Guidelines·Consensus｜Expert consensus on the emergency diagnosis and treatment of acute pancreatitis (2021)

Acute pancreatitis (acute pancreatitis, AP) is a disease characterized by acute inflammation of the pancreas and destruction of acinar cells in histology.
It is one of the common digestive system emergencies.
It often develops locally and affects systemic organs and systems to become severe acute pancreas.
Inflammation (severe acute pancreatitis, SAP).

Background Acute pancreatitis (AP) is a disease characterized by acute inflammation of the pancreas and the destruction of acinar cells in histology.
It is one of the common digestive system emergencies.
It often develops locally and affects systemic organs and systems and becomes severe acute.
Pancreatitis (severe acute pancreatitis, SAP).

The annual incidence of AP worldwide is 13~45/100,000.
The incidence in China has increased from 0.
19% to 0.
71% in 20 years.
80%~85% of patients have mild acute pancreatitis (MAP).
Limitations, the fatality rate is less than 1% to 3%, but about 20% of patients will develop moderate or severe pancreatitis, and the fatality rate can reach 13% to 35%.

Therefore, timely diagnosis or early prediction of the occurrence and development of severe acute pancreatitis (SAP) and the emergence of complications are very important.

In recent years, in the field of acute pancreatitis treatment, a multidisciplinary comprehensive treatment model based on non-surgical treatment has gradually formed.

1.
Epidemiology of acute pancreatitis The most common causes of AP are biliary tract disease, hyperlipidemia, and alcohol consumption.

Other uncommon causes include drugs, pancreatic cystic malignancies, viral infections [new coronavirus, human immunodeficiency virus, mumps, cytomegalovirus, Coxsackie B virus and influenza A (H1N1)] , Metabolic factors (such as hyperparathyroidism, hypercalcemia), vasculitis, autoimmunity, pregnancy, trauma, iatrogenic factors, etc.

Endoscopic retrograde cholangiopancreatography (ERCP) is the most common iatrogenic cause of AP.
Measures to prevent pancreatitis after ERCP include: preoperative or postoperative application of non-steroidal anti-inflammatory drugs anal suppositories ( Indomethacin suppository 50 mg or 100 mg), preoperative somatostatin intravenous drip, pancreatic duct stent placement.

A large multi-center, retrospective study in my country showed that the fatality rate of SAP within one week of the course of SAP is even as high as 67%, and its etiology and predisposing factors are diverse.
Biliary tract disease is the main cause of SAP, accounting for 58.
7%; idiopathic SAP accounts for 58.
7%.
25.
2%; SAP caused by alcohol abuse accounted for 9.
0%; other causes accounted for 7.
1%.

The occurrence of hyperlipidemic pancreatitis (HLP) has nothing to do with serum cholesterol levels, but is closely related to the significant increase in serum triglycerides (TG) levels, so it is also called hyperlipidemic pancreatitis ( hpertriglyceridemia pancreatitis, HTGP).

In recent years, the incidence of HTGP has been on the rise, and often leads to more serious clinical processes.

A large sample study in Jiangxi Province analyzed the incidence trend of AP from 2005 to 2012, showing that hyperglyceremia has surpassed alcohol as the second leading cause of biliary diseases (14.
3%), and the fatality rate of severe HTPG is significantly higher than Severe biliary pancreatitis.

A large sample study in developed areas in China showed that the proportion of hyperlipidemia in the cause of AP has jumped to 25.
6%.

In addition, HTGP mostly occurs in young men, especially those with obesity, alcoholism and diabetes.

2.
Acute pancreatitis diagnosis 2.
1 Clinical manifestations ① Onset of abdominal pain: sudden onset of abdominal pain, the pain peaks within 30 minutes; the onset is often related to eating and drinking.

②The nature of abdominal pain: dull or sharp pain, persistent and severe.

③Position of abdominal pain: the upper abdomen is mostly, followed by the left upper abdomen, which can radiate to the back, chest, and left abdomen.

④The degree of abdominal pain: it is usually difficult to tolerate and does not relieve for more than 24 hours.
Some patients may be relieved in a curled up position or leaning forward position.

⑤ Accompanying symptoms: may be accompanied by nausea, vomiting, abdominal distension, jaundice, fever, and changes in consciousness.

Complicated with sepsis, organ failure, intra-abdominal hypertension or abdominal compartment syndrome, pancreatic encephalopathy.

2.
2 On physical examination, patients with mild upper abdominal tenderness and mild muscle tension were not severe.

Severe patients present with localized peritonitis or pan-abdominal peritonitis, and may have Grey-Turner sign and Cullen sign.

Most patients with jaundice are biliary pancreatitis.

2.
3 Diagnostic criteria The diagnosis of AP needs to meet at least two of the following three criteria: ① Abdominal pain consistent with the onset; ② Biochemical evidence of pancreatitis [serum amylase and/or lipase greater than 3 times the upper limit of normal]; ③ Typical appearance of abdominal imaging (pancreatic edema/necrosis or effusion around the pancreas).

3.
Differential diagnosis of acute pancreatitis Common clinical acute abdomen will have abdominal pain, and serum amylase and lipase levels may also increase, which often confuses or delays the diagnosis of AP.
Therefore, it is necessary to treat common acute abdomen in the emergency department.
Distinguish the disease and AP.

3.
1 Acute cholecystitis Severe right upper abdominal pain, which can radiate to the right scapular area; pain may increase after eating a large amount of and/or high-fat food, and serum amylase and lipase levels are within the reference range or only slightly increase .

Diagnosis basis: Murphy's sign is positive, right upper abdominal tenderness during physical examination, may be accompanied by muscle guarding and rebound pain, or Murphy's sign is positive.

Abdominal ultrasound showed enlarged gallbladder, thickened wall and edema, which may be accompanied by gallbladder stones.

3.
2 Common bile duct stones are intermittently strong, dull pain or colic in the right upper abdomen or under the xiphoid process, which can radiate to the right scapular area; jaundice, clay-colored stool; may have fever; serum amylase and lipase levels may increase.

Diagnosis basis: The level of bilirubin is elevated, and direct bilirubin is the main factor.
The abdominal ultrasound and or CT/MRI examinations suggest that the common bile duct is widened, and the image of stones can be seen.

3.
3 Peptic ulcer disease: Indigestion, heartburn, abdominal distension, nausea and (or) vomiting 2 to 3 hours after a meal, upper abdominal pain.

Diagnosis basis: upper gastrointestinal endoscopy.

