1. Rao, Sheldon MD
  2. Baltaji, Stephanie MD
  3. Crow, Kyle BSN, RN
  4. DiSilvio, Briana MD
  5. Cheema, Tariq MD, FCCP, MMM


Gastrointestinal (GI) emergencies and disorders are among the most common reasons to be admitted to an intensive care unit (ICU). In addition, critically ill patients admitted to the ICU for non-GI-related diseases are frequently at risk of developing GI complications during their hospitalization. This article details the epidemiology/etiology, clinical presentation, diagnostic assessment, and management of the following GI emergencies: upper and lower GI bleed, acute pancreatitis, and ascending cholangitis.


Article Content


Gastrointestinal bleeding (GIB) can be categorized as upper or lower in location based on whether the site of the bleed is proximal or distal to the ligament of Trietz, respectively.1


Upper gastrointestinal bleeding

Epidemiology and etiology

Upper gastrointestinal bleeding (UGIB) is a common condition resulting in frequent admissions to the intensive care unit (ICU) and is associated with substantial morbidity and mortality. The annual incidence of hospitalization for acute UGIB in the United States is approximately 65 per 100 000 individuals.2 UGIB is more common in men than in women. The most frequent causes of UGIB are detailed in Table 1.

Table 1 - Click to enlarge in new windowTable 1. Etiology and Risk Factors for Upper Gastrointestinal Bleeding

Clinical presentation

The most common symptoms of UGIB are hematemesis (vomiting of frank blood or coffee-ground material) and melena (described as black, tarry stools). Some patients could also have concomitant abdominal pain. Between 5% and 10% of UGIB cases can present as hematochezia, which is frank red/maroon blood in the stool.3 About 60% of patients will have a history of a prior UGIB and will commonly be bleeding from the same site. Other pertinent history includes specific comorbid conditions that predispose to UGIB such as cirrhosis or medication use such as anticoagulants. Physical examination may be useful to assess the intravascular depletion associated with UGIB. Tachycardia, orthostatic hypotension, and supine hypotension have been associated with less than 15%, more than 15%, and more than 40% volume loss, respectively.4



Initial blood work for suspected UGIB patient should involve a complete blood cell count, a chemistry panel, liver function tests (LFTs), and coagulation studies along with a type and cross sample sent to the blood bank. Of note, hemoglobin values in a brisk UGIB episode may not be reflective of ongoing blood loss and should not be used as the sole indicator of patient stability. Hemoglobin values should therefore be repeated every 2 to 8 hours based on clinical judgment. In patients with UGIB, an elevated blood urea nitrogen (BUN)-to-creatinine ratio of more than 30:1 may be seen.5


The use of nasogastric tube (NGT) lavage is not currently recommended as studies have failed to show a mortality benefit, improvement in other clinical outcomes such as length of hospital stay, or transfusion requirement.6 This is because NGT lavage may not be positive if the bleeding has stopped or the site is beyond the pylorus. However, despite these recommendations, NGT lavage is common practice in some institutions to confirm ongoing bleed in the stomach or to remove food residue or old blood from the stomach prior to endoscopy.6


Glasgow Blatchford score (GBS) is a risk score used to assess severity of an UGIB episode and need for endoscopic intervention. It is calculated using the hemoglobin, BUN, systolic blood pressure, pulse, and the presence of melena, syncope, hepatic disease, and/or cardiac failure. GBS ranges from 0 to 23, and a higher score indicates the need for more urgent intervention.7


