients may develop pancreatic encephalopathy, manifested as abnormal mental and disordered states, lack of orientation, accompanied by illusions, hallucinations, and mania.

　　Two, Signs

　　1, Patients with acute edematous pancreatitis have mild abdominal signs, often inconsistent with the patient's complaints, due to the pancreas being a retroperitoneal organ. Patients present with upper abdominal tenderness, without rebound pain or muscle tension, and may be accompanied by abdominal distension and reduced bowel sounds.

　　2, Hemorrhagic and necrotic pancreatitis often presents with signs of acute peritonitis, such as abdominal muscle tension, abdominal tenderness, and rebound pain. In patients with paralytic ileus, bowel sounds are weak or absent. Some patients may develop ascites, which is usually hemorrhagic, and positive shifting dullness in the abdomen. A few patients may exhibit Grey-Turner sign and Gullen sign, which are due to enzymes, necrotic tissue, and bleeding infiltrating through the peritoneal spaces and muscle layers into the subcutaneous tissue under the abdominal wall, reaching the lateral abdominal area and periumbilical region on both sides, leading to changes in skin color. Patients with concurrent pancreatic abscess or cyst may palpate a mass in the upper abdomen. Early jaundice in patients is due to inflammatory edema of the pancreatic head and obstruction of the common bile duct or ampulla by ascaris, while later jaundice is usually due to compression of the common bile duct or liver cell damage by pancreatic abscess or cyst, and clinical symptoms of hypocalcemia may appear when severe pancreatic necrosis calcifies, leading to hypocalcemia.

　　Parasitic acute pancreatitis should be treated with comprehensive measures. The specific preventive measures are described as follows.

　　1. Handling feces, managing water sources, and preventing infection are several aspects.

　　2. Strengthen propaganda and education, popularize health knowledge, pay attention to dietary and personal hygiene, wash hands before meals and after defecation, do not eat uncleaned vegetables and fruits, do not drink unboiled water, prevent the ingestion of ascaris eggs, and reduce the chance of infection.

　　3. Using harmless human feces as fertilizer is an important measure to prevent fecal pollution of the environment and to cut off the transmission route of ascaris.

　　In areas where water and manure are used as fertilizer, the five-tank three-pool storage method can be used to make most of the eggs settle at the bottom of the pool. Especially in rural areas, if the infection rate of parasites such as ascaris exceeds 60% in the population, deworming treatment can reduce the incidence of ascaris pancreatitis.

　　The examination for parasitic acute pancreatitis includes blood tests, abdominal X-ray, abdominal ultrasound, CT, and endoscopy. The specific examination methods are described as follows.

　　1. White blood cell count

　　There is an increase in white blood cells and left shift of neutrophil nuclei.

　　2. Amylase measurement

　　In normal people, there are two types of amylase in the blood: salivary and pancreatic. The amylase that increases during acute pancreatitis is mainly of the pancreatic type. The rapid test currently used in clinical practice can inhibit the salivary amylase in serum and only measure the pancreatic amylase, thus having a high specificity. Serum amylase begins to rise 6 to 12 hours after onset and starts to decline after 48 hours, lasting for several days. Serum amylase exceeding five times the normal level can confirm the disease. It is noteworthy that the level of serum amylase does not necessarily parallel the patient's condition. The amylase in hemorrhagic necrotizing pancreatitis may be lower than normal or normal. For other diseases such as acute gastrointestinal perforation, acute cholecystitis, cholelithiasis, and acute intestinal obstruction, the serum amylase can also rise, but generally not more than twice the normal level. The increase in urinary amylase is about 6 hours later than that of serum amylase and is greatly affected by the patient's urine volume.

　　3. Ratio of amylase to endogenous creatinine clearance rate (cam/ccr%)

　　The normal range of Cam/ccr% in clinical tests is 1% to 4%. During acute pancreatitis, the kidney's clearance of amylase increases, while the clearance of creatinine remains unchanged, resulting in an increased ratio, which is usually three times higher. For other causes of hyperamylasemia, this value is generally normal or lower than normal. However, in patients with diabetic ketoacidosis and renal insufficiency, this ratio may increase.

　　4. Serum lipase

　　The elevation time of serum lipase is about 24 hours later than that of serum amylase, and its duration is longer than that of serum amylase. It is often used to measure for diagnosis in patients who seek medical attention late.

　　5. Serum metmyoglobin

　　When there is intra-abdominal hemorrhage, hemoglobin in red blood cells undergoes a series of changes to form metmyoglobin, which can appear 72 hours after onset, and a positive result indicates that the patient has severe hemorrhagic necrotizing pancreatitis.

　　6. Biochemical examination

　　Patients often have transiently elevated blood glucose levels, which usually return to normal within 3 to 5 days. If the blood glucose level remains elevated above 10 mmol/L, it indicates severe pancreatic necrosis with poor prognosis. Clinically, elevated transaminases and lactate dehydrogenase can also be commonly observed. In addition, there is often transient hypocalcemia, such as when the blood calcium level is below 1.75 mmol/L and the patient has tetany, it indicates hemorrhagic necrotizing pancreatitis. If the PaO2 is below 60 mmHg, clinical caution should be exercised for the occurrence of adult respiratory distress syndrome.

