Upper Gastrointestinal Bleeding (2024)

by Resshme Kannan Sudha & Thiagarajan Jaiganesh

You have a new patient!

A 55-year-old male with alcoholic liver cirrhosis was brought to the emergency department by his wife, presenting with two episodes of haematemesis (containing fresh blood) and light-headedness. This is the first occurrence of such symptoms. Vital signs: Temperature: 36.8°C, Heart Rate: 115 bpm, SpO₂: 95%, BP: 88/65 mmHg. On examination, the patient appears pale, lethargic, and jaundiced, with abdominal distension noted.

The image was produced by using ideogram 2.0.

What do you need to know?

Upper gastrointestinal (GI) bleeding is defined as bleeding occurring above the level of the ligament of Treitz. It is more common than lower GI bleeding [1]. Upper GI bleeding is a significant clinical condition that can lead to morbidity and mortality if not promptly diagnosed and managed. It encompasses bleeding from the esophagus, stomach, or duodenum, often presenting as hematemesis or melena. The importance of recognizing and treating upper GI bleeding lies in its potential to indicate serious underlying conditions. Early intervention is crucial, as the severity of bleeding can lead to hypovolemic shock, necessitating urgent medical care. Upper GI bleeding is a common emergency, with an estimated incidence of 50 to 150 cases per 100,000 individuals annually [2]. The prevalence varies based on demographic factors such as age, gender, and geographical location. The condition is more prevalent in older adults, particularly those over 60 years.

The most common cause is peptic ulcer disease, with duodenal ulcers being the most frequent. Other causes include varices, erosive esophagitis, duodenitis, Mallory-Weiss tear, gastrointestinal malignancies, and arterial and venous malformations (e.g., aorto-enteric fistula, Dieulafoy lesion) [1,3]. Causes of peptic ulcer disease include NSAID (Non-Steroidal Anti-inflammatory Drug) intake, Helicobacter pylori infection, and stress ulcers. In recent years, the incidence of upper gastrointestinal bleeding admissions due to peptic ulcer disease has decreased in the USA. This trend has been attributed to the use of triple therapy for Helicobacter pylori and the co-administration of proton pump inhibitors with NSAIDs [4].

Clinical manifestations include vomiting coffee ground material or fresh blood, and/or passing fresh blood in the stool or black, tarry stool (melena) [1].

Goals in the management of a patient with upper gastrointestinal bleeding include identifying the site and nature of the bleeding, stabilizing the patient, and controlling the source of the bleed [4].

Medical History

After performing a primary survey and stabilizing the patient, it is important to fine-tune your history, physical examination, and investigations to identify the source of bleeding and guide further management and disposition.

Upper GI bleeding commonly presents with haematemesis (coffee-ground or fresh blood), haematochezia, and/or melena [4]. Certain foods, such as beets, and medications like cefdinir, can cause red-colored stool, while bismuth and iron supplements may cause black-colored stool [4].

Associated Symptoms
  • Peptic ulcer disease may be associated with epigastric pain (gastric ulcer) and dysphagia, gastroesophageal reflux disease (GERD), or odynophagia (esophageal ulcer).
  • Haematemesis associated with retching may indicate a Mallory-Weiss tear.
  • The presence of jaundice and ascites suggests variceal bleeding [4].

A prior history of GI bleeding should be assessed, as patients are more likely to bleed from the same lesion.

Key Past Medical History and Risk Factors

Peptic Ulcer Disease:

  • Ulcers can occur in the esophagus, stomach, or duodenum, with duodenal ulcers being more common.
  • However, gastric ulcers account for a higher incidence of bleeding.
  • Known causes include Helicobacter pylori, NSAIDs, alcohol, and steroid use.
  • Symptoms may include epigastric pain, nausea, vomiting, upper GI bleeding (painless haematemesis and melena), and signs of anaemia.
  • Upper GI bleeding after NSAID use, stress, or a history of dyspepsia may indicate erosive gastritis [5,6].

Esophageal Varices:

  • Caused by portal hypertension secondary to liver diseases such as cirrhosis.
  • Symptoms include jaundice, spider angiomata, palmar erythema, hepatic encephalopathy (confusion), coagulopathy (petechiae/purpura), ascites, and variceal bleeding (painless haematemesis with large amounts of fresh blood) [6].
  • Ask about chronic alcohol use, hepatitis, and hepatocellular carcinoma.
  •  

Mallory-Weiss Syndrome:

  • Caused by forceful retching or vomiting, often after heavy alcohol intake.
  • Leads to a tear in the esophagus or stomach, resulting in haematemesis (large amounts of fresh blood).
  • This condition is usually self-limiting [6].

Malignancy:

  • Gastric cancers may present with haematemesis, anaemia, and dyspepsia [6].
  • Enquire about sudden weight loss, loss of appetite, and risk factors like prior Helicobacter pylori infection.

Angiodysplasia:

  • Dieulafoy’s disease is a rare vascular malformation affecting young individuals.
  • It involves small aneurysms in the stomach that rupture, leading to massive spontaneous haematemesis [6].

Aorto-enteric Fistula:

  • A rare condition, usually occurring post-repair of an abdominal aortic aneurysm.
  • Presents with profuse haematemesis and rectal bleeding [6].

Gastro-enteric Anastomosis:

  • Ulcers may develop at the site of gastro-enteric anastomosis, presenting with upper GI bleeding [7].
Comorbid Illnesses

Enquire about conditions such as:

  • Ischemic heart disease or pulmonary conditions (higher haemoglobin levels required).
  • Coagulopathies (may necessitate additional therapies).
  • Dementia or hepatic encephalopathy (risk of aspiration due to altered mental state).
  • Heart failure or renal failure (risk of fluid overload during blood transfusion).
Medication History

Assess for [8]:

  • NSAIDs (associated with peptic ulcers).
  • Anticoagulants and antiplatelets.
  • Chemotherapeutic agents.
  • Iron supplements (black stool).
Symptoms of Severe Bleeding and Poor Prognosis [1,4,7,9]
  • Light-headedness, confusion, syncope (cerebral hypoperfusion).
  • Chest pain and palpitations (coronary hypoperfusion) .

Physical Examination

The severity of bleeding should be assessed based on clinical signs of shock rather than the color of the blood [4]. Upper GI bleeding typically presents with haematemesis (frank blood or coffee-ground emesis) and/or melena [4]. In cases of brisk upper GI bleeding, the patient may present as vitally unstable with haematochezia [4].

Vital Signs

Monitor for signs of hemodynamic instability, including:

  • Tachycardia, tachypnea, and hypotension [1,7].
  • Supine hypotension is associated with greater blood loss than orthostatic hypotension [1].

General Examination

  • Confusion may indicate hemodynamic instability.
  • Gynecomastia may be seen in patients with liver disease [10].
  • Haematemesis strongly suggests an upper GI bleed [4].

ENT Examination

  • Inspect the nose for epistaxis, which can present as haematemesis if the blood is swallowed [11].

Skin Examination

  • Palmar erythema, spider angiomata, caput medusae, and jaundice are suggestive of liver disease [11].

Abdominal Examination

  • Abdominal tenderness, guarding, rigidity, and rebound tenderness may indicate perforation.
  • The presence of ascites suggests liver disease [4,7].

Rectal and Stool Examination

  • A digital rectal examination and stool analysis can help identify the location of the bleed:
    • Melena typically indicates an upper GI bleed.
    • Haematochezia may suggest a lower GI bleed or a massive upper GI bleed [4].

Alternative Diagnoses

The differential diagnosis for gastrointestinal bleeding includes several conditions that may mimic an upper or lower GI bleed:

  1. Epistaxis: Bleeding from the nose can present as haematemesis if the blood is swallowed. Careful examination of the nasal cavity is essential to rule this out.

  2. Vaginal Bleeding: In some cases, vaginal bleeding can be mistaken for haematochezia. A thorough history and physical examination can help differentiate these sources.

  3. Food-Induced Discoloration: Certain foods may alter the color of stool, leading to a false suspicion of GI bleeding. For example, beets can cause red-colored stools, which may mimic haematochezia.

  4. Medication-Induced Changes: Some medications can also discolor stool:

    • Cefdinir may produce red-colored stool.
    • Iron supplements and bismuth-containing products can result in black stool, resembling melena [4].
  5. Neonatal Swallowed Blood: In neonates, vomiting swallowed maternal blood during delivery or breastfeeding may be mistaken for upper GI bleeding [12].

Acing Diagnostic Testing

Bedside Tests

Several bedside tests can aid in the initial evaluation of upper GI bleeding:

  • Point-of-care venous blood gas: Useful for detecting acidosis, electrolyte disturbances, and haemoglobin levels. Haemoglobin levels < 8 g/dL in previously healthy patients, or < 9 g/dL in patients with known coronary artery disease or anaemia-related complications, suggest the need for blood transfusion [4].
  • Point-of-care PT (Prothrombin Time) and INR (International Normalized Ratio): Essential for patients taking medications like warfarin to determine the need for reversal agents.
  • Bedside ultrasound: Helpful in identifying ascites, which may aid in diagnosing variceal bleeding.
Ascites in Cirrhotic Patient

Laboratory Tests

The following blood tests are useful when there is a clinical suspicion of upper GI bleeding [4,6,11,13]:

  • Complete Blood Count (CBC): To assess haemoglobin and haematocrit levels.
  • Blood Urea Nitrogen (BUN), Creatinine, and electrolytes: A BUN:Creatinine ratio > 35 is highly suggestive of upper GI bleeding (90%).
  • Coagulation Screen: INR levels are important in patients on anticoagulant therapy (e.g., warfarin) to guide reversal strategies.
  • Liver Function Tests: Elevated parameters are suggestive of liver disease and potential variceal bleeding.
  • Type and Crossmatch: Crucial for patients who may require blood transfusion.

Imaging

Radiological imaging is rarely needed in hemodynamically unstable patients as it may delay resuscitation. In such cases, endoscopy should take precedence [4].

  • Upright chest X-ray: Helpful in detecting free air under the diaphragm, which is suggestive of perforation.
  • CT Angiography: Recommended for hemodynamically stable patients when identifying the bleeding etiology before endoscopy is crucial. It can detect slow bleeding (approximately 0.3 mL/min) and guide management decisions (endoscopy, surgery, or angiography). However, it is not suitable for unstable patients due to delays in management. In such cases, conventional angiography with embolization is preferred [4].