General management

All patients with suspected or ongoing UGIB with hemodynamic instability should be closely monitored, and resuscitation should be begun prior to transfer to an ICU. Vital signs including urine output and airway status should be regularly reassessed. Adequate intravenous access via 2 peripheral 18-gauge or larger catheters or central venous access must be placed and maintained at all times. Intravenous fluid resuscitation must be based on clinical judgment as well as the patient's known comorbid conditions such as cardiac or liver disease. Blood transfusion should be guided by hemodynamic monitoring and blood pressure measurements rather than a hemoglobin value. Restrictive transfusion strategies (targeting a hemoglobin level of 7 g/dL in most individuals and 8 g/dL in individuals with ongoing chest pain or coronary artery disease) are associated with similar ICU outcomes with regard to morbidity and mortality when compared with more liberal transfusion strategies. Restrictive transfusion strategies, however, are associated with a reduction in the number of red blood cell products transfused.8 A platelet goal of more than 50 000 cells/mm3 should be achieved in any patient with an ongoing bleed or hemodynamic instability. International normalized ratio (INR) targets are dependent on the patient's thromboembolism risk; however, in the setting of an active hemodynamically unstable bleed, all efforts should be made to keep the INR as close to 1.5 as possible.9 Patients should receive nothing by mouth (NPO) and are often electively intubated prior to any planned procedure, especially if there is ongoing hematemesis or severe hemodynamic instability.4



Patients admitted with UGIB are typically treated with intravenous formulations of a proton pump inhibitor (PPI). Current practice in most institutions is empiric initiation of high-dose bolus of a PPI, followed by continuous PPI infusion. We note, however, that the most recent recommendations do not specify that acid suppression therapy should be started prior to endoscopic intervention.10 Recent studies have compared the efficacy of intermittently dosed PPIs to continuous PPI infusions. While intermittently dosed PPIs were noted to be noninferior in those studies, this practice is yet to be widely accepted.11 It is additionally recommended to use prokinetic agent such as erythromycin, if possible, to improve gastric visualization during endoscopy. The use of medications in variceal bleeding is discussed later in the text. Tranexamic acid has been used successfully in traumatic bleeding; however, studies have shown no benefit in patients with UGIB.12


Diagnostic studies

Upper gastrointestinal (GI) endoscopy is the diagnostic modality preferred in an acute UGIB episode. This is because endoscopy has the benefit of offering therapeutic interventions at the same time as diagnostic evaluation. Patients with suspected UGIB are expected to have endoscopic evaluation within 24 hours of presentation; however, in variceal bleeds, it is prudent to be done sooner.10 Other diagnostic modalities involve computed tomography angiography (CTA), small bowel enteroscopy, and, rarely, intraoperative enteroscopy.13



Most endoscopic interventions are dependent upon visualization of the site of active bleed. Currently, endoscopic interventions include the use of bipolar electrocoagulation, argon plasma coagulation, heater probes, epinephrine injections, as well as hemostatic clips for actively bleeding ulcers, vascular lesions, or nonbleeding visible vessels.4 If a lesion is suspected to be rebleeding after having achieved successful hemostasis on initial endoscopy, repeat endoscopic therapy is advised.10 Arterial embolization with Interventional Radiology (IR) is recommended for those UGIB patients in whom endoscopic interventions were unsuccessful or recurrent bleeding has occurred despite a second endoscopic evaluation. Surgery is the last resort for an uncontrolled UGIB episode and carries with it the risk of even greater morbidity and mortality.10


Special conditions


i. Variceal bleeds: Variceal bleeds are a major cause of death in cirrhotic patients. The general principle of management for variceal bleeds remains the same as other causes of UGIB. However, fluid resuscitation and blood transfusion strategies must be closely monitored as excessive volume can increase portal pressures causing increased bleeding. In addition to a PPI, a continuous infusion of a somatostatin analogue such as octreotide is often used. In addition, prophylactic antibiotics-such as a third-generation cephalosporin-are used as they are shown to reduce the rate of spontaneous bacterial peritonitis.14 Often, in uncontrolled variceal hemorrhage, protecting the airway via endotracheal intubation is of paramount importance. The utilization of balloon tamponade as a temporary stabilization measure for ongoing variceal hemorrhage can be done using one of the 3 tubes-the Sengstaken-Blakemore tube, the Minnesota tube, and the Linton-Nachlas tube. Endoscopic interventions include variceal ligation and sclerotherapy. If endoscopic intervention fails, transjugular intrahepatic portosystemic shunt (TIPS) may be performed by IR. TIPS is also a treatment modality of choice for variceal rebleeding.14


ii. Anticoagulant use: When possible, anticoagulants should be held in patients with UGIB. In patients with hemodynamic instability and ongoing severe bleeding, a reversal agent or intravenous prothrombin complex concentrate (PCC) may be used. The decision to discontinue medications or administer reversal agents needs the coordination of multiple specialties and should be individualized.9


Lower gastrointestinal bleeding

Epidemiology and etiology

Lower gastrointestinal bleeding (LGIB) refers to bleeding from a site distal to the ligament of Trietz.1 A cohort study from 1998 estimated an annual incidence rate for acute LGIB of 20.5 patients per 100 000.15 The most frequent causes of LGIB are detailed in Table 2.