　　7. Abdominal X-ray

It can exclude other acute abdominal conditions such as perforation, and can also detect intestinal paralysis or diagnose paralytic ileus.

　　8. Abdominal ultrasound

Ultrasound has diagnostic significance for the enlargement of the pancreas, pancreatic abscess, and pseudocyst. When the pancreatic duct is blocked by parasites, a solid parallel bright band can be seen within the pancreatic duct, without an acoustic shadow behind it. Real-time dynamic observation often shows no significant peristalsis of the band.

　　9. CT

CT examination can clearly show the lesions of the pancreas and surrounding organs without being affected by intestinal gas, and can distinguish between edematous and necrotic pancreatitis and their severity.

　　10. Endoscopic examination

In the past, emergency endoscopic examination was considered a contraindication for acute pancreatitis, but this view has changed. Endoscopic examination can detect the blockage of the pancreatic and bile ducts by parasites and can remove them, which is particularly suitable for elderly patients and those who cannot tolerate surgical treatment.

　　For patients with parasitic acute pancreatitis, it is advisable to eat light, low-fat, and easily digestible foods; to consume vegetable oils; to consume fruits and vegetables rich in dietary fiber and vitamins. It is forbidden to eat spicy and刺激性 foods; to avoid animal fats and other high-fat foods; to avoid greasy foods; and to avoid foods that are prone to cause bloating.

　　First, what kind of food is good for the body in acute pancreatitis?

　　1. It is advisable to eat light, nutritious, and liquid foods, such as rice gruel, vegetable soup, lotus root starch, egg flower soup, and noodles.

　　2. In addition to liquid food, it also includes rice porridge, vegetarian noodles, vegetarian wontons, bread, biscuits (low in oil), and a small amount of minced soft vegetables and fruits.

　　3. After the abdominal pain and vomiting have basically disappeared, and the white blood cells and amylase have decreased to normal levels, pure carbohydrate-rich food without fat can be provided, including rice gruel, thin lotus root starch, almond tea, fruit juice, jelly, and other sugar-containing foods. As these foods have no stimulating effect on the exocrine function of the pancreas, they can be used as the main source of energy supplement for acute pancreatitis.

　　4. It is appropriate to increase the intake of sieved congee, steamed egg white, and a small amount of soybean milk soup food.

　　5. Choose vegetable oils, and use cooking methods such as boiling, steaming, pickling, roasting, stewing, braising, and simmering.

　　Second, What Foods Should Not Be Eaten for Acute Pancreatitis

　　1. Absolute abstinence from alcohol: general recovery takes 2 to 3 months, and to prevent recurrence, it is necessary to avoid eating foods rich in fat for a long time.

　　2. Avoid greasy foods. Greasy foods are difficult to digest and can promote bile secretion, and bile can activate digestive enzymes in the pancreas, which can worsen the condition. Therefore, foods with a high fat content, such as fatty meat, peanuts, sesame seeds, fried snacks, fried foods, etc., should be prohibited.

　　3. Avoid foods containing fat, such as broths, fish soups, chicken soups, milk, egg yolks, etc.

　　4. Avoid spicy and stimulating seasonings, such as chili, Sichuan pepper, cumin powder, etc.

　　Acute pancreatitis caused by ascaris can be treated medically or surgically, and the specific treatment methods are described as follows.

　　First, Medical Treatment

　　Early nutritional support treatment should be provided for severe patients; antispasmodic analgesic treatment should be given, and atropine can be given to patients without paralytic intestinal obstruction; for severe pain patients, pethidine should be added; at the same time, the external secretion of the pancreas should be reduced, and the following methods are generally used in clinical practice, such as fasting, gastrointestinal decompression, H2 receptor antagonists, or proton pump inhibitors. The use of somatostatin such as octreotide can inhibit pancreatic secretion caused by various reasons, reduce postoperative pancreatic fistula and other complications, and shorten hospital stay. Antibiotics can be given to prevent and control concurrent infections. Parenteral nutritional support should be provided during fasting.

　　Second, Endoscopic Treatment

　　Endoscopic vermifuge treatment has been carried out in China outside, and it may be limited in cases of concomitant gallstones, vermiform displacement within the pancreatic duct, and pancreatic necrosis, and surgical treatment may be considered.

　　Third, Surgical Treatment

　　Surgical treatment must be considered under the following conditions:

　　1. The diagnosis of acute pancreatitis is clear, and the condition still progresses to acute peritonitis after active medical treatment.

　　2. Ascaris obstruction of the pancreatico-biliary duct requires relief of obstruction and endoscopic extraction of the worm has not been successful.

　　3. The diagnosis of acute hemorrhagic necrotizing pancreatitis is unclear, and it cannot be ruled out that other acute abdominal emergencies requiring laparotomy for non-surgical conditions.

　　4. Pancreatic abscess and pseudocyst with concomitant gallstones, vermiform displacement within the pancreatic duct, and pancreatic necrosis may limit endoscopic vermifuge treatment, and surgical treatment may be considered.