Endoscopy

Endoscopy is both diagnostic and therapeutic [14,15]:

  • There is no evidence to support that emergent endoscopy is superior to routine endoscopy.
  • Immediate gastroenterology consultation for emergent endoscopy is advised in patients with ongoing severe upper GI bleeding.
  • Endoscopy is recommended within 24 hours for all admitted patients with UGIB after stabilizing hemodynamic parameters and addressing other medical issues.
  • Patients with high-risk clinical features such as tachycardia, hypotension, haematemesis, or blood in nasogastric aspirate should undergo endoscopy within 12 hours, as this may improve clinical outcomes.

Additional Considerations

  • A screening ECG is recommended in patients > 35 years of age with cardiac risk factors, as co-existing acute coronary syndrome may complicate GI bleeding [4].
  • Nasogastric lavage is generally not recommended due to risks of perforation, pneumothorax, and aspiration [4].
  • Erythromycin can be used as an alternative prokinetic to clear gastric contents before endoscopy [4,8].

Risk Stratification

To effectively manage gastrointestinal (GI) bleeding, patients must be categorized into high-risk and low-risk groups. High-risk patients require prompt intervention, whereas low-risk patients can be managed through outpatient treatment [4]. A combination of clinical, endoscopic, and laboratory features, along with risk scores, can aid in risk stratification. While risk scores may not always predict high-risk patients accurately, they are effective in identifying patients at very low risk of harm. When selecting patients for outpatient management, ensuring high sensitivity is essential to prevent the inadvertent discharge of high-risk individuals [16].

Risk Assessment Tools

Commonly used scoring systems for GI bleeding include:

  1. Glasgow-Blatchford Score (GBS)
  2. Rockall Score
  3. AIMS65 Score

The AIMS65 score assesses parameters such as:

  • Albumin < 3 mg/dL
  • International Normalized Ratio (INR) > 1.5
  • Altered mental status
  • Systolic blood pressure < 90 mmHg
  • Age > 65 years

Studies show that the GBS is more effective at predicting a combined outcome of intervention or death [16].

Glasgow-Blatchford Score (GBS)

The Glasgow-Blatchford Score is particularly useful for predicting the need for intervention, hospital admission, blood transfusion, surgery, and mortality. A significant advantage of the GBS is that it can be calculated at the time of patient presentation, as it does not require endoscopic data (unlike the Rockall score).

The GBS includes the following parameters:

  • Blood urea nitrogen (BUN)
  • Haemoglobin levels
  • Systolic blood pressure
  • Pulse rate
  • Symptoms such as melena, syncope, and a history of hepatic disease or cardiac failure.

The score ranges from 0 to 23, with a higher score indicating a greater risk of requiring endoscopic intervention [4].

Glasgow-Blatchford Risk Score

CategoryScore
BUN in mg/dL
18.2 to 22.42
22.5 to 283
28.1 to 704
70.1 or greater6
Hemoglobin, men g/dL
12 to 131
10 to 11.93
9.9 or less6
Hemoglobin, women g/dL
10 to 121
9.9 or less6
Systolic Blood Pressure, mmHg
100-1091
90-992
<903
Heartrate >100 peats per minute1
Melena1
Syncope2
Hepatic Diseases2
Heart failure2
Glasgow-Blatchford Risk Score is useful for predictive of inpatient mortality, blood transfusions, re-bleeding, ICU monitoring, and hospital length of stay. Patients with a score of zero may be discharged home, those with score 2 or higher are usually admitted, and those with score of 10 or more are at highest risk for morbidity and resource utilization. Maximum score is 23.
Outpatient Management

Patients with a Glasgow-Blatchford Score of 0 are considered at low risk for rebleeding. According to international consensus guidelines, these patients may be safely discharged with early outpatient follow-up [8,17].

Management

Initial Stabilization

Airway and Breathing:
Patients with massive upper GI bleeding presenting with uncontrollable haematemesis, respiratory distress, or severe shock require immediate airway protection and intubation. It is essential to improve hemodynamic status before administering induction and paralytic drugs for intubation and initiating positive pressure ventilation, as this can mitigate a sharp decrease in cardiac output. However, intubation is associated with poor outcomes and should only be performed when absolutely necessary [4].

Circulation:
Massive GI haemorrhage is characterized by ongoing active bleeding (haematemesis or haematochezia), signs of hemodynamic compromise (e.g., tachycardia, hypotension, altered mental status), or a shock index ≥ 0.9 [4].

Immediate volume resuscitation is critical and includes:

  • Placement of two large-bore IV catheters.
  • Infusion of balanced isotonic crystalloids (e.g., 2 liters of normal saline or Plasmalyte over 30 minutes).
  • Transfusion of uncrossmatched blood, if required [4].
Transfusion Strategies

For stable patients, a restrictive transfusion strategy is recommended. While the ideal haemoglobin target is not universally defined:

  • In stable patients without known coronary artery disease (CAD), maintain haemoglobin ≥ 8 g/dL.
  • For patients with known CAD, a higher target of ~9 g/dL is appropriate to reduce the risk of anaemia-related complications [4].

In patients requiring massive transfusion (more than 4 units of PRBCs), a balanced transfusion ratio of 1:1:1 (PRBC:Platelets:Fresh Frozen Plasma) is advised. Cryoprecipitate should be administered if fibrinogen levels remain < 1.5 g/L [18]. A platelet count > 50,000 platelets/μL should be maintained [4].

Coagulation Management
  • Vitamin K antagonists (e.g., warfarin) should be stopped and reversed to achieve a target INR of 1.5–2.5. Treatment options include Fresh Frozen Plasma (FFP) and Prothrombin Complex Concentrate (PCC). Vitamin K is an appropriate choice for hemodynamically stable GI bleeding.
  • Direct oral anticoagulant reversal:
    • Idarucizumab for dabigatran reversal.
    • PCC or coagulation factor Xa (recombinant/inactivated-zhzo) for factor Xa inhibitors.
  • For heparin reversal, protamine sulfate may be used.

Before administering reversal agents, the risks of reversing anticoagulant therapy must be carefully weighed against the risk of thromboembolism [19].

PCC is preferred over FFP for rapid coagulopathy correction, especially in patients at risk of fluid overload, as it requires lower volume administration [4]. Over-transfusion or empiric correction of PT/INR with FFP or PCC in portal hypertension may worsen portal hypertension and exacerbate bleeding [4].

Medications

Proton Pump Inhibitors (PPIs)

PPIs are the mainstay in the management of acute GI bleeding. They work by inhibiting the hydrogen potassium ATPase pump, thereby reducing gastric acid secretion [20]. Studies have shown that PPIs reduce the risk of re-bleeding, the need for surgery, and mortality in patients with bleeding ulcers [4].

Both intermittent PPI therapy and continuous infusion are equally effective in reducing bleeding [8]. Available IV formulations include esomeprazole and pantoprazole. The recommended dose is:

  • Pantoprazole or esomeprazole: 80 mg IV as a single initial dose, followed by either:
    • Continuous infusion at 8 mg/hr, or
    • 40 mg IV BID [8].

If IV formulations are unavailable, oral alternatives such as 40 mg of esomeprazole twice daily may be used [8].

PPIs are classified as Category B in pregnancy, except for omeprazole, which is Category C [21]. Caution should be exercised due to the risk of Clostridium difficile infection, Steven Johnson syndrome, kidney and liver impairment, and pancreatitis [20]. Omeprazole is particularly associated with the risk of acute interstitial nephritis [22].

Somatostatin Analogues

Somatostatin and its synthetic analogue, octreotide, are predominantly used in variceal bleeding. These agents reduce the risk of bleeding, need for transfusion, and portal hypertension. Indications include acute GI bleeding in patients with variceal bleeding, abnormal liver function tests, liver disease, or alcoholism [4].

The dosing regimen for octreotide is:

  • Adults: 50 mcg IV bolus, followed by 25–50 mcg/hr continuous infusion [23,24].
  • Paediatrics: 1 mcg/kg IV bolus (maximum: 100 mcg), followed by 1 mcg/kg/hr infusion [23,24].

Octreotide crosses the placenta and is expressed in breast milk. Common adverse effects include arrhythmias, pancreatitis, abnormal glucose regulation, and low platelet count [23]. It also crosses the blood-brain barrier [23].

Terlipressin

Terlipressin is a synthetic vasopressin receptor agonist that causes splanchnic vasoconstriction, thereby reducing portal hypertension. It is primarily indicated for variceal bleeding [25].

The recommended dose is 2 mg IV every 6 hours [26]. Terlipressin may cause teratogenic effects (limited data available) [27] and can result in painful hands and feet due to peripheral vasoconstriction [26]. While studies suggest that terlipressin, somatostatin, and octreotide have similar efficacy, data regarding their use in paediatric patients remains limited [24,28].

Prokinetic Agents (Erythromycin and Metoclopramide)

Prokinetic agents are used to improve visualization during endoscopy by clearing gastric contents.

  • Erythromycin:

    • Adult dose: 3 mg/kg IV, administered over 20–30 minutes, 20–90 minutes before endoscopy [29].
    • Classified as Category B in pregnancy and is safe for breastfeeding mothers [29].
    • Adverse effects include QT prolongation, pseudomembranous colitis, seizures, and hypertrophic pyloric stenosis [4,29].
  • Metoclopramide:

    • Adult dose: 10 mg IV.
    • Paediatric dose: 0.1–0.2 mg/kg IV [30].
    • Classified as Category B in pregnancy [30].
    • Caution is advised in patients with a history of extrapyramidal symptoms due to its association with extrapyramidal side effects [30].

Tranexamic Acid

Tranexamic acid is an antifibrinolytic agent. However, according to the HALT-IT Trial, it has not been shown to reduce mortality associated with gastrointestinal bleeding. As a result, its routine use in GI bleeding is not recommended [31].

Antibiotic Prophylaxis

Antibiotic prophylaxis is recommended for patients with cirrhosis or suspected cirrhotic liver disease to reduce the risk of infection and mortality [4].

The recommended antibiotics include:

  • Fluoroquinolones (e.g., ciprofloxacin 400 mg IV)

  • Third-generation cephalosporins (e.g., ceftriaxone 1–2 g IV) [4].