Table 2 - Click to enlarge in new windowTable 2. Etiology and Risk Factors for Lower Gastrointestinal Bleeding

Clinical presentation

Patients with LGIB typically have hematochezia described as maroon, bright-red blood, or blood clots per rectum. It is often observed that bleeding from the left side of the colon tends to be bright red while blood loss from the right side of the colon is darker or more maroon-colored. UGIB can occasionally present with hematochezia, especially if bleeding is massive with rapid transit through the GI tract. It becomes important to quickly distinguish the source of hematochezia in a hemodynamically unstable patient as the interventions to treat the cause may vary. Again, a history of LGIB becomes useful as patients can commonly bleed from either the same site or similar disease state. As mentioned earlier, physical examination is vital to assess for intravascular volume depletion associated with LGIB.4



Initial blood work for suspected LGIB patient should involve a complete blood cell count, a chemistry panel, LFTs, and coagulation studies along with a type and cross sample sent to the blood bank. Similar to UGIB, hemoglobin values in LGIB may not reflect the severity of a bleed. Unlike UGIB patients, patients with LGIB typically do not have an elevated BUN-to-creatinine ratio of more than 30:1. The biggest consideration in a patient with ongoing hematochezia and hemodynamic instability is to rule out a brisk UGIB episode as an urgent upper endoscopy may be indicated.


General management

The general management of patients with LGIB is similar to UGIB and includes ongoing resuscitation and close monitoring of vital signs even before transfer to an ICU. Restrictive transfusion strategies similar to UGIB may be employed. Patients should receive NPO as well. Four-factor PCC, fresh frozen plasma, and vitamin K may be used to correct underlying coagulopathy in patients with an elevated INR of more than 1.6. Specific reversal agents for newer direct-acting anticoagulants can be individualized on the basis of a patient's clinical presentation and comorbidities.9


Diagnostic studies

Colonoscopy is the diagnostic modality preferred in an acute LGIB episode once UGIB has been ruled out as it can offer diagnostic assessment as well as therapeutic interventions if needed. The biggest drawback of a colonoscopy is the need for bowel preparation with polyethylene glycol. On occasion, flexible sigmoidoscopies after enemas have also been used to evaluate and manage LGIB. Other diagnostic modalities involve CTA, radionuclide imaging, and push enteroscopy.16



Most colonoscopic interventions depend upon the cause and site of the bleed. Most specialists will use epinephrine injections, thermal or electrical coagulation, and hemostatic clips for actively bleeding sites. Transcatheter arterial embolization by IR is useful for bleeds that persist despite colonoscopic interventions or are unamenable to endoscopic procedures. Arterial embolization, however, does carry the major risk of large bowel infarction. Finally, colectomy may be required in select patients with uncontrolled LGIB who are good surgical candidates.16



Acute pancreatitis is inflammation of the pancreas and is a leading GI cause of hospitalization in the United States.17


Epidemiology and etiology

Around 80% of patients with acute pancreatitis have mild self-limiting disease that may require hospitalization only for a few days. Overall mortality of acute pancreatitis is approximately 2%, with certain subgroups of patients, such as the elderly, obese, or those with multiple comorbid conditions, at higher risk.18 In this review, we primarily discuss severe episodes of acute pancreatitis that are characterized by persistent failure of 1 or more organ systems or infected pancreatic necrosis. The etiology of acute pancreatitis can be readily identified in 75% to 85% of cases.19Table 3 lists some of the causes of acute pancreatitis.