3.
4 Sudden and severe abdominal pain due to perforation of the digestive tract; during palpation, the patient may have flat abdomen, involuntary muscle guarding, and obvious tenderness and diffuse rebound pain; hypotension, shortness of breath, tachycardia, fever, etc.
may occur; serum The levels of amylase and lipase may be elevated.

Diagnosis basis: abdominal X-ray/CT showed free gas in the abdominal cavity.

3.
5 Acute mesenteric ischemia, severe diffuse abdominal pain, abdominal distension, nausea, vomiting, diarrhea or blood in the stool.

Diagnosis basis: when there is no bowel necrosis, it can only manifest as periumbilical tenderness, with severe symptoms and mild signs; when combined with bowel necrosis, peritonitis manifests, bowel sounds disappear, white blood cell count increases, colonoscopy suggests ischemic bowel disease, Contrast-enhanced CT of the abdomen shows filling defects of mesenteric angiography, which may have intestinal wall edema and intestinal necrosis.

Angiography can be distinguished, but it is not routinely used.

3.
6 Intestinal obstruction Intermittent abdominal cramps, bloating, accompanied by nausea, vomiting, gas, reduced or stopped defecation.

Diagnosis basis: abdominal X-ray/CT shows gas-liquid level, isolated bowel loops, spring signs, etc.

3.
7 Myocardial infarction (acute coronary syndrome) severe and continuous retrosternal pain, which can radiate to the neck, shoulders, jaw and left arm, occasionally epigastric pain or epigastric discomfort, fatigue, sweating, nausea and vomiting, breathing Difficulties etc.

Diagnosis basis: dynamic changes of ECG ST-T, increased levels of cardiac biomarkers (such as troponin I levels), coronary CTA/coronary angiography can confirm the diagnosis.

3.
8 Diabetic ketoacidosis is about 20%~30% Diabetes patients are complicated with acute abdominal pain, and amylase is slightly elevated, which is easy to be misdiagnosed as AP.
Abdominal CT can confirm the diagnosis.

However, it is not uncommon for patients with diabetic ketoacidosis to have AP at the same time.

Patients may have polydipsia, polyuria, nausea, vomiting, lethargy, and even coma.

Various signs of dehydration can be seen, such as dry skin, sunken eyeballs, decreased blood pressure, cold limbs, and shock.

Urinary glucose and urine ketone bodies are strongly positive, and blood sugar is significantly elevated, generally 16.
7-27.
8 mmol/L (300-500 mg/dL), carbon dioxide binding capacity is reduced, and blood gas indicates metabolic acidosis.

Fourth, the risk of wind layer (scoring) Most of the scores are based on the patient's clinical characteristics, laboratory parameters or imaging characteristics, and are evaluated at the time of admission or within 48 hours.

Including: Ranson criteria (1974), Glasgow-Imrie score (1978), Acute Physiology and Chronic Health Assessment II (APACHE II), Simplified Acute Physiology Score (SAPS II) (1984), Sequential Organ Failure Assessment (SOFA), CT Severity Index (CTSI), Acute Pancreatitis Bedside Severity Index (BISAP) Score (2008) and Japan AP Severity Score (JSS), etc.

Currently, there is no "gold standard" to predict the prognosis of severe acute pancreatitis.

Bedside AP severity score (bedside index for severity in acute pancreatitis, BISAP) is a new simple, easy and accurate assessment standard for acute pancreatitis proposed in 2008.

There are 5 variables that predict hospital mortality (Table 1): blood urea nitrogen (BUN), impaired mental status, systemic inflammatory response syndrome (SIRS), age (Age) and pleural effusion (Pleural) effusion), and stipulated that the BISAP score ≥3 is divided into SAP; the sensitivity of the diagnosis of SAP is 38%, the specificity is 92%, the positive predictive value is 58%, and the negative predictive value is 84%.

The BIASP score was performed on AP patients within 24 hours of admission.
When the BISAP score was less than 2, the fatality rate was <1%, and when the BISAP score was 2, 3, 4, and 5, the fatality rate was 1.
6%, 3.
6%, and 7.
4%, respectively.
, 9.
5%, the most prominent advantage of BISAP score is that it is simple and easy to implement, and can predict severity, death and organ failure.

Only composed of 5 easily accessible indicators and no additional calculations are required.
BISAP simplifies mental disorders to be positive as long as there is a decline in orientation or other mental behavior abnormalities.

Secondly, BISAP scores can be performed multiple times during the course of the disease to dynamically monitor changes in the condition.

Recommendation 1 The BISAP score is simple and easy to implement, with high accuracy.
Emergency physicians should complete the BISAP score within 24 hours of admission to predict the severity of acute pancreatitis in the early stage.

V.
Classification of acute pancreatitis.
In 2012, the International Association of Pancreatology (IAP) issued the "Atlanta Classification Standard (Revised Edition)".
In the same year, it also proposed a classification method based on the severity of determinants for the assessment of disease severity.

5.
1 The Revised Atlanta Classification 2012 (the Revised Atlanta Classification, RAC) This classification method divides the severity of the disease into 3 levels according to the presence or absence of organ failure and complications: ①Mild acute pancreatitis (MAP): AP It is not accompanied by organ failure, local or systemic complications, and the fatality rate is extremely low.

②Moderately severe acute pancreatitis (MSAP): AP is accompanied by transient organ failure (within 48 hours) or local or systemic complications, and the fatality rate is <5%.

③Severe acute pancreatitis (SAP): AP is accompanied by persistent organ failure (>48 h), and the fatality rate is 36%-50%.

5.
2 Determinant-Based Classification of Acute Pancreatitis Severity (DBC) based on determinants.
In addition to the classification of organ failure, the classification method will also include the presence or absence of pancreatic tissue necrosis and its status (sterility).
Or infectious necrosis) The severity of the disease is divided into 4 levels, namely ①mild: no organ failure and pancreatic/peripancreatic necrosis; ②moderate: transient organ failure and/or aseptic pancreas ( Peripheral necrosis; ③severe: persistent organ failure or infectious pancreatic (peripheral) necrosis; ④critical: persistent organ failure with infectious pancreatic necrosis.

Studies have shown that the two classification methods have similar efficacy in the diagnosis and severity of AP.

RAC has a broader overview than DBC, and the Critical classification of DBC determines the severity of the disease; DBC is slightly better in judging the length of hospital stay.

Recommendation 2 Patients with persistent organ failure and infectious necrosis are at the highest risk of death.

6.
Early warning markers for diagnosis of acute pancreatitis In AP, amylase, lipase, elastase and trypsin are released into the blood at the same time.

Serum amylase levels usually increase within 6-12 hours, reach a peak within 24-48 hours, and then fall to normal or close to normal levels within 3-7 days.