  • Ceftriaxone: Classified as Category B in pregnancy but contraindicated in hyperbilirubinemic neonates due to the risk of kernicterus and those receiving IV calcium-containing solutions due to ceftriaxone–calcium precipitation [32].

  • Ciprofloxacin: Classified as Category C in pregnancy. Adverse effects include Clostridium difficile infection, dysglycemia, tendon rupture, neurotoxicity, QT prolongation, hepatotoxicity, and Stevens-Johnson syndrome/toxic epidermal necrolysis [33].

Procedures

Balloon tamponade [4,6,34], using devices such as the Sengstaken-Blakemore tube, Minnesota tube, or Linton-Nachlas tube, can serve as a temporizing measure for suspected life-threatening variceal bleeding when endoscopy is not immediately available. These devices must be stored in refrigerators to maintain readiness.

Before the procedure, patients must be intubated to reduce the risk of aspiration. The device is inserted through the mouth, passed via the esophagus into the stomach. The tube consists of two balloons—a gastric balloon and an esophageal balloon:

  • The gastric balloon of the Sengstaken-Blakemore tube can be inflated with 250–300 cc of air, while the Minnesota tube can accommodate up to 450–500 cc to secure the tube in place.
  • The esophageal balloon can be inflated to a pressure of 20–40 mmHg, with a strict upper limit of 45 mmHg to avoid injury. Pressure should be carefully monitored using a manometer.

Balloon tamponade is a temporary measure, and definitive management, such as endoscopic therapy, should be arranged as soon as possible. The procedure is associated with significant risks, including ulceration, esophageal rupture, and aspiration [4].

Special Patient Groups

Paediatrics

The causes of upper GI bleeding in the pediatric population are generally similar to those seen in adults [12,15,35]. However, there are additional causes specific to neonates and infants that require consideration. In neonates, vitamin K deficiency, also referred to as the haemorrhagic disease of the newborn, is an important cause. Other causes include congenital vascular anomalies, such as telangiectasia, and coagulopathy, which may result from infections, liver disease, or coagulation factor deficiencies. Milk protein intolerance is also a recognized cause of upper GI bleeding in this age group. During the neonatal period and the first few months of life, it is crucial to differentiate swallowed maternal blood from true upper GI bleeding. The Apt-Downey test is a reliable diagnostic tool used to confirm the presence of fetal blood and rule out swallowed maternal blood as the source.

The management of upper GI bleeding in children largely follows the same principles as in adults, with necessary adaptations for the pediatric population. Intravenous proton pump inhibitors (IV PPIs) are effective and can be administered to reduce gastric acid secretion, thereby promoting hemostasis. In cases of suspected variceal bleeding, somatostatin analogues can be given to reduce portal hypertension and minimize bleeding risk. When severe acute bleeding is ongoing, endoscopy plays a key role in diagnosis and intervention. It is recommended that endoscopy be performed within 24 to 48 hours of presentation. However, it is critical to ensure that the patient is as hemodynamically stable as possible before proceeding with the procedure to minimize complications.

In cases where endoscopy cannot control the bleeding or fails to identify the source, further interventions may be necessary. Angiography with embolization is a useful modality in such instances, as it can help detect and address underlying vascular abnormalities contributing to the bleeding. This approach is particularly helpful when other methods have proven unsuccessful.

Overall, a multidisciplinary approach that includes appropriate stabilization, pharmacologic therapy, and procedural intervention is essential to effectively manage upper GI bleeding in the pediatric population [12,15,35].

Geriatrics

Upper GI bleeding in elderly patients presents unique challenges due to the high-risk nature of this population and the limitations of existing risk assessment tools. Studies indicate that traditional pre-endoscopic risk scores, such as the Glasgow-Blatchford and AIMS65, often fail to accurately predict outcomes like mortality and hospital stay length in geriatric patients, particularly those aged 82 and older, suggesting a need for age-adjusted scoring systems [36]. Despite these challenges, emergency oesophagogastroduodenoscopy is generally safe for elderly patients, with a high survival rate at 90 days post-procedure, although a significant proportion of OGDs yield normal findings, highlighting the importance of careful patient selection [37]. The management of Upper GI bleeding in the elderly is further complicated by recurrent bleeding, as seen in cases involving peptic ulcer disease, which necessitate a multidisciplinary approach and close monitoring to improve outcomes [38]. Recent efforts to develop novel risk scores tailored for the elderly have shown promise, with a new score incorporating factors like comorbidity index and blood pressure demonstrating good discriminative performance for identifying patients suitable for outpatient management [39].

Pregnant Patients

The causes of upper GI bleeding in pregnant women are similar to those in the general population, including conditions such as esophageal ulcers, gastroesophageal reflux disease, and portal vein thrombosis leading to esophageal varices [40]. Haematemesis, or the vomiting of blood, is a common manifestation of upper GI bleeding and can present as bright red or coffee-ground emesis, indicating bleeding from the upper gastrointestinal tract [1, 40]. In rare cases, UGIB in pregnancy can be caused by gastrointestinal stromal tumors (GISTs), as illustrated by a case where a pregnant woman presented with coffee-ground vomiting and was diagnosed with a bleeding GIST at the stomach cardia [41]. Endoscopy is a critical diagnostic and therapeutic tool for upper GI bleeding, but its use in pregnant women is generally reserved for severe or persistent cases due to potential risks to the mother and fetus [42]. Despite the need for endoscopic evaluation in over 12,000 pregnant women annually in the U.S., research on the safety and outcomes of such procedures remains limited [43]. Therefore, careful consideration of the risks and benefits is essential when managing upper GI bleeding in pregnant patients.

When To Admit This Patient

Admission is required for elderly patients over the age of 60 years, those who require blood transfusions, and patients with a Glasgow-Blatchford Score (GBS) greater than 0 [4,8]. Patients with high-risk bleeding sources should be admitted to a monitored setting or an intensive care unit (ICU) to allow close monitoring for signs of rebleeding and other potential complications.

The decision to discharge a patient following endoscopy depends on the identification of the bleeding source and the associated risk of rebleeding. Patients can be considered for discharge if they meet all of the following criteria: a GBS of 0, blood urea nitrogen (BUN) less than 18 mg/dL, haemoglobin >13 g/dL in men and >12 g/dL in women, heart rate less than 100 beats per minute, systolic blood pressure greater than 110 mmHg, no evidence of melena or syncope since the initial presentation, absence of heart failure or liver failure, and prompt access to outpatient follow-up care.

However, it is important to note that this recommendation is based on low-quality evidence, and clinical judgment should play a significant role in the final decision to discharge a patient. Clinicians should carefully assess each patient’s overall condition, risk of rebleeding, and ability to follow up in an outpatient setting to ensure safe discharge planning [15].

Revisiting Your Patient

In managing this patient, the immediate priority is to assess airway, breathing, and circulation and provide stabilization. Given the patient’s vital instability, they should be promptly transferred to the resuscitation bay for further management.

The image was produced by using ideogram 2.0.

Airway and Breathing: The patient’s airway is currently patent, and they are communicating comfortably, with no signs of obstruction such as pooling of blood or secretions. There have been no further episodes of haematemesis, and the patient is maintaining adequate oxygen saturation on room air. Chest auscultation is clear. At this time, the patient does not require airway adjuncts or intubation, but close observation is essential to detect any deterioration.

Circulation: The patient is hypotensive, indicating the need for immediate intervention. Two large-bore IV cannulas should be inserted to initiate intravenous fluid resuscitation. Crossmatched and uncrossmatched blood should be arranged as a precaution. A point-of-care venous blood gas test must be performed to quickly evaluate acidosis, haemoglobin levels, and other critical parameters. Care should be taken to avoid fluid overload, especially in patients with underlying liver disease.

Further History and Review of Systems: On further evaluation, the patient denies haematochezia, haemoptysis, epistaxis, melena, chest pain, palpitations, syncope, loss of consciousness, or confusion.

Past Medical and Surgical History and Risk Factors: The patient has a history of alcoholic liver disease and is a smoker. There is no history of chronic NSAID use, Helicobacter pylori infection, recent forceful retching, or ingestion of foods or medications that might cause red-colored secretions. There are no known coagulopathies, recent anticoagulant use, vascular abnormalities, weight loss, or loss of appetite. Additionally, the patient has no history of prior surgery.

Examination: Clinical signs of hemodynamic instability, such as hypotension, suggest hypovolemic shock, requiring prompt management with IV fluids and blood transfusion. Examination findings of jaundice, abdominal distension with shifting dullness, and caput medusae are consistent with alcoholic liver disease and indicate probable variceal bleeding. There is no abdominal tenderness, guarding, rigidity, or rebound tenderness to suggest another abdominal pathology.

Laboratory Investigations: Laboratory tests sent include a complete blood count, urea, electrolytes, creatinine, coagulation screen, liver function tests, and type and crossmatch for transfusion. The point-of-care venous blood gas reveals acidosis, haemoglobin <8 g/dL, negative base excess, and elevated lactate, indicating ongoing active bleeding. These findings necessitate urgent gastroenterology consultation for endoscopic intervention and the arrangement of blood transfusion. In addition, the patient must be monitored for liver disease-induced coagulopathy, and a haematology consultation is warranted.

Diagnostic Test: The patient’s Glasgow-Blatchford Score is greater than 0, further confirming the need for urgent endoscopy to identify and control the source of bleeding, which is most likely esophageal varices. Simultaneously, resuscitation measures must continue.

Medications: Given the patient’s history of alcoholic liver disease and suspected variceal bleeding, appropriate pharmacological management should include vasoactive agents such as somatostatin, octreotide, or terlipressin to reduce portal pressure. Empirical antibiotics (fluoroquinolones or third-generation cephalosporins) should be administered to reduce the risk of infection. Additionally, proton pump inhibitors (PPIs) should be started as part of the management protocol.

Disposition: This patient requires urgent gastrointestinal consultation for endoscopy to achieve source control of the bleeding. Admission is necessary to allow for close monitoring of potential complications, including rebleeding and complications of alcoholic liver cirrhosis, such as hepatic encephalopathy and renal failure.

