Summary: Acute pancreas is a common acute abdominal condition with a complex mechanism and a high degree of severity. The purpose of this document is to increase public awareness of the disease, promote early diagnosis, effective treatment and active prevention and reduce its incidence and mortality.
Introduction
Acute pancreas can occur at any age, with acute conditions, often associated with severe abdominal pain, nausea and vomiting, which seriously affect the quality of life of patients and, in serious cases, can cause complications such as general inflammation syndrome, multi-organ failure and endanger life. Knowledge of acute pancreas is of great importance, both for disease prevention in the general public and for early identification and timely treatment of patients.
II. Epidemiology and morbidity mechanisms
(i) Causes
1. Cholesterol: Cholesterol is the most common cause of acute pancreas in the country. When cholesterol blockes the common passage between the cholesterol and the pancreas, the cholesterol goes backwards into the pancreas, activates the pancreas, leads to the internal digestion of the pancreas and causes acute pancreasitis. In addition, cholesterol infections, aphids, etc. can induce acute pancreas.
2. Alcoholic and violent consumption: A large amount of alcohol can stimulate pancreas gestation, while causing edema and Oddi ‘ s stasis, obstructing the discharge of pancreas and increasing pressure within the pancreas, causing damage to the pancreas. Insulin and cholesterol can contribute to high levels of insulin and cholesterol, and can lead to increased pressure within the mesoplasmic intestine, further increasing the risk of insulin reversal.
Insulin blockage: Insulin blockage, narrowness, tumours, etc. can lead to insulin blockage, incubation of insulin, increased pressure within the insuline, causing pancreas bubbles to burst, and the release of pancreas, leading to acute pancreasitis.
4. Surgery and trauma: abdominal surgery, particularly in pancreas, chords, stomachs, etc., may directly damage pancreas tissue or affect the blood supply of pancreas, leading to acute pancreasitis. In addition, abdominal injuries such as car accident injuries, violent impactes, etc. can cause inflammation and inflammation.
5. Endocrine and metabolic factors: high calcium haemorrhagic conditions allow calcium salt to be deposited in insulin, block incubation of insulin, while promoting incubation and activation of pancreas and increasing the risk of acute pancreas disease. High lipid haematosis can cause microcircle disorders in pancreas, and fatty acid can damage pancreas cells and is one of the contributing factors to acute pancreasitis.
6. Drug factors: Certain drugs, such as gills, sulfur, sugar cortex hormones, may cause acute pancreasitis, the mechanisms of which may be related to drug-induced increases in pancreas, pancreas vascular constrictions or the direct toxic effects of the drug.
(ii) Incidence mechanisms
Under normal conditions, the pancreas contain various digestive enzymes, which are present in the pancreas in the form of inactivated enzymes, which only function as digestive foods when the pancreas enters the incubine and is activated by substances such as intestinal hormones. In the case of acute pancreas, due to the above-mentioned causes, the pancreas were abnormally activated in the pancreas, and active pancreas, such as pancreas, fat enzyme, starchase, etc. began to digest the pancreas ‘ own tissue, leading to changes in the pathology of pancreas edema, haemorrhage and necrosis. At the same time, inflammatory responses in pancreas can activate inflammation cells and release a large number of inflammatory media, such as the cancer cause of death – alpha, white cell inflammation -1 etc., which enter the blood cycle and cause a general inflammation syndrome, thus affecting the functioning of multiple organ systems and leading to multi-organ failure.
III. Clinical performance
Abdominal pain
Abdominal pain, most of the most prevalent symptoms of acute pancreas, is found in the upper abdomen, often with persistent acute pain and can be radiationed from the back of the left. The degree of pain varies from one person to another, to a blunt pain, which can be seen in the form of strangulation, which generally occurs after a severe or drink, and can be mitigated by bending over to the knee.
Disgusting, vomiting
Almost all patients suffer from nausea, vomiting and vomiting, which is frequent and intense, most of the vomiting is a stomach content and can excite the juice when it is serious. The abdominal pain after vomiting is generally not abated, unlike the general gastrointestinal disease.
(iii) Heating
Most patients have moderate fever at the onset of the disease, and the temperature is generally between 38°C and 39°C, lasting 3-5 days. If the fever persists or the body temperature exceeds 39°C, it may suggest that pancreas are bad, infected or combined with other infectious diseases.
(iv) Yellow
Some patients can experience yellow stings, which may be the result of a lack of cholesterol excretion as a result of cholesterol or pancreas inflammation and cholesterol. Yellow bellows are of varying degrees and can be light membrane dyes, as well as in the form of yellow dyes of the whole skin, increased urine.
(v) Other symptoms
Patients may also experience abdominal swelling, peritoneal tractions (e.g. abdominal pain, anti-fault pain, abdominal muscle stress). Severe acute pancreas can cause shock, and the patients suffer from a combination of pale skin, wet skin, pulsary velocities, blood pressure drops, etc., as a result of massive fluid seepage, haemorrhage, and vascular expansion and myocardial inhibition caused by inflammatory media.
Diagnosis
(i) Clinical symptoms and signs
Based on the patient ‘ s typical clinical behaviour of upper abdominal pain, nausea, vomiting and fever, there is a prima facie suspicion of acute pancreasitis in combination with abdominal pain and anti-tiring pain. However, these symptoms and signs are not specific and need to be examined and confirmed.
(ii) Laboratory inspection
Serum starch enzyme and fat enzyme determination: The serosol starch enzyme starts to rise in 2 – 12 hours after the onset of the disease, reaches its peak 24 hours, starts to decline 48 hours later and lasts 3-5 days. The serofatase rises later, often 24 – 72 hours after the onset of the disease and lasts 7 – 10 days. Both exceeded the normal upper limit by more than three times, with significant diagnostic value, but the extent of the increase in serosol and fatase is not entirely relevant to the severity of the condition.