Lipase rises within 4 to 8 hours, reaches a peak in 24 hours, and drops to a normal or close to normal level in the next 8 to 14 days.

Serum lipase is considered to be a more reliable AP diagnostic biomarker than serum amylase.

A large sample survey in 2020 shows that people with BMI>22 have an increased risk of AP, and as BMI increases, the risk of disease increases.

And the independent risk factors of AP were screened out, including BMI increased by 1 kg/m2, triglyceride increased by 1 mmol/L (89mg/dL), smoking, and cholelithiasis.

C-reactive protein (CRP), an inflammatory marker, is an important indicator for disease severity assessment.
Others include blood urea nitrogen (BUN)>20 mg/dL (>7.
14 mmol/L), hematocrit (HCT) increased> 44% etc.

In 2020, studies have shown that lactate dehydrogenase, white blood cell count, and percentage of immature granulocytes can be used to predict the severity of AP.

Some scholars use a scoring system composed of lactate dehydrogenase, creatinine, albumin, and blood calcium to predict the incidence and mortality of AP organ failure, and the results show that the prediction accuracy is high.

In addition, chest CT quantitatively assesses the amount of pleural effusion and the number of pulmonary consolidation lobes, which can predict SAP and organ failure early.

Procalcitonin is currently a sensitive marker for detecting pancreatic infection.

Recommendation 3 Use procalcitonin to detect pancreatic infections.

C-reactive protein level ≥150 mg/L on day 3 can be used as a prognostic factor for severe acute pancreatitis.

Hematocrit>44% is an independent risk factor for pancreatic necrosis.

Blood urea nitrogen >20 mg/dL (7.
14 mmol/L) is an independent predictor of death.

7.
Imaging examination of acute pancreatitis.
Ultrasonography should be performed on admission to determine the cause of acute pancreatitis (biliary tract).

Under ultrasound, the volume of the pancreas diffusely increases, the internal echo is reduced, and the surrounding boundary is unclear.

When the diagnosis is in doubt, CT provides good evidence for the diagnosis of pancreatitis.

In terms of distinguishing AP from other acute abdomen, CT is better than ultrasound.

The best time for the first enhanced CT evaluation is 72 to 96 hours after the onset of onset.
The modified CT severity index (MCTSI) (Table 2) helps to assess the severity of AP.

Abdominal ultrasound or CT examination is unreliable for the early detection of choledocholithiasis in biliary pancreatitis.
Therefore, for patients with unknown etiology, magnetic resonance cholangiopancreatography (MRCP) or endoscopic ultrasonography should be considered for occult gallbladder Explorer stones.

For patients with atypical symptoms of AP, critically ill patients, patients suspected of co-infection, and patients with necrotizing pancreatitis whose clinical status has significantly deteriorated (such as sudden drop in hemoglobin or hematocrit (pseudoaneurysm rupture), hypotension, tachycardia, breathing Urgent], more than 4 weeks of pancreatic or peripancreatic effusion in patients with gastrointestinal obstruction symptoms, abdominal and pelvic enhanced CT and abdominal MRI + MRCP examination should be performed: Diffusion-weighted imaging (DWI), T1 imaging, T2 imaging can be used for AP Quantitative analysis.

DWI can quantify the diffusion of water molecules, and a lower apparent diffusion coefficient (ADC value) is associated with an increase in the severity of AP.

DWI can distinguish between edematous and necrotizing pancreatitis, and distinguish between aseptic necrosis and infectious necrotic pancreatitis.

NMR T1 imaging can diagnose chronic pancreatitis and autoimmune pancreatitis, and T2 imaging is used to quantify the degree of pancreatic edema and inflammatory changes, and to predict prognosis.

Recommendation 4 The best time for the first enhanced CT evaluation is 72~96h after the onset of disease.

For critically ill patients, complete abdominal and pelvic enhanced CT and abdominal MRI+MRCP 48 to 72 hours after the onset of symptoms.

For patients with signs of infection, significant clinical deterioration, and gastrointestinal obstruction or signs of infection with peripancreatic effusion over 4 weeks, the abdominal and pelvic-enhanced CT and abdominal MRI+MRCP should be rechecked.

MRCP or EUS is used to screen for occult choledocholithiasis.

MRI helps to determine the status of pancreatic necrosis (sterile and infectious).

8.
Local Complications of Acute Pancreatitis 8.
1 Acute peripancreatic fluid collection (APFC) is a uniform accumulation of peripancreatic fluid without walls, which is limited by the normal anatomical plane and usually resolves spontaneously; if it continues More than 4 to 6 weeks, it may develop into a pseudocyst with clear walls.

8.
2 Pancreatic pseudocyst (PPC) is a liquid aggregate with a clear wall around it and does not contain solid matter; it usually occurs more than 4 weeks after pancreatitis.

Pseudocysts usually appear as thin-walled (1~2 mm), round or oval cystic lesions with a density of <20 HU.

8.
3 Acute necrotic collection (acute necrotic collection, ANC) The pancreas and the surrounding tissues of the pancreas have acute necrosis without a clear tissue wall.

It usually appears two to three weeks after the onset of illness, and the image shows solid or semi-solid (partially liquefied).

8.
4 Walled-off necrosis (WON) Approximately 4 weeks after the onset of ANC, the cystic margin appears in the fat necrosis lesion.
The shape of WON is irregular, and it can not only extend to the peripancreatic tissue and mesangial colon, but also to the colon.
Side ditch.

Their walls are thick and irregular, and calcification occurs over time.

There is a mixture of liquid, necrotic material, and adipose tissue inside WON, which makes the CT imaging level higher than the water concentration, and in many cases it is not uniform.
This is an important feature that distinguishes PPC from WON.

Each of the above local complications is divided into infective and aseptic situations, as shown in Table 3.

9.
Systemic complications of acute pancreatitis 9.
1 Sepsis SAP is complicated by sepsis, and the fatality rate increases by 50% to 80%.

Sequential Organ Failure Assessment (SOFA) ≥ 2 points after infection is used as the clinical judgment standard for sepsis (Table 4); at the same time, it is recommended to use the rapid SOFA score (qSOFA) ≥ 2 points for out-of-hospital, emergency department and general ward Screening criteria for sepsis (Table 5).

9.
2 Acute respiratory distress syndrome SAP is complicated by acute respiratory distress syndrome (ARDS), and the case fatality rate has risen sharply to more than 50%.

The Berlin diagnostic criteria for ARDS are shown in Table 6.

9.
3 Organ failure is assessed according to the Marshall score (Table 7).

An organ score ≥ 2 points is defined as organ failure.