Table 3 - Click to enlarge in new windowTable 3. Causes of Acute Pancreatitis

Clinical presentation

Patients with acute pancreatitis present with acute-onset epigastric or left upper-quadrant abdominal pain. This pain is often described as "radiating to the back." Pain persists for several hours to days and may be partially relieved by sitting up or bending forward. Patients may also have concomitant nausea and vomiting. Patients with severe acute pancreatitis may have dyspnea due to diaphragmatic inflammation, pleural effusions, or acute respiratory distress syndrome. Approximately 5% to 10% of patients with acute severe pancreatitis may have painless disease and have unexplained hypotension (seen in critically ill patients or dialysis-dependent patients).20 Ecchymosis may be observed in the periumbilical region (Cullen's sign) or along the flank (Grey-Turner sign) in about 3% of patients and is associated with a mortality of about 37%.21 Physical examination may also provide clues to the etiology of the pancreatitis episode-hepatomegaly may be present in patients with alcoholic pancreatitis, xanthomas in hypertriglyceridemia-induced pancreatitis, and jaundice/scleral icterus in patients with choledocholithiasis.22


Assessment and diagnosis

History should be obtained to evaluate the cause of acute pancreatitis including past episodes and their severity. All patients with acute pancreatitis should get a complete blood cell count, a basic metabolic panel, LFTs, coagulation profile, and a C-reactive protein (CRP) as part of their initial laboratory workup. An arterial blood gas analysis should be performed in patients with hypoxia. The elevation of pancreatic enzymes (lipase and amylase) released from inflamed pancreatic tissue is the cornerstone of biochemical diagnosis. Lipase is considered to be more sensitive and specific than amylase for diagnostic purposes.22


Various modalities of imaging are useful in acute pancreatitis. Abdominal radiographs may show localized ileus of the small bowel. Approximately one-third of patients with acute pancreatitis have abnormalities visible on a chest radiograph such as elevation of a hemidiaphragm, pleural effusions, or acute respiratory distress syndrome.23 Abdominal ultrasound scan may reveal the pancreas to be diffusely enlarged and hypoechoic. Gallstones may be visualized in the gallbladder. Peripancreatic fluid appears as an anechoic collection on abdominal ultrasound scan. Contrast-enhanced CT scan of the abdomen and magnetic resonance imaging (MRI) of the abdomen are the best imaging modalities for visualization of pancreatic pathology. Note that these tests are not routinely indicated in patients with mild pancreatitis. The classic feature seen is the presence of focal or diffuse enhancement of the pancreas. If performed 3 or more days after the onset of abdominal pain, contrast-enhanced CT scan can reliably establish the presence and extent of pancreatic necrosis and local complications and predict the severity of the disease. CT scans may occasionally detect a common bile duct stone or pancreatic structural abnormalities, indicating the etiology of the episode as well.


Accurate diagnosis of acute pancreatitis requires at least 2 of the following 3 diagnostic features: abdominal pain consistent with acute pancreatitis, serum lipase or amylase levels that are at least 3 times the upper limit of the reference range, and findings of acute pancreatitis on cross-sectional imaging (CT or MRI).19


The determination of the severity of acute pancreatitis is one of the most important first steps in management. It helps in selecting appropriate treatments, ensuring proper patient triage, initiation of applicable therapies, and stratifying patient risk for complications. Several tools and scoring systems have been developed to assess the severity of acute pancreatitis. These scoring systems have been summarized in Table 4.

Table 4 - Click to enlarge in new windowTable 4. Risk Stratification of Acute Pancreatitisa


The cornerstones of management include aggressive early intravenous hydration, pain control, appropriate nutrition, and other specific interventions if needed for complications.