General blood testing: White cell count rises, usually between (10 – 20) x 109/L, and the percentage of neutral particles increases, prompting inflammation.
3. Blood biochemical examination: there can be an increase in blood sugar, a decrease in calcium blood, an increase in triester blood glycerine, abnormal liver function, etc. Declination of calcium is related to the severity of the condition, and calcium is below 1.75mmol/L. In addition, indicators such as urea nitrogen and acetic anhydride may reflect the kidney function of the patient and may be useful in assessing the condition and the prognosis.
(iii) Visual inspection
1. Abdominal ultrasound: a preliminary observation of pancreas morphology, size, echoes, etc., can be made, along with an examination of the cholesterol system for the presence of stones, expansion, etc. However, due to intestinal gas interference, the evidence for pancreas may not be clear enough, especially when acute pancreas is more severe, and its diagnostic value is limited.
Diagnosis of the abdominal CT: is an important visual tool for the diagnosis of acute pancreas. In the early years of acute pancreas disease, CT can show changes in pancreas swelling, blurring edges, percolosis, etc. C.T. has a high degree of accuracy in determining the extent and extent of pancreas necrosis, helps to distinguish light and acute pancreas disease, and can detect complications around pancreas, such as pancreas sepsis, false cysts, etc. Enhanced CT scans provide a clearer picture of pancreas blood supply and are particularly important for the diagnosis of pancreas deaths.
Treatment
(i) General treatment
Patients should immediately fast and water to reduce pancreas. The reduction of gastrointestinal pressure, the extraction of gas and gas from the stomach, the reduction of abdominal swelling and vomiting symptoms, and the reduction of the stimuli of stomach acid to pancreas. The water, electrolyte balance and nutritional support of patients are maintained through intravenous rehydration, electrolytics and nutrients to correct shock and acid alkali balance disorders.
(ii) Drug treatment
1. Insulin control drugs: Common drugs have growth inhibitors and their analogues, such as occurate, which can inhibit incubation of pancreas, high insulin, cholesterol, etc., and reduce ingestion of pancreas.
Insulin-activated drugs, such as ustratin, Gaberone etc., can inhibit the activity of insulinase, fat enzymes, etc. and reduce inflammation of pancreas.
3. Painal treatment: For patients with severe abdominal pain, painkillers such as thorium may be given, but morphine is prohibited, as it can cause Oddi absemic convulsions and aggravates increas.
Antibiotic treatment: In the case of acute pancreas disease, no routine use of antibiotics is generally required. However, in cases of severe acute pancreasitis or associated cholesterol infections, antibiotic treatment should be provided in a timely manner, with the selection of broad-spectral antibiotics, such as joint nitrazine, which can cover grenacella and anaerobic bacteria.
(iii) Surgery
Surgical treatment applies mainly to:
1. Caution: If acute pancreasitis is caused by cholesterol, as soon as the condition permits, the operation or under-simulation should be carried out as soon as possible to remove the choreography and prevent the recurrence of pancreas.
2. Pancreas necrosis: In cases of acute pancreas inflammation and pancreas necrosis, where conservative treatment is ineffective, the operation is required to lead to the initiation, removal of the defacing tissue and control of the infection.
3. Pancreatic pseudocysts: Large pancreatic pseudocysts (greater than 6 cm in diameter) with no signs of self-absorption observed during the week 4-6 weeks, or complications such as cystic oppression of the surrounding tissue organs, cyst fractures, haemorrhage, etc., may be considered for surgical treatment or hypothylene induction.
Prevention
(i) Active treatment of daring diseases
Treatment should be provided in a timely manner to persons suffering from cholesterol diseases, such as pharmacological solubles, in vitro shocks, and surgery to extract stones to prevent acute pancreas.
(ii) Adapting lifestyles
Avoid alcohol consumption, control alcohol consumption, and minimize alcohol or non-drink consumption. To develop good eating habits, to avoid heavy consumption, to follow the principle of a time-quantified diet, to reduce intake of high fats, high cholesterol foods and to eat more of foods rich in diet fibres, such as vegetable fruits and fruits and whole grain foods.
(iii) Control of basic diseases
For people suffering from basic diseases such as hyperlipplasia and calcium haemorrhagicemia, there should be active treatment of primary diseases, and indicators such as blood resin and calcium should be kept within normal limits through dietary control, physical exercise and medication. For example, high-fat haemorrhagic disease can be administered to people with high-fat, and high-calcium haemorrhagic disease can be treated for causes, such as surgery for patients with hyperthyroidism.
(iv) Prudence
In the use of drugs that may induce acute pancreas, such as gills, sulfur, etc., close observation of abdominal pain, nausea, vomiting, etc. should be made in strict compliance with the doctor ‘ s advice, and in case of abnormalities should be stopped and treated in a timely manner.
Conclusion
Acute pancreas is a serious disease of the digestive system, with complex and diverse causes, and the system of morbidity involves the own digestion of the pancreas and the response to systemic inflammation. Clinical performance is characterized by abdominal pain, nausea, vomiting, etc. The diagnosis requires a combination of clinical symptoms, signs, laboratory examinations and visual examinations. Treatment should be based on the severity of the condition, including general treatment, medication and surgical treatment. The key to the prevention of acute pancreas is active treatment of cholesterol diseases, lifestyle adjustments, control of underlying diseases and prudent use of medication. By raising awareness of acute pancreas, increasing public health awareness and prevention capabilities, and timely and accurate diagnosis and treatment, the incidence and mortality of acute pancreas can be effectively reduced and the health of patients ensured.
Acute pancreasitis