Organ function recovery within 48 hours is transient organ failure, otherwise it is persistent organ failure.

9.
4 Intra-abdominal hypertension and abdominal compartment syndrome usually use bladder pressure to measure intra-abdominal pressure (IAP) indirectly.

Continuous or repeated IAP >12 mmHg is defined as intraabdominal hypertension (IAH).

IAH is divided into four levels: Level I: intra-abdominal pressure 12-15 mmHg; Level II: 16-20 mmHg; Level III: 21-25 mmHg; Level IV> 25 mmHg.

When IAH>20mmHg, accompanied by new organ dysfunction or failure, the diagnosis of abdominal compartment syndrome (abdominal compartment syndrome, ACS).

10.
Treatment of acute pancreatitis AP has the characteristics of rapid disease progression, many complications, and high mortality.
In the past, surgical treatment was advocated.
However, some scholars have found that early surgery may increase the risk of multiple organ dysfunction and lead to death.

In recent years, medical researchers have gained a new understanding of AP.
Comprehensive treatment during the acute reaction period can prevent organ dysfunction and reduce the mortality rate.

The concept of multidisciplinary diagnosis and treatment (MDT) is a new type of diagnosis and treatment model that can solve when, where, who and what technology to deal with patients' problems.

It advocates that multiple disciplines should be combined to diagnose and treat patients, which can realize the optimal allocation of medical resources.
Staff from all departments should jointly discuss diagnosis and treatment plans, enrich treatment ideas, brainstorm and formulate optimal treatment plans.

MDT can make up for the shortcomings of individual diagnosis and treatment, and is conducive to giving full play to the advantages of each technology, promoting the improvement of diagnosis and treatment and improving the efficacy.

The treatment process of AP includes fluid management, analgesia and sedation management, the use of antibiotics, emergency ERCP, nutritional support, organ function support, management of abdominal compartment syndrome, treatment of local complications, TCM treatment, etc.
Specific plans for each stage The formulation of the emergency department, ICU, gastroenterology, surgery, ultrasound, interventional, anesthesiology, nutrition, traditional Chinese medicine, imaging, rehabilitation and other disciplines close collaboration.

Patients with organ failure (defined according to the RAC classification criteria) need to be urgently transferred to the intensive care unit (ICU).

The indication for transfer to ICU is organ failure for more than 48 hours.

Therefore, patients with temporary organ failure may not need to be transferred to ICU, but if fatal multiple organ failure occurs, they need to be transferred to ICU in time.

Recommendation 5 Emergency physicians should use multidisciplinary diagnosis and treatment concepts and models at the beginning of admission for AP patients.
The indication for transfer to the ICU is that the organ failure exceeds 48 hours.
If fatal multi-organ failure occurs, they need to be transferred to the ICU in time.

10.
1 The drop in AP fatality rate observed in the liquid treatment program in the past ten years may be due to more extensive fluid resuscitation to prevent pancreatic necrosis by maintaining microcirculation.
The treatment is mainly divided into two stages: rapid expansion and adjustment of fluid distribution in the body.

10.
1.
1 Timing of fluid resuscitation Early fluid resuscitation can optimize tissue perfusion goals without waiting for hemodynamic deterioration.

Early active intravenous fluids in the first 12-24 hours is the most beneficial.
It plays a key role in improving tissue oxygenation and microcirculation perfusion.
It not only helps to protect the perfusion of the pancreas, but also improves the microcirculation of organs such as the kidney and heart.
Early fluid resuscitation is accompanied by a lower rate of pancreatic necrosis, a lower incidence of MODS, and a mortality rate.

10.
1.
2 Liquid selection Isotonic crystal liquid is the preferred liquid.

Extracellular solutions (Ringer's lactic acid solution, etc.
) may be related to anti-inflammatory effects, but the evidence based on randomized trials is insufficient to prove that Ringer's lactic acid is superior to normal saline.

Due to the increased risk of organ failure, artificial colloidal solutions such as hydroxyethyl starch (HES) are not recommended.

At the same time correct the blood potassium level.

The speed of fluid resuscitation follows the principle of "individualization, precision, and restriction".
The fluid volume must be adjusted according to the patient's age, body weight, and pre-existing kidney and/or heart conditions.

For patients with early shock or dehydration in AP, it is recommended that the fluid velocity be 5-10 mL/(kg·h) within 24 hours of admission, of which 20 mL/kg can be infused in the first 30-45 minutes.
Crystal liquid/colloid liquid=3:1.

Patients without dehydration should be closely monitored and appropriate infusions should be given.

Active fluid resuscitation, vasoactive drugs, and sedative drugs cause increased systemic vascular permeability, leading to pulmonary edema, intestinal failure, and increased intra-abdominal pressure.
The use of fluids, vasoactive drugs, and sedative drugs should be minimized.

Fluid overload or interstitial edema can increase the ratio of colloids (1:1-2) and use diuretics in small doses.

The value of fluid resuscitation goal early goal-directed therapy (EGDT) for AP is not yet clear.
It can be evaluated every 4-6 hours whether AP patients have achieved the following resuscitation goals: ①Central venous pressure (CVP) 8-12 mmHg; ②Mean arterial Pressure ≥65 mmHg; ③Urine output per hour ≥0.
5 mL/(kg·h); ④Mixed venous blood oxygen saturation ≥70%.

Hematocrit, blood urea nitrogen, creatinine, and lactic acid are laboratory indicators of blood volume and adequate tissue perfusion and should be monitored.

Recommendation 6 For patients with early shock or acute pancreatitis accompanied by dehydration, it is recommended to perform rapid fluid resuscitation in a short time.

Give appropriate infusions to patients who are not dehydrated.

Early active intravenous fluids in the first 12 to 24 hours is the most beneficial.

Liquid overload can have harmful effects, so the volume and speed of infusion should be adjusted dynamically with reference to hematocrit, blood urea nitrogen, creatinine and lactic acid levels.

The first choice is isotonic crystal rehydration.

10.
2 Analgesia and sedation management AP pain includes: abdominal pain and pain outside SAP-related diseases (various monitoring, invasive operations, prolonged bed immobilization, etc.
), AP patients need appropriate analgesia and sedation to improve the patient It can provide comfort, reduce oxygen consumption and stress response, tolerate invasive operations, and reduce clinical symptoms.

AP patients should receive analgesic treatment within 24 hours after admission to avoid affecting the patient's quality of life.

Traditionally, morphine is believed to contract the oddis sphincter, and cholinergic receptor antagonists such as anisodamine (654-2) can induce or aggravate intestinal paralysis.
However, a meta-analysis of 5 RCTs of 227 patients found that opioids suppressed There is no difference between pain medication and non-opioid analgesics in the risk of complications of pancreatitis and other serious adverse events.