Authors

Picture of Resshme Kannan Sudha

Resshme Kannan Sudha

Resshme Kannan Sudha graduated from RAK Medical and Health Sciences University and is currently an Emergency Medicine Graduate Resident at STMC Hospital, Al Ain. She is a keen follower of FOAMed projects and an enthusiastic educator. Her special interests include critical care, POCUS, global health, toxicology and wilderness medicine.

Picture of Thiagarajan Jaiganesh

Thiagarajan Jaiganesh

STMC Hospital, Al Ain

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References

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  6. Leach T. Upper GI bleed. Almostadoctor. Published December 5, 2020. Accessed April 8, 2023. https://almostadoctor.co.uk/encyclopedia/upper-gi-bleed
  7. Pace R. Upper GI bleeding. Core EM. Published January 24, 2018. Accessed March 20, 2023. https://coreem.net/core/upper-gi-bleeding/
  8. Undifferentiated upper gastrointestinal bleeding – WikEM. WikEM. Accessed March 23, 2023. https://www.wikem.org/wiki/Undifferentiated_upper_gastrointestinal_bleeding
  9. Kaur G. Upper gastrointestinal bleeding: Evaluation, management, and disposition. emDOCs.net – Emergency Medicine Education. Published June 7, 2021. Accessed April 11, 2023. https://www.emdocs.net/upper-gastrointestinal-bleeding-evaluation-management-and-disposition/
  10. Chen ZJ, Freeman ML. Management of upper gastrointestinal bleeding emergencies: evidence-based medicine and practical considerations. World J Emerg Med. 2011;2(1):5-12. doi:10.5847/wjem.j.1920-8642.2011.01.001
  11. (Sokolosky MC. Gastrointestinal bleeding. In: Tintinalli’s Emergency Medicine Manual. New York, NY: McGraw-Hill Education; 2018:237-238.
  12. Donaldson R, Swartz J, Claire, et al. Gastrointestinal bleeding (peds) – WikEM. WikEM. Updated March 29, 2022. Accessed April 10, 2023. https://www.wikem.org/wiki/Gastrointestinal_bleeding_(peds)
  13. Wilkins T, Wheeler B, Carpenter M. Upper gastrointestinal bleeding in adults: Evaluation and management. American Family Physician. Published March 1, 2020. Accessed March 20, 2023. https://www.aafp.org/pubs/afp/issues/2020/0301/p294.html
  14. 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. doi:10.14309/ajg.0000000000001245
  15. Woodfield A, Donaldson R, Reynolds C, Young N. Upper GI bleeding guidelines. WikEM. Published March 12, 2022. Accessed March 20, 2023. https://www.wikem.org/wiki/Upper_GI_bleeding_guidelines
  16. Stanley AJ, Laine L. Management of acute upper gastrointestinal bleeding. BMJ. 2019;364:l536. Published March 25, 2019. Accessed February 15, 2023. https://www.bmj.com/content/364/bmj.l536
  17. 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. doi:10.7326/m19-1795
  18. Farkas J. GI bleeding. EMCrit Project. Published September 18, 2021. Accessed April 11, 2023. https://emcrit.org/ibcc/gib/
  19. Gnanapandithan K, Muniraj T. Management of antithrombotics around gastrointestinal procedures. PubMed. Published 2023. Accessed April 11, 2023. https://www.ncbi.nlm.nih.gov/books/NBK553210/
  20. Carmen Fookes B. List of proton pump inhibitors + uses, side effects. Drugs.com. Accessed April 11, 2023. https://www.drugs.com/drug-class/proton-pump-inhibitors.html
  21. Richter JE. Gastroesophageal reflux disease during pregnancy. Gastroenterol Clin North Am. 2003;32(1):235-261. doi:10.1016/s0889-8553(02)00065-1
  22. Reynolds C, Cunningham R, Ostermayer D, Donaldson R, Young N. Omeprazole. WikEM. Updated March 5, 2021. Accessed April 11, 2023. https://wikem.org/wiki/Omeprazole
  23. Ostermayer D, Murray B, Lee E, Donaldson R, Cunningham R. Octreotide. WikEM. Published February 10, 2021. Accessed March 20, 2023. https://wikem.org/wiki/Octreotide
  24. Sandostatin, Sandostatin LAR (octreotide) dosing, indications, interactions, adverse effects, and more. Medscape. Accessed April 11, 2023. https://reference.medscape.com/drug/sandostatin-lar-octreotide-342836
  25. Nickson C. Terlipressin. Life in the Fast Lane. Published January 4, 2019. Accessed April 11, 2023. https://litfl.com/terlipressin/
  26. Tripathi D, Stanley AJ, Hayes PC, et al. UK guidelines on the management of variceal haemorrhage in cirrhotic patients. Gut. 2015;64(11):1691-1692. doi:10.1136/gutjnl-2015-309262
  27. Terlivaz. Medscape. Published July 15, 2024. Accessed December 7, 2024. https://reference.medscape.com/drug/terlivaz-terlipressin-4000107#6
  28. Seo YS, Park SY, Kim MY, et al. Lack of difference among terlipressin, somatostatin, and octreotide in the control of acute gastroesophageal variceal hemorrhage. Hepatology. 2014;60(3):962. doi:10.1002/hep.27006
  29. Donaldson R, Claire, Lee E, Ostermayer D, Holtz M. Erythromycin. WikEM. Published September 22, 2019. Accessed March 20, 2023. https://www.wikem.org/wiki/Erythromycin
  30. Fernando T, Donaldson R, Grove G, et al. Metoclopramide. WikEM. Updated March 7, 2021. Accessed April 11, 2023. https://www.wikem.org/wiki/Metoclopramide
  31. Roberts I, Shakur-Still H, Afolabi A, et al. 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. doi:10.1016/s0140-6736(20)30848-5
  32. Donaldson R, Shah M, Ostermayer D, Young N, Claire. Ceftriaxone. WikEM. Updated September 19, 2019. Accessed April 10, 2023. https://www.wikem.org/wiki/Ceftriaxone
  33. Donaldson R, Gausepohl A, Janeway H, et al. Ciprofloxacin. WikEM. Updated October 17, 2021. Accessed April 11, 2023. https://wikem.org/wiki/Ciprofloxacin
  34. Balloon tamponade for massive GI bleeding – WikEM. WikEM. Accessed March 23, 2023. https://www.wikem.org/wiki/Balloon_tamponade_for_massive_GI_bleeding
  35. Lirio RA. Management of upper gastrointestinal bleeding in children. Gastrointest Endosc Clin N Am. 2016;26(1):63-73. doi:10.1016/j.giec.2015.09.003
  36. Di Gioia G, Sangineto M, Paglia A, et al. Limits of pre-endoscopic scoring systems in geriatric patients with upper gastrointestinal bleeding. Sci Rep. 2024;14(1). doi:10.1038/s41598-024-70577-2.
  37. McWhirter A, Mahmood S, Mensah E, Nour H, Olabintan O, Mrevlje Z. Evaluating the safety and outcomes of oesophagogastroduodenoscopy in elderly patients presenting with acute upper gastrointestinal bleeding. Cureus. 2023. doi:10.7759/cureus.47116.
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  42. Bjorkman DJ. Is endoscopy safe for pregnant women with upper gastrointestinal bleeding. NEJM J Watch. 2011. doi:10.1056/JG201101070000004.
  43. Rabiee A, Moshiree B. Upper and lower endoscopy for gastrointestinal (GI) bleeding in pregnancy. In: Gastrointestinal Bleeding. Springer; 2019:155-164. doi:10.1007/978-3-319-90752-9_12.

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Acute Mesenteric Ischaemia (2024)

You have a new patient!

An 80-year-old gentleman presents to our department with a two-day history of abdominal pain accompanied by diarrhea and nausea. He describes the pain as recurrent, having occurred periodically over the past two years, with a crescendo pattern. However, this current episode has not been resolved and is excruciating.

a-photo-of-an-80-year-old-male-patient-(the image was produced by using ideogram 2.0)

A review of his medical records reveals a history of hypertension, dyslipidemia, a previous transient ischemic attack, and atrial fibrillation (AF). He underwent cholecystectomy many years ago for biliary colic. There is no other significant medical history.

On examination, his vital signs are as follows:

  • Blood pressure is 95/57 mmHg.
  • Pulse is 126 beats per minute.
  • Respiratory rate is 26 breaths per minute.
  • Oxygen saturation is 95%.
  • He is afebrile.

The patient appears pale, diaphoretic, and in significant discomfort. There is no clinical jaundice. Abdominal examination reveals diffuse tenderness, most prominent centrally, without guarding. Bowel sounds are sluggish. A cholecystectomy scar is noted in the right hypochondrium. Cardiac examination reveals irregular tachycardia, and the lungs are clear. Examination of the lower limbs is unremarkable, with no swelling. Stool is brown, with no visible blood or melena.

How would you proceed with further evaluation for this patient?

What do you need to know?

Acute mesenteric ischemia (AMI) refers to the sudden loss of blood flow to the small intestine, typically due to arterial insufficiency caused by an embolus or thrombus. AMI falls under the broader category of intestinal ischemia, which includes ischemia of the colon and, more rarely, the stomach and upper gastrointestinal tract. Other forms of intestinal malperfusion include venous occlusion as well as chronic or non-occlusive mesenteric ischemia [1].

Importance

Acute mesenteric ischemia carries an alarmingly high mortality rate, estimated between 60–80%. This is exacerbated by its nonspecific presentation, which often delays diagnosis and increases the likelihood of complications. Early recognition, timely resuscitation and treatment, and prompt advocacy for intervention are essential to improving outcomes [2,3].

Epidemiology

The incidence of AMI in developed countries is approximately 5 per 100,000 people annually, with a prevalence of around 0.1% of all hospital admissions.

AMI primarily occurs in patients with pre-existing atherosclerotic disease of arteries, often associated with risk factors such as advanced age, hypertension, diabetes, and atrial fibrillation [4].

A non-exhaustive list of risk factors includes [1]:

  • Cardiac conditions (e.g., atrial fibrillation, recent myocardial infarction)
  • Aortic surgery or instrumentation
  • Peripheral artery disease
  • Haemodialysis
  • Use of vasoconstrictive medications
  • Prothrombotic disorders
  • Systemic inflammation or infections
  • Hypovolaemic states
  • Bowel strangulation (e.g., volvulus, hernias)
  • Vascular compression syndromes.