Intravascular volume depletion from fluid sequestration associated with pancreatic, peripancreatic, and systemic edema is characteristic of patients with acute pancreatitis. Vigorous fluid therapy is most important during the first 12 to 24 hours after the onset of symptoms and is of little value after 24 hours. Administration of a balanced crystalloid solution has been recommended at a rate of 200 to 500 mL per hour or 5 to 10 mL per kilogram of body weight per hour. This usually amounts to 2500 to 4000 mL within the first 24 hours. One trial suggested the superiority of Ringer's lactate as compared with normal saline in reducing inflammatory markers.25 The main risk of intravenous fluid therapy is volume overload. Excessive fluid administration results in increased risks of abdominal compartment syndrome, sepsis, need for intubation, and death. Fluid therapy needs to be tailored to the degree of intravascular volume depletion and the cardiopulmonary reserve of the patient.22


The provision of nutrition is an important component in the care of patients with acute pancreatitis. Moderately severe acute pancreatitis and severe acute pancreatitis elicit an intense systemic inflammatory response resulting in a catabolic state, increasing caloric and nutritional requirements. Most patients with mild acute pancreatitis can be started on a low-fat diet soon after admission, in the absence of severe pain, nausea, vomiting, and ileus. A need for artificial enteral feeding may be predicted on the basis of unrelenting symptoms that continue to be severe or an inability to tolerate attempts at oral feeding. Although nasojejunal tube feeding is best for minimizing pancreatic secretions, randomized trials and a meta-analysis have shown that nasogastric or nasoduodenal feeding is clinically equivalent.26 Total parenteral nutrition should be reserved for the rare cases in which enteral nutrition is not tolerated or nutritional goals are not met.22


Opioids remain the first-line choice of pain medication. Recent studies showed no differences in the risk of complications related to pancreatitis or adverse events when comparing different opioids and routes of administration.27


There is no role for prophylactic antibiotics in acute pancreatitis. Antibiotics are useful in patients with infected pancreatitis. Infected pancreatitis occurs later in the course of the disease (after 2 weeks) and should be suspected in patients with clinical deterioration despite appropriate treatment. This commonly presents as fever, increasing white blood cell count or hemodynamic instability.28 In these patients, empiric treatment should be aimed against the following common pathogens: Escherichia coli, Bacteroides species, Enterobacter species, Klebsiella species, Streptococcus faecalis, Staphylococcus epidermidis, and Staphylococcus aureus. Appropriate antibiotic choices include carbapenems, quinolones, and metronidazole, which are all known to penetrate pancreatic necrosis and target these bacteria. Infected pancreatic collections can be aspirated and sent for bacterial culture to target antibiotics appropriately.28


Endoscopic retrograde cholangiopancreatography (ERCP) is used primarily in patients with gallstone pancreatitis and is indicated in those who have evidence of cholangitis superimposed on gallstone pancreatitis. This procedure is also a reasonable treatment option for patients with documented choledocholithiasis on imaging or findings strongly suggestive of a persistent bile duct stone.


Indications for surgical intervention include the presence of gallstones in the gallbladder or biliary tree, infected necrosis preferably for more than 4 weeks after antibiotics if stable, and necrosectomy in symptomatic patients. Cholecystectomy when done during the initial hospitalization for pancreatitis due to gallstones reduces the rate of subsequent gallstone-related complications by almost 75%, as compared with cholecystectomy performed 25 to 30 days after discharge.29



The local complications and their treatment options have been detailed in Table 5.

Table 5 - Click to enlarge in new windowTable 5. Local Complications of Acute Pancreatitisa

Nearly 60% of patients with necrotizing pancreatitis can be treated conservatively. For patients in whom infected necrosis develops, treatment consists of antibiotic administration, percutaneous drainage as needed, and, after a delay of several weeks, minimally invasive debridement, if required. A number of minimally invasive techniques (eg, percutaneous, endoscopic, laparoscopic, and retroperitoneal approaches) are available to debride infected necrotic tissue in patients with walled-off pancreatic necrosis. A small proportion of patients with infected necrosis can be treated with antibiotics alone.26



Pancreatic exocrine and endocrine dysfunction develops in approximately 20% to 30% of patients, and chronic pancreatitis develops in about 5% to 10% of those patients.22



Biliary emergencies in the ICU include acute cholangitis, acute cholecystitis, as well as postoperative complications of biliary surgery. There are different types of cholangitis, which include primary biliary cholangitis, primary sclerosing cholangitis, IgG4-related autoimmune cholangitis, and recurrent pyogenic cholangitis. Here, we discuss ascending cholangitis, also known as acute bacterial cholangitis. It is a disorder caused by bacterial infection of the biliary system, most commonly secondary to partial or complete obstruction of the bile duct or hepatic ducts.29