In most institutions, for patients without tracheal intubation, hydromorphone hydrochloride is superior to morphine or fentanyl.

For SAP patients who need high-dose opioids for long-term pain relief, epidural analgesia can be considered.

Recommendation 7 AP patients should receive analgesia within 24 hours after admission.

There is no evidence or recommendation for any restrictions on pain medications.

Acute kidney injury should avoid the use of non-steroidal anti-inflammatory drugs.

In non-tracheal intubation patients, dihydromorphone hydrochloride has better analgesic effects than morphine or fentanyl.

10.
3 Antibiotic use The preventive use of antibiotics in AP patients is not associated with a significant reduction in mortality or morbidity.

Therefore, the routine preventive use of antibiotics is not recommended for all AP patients.

Antibiotic application indications Patients with acute cholangitis or confirmed extra-pancreatic infection should use antibiotics.
For patients with signs of sepsis or positive puncture culture of bacteria from infectious necrosis, antibiotics must be used in time.

The peak of the secondary infection time of AP is in the second to fourth weeks after the occurrence of pancreatitis.
PCT is considered to be an effective predictor of the severity of AP and the risk of pancreatitis.

Air bubbles in the pancreas and surrounding tissues during CT scan can be considered as evidence of infection.

Infection with common pathogenic microorganisms The pathogenic bacteria of pancreatic infections are mostly gram-negative bacteria in the gastrointestinal tract (Escherichia coli, Proteus, Klebsiella pneumonia), which occur by destroying the intestinal flora and destroying the intestinal mucosa.

The body's defense function is impaired, which can easily lead to the translocation of gastrointestinal microorganisms and toxins, and then cause secondary pancreatic infection.

Gram-positive bacteria (Staphylococcus aureus, Streptococcus faecalis, Enterococcus), anaerobic bacteria are also often seen, and occasionally fungi can be found.

Selection of antibiotics For patients with infectious necrosis, antibiotics known to penetrate the necrotic pancreas should be used.
The antibacterial spectrum should include aerobic and anaerobic gram-negative and gram-positive bacteria.

The third-generation cephalosporin has a moderate osmotic effect on pancreatic tissue and can cover most of the gram-negative bacteria in pancreatic infections.

Piperacillin/carbapenem drugs all show good pancreatic tissue permeability and can cover anaerobic bacteria.

However, due to the high drug resistance rate of quinolones worldwide, quinolones are generally only used for patients who are allergic to β-lactam drugs.

Due to the increasing number of drug-resistant Klebsiella pneumoniae, carbapenems are only used in critically ill patients.

In addition, the antibacterial spectrum of metronidazole is almost only for anaerobic bacteria, and it can penetrate into the pancreas well.

Recommendation 8 Routine preventive use of antibiotics is not recommended.

For patients who show signs of sepsis or who have positive puncture culture of bacteria from infectious necrosis, they must use drug-sensitive antibiotics in time.

Recommendation 9 For patients with infectious necrosis, antibiotics that can penetrate the necrotic pancreas should be selected, and the antibacterial spectrum should cover aerobic and anaerobic gram-negative and gram-positive bacteria.

Quinolone and carbapenem drugs have good pancreatic tissue permeability and can cover anaerobes.

Due to the high drug resistance rate, quinolones are generally only used for patients who are allergic to β-lactam drugs, and carbapenems are only used for critically ill patients.

The third-generation cephalosporin has a moderate osmotic effect on pancreatic tissue.

Piperacillin/tazobactam is effective against gram-positive bacteria and anaerobes.

10.
4 The role of other drugs in the treatment of acute pancreatitis Somatostatin and its analogues (octreotide) can exert their effects by directly inhibiting pancreatic exocrine secretion.

Proton pump inhibitors can indirectly inhibit pancreatic secretion by inhibiting gastric acid secretion, and can also prevent the occurrence of stress ulcers.

Protease inhibitors (Ulinastatin, Gabexate) can broadly inhibit pancreatic enzyme activity related to AP progression, stabilize lysosomal membranes, improve pancreatic microcirculation, and reduce AP complications.

Gabexic acid mesylate may reduce additional invasive interventions, octreotide may reduce organ failure, and lesipadan may reduce the risk of sepsis.

Advocate the early and adequate application of somatostatin and its analogues and protease inhibitors.

Recommendation 10 Early and adequate use of somatostatin and its analogues and protease inhibitors.

10.
5 Nutritional support 10.
5.
1 The purpose of early enteral nutrition Early use of enteral nutrition helps protect the intestinal mucosal barrier and reduce bacterial translocation, thereby reducing the risk of infection and other serious complications.

Timing of enteral nutrition AGA recommends early oral intake (usually within 24 hours) if it can be tolerated, rather than instructing patients to fast.

If oral diet cannot be tolerated, enteral nutrition (EN) treatment should be started as soon as possible within 72 hours after admission to prevent intestinal failure and infectious complications, and to avoid total parenteral nutrition as much as possible.

If AP patients need EN, they are given via a naso-gastric tube.

In the case of digestive intolerance, it is best to administer via a nasal-jejunal tube.

Continuous feeding is better than one-time feeding.

The method of enteral nutrition support should follow the principle of "individualization".
The method of nutrition support for severe pancreatitis patients should be determined according to the patient's intra-abdominal pressure (IAP) and intestinal function: ① IAP<15 mmHg, early EN through nasal-jejunum or nasogastric tube Start as the preferred method.

Continuously monitor the IAP and the patient's clinical condition during EN.

② In patients with IAP>15 mmHg, the rate starts from 20 mL/h through the nasal-jejunal tube, and the rate is increased according to tolerance.

When the IAP value further increases under EN, EN should be temporarily decreased or suspended.

③ Patients with IAP>20 mmHg or abdominal compartment syndrome (ACS) or intestinal failure should stop EN and start parenteral nutrition (PN).

Enteral nutrition.
Patients with mild AP should be given a low-fat, soft food when they retake the oral diet.

Both the elemental diet and the whole protein diet are well tolerated by patients with pancreatitis and are also recommended.

Enteral nutrition can first adopt short peptide preparations, and then gradually transition to whole protein preparations.

Intestinal feeding with immune-enhancing ingredients (arginine, glutamine, nucleotides and omega-3 fatty acids) to regulate host inflammation and immune response has recently attracted great interest in the medical community, but the results of published trials are different Larger.

Currently, there is insufficient evidence to support AP patients benefiting from the use of immune enhancers (arginine, fish oil, glutamine, etc.
).