Pathophysiology

The intestinal system exhibits relatively low oxygen extraction; residual oxygenated blood from intestinal veins is delivered to the liver via the portal vein. For ischaemic damage to occur, blood flow must be reduced by at least 50% of normal levels [1].

Interestingly, mesenteric arteries are less affected by atherosclerosis compared to other similarly sized vessels, likely due to protective hemodynamic factors. As a result, patients with AMI often have concurrent atherosclerotic conditions elsewhere, such as cerebrovascular disease, ischaemic heart disease, or peripheral vascular disease. Regarding the mechanism,

  • Embolism of the mesenteric artery accounts for ~50% and
  • Thrombosis of the mesenteric artery accounts for ~25% of AMI cases.

Mesenteric venous thrombosis can mimic AMI in a minority of cases, often presenting as nonspecific abdominal pain with diarrhea lasting 1–2 weeks. In some instances, these thrombi resolve spontaneously.

Medical History

The primary symptom of acute mesenteric ischemia (AMI) is central and severe abdominal pain, classically described as being “out of proportion” to physical examination findings. The initial pain is due to visceral ischemia, which initially spares the parietal peritoneum. Peritonism with abdominal rigidity typically develops later, indicating full-thickness ischemia, necrosis, or perforation [5].

Early symptoms may include persistent vomiting and defecation. As the condition progresses, passage of altered blood may occur. Unfortunately, associated gastrointestinal symptoms such as nausea, vomiting, and diarrhea can mimic infective causes, potentially leading to misdiagnosis. While bloody diarrhea is more commonly associated with colonic ischemia, it is less frequent in small bowel ischemia.

In some cases, AMI is preceded by symptoms of chronic non-occlusive mesenteric ischemia. Patients often report recurrent, postprandial abdominal pain resulting from an inability to increase blood flow to meet intestinal vascular demands. This may lead to a fear of eating and significant weight loss. In patients with chronic non-occlusive mesenteric ischemia, symptoms tend to be even more vague. Pain may be less severe and poorly localized, and patients may present with subtle signs such as abdominal distension or occult gastrointestinal bleeding [6].

In addition to embolic causes, mesenteric ischemia can be worsened by systemic conditions that restrict blood flow, such as hemorrhage, hypovolaemia, shock, and low-output cardiac states.

Physical Examination

In the early stages of AMI, physical examination findings are often sparse. The patient will typically appear to be in severe pain without relief, and abdominal tenderness is common. Suspicion should be heightened in frail patients of advanced age who may lack sufficient abdominal musculature to produce guarding during the examination.

Patients may appear pale due to pain or anemia, but specific physical signs are limited in this condition. Diagnosis often relies on a combination of clinical history and thorough investigation.

AMI is a critical condition characterized by reduced blood flow to the intestines, leading to severe complications if not diagnosed early. The physical examination findings should be combined with clinical history and specific symptoms. Understanding these findings is essential for timely intervention.

Key Findings

  • Severe Abdominal Pain: Patients typically present with a sudden onset of severe abdominal pain, which is a hallmark symptom of AMI.
  • Painless Interval: Following the initial pain, a transient painless period may occur, potentially misleading the diagnosis.
  • Signs of Peritonitis: Physical examination may reveal tenderness, guarding, or rebound tenderness, indicating peritoneal irritation and necessitating immediate surgical evaluation.
  • Bowel Sounds: Diminished or absent bowel sounds can suggest intestinal ischemia.

Importance of Clinical History to Guide Physical Exam

  • Risk Factors: A thorough history should include predisposing factors such as cardiovascular disease, recent surgeries, or conditions leading to hypercoagulability.
  • Chronic Symptoms: In cases of arterial thrombosis, patients may report a history of intermittent abdominal pain, weight loss, or diarrhea.

Alternative Diagnoses

The nonspecific symptoms of AMI mean it can be mimicked by many other conditions that are not easily excluded based on history and examination alone. Risk factors such as advanced age, prothrombotic states, atherosclerosis, and conditions causing hypovolaemia should raise clinical suspicion.

Differential diagnoses include:

  • Acute gastroenteritis: Main differential due to similar gastrointestinal symptoms (nausea, diarrhea, vomiting), especially at the initial stages of AMI, but pain and tenderness are typically less severe, more intermittent, and responsive to analgesia. Gastroenteritis is also less likely to cause metabolic acidosis or other significant biochemical abnormalities.
  • Acute cholecystitis: Presents with pain mainly in the right upper quadrant (RUQ) radiating to the right shoulder, often triggered by fatty meals, with accompanying nausea, vomiting, and fever. Murphy’s sign (pain and inspiratory arrest on palpation of the gallbladder) is often positive, particularly in those with a history of gallstones or biliary colic.
  • Acute pancreatitis: Epigastric pain radiating to the back, along with nausea and vomiting, is common. Associated with gallstones or alcohol use. Physical findings include epigastric tenderness, reduced bowel sounds, and, in severe cases, Grey-Turner’s or Cullen’s sign. Diagnosis is supported by elevated serum lipase or amylase levels.
  • Peptic ulcer disease: Characterized by burning or gnawing epigastric pain, often relieved by food or antacids. Common risk factors include NSAID use and Helicobacter pylori infection. Examination is typically unremarkable unless perforation occurs, which may result in acute peritonitis.
  • Bowel perforation: Sudden severe, diffuse abdominal pain with signs of peritonitis (rebound tenderness, guarding), fever, and tachycardia. A history of PUD or diverticulitis may be present. Diagnosis is supported by imaging, showing free air under the diaphragm on X-ray.
  • Diverticulitis: Presents with localized left lower quadrant (LLQ) pain, fever, and altered bowel habits (diarrhea or constipation). LLQ tenderness or a palpable mass is often noted in older patients.
  • Bowel obstruction: Crampy, intermittent abdominal pain, nausea/vomiting, abdominal distension, and constipation, potentially progressing to obstipation. Examination reveals a distended abdomen with high-pitched or absent bowel sounds. Plain X-rays typically show air-fluid levels and dilated bowel loops.
  • Ureteric calculus: Sudden colicky flank pain radiating to the groin, often with hematuria, nausea, and vomiting. A history of kidney stones is common. Findings include costovertebral angle tenderness, with a generally unremarkable abdominal exam. Hematuria is detected on urinalysis.

Acing Diagnostic Testing

Bedside Tests

Bedside diagnostics are limited but can provide valuable clues:

  • ECG: May reveal atrial fibrillation, a common risk factor.
  • Blood glucose: Hyperglycaemia due to physiological stress.
  • Point-of-Care Testing (POCT) for lactate: Elevated levels may indicate tissue hypoxia, though not specific to AMI.
  • Ultrasound: Limited in diagnosing AMI but useful for ruling out other causes of abdominal pain (e.g., cholecystitis, abdominal aneurysm, or ureteric colic). Ultrasound can also assess fluid status and response to fluid resuscitation via the inferior vena cava (IVC) and right heart function, particularly in patients with cardiac or renal comorbidities or failure.
An ECG sample in an abdominal pain patient - Rapid ventricular rate, atrial fibrillation.

Laboratory Tests

No serum markers are sufficiently sensitive or specific to diagnose AMI reliably:

  • Complete blood count (CBC): It may reveal haemoconcentration or leukocytosis but lacks specificity.
  • Serum lactate: Highly sensitive in bowel infarction but nonspecific; elevated levels may not occur in the early stages.

Leucocytosis and elevated lactate levels are the two most frequently observed abnormalities in acute mesenteric ischemia; however, both lack specificity for this condition [7,8].

  • Blood gas analysis: Metabolic acidosis is a late finding; its presence should heighten suspicion in the appropriate clinical context.
  • Serum amylase: Moderately elevated in more than half of cases; highly elevated levels suggest pancreatitis, which should guide further diagnostic steps.

Imaging

  • X-rays (Chest/Abdomen): Chest and abdominal X-rays are often normal in the early stages of acute mesenteric ischemia but are useful for identifying complications or alternative diagnoses (e.g., perforation, ureteric calculus) [9]. Early findings may include adynamic ileus, distended air-filled bowel loops, or bowel wall thickening. Late findings such as pneumatosis or portal venous gas strongly suggest bowel infarction.
  • CT Scanning: The primary imaging modality in diagnosing AMI. When enhanced with contrast, CT can detect bowel wall edema, mesenteric edema, abnormal gas patterns, intramural gas, ascites, and mesenteric venous thrombosis. Sensitivity and specificity are high (82.8–97.6% and 91.2–98.2%, respectively), though contrast use may be limited by renal function [10]. However, delaying diagnosis poses greater risks than the small chance (~1%) of contrast-induced nephropathy requiring dialysis [11].
The CT image shows bowel wall thickness.
  • Catheter Angiography: is considered the gold standard but rarely available in emergency settings [10]. It may still be necessary if CT is inconclusive and clinical suspicion remains high.
  • Diagnostic Laparotomy: it may be required for definitive diagnosis in cases of high suspicion when imaging is non-diagnostic.

Risk Stratification

No validated tools exist for risk stratification in AMI. However, specific features indicate late-stage disease and worse prognosis:

  • Prolonged symptoms before presentation.
  • Evidence of bowel necrosis or perforation.
  • Severe biochemical derangements (e.g., high lactate, metabolic acidosis).
  • Hemodynamic instability, such as septic or hemorrhagic shock.

Management

Initial Stabilization

Initial stabilization of the patient, if required, is straightforward but must follow a systematic approach, following airway, breathing, circulation, disability, and exposure.

Airway and Breathing:

The airway should be secured if necessary, especially in cases where the patient appears drowsy due to cerebral hypoperfusion or septic encephalopathy, or if they are actively vomiting and at high risk of aspiration. Rapid correction of hypovolaemia before administering sedatives or paralytics is recommended. Breathing is not commonly compromised in this condition; however, supplemental oxygen may be required for patients experiencing atelectasis or tachypnoea secondary to pain.

C: Circulation – Circulation management necessitates aggressive and rapid resuscitation with fluids or blood products. Fluid resuscitation should not be delayed due to difficulty in obtaining IV access. Ultrasound guidance can be used if venous access proves challenging. If the patient is hypotensive, an initial 10–20 mL/kg (Crystalloids: Normal saline / Hartmann’s / Ringer’s lactate / Plasmalyte etc.) bolus delivered rapidly over 5–15 minutes is appropriate. This usually requires at least one large-bore IV line (20G or larger).