Etiology and epidemiology

The most frequent causes of biliary obstruction in patients with acute cholangitis are biliary calculi, benign biliary stricture, and malignancy. Malignant obstruction may be due to the presence of tumor in the gallbladder, bile duct, ampulla, duodenum, or pancreas. Benign biliary strictures may be congenital, postinfectious, or inflammatory. Post-ERCP acute cholangitis can occur in 0.5% to 2.4% of cases.30 The average age of patients presenting with acute cholangitis is 50 to 60 years. Fewer than 200 000 cases of cholangitis occur per year in the United States.31


Clinical presentation

Classically, patients with ascending cholangitis present with fever, abdominal pain, and jaundice (Charcot triad). In cases of severe acute cholangitis, patients are additionally hypotensive and confused (Reynold pentad). Although the presence of Charcot triad is suggestive of acute cholangitis, it is not diagnostic. Charcot triad is present in 26.4% to 72% of patients with acute cholangitis.32 Patients with acute cholangitis can also present with complications from bacteremia, including hepatic abscess, sepsis, multiorgan system dysfunction, and shock.



Acute cholangitis should be suspected in patients with Charcot triad. Laboratory evaluation shows leukocytosis and elevated LFTs, especially an increase in the serum alkaline phosphatase, [gamma]-glutamyl transpeptidase, and bilirubin (predominantly conjugated portion). Blood cultures should be drawn to assess for bacteremia and help narrow the antibiotic regimen if possible.


Imaging studies may include ultrasound scan of the abdomen, CT, magnetic resonance cholangiopancreatography (MRCP), and endoscopic ultrasonography (EUS). Among these, MRCP (82.2% accuracy in detecting choledocholithiasis) and EUS (96.9% accuracy in detecting choledocholithiasis) are the most sensitive imaging modalities.23



Patients with acute cholangitis require intravenous hydration and pain control. In addition, they should be monitored closely for organ dysfunction and clinical deterioration. Antibiotics should be started without any delay. Empiric regimens for intra-abdominal infections include antimicrobials with activity against enteric streptococci, coliforms, and anaerobes. The choice of antibiotics should take into consideration whether the infection is community-acquired versus health care-associated, as well as individual risk factors for infection. The choice of empiric antibiotics should cover both gram-negative and anaerobic organisms. The following antibiotics are recommended: piperacillin-tazobactam, ticarcillin-clavulanate, ceftriaxone plus metronidazole, or ampicillin-sulbactam. Antibiotics should be tailored to biliary or blood culture results if available.


Biliary drainage is often required for source control owing to impaired biliary secretion of antibiotics. Timing of the procedure often depends on clinical severity of the patient but is frequently done within 48 hours. Therapeutic ERCP is the procedure of choice. Endoscopic sphincterotomy along with stone extraction using a basket or extractor catheter is often used for calculi. In other cases, endoscopic stents are placed to facilitate biliary drainage and relieve intraductal pressure. Another alternative to ERCP for biliary drainage is EUS-guided cholangiopancreatography with biliary drainage and stent placement in patients at high risk for complications with ERCP or if ERCP is not possible due to altered surgical anatomy. In the event endoscopic drainage is not possible due to failed prior attempts or presence of unfavorable comorbidities, percutaneous biliary drainage can be employed. A percutaneous cholecystostomy tube can be placed in patients with an intact gallbladder. Percutaneous transhepatic biliary drainage places a tube directly into a bile duct. Surgical drainage tends to be a last resort for ICU patients and is reserved for when other modalities of biliary drainage are contraindicated or fail. Surgical intervention, however, carries high rates of morbidity and mortality. If the cause of cholangitis is gallbladder stones, laparoscopic cholecystectomy offers definitive management.