If the parenteral route cannot be fully tolerated, some parenteral nutrition should be considered to meet the caloric and protein requirements.

Parenteral nutrition should be supplemented with L-glutamine at 0.
20 g/kg per day.

Otherwise, immunonutrition does not work in acute severe pancreatitis.

For mild patients who are considering being discharged directly from the emergency department, it is necessary to provide oral nutrient solutions for emergency patients to ensure that patients can use liquid food at home.

Recommendation 11 Early oral eating (usually within 24 hours) should be tolerated instead of fasting.

If the oral diet cannot be tolerated, enteral nutrition (EN) treatment should be started as soon as possible within 72 hours after admission.

EN can be administered through a naso-gastric tube.

In case of digestive intolerance, it is administered via a nasal-jejunal tube.

For SAP patients, the nutritional support method should be determined based on intra-abdominal pressure and bowel function.

Recommend element diet and whole protein diet.

10.
6 Management of biliary pancreatitis A systematic review of 7 randomized controlled trials with 757 subjects showed that there is no evidence to support routine retrograde cholangiopancreatography (ERCP) for all patients with acute biliary pancreatitis.

ERCP indications: AP patients with acute cholangitis (acute cholangitis) or biliary obstruction should undergo emergency endoscopic retrograde cholangiopancreatography (ERCP) within 24 hours of admission, and duodenal papilla if necessary Sphincterotomy (duodenal papillary sphincterotomy, EST).

Patients with biliary pancreatitis without obstructive jaundice or acute cholangitis do not need early ERCP.

For patients who are highly suspected of having common bile duct stones without cholangitis or jaundice, magnetic resonance cholangiopancreatography MRCP or endoscopic ultrasound (EUS) can be used, and diagnostic ERCP is not required for diagnostic screening.

Regarding the prevention of post-ERCP pancreatitis, the European Society of Gastrointestinal Endoscopy (ESGE) recommends that all patients without contraindications be given 100 mg of diclofenac or indomethacin rectally before or immediately after ERCP, and pancreatic duct stents should be placed in high-risk patients.

For patients with mild biliary pancreatitis with gallbladder stones, laparoscopic cholecystectomy should be performed during the hospital stay to prevent the recurrence of biliary pancreatitis.

For severe acute biliary pancreatitis with peripancreatic effusion, cholecystectomy should be postponed until the inflammation is relieved, the accumulation of peripancreatic fluid subsides or the operation is delayed for 6 weeks.

Recommendation 12 For AP patients with acute cholangitis or biliary obstruction, emergency ERCP or EST should be performed within 24 hours of admission.

Patients with biliary pancreatitis without obstructive jaundice or acute cholangitis do not need early ERCP.

For patients who are highly suspected of having common bile duct stones without cholangitis or jaundice, MRCP or EUS is performed to confirm the diagnosis.

Recommendation 13 To prevent post-ERCP pancreatitis, if there are no contraindications, NSAIDs should be administered rectally immediately before or after ERCP, and pancreatic duct stents should be placed in high-risk patients.

Recommendation 14 For mild biliary pancreatitis with gallbladder stones, laparoscopic cholecystectomy should be performed during the current hospital stay.

For severe acute biliary pancreatitis with peripancreatic effusion, surgery should be postponed for 6 weeks.

10.
7 Hyperlipidemia pancreatitis management 10.
7.
1 Clinical features Compared with non-HTGP, HTGP patients have severe clinical symptoms, easy to relapse, pseudohyponatremia, pseudopancreatin (blood and urine amylase) normal, Features of poor prognosis.

Due to the blood lipid volume effect, HTGP can cause pseudohyponatremia, making the measured blood sodium value 10 mmol/L lower than the actual value.

TG levels> 5.
65 mmol/L can lead to pseudo-normal blood and urine amylase levels.

At this time, compared with amylase, serum lipase has higher specificity and sensitivity, and higher diagnostic value.

10.
7.
2 The diagnostic criteria of HTGP meet the diagnosis of AP, and the serum TG level at the onset of the patient is ≥ 11.
3 mmol/L (> 1000 mg/dL); or TG is between 5.
65 and 1.
3 mmol/L, and other causes such as cholelithiasis, AP caused by alcoholism.

10.
7.
3 It is forbidden to import any fat emulsion within 72 hours of onset of HTGP treatment.

It takes a short time to reduce the TG level and try to reduce it to below 5.
65 mmol/L.

When the patient's symptoms are relieved and blood TG is ≤ 5.
65 mmol/L, and it is difficult to control blood sugar by intravenous infusion of high glucose and energy supplementation, the short and medium-chain fat emulsion directly metabolized by the portal vein can be considered.

Conventional lipid-lowering drugs: A standardized lipid-lowering drug program should be implemented as soon as possible under the patient's tolerance.
Fibrates can significantly reduce TG and increase high-density lipoprotein levels, and can be the first choice for HTGP treatment.

Heparin and insulin: The bleeding risk of low-molecular-weight heparin is much lower than that of unfractionated heparin, and it can significantly reduce the incidence of pancreatic encephalopathy and improve the survival rate of severe AP.

The combination of the two treatments for HTGP has been clinically recognized.
It has a positive effect in reducing TG concentration, relieving symptoms, reducing recurrence rate and mortality, and can be used as the first-line treatment of severe HTGP.

Blood purification: When the above measures are not effective, blood purification is a common method for clinical treatment of severe HTGP.

It can quickly clear the chylomicrons in the plasma, reduce the concentration of TG and pancreatin, reduce the damage of inflammatory factors to the pancreas and systemic organs, and significantly reduce the clinical symptoms of HTGP patients.

10.
8 Intensive care and supportive care Generally speaking, patients with persistent organ failure for more than 48 hours need to be urgently transferred to the ICU.

It is not necessary to routinely transfer patients with transient organ failure to the ICU, but similar patients still require close monitoring.

Severe patients with organ failure within 48 hours who need ventilator, CRRT, etc.
, should also be transferred to ICU.

Define organ failure according to the modified Marshall scoring system, which has the ability to be simple, universally applicable in international centers, and easily and objectively stratify the severity of the disease.

The improved Marshall scoring system is superior to the SOFA scoring system, which is more suitable for intensive care unit management.

10.
8.
1 Treatment of ARDS caused by SAP ARDS is one of the common forms of organ damage in SAP.
Treatment strategies include: early identification of ARDS: The clinical features of ARDS are progressive hypoxemia and respiratory distress.

The organ protection measures of ARDS include: ①Control the amount of fluid replacement.