Many of these patients have comorbidities such as congestive heart failure (CHF), which requires judicious fluid management. Careful hemodynamic monitoring, including repeated clinical assessments and sonographic evaluation of inferior vena cava (IVC) collapsibility, is crucial. If required, more invasive hemodynamic monitoring may be employed.

Vasoactive agents should be avoided due to their role as predisposing factors; however, if vasopressors are essential, it is advisable to avoid alpha-agonist medications.

D: Disability – In patients with acute mesenteric ischemia (AMI), mental status may become altered if ischemia progresses to sepsis or shock, leading to cerebral hypoperfusion. This may present as confusion, agitation, or lethargy. Tools such as the AVPU scale or Glasgow Coma Scale (GCS) are valuable for assessing consciousness and monitoring neurological status during treatment. Clinicians should also consider the presence of sequelae from prior strokes, as these may indicate underlying atherosclerotic disease, which is a risk factor for AMI. Additionally, severe pain can interfere with the patient’s ability to engage fully in the assessment, even when mental status remains intact.

E: Exposure – The patient should be fully exposed to enable a thorough examination, while ensuring measures are taken to maintain warmth and prevent hypothermia, as this can worsen shock. A systematic palpation of the abdomen is critical to identify tenderness, guarding, or masses. In the early stages of AMI, there may be no external signs, but central or generalized abdominal tenderness is typically present. As the condition advances, abdominal distension and signs of peritonitis, such as rebound tenderness and rigidity, may develop.

Clinicians should also observe for secondary indicators, including surgical scars or stomas, which may suggest a history of abdominal pathology. Systemic signs of hypoperfusion and shock, such as mottled skin or cool extremities, should also be noted. Regular and frequent reassessment is essential to detect any progression or subtle changes in the patient’s condition, ensuring timely and appropriate intervention.

Early and empirical administration of broad-spectrum antibiotics is critical and should not be delayed for blood culture collection, as the risk of bacterial translocation across the bowel wall is high. Oral intake must be avoided since these patients are likely to undergo urgent surgery under general anesthesia. Electrolyte imbalances should also be corrected promptly.

Antibiotic Administration

Ceftriaxone

  • Dose per kg: 1–2 g
  • Frequency: Stat (given immediately)
  • Maximum Dose: 2 g
  • Category in Pregnancy: Category B (safe for all trimesters)
  • Cautions/Comments: None specified.

Metronidazole

  • Dose per kg: 500 mg
  • Frequency: Stat (given immediately)
  • Maximum Dose: 500 mg
  • Category in Pregnancy: Category B (safe for all trimesters)
  • Cautions/Comments: None specified.

An urgent surgical consultation is imperative, as acute mesenteric ischemia is a time-sensitive condition. Delays to definitive treatment significantly increase morbidity and mortality. High clinical suspicion alone should prompt surgical involvement, even before imaging results are available. In critically ill patients, surgical teams may decide to proceed directly to the operating theatre without advanced imaging. Such decisions are typically made collaboratively by the emergency department, surgical, anesthetic, and intensive care teams.

The definitive treatment for acute mesenteric ischemia depends on the underlying cause and whether necrotic bowel is present. Necrotic bowel or signs of peritonitis necessitate immediate resection. Specific interventions include embolectomy with distal bypass grafting for mesenteric artery embolism, bypass grafting or stenting for mesenteric artery thrombosis, and removal of underlying stimuli in nonocclusive ischemia, sometimes supplemented with direct transcatheter papaverine infusion. Mesenteric venous thrombosis typically requires anticoagulation [7].

Special Patient Groups

Special populations, such as those with communication barriers or cognitive impairments, may require a lower threshold for advanced imaging since history-taking and physical examination may be unreliable. Pregnant and pediatric patients are rarely affected by this condition.

When To Admit This Patient

Given the critical nature of acute mesenteric ischemia and its high mortality rates, all affected patients should be admitted to the intensive care unit for postoperative management following surgery.

Revisiting Your Patient

Our patient was triaged to a high-acuity area of the emergency department (ED) and placed on continuous monitoring, including cardiac leads, blood pressure, and oximetry. Stabilization proceeded in a structured, prioritized manner, focusing on critical areas from A to E:

  • Airway and Breathing: The patient’s airway was intact, and there were no signs of active vomiting. Mild dyspnoea was reported, so supplemental oxygen was administered via nasal cannula.
  • Circulation: Two large-bore intravenous cannulae were inserted, and a liter of crystalloids was infused. This led to visible hemodynamic improvement, including better IVC collapsibility observed on ultrasound.
  • Disability and Exposure: Disability and exposure did not reveal anything abnormal except for a generalized tenderness on the abdomen.

With the patient stabilized, the team moved on to investigations. Blood samples were taken, including a point-of-care venous gas test with serum lactate, coagulation profile, and a group and cross-match. Leucocytes were elevated at 12,000, and serum lactate was elevated at 8. Cardiac monitoring revealed atrial fibrillation. Bedside ultrasound did not reveal other causes of abdominal pain, such as a ruptured aneurysm or cholecystitis. Chest and abdominal X-rays were normal.

Based on the clinical presentation, risk factors, and lab results, the treating team suspected acute mesenteric ischemia. A surgical consult was requested, and a CT scan of the abdomen and pelvis was ordered. Maintenance IV crystalloids and broad-spectrum antibiotics (ceftriaxone and metronidazole) were started empirically. A urinary catheter was placed to monitor fluid balance.

The CT scan revealed:

  • A thickened small bowel wall with dilated bowel loops
  • An embolism in the superior mesenteric artery

The patient was immediately taken to the operating theatre for definitive treatment.

In summary, the role of the ED physician is to:

  1. Stabilize the patient through targeted resuscitation
  2. Make an early diagnosis based on clinical suspicion supported by available investigations
  3. Understand the limitations of laboratory tests in ruling out acute mesenteric ischemia
  4. Prioritize aggressive resuscitation and management
  5. Ensure urgent surgical involvement

Authors

Picture of Colin NG

Colin NG

Woodlands Health

Listen to the chapter

References

  1. Tendler DA, Lamont JT. Overview of intestinal ischemia in adults. UpToDate. https://www.uptodate.com/contents/overview-of-intestinal-ischemia-in-adults Updated January 29, 2024. Accessed December 9, 2024.
  2. McKinsey JF, Gewertz BL. Acute mesenteric ischemia. Surg Clin North Am. 1997;77(2):307-318.
  3. Oldenburg WA, Lau LL, Rodenberg TJ, Edmonds HJ, Burger CD. Acute mesenteric ischemia: a clinical review. Arch Intern Med. 2004;164(10):1054-1062.
  4. Szuba A, Gosk-Bierska I, Hallett RL. Thromboembolism. In: Rubin GD, Rofsky NM, ed. CT and MR Angiography: Comprehensive Vascular Assessment. Philadelphia, PA, USA: Lippincott Williams & Wilkins; 2009: 295-328.
  5. Marc Christopher Winslet. Intestinal Obstruction. In: R.C.G. Russell ed. Bailey & Love’s Short Practice Of Surgery 24th ed. London, UK: Arnold; 2004:1202.
  6. Tendler DA, Lamont JT. Nonocclusive mesenteric ischemia. UpToDate. https://www.uptodate.com/contents/nonocclusive-mesenteric-ischemia Updated December 13, 2023. Accessed December 9, 2024.
  7. Park WM, Gloviczki P, Cherry KJ Jr, et al. Contemporary management of acute mesenteric ischemia: Factors associated with survival. J Vasc Surg. 2002;35(3):445-452.
  8. Cudnik MT, Darbha S, Jones J, Macedo J, Stockton SW, Hiestand BC. The diagnosis of acute mesenteric ischemia: A systematic review and meta-analysis. Acad Emerg Med. 2013;20(11):1087-1100.
  9. Smerud MJ, Johnson CD, Stephens DH. Diagnosis of bowel infarction: a comparison of plain films and CT scans in 23 cases. AJR Am J Roentgenol. 1990;154(1):99-103.
  10. Menke J. Diagnostic accuracy of multidetector CT in acute mesenteric ischemia: systematic review and meta-analysis. Radiology. 2010;256(1):93-101.
  11. Mehran R, Aymong ED, Nikolsky E, et al. A simple risk score for prediction of contrast-induced nephropathy after percutaneous coronary intervention: development and initial validation. J Am Coll Cardiol. 2004;44(7):1393-1399.

FOAM and Further Reading

CDEM Curriculum – Patel S, Mesenteric Ischemia – June 2018, https://cdemcurriculum.com/mesenteric-ischemia/ Accessed May 2023

EMdocs – Seth Lotterman. Mesenteric Ischemia: A Power Review. Nov 2014. http://www.emdocs.net/mesenteric-ischemia-power-review/ Accessed May 2023

Reviewed and Edited By

Picture of Elif Dilek Cakal, MD, MMed

Elif Dilek Cakal, MD, MMed

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Question Of The Day #100

question of the day
Which of the following is the most appropriate next step in management for this patient’s condition?

This patient arrives to the Emergency department with 1 week of melena and fatigue.  His medication list includes an antiplatelet and an anticoagulant medication.  There is tachycardia and melena noted on examination.  This patient likely has an upper GI bleed based on his signs and symptoms with peptic ulcer disease as the most common cause.  The patient’s anticoagulation serves as a risk factor for GI bleeding and is an important contributing factor in this scenario.  Please refer to the chart below for a list of causes of GI bleeding, GI bleeding signs and symptoms, and the initial Emergency Department treatment of GI bleeding. 