Acute mesenteric ischemia is caused by reduced blood flow to the visceral organs that is inadequate to meet their metabolic demands. The severity of the ischemia and its consequences depend on the affected vessel and the extent of collateral blood flow. Acute mesenteric ischemia is a surgical emergency and is detailed in "Surgical Emergencies in the ICU."33



GI emergencies such as acute GI bleeding, severe pancreatitis, and ascending bacterial cholangitis are associated with severe morbidity and mortality if not recognized early and treated promptly. Hemodynamic stabilization is fundamental to management of the aforementioned conditions and includes adequate resuscitation with intravenous fluid and/or blood products, followed by targeted treatment of the underlying pathology once diagnosed. The ICU offers a closely monitored environment where these volatile clinical conditions can be effectively treated by a multidisciplinary team of providers.




1. Zuccaro G Jr. Management of the adult patient with acute lower gastrointestinal bleeding. American College of Gastroenterology. Practice Parameters Committee. Am J Gastroenterol. 1998;93(8):1202-1208. [Context Link]


2. Wuerth BA, Rockey DC. Changing epidemiology of upper gastrointestinal hemorrhage in the last decade: a nationwide analysis. Dig Dis Sci. 2018;63(5):1286-1293. [Context Link]


3. Jensen DM, Machicado GA. Diagnosis and treatment of severe hematochezia. The role of urgent colonoscopy after purge. Gastroenterology. 1988;95(6):1569-1574. [Context Link]


4. Cappell MS, Friedel D. Initial management of acute upper gastrointestinal bleeding: from initial evaluation up to gastrointestinal endoscopy. Med Clin North Am. 2008;92(3):491-509. [Context Link]


5. Srygley FD, Gerardo CJ, Tran T, Fisher DA. Does this patient have a severe upper gastrointestinal bleed? JAMA. 2012;307(10):1072-1079. [Context Link]


6. Gralnek IM, Stanley AJ, Morris AJ, et al Endoscopic diagnosis and management of nonvariceal upper gastrointestinal hemorrhage (NVUGIH): European Society of Gastrointestinal Endoscopy (ESGE) guideline-update 2021. Endoscopy. 2021;53(3):300-332. [Context Link]


7. Holst LB, Petersen MW, Haase N, Perner A, Wetterslev J. Restrictive versus liberal transfusion strategy for red blood cell transfusion: systematic review of randomised trials with meta-analysis and trial sequential analysis. BMJ. 2015;350:h1354. [Context Link]


8. Barkun AN, Almadi M, Kuipers EJ, et al Management of nonvariceal upper gastrointestinal bleeding: guideline recommendations from the International Consensus Group. Ann Intern Med. 2019;171(11):805-822. [Context Link]


9. Veitch A M, Vanbiervliet G, Gershlick AH, et al Endoscopy in patients on antiplatelet or anticoagulant therapy, including direct oral anticoagulants: British Society of Gastroenterology (BSG) and European Society of Gastrointestinal Endoscopy (ESGE) guidelines. Endoscopy. 2016;48(4):385-402. [Context Link]


10. Laine L, Barkun AN, Saltzman JR, Martel M, Leontiadis GI. ACG clinical guideline: upper gastrointestinal and ulcer bleeding. Am J Gastroenterol. 2021;116(5):899-917. [Context Link]


11. Sachar H, Vaidya K, Laine L. Intermittent vs continuous proton pump inhibitor therapy for high-risk bleeding ulcers: a systematic review and meta-analysis. JAMA Intern Med. 2014;174(11):1755-1762. [Context Link]


12. HALT-IT Trial Collaborators. Effects of a high-dose 24-h infusion of tranexamic acid on death and thromboembolic events in patients with acute gastrointestinal bleeding (HALT-IT): an international randomised, double-blind, placebo-controlled trial. Lancet. 2020;395(10241):1927-1936. [Context Link]


13. Barth KH. Radiological intervention in upper and lower gastrointestinal bleeding. Baillieres Clin Gastroenterol. 1995;9(1):53-69. [Context Link]


14. Garcia-Tsao G, Abraldes JG, Berzigotti A, Bosch J. Portal hypertensive bleeding in cirrhosis: risk stratification, diagnosis, and management: 2016 practice guidance by the American Association for the Study of Liver Diseases. Hepatology. 2017;65(1):310-335. [Context Link]