② Analgesia and sedation treatment.

③Supplement albumin preparations.

④ Give diuretics appropriately.

The organ function support measures of ARDS include: ① Mechanical ventilation is feasible when oxygen inhalation with nasal cannula or mask is ineffective to correct dyspnea.

Both non-invasive and invasive ventilator can be used, but when the removal of bronchial secretions is ineffective and/or the patient feels tired, invasive ventilation is required.

When using mechanical ventilation, a lung-protective ventilation strategy should be used.

The tidal volume is 6 mL/kg, the upper limit of the plateau pressure is 30cmH2O, and the high positive end-expiratory pressure (PEEP).

②Minimally invasive drainage For patients with pleural and ascites, timely minimally invasive drainage of pleural fluid and ascites can increase lung volume, improve hypoxia, and reduce systemic inflammation.

③ Other supportive treatments such as turning over and patting the back, chest tapping vibration, assisted coughing, and respiratory function training.

10.
8.
2 Acute kidney injury caused by SAP Diagnosis and treatment of acute kidney injury (acute kidney injury, AKI) is one of the common complications of SAP.
Approximately 70% of SAP patients have AKI.
Although SAP improves clinically after treatment, there are still some Patients with poor recovery of renal function, it has been reported in the literature that the mortality rate of these patients can be as high as 75%.

AKI diagnostic criteria: serum creatinine (sCr) level increased ≥ 0.
3 mg/dL (≥ 26.
5 μmol/L) within 48 hours; or sCr increased to ≥ 1.
5 times the basic value or more, and it was clear or inferred to occur Within 7 days before; or for 6 hours, urine output <0.
5 mL/(kg·h).

SAP complicated by acute kidney injury should be treated with continuous renal replacement therapy (CRRT) when adequate fluid resuscitation is ineffective or when abdominal compartment syndrome (ACS) occurs.

CRRT indications are with acute renal failure or urine output ≤0.
5 mL/(kg·h); early with 2 or more organ dysfunctions; systemic inflammatory response syndrome with tachycardia and shortness of breath, after general treatment The effect is not obvious; with severe water and electrolyte disturbances; with pancreatic encephalopathy.

CRRT treatment modes currently used for SAP: continuous venous-venous hemofiltration (CVVH), continuous venous-venous hemodiafiltration (CVVHDF), high-volume hemofiltration (HVHF), hemosorption, plasma filtration combined adsorption, And peritoneal dialysis (PD) and so on.

The efficacy of CRRT in the treatment of severe acute pancreatitis SIRS is uncertain, and routine use is not recommended.

Recommendation 15 A modified Marshall scoring system of 2 or more is defined as organ failure.

When mechanically ventilated, a lung-protective ventilation strategy should be used.

CRRT is used for acute kidney injury in SAP.

10.
9 Management of abdominal compartment syndrome 10.
9.
1 Intra-abdominal hypertension (IAH) definition IAP>12 mmHg (>16 cm H2O) continuous or repeated increase.

In SAP, intra-abdominal hypertension is associated with retroperitoneal edema, fluid accumulation, peritoneal effusion, and intestinal obstruction caused by inflammation, partly due to drug intervention, especially excessive fluid resuscitation.

10.
9.
2 Abdominal compartment syndrome (ACS) defines continuous intra-abdominal pressure (IAP)> 20 mmHg (>27 cmH2O) with organ failure.

For cases with a large amount of fluid infusion, SAP combined with renal and respiratory complications, and a large amount of abdominal effusion found on CT, it is recommended that IAP be measured routinely, and IAP can be measured and monitored through a bladder catheter.

The emergence of ACS will increase the fatality rate of such cases.

10.
9.
3 Treatment of intra-abdominal hypertension When IAP≥12 mmHg persists or recurs, the abdominal pressure should be controlled in time, including restriction of infusion, moderate analgesia and sedation, gastrointestinal decompression, drainage of ascites, improvement of gastrointestinal motility, catharsis (health Rhubarb, glycerin, mirabilite, magnesium sulfate, lactulose) promote intestinal peristalsis.
External application of traditional Chinese medicine reduces intestinal edema.
Neostigmine Zusanli acupoint injection promotes intestinal peristalsis in patients with paralytic intestinal obstruction; if fluid overload is considered, it can be Limit fluid intake, diuresis or blood ultrafiltration, improve abdominal wall compliance and circulation management.

With severe organ failure and conservative treatment is ineffective, surgical decompression can be considered.

Recommendation 16 It is recommended that IAP be measured routinely for patients with a large amount of fluid infusion, SAP with renal and respiratory complications, and a large amount of abdominal effusion found on CT.

When IAP≥12mmhg persists or recurs, the abdominal pressure should be controlled in time.

When there is severe organ failure and conservative treatment is not effective for the patient, surgical decompression can be considered.

10.
10 Treatment of local complications 10.
10.
1 Treatment of aseptic pancreatic (peripancreatic) necrosis 70% of necrotizing pancreatitis is sterile, and conservative treatment is required.

If encapsulated necrosis causes gastrointestinal obstruction and bile duct obstruction after 4 to 8 weeks, intervention should be made.

If the patient has persistent pain and "hyperplasia" of the necrotic cyst wall, it is recommended to intervene after 8 weeks.

10.
10.
2 Treatment of infectious pancreatic (peripancreatic) necrosis The diagnosis of suspected pancreatic necrosis of the pancreas does not require routine fine needle aspiration (FNA), and should be judged in combination with clinical and CT.

Although the FNA used for Gram staining and culture under CT guidance can guide clinicians to choose the appropriate individualized antibiotic regimen.

However, due to the high rate of false negative detection, some places have abandoned the routine use of FNA.

10.
10.
3 Timing of treatment of infectious necrosis: For infectious necrosis, delay the intervention as much as possible to at least 4 weeks after the first appearance.

The 4-week delay can make the boundary between necrotic tissue and normal tissue clear, thereby making drainage and necrosis resection easier, and reducing the risk of complications after intervention.

10.
10.
4 Intervention for infectious necrosis: A multidisciplinary minimally invasive step-up method is adopted.
Compared with open surgical necrosis (OSN), this method can reduce the mortality rate by 5 times.

The multidisciplinary minimally invasive step-up method in order of priority is percutaneous ultrasound-guided puncture and drainage, endoscopic transgastric necrosis, video-assisted retroperitoneal debridement, nasal endoscopic necrosis, and open surgery Necrosis resection.

Recommendation 17 For aseptic necrosis, if encapsulated necrosis causes gastrointestinal obstruction and bile duct obstruction after 4-8 weeks, intervention should be made.