Gastroenterology consultation for emergent endoscopy (Choice B) is not necessary as the patient is not acutely unstable.  He may need a diagnostic and therapeutic endoscopy during an inpatient admission, but the GI consultants do not need to be called emergently for this procedure.  An acutely unstable upper GI bleed patient, such as a patient with hemodynamic instability, requiring intubation for airway protection, receiving multiple blood product transfusions, or with brisk (rapid) bleeding on exam should prompt GI consultation for an emergent endoscopy for source control.  Surgery consultation for gastrectomy (Choice C) is not a first-line treatment for upper GI bleeding.  Gastroenterology should first perform a diagnostic and therapeutic endoscopy for most upper GI bleed patients.  Surgical esophageal transection, gastrectomy, colectomy, and other surgical procedures are last resort measures to control GI bleeding.  Administration of IV Ceftriaxone (Choice D) is not needed in this scenario and should not be given routinely in upper GI bleeds.  This patient has no infectious signs or symptoms.  Antibiotics, such as Ceftriaxone or quinolones, should be given to upper GI bleed patients with chronic liver disease (i.e., cirrhosis), or presumed gastroesophageal variceal bleeds.  Antibiotics have been found to have a mortality benefit in this patient population with GI bleeds. 

The best next step in management is to treat the patient’s tachycardia with normal saline (Choice A) for volume resuscitation.  This patient may eventually need blood products, but crystalloid IV fluids are okay to start until the Complete Blood Count results return.  This patient is not in overt hemorrhagic shock, so blood products can be held until there is evidence that the hemoglobin is below 7g/dL.  Reversal of the patient’s anticoagulation with Vitamin K and fresh frozen plasma may also be needed depending on the INR level.  Reversal can wait until coagulation studies are complete since the patient is not acutely unstable. An unstable patient should have their anticoagulant reversed immediately. Correct Answer: A

References

 
 
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Question Of The Day #99

question of the day

Complete Blood Count

Result

(Reference Range)

BUN

36.2

5 -18 mg/dL

Creatinine

1.1

0.7 – 1.2 mg/dL

Hemoglobin

9.2

13.0 – 18.0 g/dL

Hematocrit

27.6

39.0 – 54.0 %

Which of the following is the most appropriate advice for this patient’s condition?

This patient arrives to the Emergency department after a single hematemesis episode.  On exam he has a borderline low blood pressure and tachycardia.  The laboratory results demonstrate an elevated BUN and a low hemoglobin and hematocrit.  The patient’s vital signs in combination with the laboratory values point towards a diagnosis of an upper GI bleed with early signs of hemorrhagic shock.  The history of alcohol abuse also should raise concern for possible gastro-esophageal variceal bleeding as the cause of the GI bleed.

Please refer to the chart below for a list of causes of GI bleeding, GI bleeding signs and symptoms, and the initial Emergency Department treatment of GI bleeding. 

Although this patient is not acutely unstable, his vital signs are abnormal and he should receive volume resuscitation and close observation in the Emergency department.  After initial resuscitation and treatment, it is sometimes difficult to know the best disposition for the patient (admit versus discharge).  The Glasgow-Blatchford Score isa validated risk satisfaction tool used to assist in determining the disposition of patients with an upper GI bleed.  The scoring criteria and instructions on how to use the score are below.

Glasgow-Blatchford Score

 

A validated risk stratification tool for patients with upper GIB

Scoring Criteria

Numerical Score

BUN (mg/dL)

<18.2

18.2-22.3

22.4-28

28-70

>70

 

0

+2

+3

+4

+6

Hemoglobin (g/dL) for men

>13

12-13

10-12

<10

 

0

+1

+3

+6

Hemoglobin (g/dL) for women

>12

10-12

<10

 

0

+1

+6

Systolic blood pressure (mmHg)

>110

100-109

90-99

<90

 

0

+1

+2

+3

Other criteria

Pulse >100 beats/min

Melena present

Syncope

Liver disease history

Cardiac failure history

 

+1

+1

+2

+2

+2

Instructions:

Low risk= Score of 0.  Any score higher than 0 is high risk for needing intervention: transfusion, endoscopy, or surgery. Consider admission for any score over 0. 

This patient has a Glasgow-Blatchford score of 15, and should not be discharged home.  A plan to discharge with gastroenterology follow up in 1 week (Choice A) or discharge with instructions to return if there are repeat hematemesis episodes (Choice B) should not be followed. This patient may have future hematemesis episodes in the Emergency department, be at risk for aspiration, require endotracheal intubation, and become more hypotensive.  A Sengstaken-Blakemore tube (Choice C) is a specialized oro-gastric tube with a gastric and esophageal balloon.  Placement of this tube is considered an invasive procedure that is only used after a patient has been endotracheally intubated to prevent aspiration.  Once placed correctly, the balloons in the tube can be inflated to tamponade any bleeding variceal vessels in the distal esophagus or stomach.  This tube is used as a last resort measure prior to endoscopic treatment for presumed gastro-esophageal variceal bleeds. 

The best advice for this patient would be to admit the patient for monitoring and endoscopy (Choice D).

References

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Question Of The Day #98

question of the day
Which of the following is the most likely cause for this patient’s condition?

This man presents to the Emergency department with epigastric pain and hematemesis.  His exam shows hypotension, tachycardia, pale conjunctiva, and a tender epigastrium and left upper quadrant.  This patient likely has an upper GI bleed based on his signs and symptoms. 

Please refer to the chart below for a list of causes of GI bleeding, GI bleeding signs and symptoms, and the initial Emergency Department treatment of GI bleeding. 

Risk factors for GI bleeds include alcohol use, anticoagulant use, NSAID (non-steroidal anti-inflammatory drug) use (i.e., ibuprofen, aspirin, naproxen), recent gastrointestinal surgery or procedures, prior GI bleeds, and a history of conditions that are associated with GI bleeds (i.e., gastritis, peptic ulcers, H. Pylori infection, ulcerative colitis, Chron’s disease, hemorrhoids, diverticulosis, or GI tract cancers).  Fatty meals (Choice A) can trigger gastroesophageal reflux disorder (GERD) symptoms or biliary colic symptoms from cholelithiasis.  However, fatty meals do not increase the risk for GI bleeding.  Physiological stress, such as sepsis or bacteremia (Choice B), can increase the risk for GI bleeding.  This patient does not have any infectious exam signs or symptoms that would support the presence of bacteremia. Acetaminophen use (Choice D) can cause liver failure if taken in excess, but acetaminophen does not cause GI bleeding.  NSAIDs, unlike Tylenol, are associated with GI bleeding. 

Systemic steroid use (Choice C) can increase the risk for GI bleeding and is the likely cause of this patient’s upper GI bleed. Correct Answer: C

References

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Question Of The Day #97

question of the day
Which of the following is the most appropriate next step in management for this patient’s condition?

This patient arrives to the Emergency department after multiple episodes of hematemesis.  Her exam shows tachycardia, borderline hypotension, and mild tachypnea.  While in the Emergency department the patient decompensates after more hematemesis episodes and develops altered mental status.  This patient has an upper GI bleed most likely from a gastroesophageal variceal bleed.  Gastro-esophageal (GE) varices are dilated blood vessels at the GE junction that result from portal hypertension.  Variceal bleeding can be catastrophic and cause hemorrhagic shock and problems with airway patency as seen in this scenario.  The management of GE variceal bleeding, like other GI bleeds, begins with management of the “ABCs” (Airway, Breathing, and Circulation).  Unlike in other causes of upper GI bleeds, IV antibiotics and IV octreotide are used in GE variceal bleeds.  IV antibiotics have a mortality benefit when used in this setting.  Early gastroenterology consultation is another important component of GE variceal bleed management for definitive diagnosis and treatment with variceal banding or ligation.  Please see the chart below for further details on general GI bleed causes, signs and symptoms, and ED management.

This patient with a depressed mental status needs to have a definitive airway established to prevent aspiration with bloody vomitus.  IV Pantoprazole (Choice B) is used in upper GI bleeds from peptic ulcers but has no role in this acutely ill variceal bleed patient.  The airway should be established prior to medications, such as pantoprazole are considered.  A cricothyrotomy (Choice D) would establish an airway, but this is an invasive approach to airway management and not the best approach in this patient.  A cricothyrotomy involves piercing a needle or scalpel in the anterior neck (cricothyroid membrane) to establish an airway surgically.  This procedure is performed in special situations where a patient cannot be intubated through the trachea (i.e., angioedema of the lips and tongue, facial mass, facial trauma) and cannot ventilate independently (i.e., depressed mental status).  This patient does not meet the criteria for this invasive procedure.  Endotracheal intubation should be attempted first on this patient.  A Sengstaken-Blakemore tube (Choice A) is a specialized oro-gastric tube with a gastric and esophageal balloon.  Once placed correctly, the balloons on the tube can be inflated to tamponade any bleeding variceal vessels in the distal esophagus or stomach.  This tube should be placed only after intubating a patient and is used as a last resort measure prior to endoscopic treatment.  The best next step in management of this patient is to perform endotracheal intubation (Choice C) for airway protection. Correct Answer: C

References

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Question Of The Day #96

question of the day
Which of the following is the most appropriate next step in management for this patient’s condition?

This patient arrives to the Emergency department with upper abdominal pain and hematemesis.  The exam demonstrated hypotension, tachycardia, pale conjunctiva, and abdominal ascites. The patient decompensates during the exam requiring endotracheal intubation for airway protection. This patient has an upper GI bleed most likely from gastro-esophageal varices given her history of liver cirrhosis and stigmata of chronic liver disease.  Gastro-esophageal (GE) varices are dilated blood vessels at the GE junction that result from portal hypertension.  Variceal bleeding can be catastrophic and cause hemorrhagic shock and problems with airway patency as seen in this scenario.  The management of GE variceal bleeding, like other GI bleeds, begins with management of the “ABCs” (Airway, Breathing, and Circulation).  Unlike in other causes of upper GI bleeds, IV antibiotics and IV octreotide are used in GE variceal bleeds.  IV antibiotics have a mortality benefit when used in this setting.  First line antibiotics are IV ceftriaxone or IV ciprofloxacin.  Early gastroenterology consultation is another important component of GE variceal bleed management for definitive diagnosis and treatment with variceal banding or ligation.  

An abdominal paracentesis (Choice A) is not the best next step in this unstable cirrhotic patient.  Antibiotics are routinely given in gastro-esophageal variceal bleeds due to their mortality benefit, so there is no need for an emergent paracentesis to evaluate for spontaneous bacterial peritonitis (SBP) with an ascitic fluid sample. IV Tranexamic acid (Choice C) is an anti-fibrinolytic agent with pro-coagulative effects.  Its use is recommended in post-partum hemorrhage and traumatic hemorrhages, but it has no utility in the setting of GI bleed.  Early gastroenterology consultation for endoscopy is preferred over general surgery consultation (Choice D).  Surgery consultants can assist in a TIPS procedure (Transjugular intrahepatic portosystemic shunt) to reduce portal hypertension, esophageal resection, or gastrectomy, but less invasive endoscopic therapies with GI specialists are preferred over these procedures.