15. Longstreth GF. Epidemiology and outcome of patients hospitalized with acute lower gastrointestinal hemorrhage: a population-based study. Am Coll Gastroenterol. 1997;92:419-424. [Context Link]


16. Triantafyllou K, Gkolfakis P, Gralnek IM, et al Diagnosis and management of acute lower gastrointestinal bleeding: European Society of Gastrointestinal Endoscopy (ESGE) guideline. Endoscopy. 2021;53(8):850-868. [Context Link]


17. Peery AF, Crockett SD, Murphy CC, et al Burden and cost of gastrointestinal, liver, and pancreatic diseases in the United States: update 2018. Gastroenterology. 2019;156(1):254-272.e11. [Context Link]


18. Garg SK, Sarvepalli S, Campbell JP, et al Incidence, admission rates, and predictors, and economic burden of adult emergency visits for acute pancreatitis. J Clin Gastroenterol. 2019;53(3):220-225. [Context Link]


19. Wang GJ, Gao CF, Wei D, Wang C, Ding SQ. Acute pancreatitis: etiology and common pathogenesis. World J Gastroenterol. 2009;15:1427-1430. [Context Link]


20. Lankisch PG, Schirren CA, Kunze E. Undetected fatal acute pancreatitis: why is the disease so frequently overlooked? Am J Gastroenterol. 1991;86(3):322-326. [Context Link]


21. Mookadam F, Cikes M. Images in clinical medicine. Cullen's and Turner's signs. N Engl J Med. 2005;353:1386. [Context Link]


22. Forsmark CE, Vege SS, Wilcox CM. Acute pancreatitis. N Engl J Med. 2016;375:1972-1981. [Context Link]


23. Ranson JH, Turner JW, Roses DF, Rifkind KM, Spencer FC. Respiratory complications in acute pancreatitis. Ann Surg. 1974;179(5):557-566. [Context Link]


24. Banks PA, Bollen TL, Dervenis C, et al Classification of acute pancreatitis-2012: revision of the Atlanta classification and definitions by international consensus. Gut. 2013;62:102-111.


25. Wu BU, Hwang JQ, Gardner TH, et al Lactated Ringer's solution reduces systemic inflammation compared with saline in patients with acute pancreatitis. Clin Gastroenterol Hepatol. 2011;9:710-717.e1. [Context Link]


26. Chang YS, Fu HQ, Xiao YM, Liu JC. Nasogastric or nasojejunal feeding in predicted severe acute pancreatitis: a meta-analysis. Crit Care. 2013;17:R118. [Context Link]


27. Basurto Ona X, Rigau Comas D, Urrutia G. Opioids for acute pancreatitis pain. Cochrane Database Syst Rev. 2013:CD009179. [Context Link]


28. Tenner S, Baillie J, DeWitt J, Vege SS; American College of Gastroenterology. American College of Gastroenterology guideline: management of acute pancreatitis. Am J Gastroenterol. 2013;108(9):1400-1416. [Context Link]


29. da Costa DW, Bouwense SA, Schepers NJ, et al Same-admission versus interval cholecystectomy for mild gallstone pancreatitis (PONCHO): a multicentre randomised controlled trial. Lancet. 2015;386:1261-1268. [Context Link]


30. Kimura Y, Takada T, Kawarada Y, et al Definitions, pathophysiology, and epidemiology of acute cholangitis and cholecystitis: Tokyo guidelines. J Hepatobiliary Pancreat Surg. 2007;14(1):15-26. [Context Link]


31. Ahmed M. Acute cholangitis-an update. World J Gastrointest Pathophysiol. 2018;9(1):1-7. [Context Link]


32. Kiriyama S, Takada T, Strasberg SM, et al TG13 guidelines for diagnosis and severity grading of acute cholangitis (with videos) J Hepatobiliary Pancreat Sci. 2013;20:24-34. [Context Link]


33. Saini V, Ashraf O, Babowice J, Hamilton HA, Khan U, Bhanot N. Surgical emergencies in the ICU. Crit Care Nurs Q. 2023;46(1):49-66. [Context Link]


cholangitis; gastrointestinal bleeding; intensive care unit; pancreatitis