If the patient has persistent pain and "hyperplasia" of the necrotic cyst wall, it is recommended to intervene after 8 weeks.

For infectious necrosis, the intervention is delayed until at least 4 weeks after the first appearance.

The intervention method adopts a multi-disciplinary minimally invasive method of ascending the ladder.

10.
11 Indications for surgical intervention: Abdominal compartment syndrome, unsuccessful interventional therapy for acute persistent bleeding, intestinal ischemia or acute necrotizing cholecystitis, intestinal fistula leading to peripancreatic effusion, etc.

Recent systematic reviews and meta-analysis have compared early surgery with late surgery, suggesting that postponing surgical intervention until 4 weeks after the onset of disease can reduce the mortality rate.

Minimally invasive surgical strategies such as endoscopic necrosis or video-assisted retroperitoneal debridement (VARD) can reduce new organ failure after surgery.

Recommendation 18 The indications for surgical intervention include abdominal compartment syndrome, unsuccessful interventional therapy for acute persistent bleeding, intestinal ischemia or acute necrotizing cholecystitis, and intestinal fistula leading to peripancreatic fluid.

10.
12 Traditional Chinese Medicine Special Treatment 10.
12.
1 External Application of Traditional Chinese Medicine Ointment External application of Chinese medicine has the effects of promoting blood circulation, removing blood stasis, reducing inflammation and relieving pain.

Choose Liuhedan, Huoxuezhitong ointment, Glauber's salt, according to the position of effusion, cyst or encapsulated necrosis in the abdominal cavity, externally apply to the corresponding abdomen, 6~8 h/time, once/d.

10.
12.
2 In accordance with the characteristics of “six-fu-organs for the purpose of generalization and reduction for smoothness”, the treatment of SAP should be used as soon as possible for the treatment of SAP.

Rhubarb: Rhubarb not only has a purgative effect, but also removes toxic substances and gases from the intestines, thereby relieving intestinal paralysis.

At the same time, it has antipyretic, anti-infective, choleretic and anti-pancreatic enzyme activity.

Usage: Rhubarb 15g, Glauber's salt 9g, Yuan ginseng 10g, licorice 6g decocted in water, 1-2 doses per day; Rhubarb decoction (30 g), oral or retention enema; Rhubarb tablets (or powder), 1.
5g each time Oral; 3.
0g Xinqingning tablets orally.

Acupoint injection: Inject 0.
5mg of neostigmine on each side of Zusanli on both sides, once/12h, and the course of treatment is 3d.

Neostigmine is contraindicated in patients with epilepsy, angina pectoris, ventricular tachycardia, mechanical intestinal obstruction, urinary tract infarction, and bronchial asthma.

Acupuncture treatment: Zusanli, Sanyinjiao, Yanglingquan, Hegu, Neiguan, Zhigou, combined with electroacupuncture, etc.

Oral treatment of traditional Chinese medicine: the treatment methods of clearing away heat and removing dampness, detoxifying and promoting blood circulation, and Tong Li Gong.

The Tongli Gongxia method represented by "Dachengqi Decoction" and "Qingyi Decoction" can promote the recovery of gastrointestinal motility.

Recommendation 19 The concept and method of integrated traditional Chinese and western medicine should be incorporated into comprehensive treatments such as abdominal abdominal surgery for patients with acute pancreatitis.

10.
13 Follow-up treatment and observation During AP recovery from treatment, transient pancreatic exocrine and endocrine insufficiency may occur.

Therefore, the function of the pancreas should be monitored.
Generally, it can return to normal after 3 months of remission of acute pancreatitis.
Pancreatic enzyme replacement therapy is usually not required.

After about 3 months, the endocrine pancreatic function should be checked (by fasting and postprandial blood glucose concentration testing, HbA1C can also be measured).

AP is often complicated by diabetes.

In addition, the cumulative risk of developing chronic pancreatitis after AP occurs is 13% within 10 years and 16% within 20 years.

Survivors of recurrent AP have an increased risk of chronic pancreatitis within two years to 38%.

Nicotine abuse greatly increases this risk.

For patients with acute alcoholic pancreatitis, simple drinking intervention is recommended during admission.

A study showed that intervention by medical staff every 6 months (organized conversations between trained nurses and patients to inform patients how and why they should abstain from alcohol) significantly reduced the recurrence rate of alcoholic pancreatitis within 2 years .

Recommendation 20 The prevention of long-term complications of AP, such as recurrent pancreatitis, chronic pancreatitis, and diabetes, should be included in the entire diagnosis and treatment of acute pancreatitis.

In short, SAP has a high fatality rate.
With the improvement of treatment methods, although the fatality rate has a downward trend, the hospital stay is still very long and expensive.
The only way to move the treatment checkpoint for pancreatitis is to provide timely refined and standardized treatment.
In order to reduce the post-operative rate of AP, the mortality rate of hospitalization, and reduce the length of hospitalization.

It is precisely the main task of emergency physicians to move the checkpoint forward and provide standardized diagnosis and treatment in the early stage of AP.

The diagnosis of AP can usually be made through medical history, physical examination, laboratory evaluation and imaging of elevated pancreatic enzymes.
Careful evaluation is essential, especially for those who are likely to develop critical illness as determined by the scoring system or clinical evaluation.
patient.

The treatment of acute pancreatitis has also become much more conservative than in the past, and the role of surgery has lost its previous role, replaced by a comprehensive treatment combining fluids, nutritional therapy, interventional radiology, endoscopic therapy, and rehabilitation physiotherapy.
system.

The source of the above content: Emergency Branch of Chinese Medical Association Beijing-Tianjin-Hebei Emergency Emergency Medicine Alliance Beijing Medical Association Emergency Branch Beijing Medical Association Emergency Physician Specialist Branch Chinese Medical and Health Cultural Association Emergency Emergency Medical Care Branch.
Expert consensus on acute pancreatitis emergency diagnosis and treatment.
Chinese Journal of Emergency Medicine .
2021.
30(2):161-172.
Source: Panoramic View Critical Illness-END-Please long press the picture below to identify the QR code and pay attention to dopamine.
Read more exciting articles "Up" "After three rescues, I regret the original efforts!" "Heaven or peace, but the world is disturbed" I used a stethoscope to measure the lives of those who met each other by the water, and the lives that flowed away in my hands were interpreted to me by the tears piled up in the corners of my eyes.
The meaning of life.

I am the last dopamine, recording sounds from the real world.

Some pictures are from the Internet.
If there is any infringement, please contact the back office in time.

Picture: source network copyright, cooperation WeChat: dba0604 Contribution email: last-dopamine@foxmail.
com