IV Ceftriaxone (Choice B) is the best next step in this scenario due to the mortality benefit of antibiotics in chronic liver disease patients with variceal bleeds.      

Please see the chart below for further details on general GI bleed causes, signs and symptoms, and ED management.

    

References

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Question Of The Day #95

question of the day

Complete Blood Count

Result

(Reference Range)

WBC Count

16.2

4.0 – 10.5 X 103/mL

Hemoglobin

10.8

13.0 – 18.0 g/dL

Hematocrit

32.4

39.0 – 54.0 %

Platelets

220

140 – 415 x 103/mL

Which of the following is the most likely diagnosis for this patient’s condition?

This patient arrives to the Emergency department with bright red bloody stools and lower abdominal pain.  The exam shows fever, tachycardia, and left-sided abdominal tenderness.  The laboratory results provided show leukocytosis and anemia.  This patient likely has a lower GI bleed based on her signs and symptoms.  Please refer to the chart below for a list of causes of GI bleeding, GI bleeding signs and symptoms, and the initial Emergency Department treatment of GI bleeding. 

All choices provided are causes of lower GI bleeding and are possible in this patient.  However, that patient’s signs, symptoms, and risk profile make certain diagnoses less likely than others.  Diverticulosis (Choice A) is the most common cause of lower GI bleeding.  Diverticulosis often occurs in older patients and should not be associated with pain or fever, which support a diagnosis of an inflammatory or infectious etiology (i.e., diverticulitis, Shigellosis, ulcerative colitis, chron’s disease, etc.).  This patient is young and has fever and leukocytosis, making diverticulosis less likely.  Colon malignancy (Choice B) is also possible but is less likely given the patient’s young age, the presence of fever, and the acute onset of symptoms over 2 days.  Colon malignancy tends to cause slow GI bleeding over a longer period of time, rather than acutely over 2 days.  Ischemic colitis (Choice C), such as mesenteric ischemia, is less likely in a young patient without any cardiac risk factors or recent abdominal surgeries. 

Ulcerative colitis (Choice D) is the most likely diagnosis in this scenario.  Peak incidence for ulcerative colitis occurs in the second and third decades of life, and women are more likely than men to have this diagnosis.  Definitive diagnosis requires a biopsy and colonoscopy, but a CT scan of the abdomen and pelvis can show findings consistent with ulcerative colitis for a new diagnosis.  Treatment of an ulcerative colitis flare includes general supportive care, IV steroids, and IV antibiotics if there is concern for a concurrent infectious process.  Intestinal perforation and toxic megacolon also should be evaluated for with CT imaging.    

References

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Question Of The Day #94

question of the day

Complete Blood Count

Result

(Reference Range)

WBC Count

4.5

4.0 – 10.5 X 103/mL

Hemoglobin

5.3

13.0 – 18.0 g/dL

Hematocrit

15.9

39.0 – 54.0 %

Platelets

138

140 – 415 x 103/mL

Which of the following is the most appropriate next step in management for this patient’s condition?

This patient arrives to the Emergency Department with bright red bloody stools in the setting of warfarin use.  His exam shows hypotension and tachycardia.  The laboratory results show a low hemoglobin and hematocrit, but no INR or other coagulation studies are provided.  This patient is in hemorrhagic shock due to a lower gastrointestinal bleed.  This patient’s condition may be due to coagulopathy from his warfarin (i.e., supratherapeutic INR), diverticulosis, or other conditions.  Initial management of this unstable patient should include management of the airway, breathing, and circulation (“ABCs”).  This includes aggressive and prompt treatment of the patient’s hypotension and tachycardia and reversal of the patient’s anticoagulation.  Please refer to the chart below for a list of causes of GI bleeding, GI bleeding signs and symptoms, and the initial Emergency Department treatment of GI bleeding. 

This patient’s platelet level is just below the lower limit of normal, so administration of a platelet transfusion (Choice A) would not be the next best step.  Platelet administration should be considered if the platelet count is below 50,000-100,000, or if a massive transfusion protocol is initiated to prevent coagulopathy.  No INR value is provided in the question stem, but prompt reversal of warfarin should not be delayed for an INR level (Choice D).  Reversal of warfarin should be promptly initiated when a patient is unstable (i.e., hypotensive GI bleed, traumatic wound hemorrhage, intracranial bleed, etc.).  Medication reversal in these settings includes both IV Vitamin K 10mg and IV Fresh Frozen Plasma 10-20cc/kg.  IV Vitamin K helps reverse the Vitamin K antagonistic effect of Warfarin, but it does not acutely provide new Vitamin K-dependent coagulation factors (Factors X, V, II, VII).  IV Vitamin K gives the liver the ‘materials’ needed to regenerate these coagulation factors, but this process takes time.  Fresh frozen plasma contains ‘ready-to-use’ coagulation factors that will help control the hemorrhage acutely.  For this reason, both Vitamin K and FFP are given together in an unstable patient.  An alternative to fresh frozen plasma (FFP) is prothrombin complex concentrate (PCC), which is a concentrated version of coagulation factors.  PCC is not broadly available in all countries, and is generally more expensive than FFP. 

The management of stable patients with a supratherapeutic INR includes holding warfarin doses and sometimes providing PO Vitamin K, depending on the INR level.  Administration of IV Vitamin K only (Choice C) is not the correct treatment in this scenario.  IV Vitamin K and IV Fresh Frozen Plasma (Choice B) is the best next step to reverse this patient’s anticoagulant. 

References

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Question Of The Day #93

question of the day

Which of the following is the most appropriate next step in management?

This patient arrives to the Emergency Department with bright red bloody stools and generalized abdominal pain.  His exam shows hypotension, tachycardia, a diffusely tender abdomen, and pale conjunctiva.  He also takes warfarin daily for anticoagulation.  This patient is in hemorrhagic shock due to a lower gastrointestinal bleed.  This patient’s condition may be due to coagulopathy from his warfarin (i.e., supratherapeutic INR), diverticulosis, ischemic colitis (i.e., mesenteric ischemia), and other conditions.  Initial management of this unstable patient should include management of the airway, breathing, and circulation (“ABCs”).  This includes aggressive and prompt treatment of the patient’s hypotension and tachycardia.  Please refer to the chart below for a list of causes of GI bleeding, GI bleeding signs and symptoms, and the initial Emergency Department treatment of GI bleeding. 

A CT Angiogram of the abdomen and pelvis (Choice A) may be helpful in clarifying the etiology and site of the patient’s bleeding, but this is not the best next step in management.  The patient’s shock state first should be managed prior to any imaging studies.  Gastroenterology consultation for colonoscopy (Choice B) may be important later in this patient’s management, but it is not the best next step in management. His shock state should be treated prior to calling any consultants. An IV Pantoprazole infusion (Choice C) is helpful in upper GI bleeds due to peptic ulcer disease.  Proton pump inhibitor medications, like pantoprazole, help reduce findings of ulcer bleeding during endoscopy.  Proton pump inhibitor use has been controversial in upper GI bleeds as there is no evidence that their use decreases mortality, decreases blood product requirements, or ulcer rebleeding, but these medications are often given due to their generally small risk profile.

 

The best next step for this patient in hemorrhagic shock is administration of packed red blood cells (Choice D).  He also should have reversal of his warfarin with IV Vitamin K and fresh frozen plasma to prevent continued bleeding.

References

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Question Of The Day #92

question of the day

Which of the following is the most likely cause of this patient’s condition?

This elderly patient arrives to the Emergency Department with painless hematochezia.  His exam shows borderline hypotension, tachycardia, and a normal abdominal exam.  This patient most likely has a lower gastrointestinal bleed based on his signs and symptoms.  A brisk (fast) upper GI bleed is also possible but is less likely.  Please refer to the chart below for a list of causes of GI bleeding, GI bleeding signs and symptoms, and the initial Emergency Department treatment of GI bleeding. 

All choices listed above are potential causes of bright red bloody stools.  Peptic ulcer disease (Choice C) is the most common cause of upper GI bleeding worldwide, not lower GI bleeding.  However, a profusely bleeding peptic ulcer can cause rapid blood transit through the GI tract to form hematochezia rather than melena.  The patient lacks any risk factors or symptoms of peptic ulcer disease, such as upper abdominal pain, hematemesis, NSAID use, or prior H. pylori infection.  Ischemic colitis, or mesenteric ischemia (Choice A), is often associated with abdominal pain and cardiac risk factors (i.e., atrial fibrillation).  Colon cancer (Choice B) is also possible, but typically colon malignancy causes slow, chronic bleeding, rather than acute large volume bloody stools with signs of shock as in this patient.  The most common cause of lower GI bleeding worldwide is diverticulosis (Choice D).  This is the most likely diagnosis in this patient with painless hematochezia.

References

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Question Of The Day #91

question of the day

Which of the following is the most likely cause of this patient’s condition?

This patient arrives to the Emergency Department with upper abdominal pain and hematemesis.  He occasionally takes ibuprofen, a non-steroidal anti-inflammatory drug (NSAID), which is a risk factor for GI bleeding. His examination shows tachycardia.  This patient likely has an upper gastrointestinal bleed given his signs and symptoms.  Please refer to the chart below for a list of causes of GI bleeding, GI bleeding signs and symptoms, and the initial Emergency Department treatment of GI bleeding.  

All choices listed above are potential causes of upper GI bleeding, with the exception of GERD (Choice D).  Erosive gastritis and esophagitis can cause an upper GI bleed, but GERD is not a cause of upper GI bleed.  The patient lacks risk factors for esophageal varices (Choice A), such as chronic liver disease, cirrhosis, or alcohol abuse.  Gastric malignancy (Choice B) is possible, but less likely given the patient’s young age and lack of risk factors mentioned in the question stem for gastric malignancy (i.e., prior H. pylori infection, tobacco smoking, chronic gastritis, weight loss, lymphadenopathy, etc.).  The most common worldwide cause of upper GI bleeding is peptic ulcer disease (Choice C).  For this reason, Choice C is the best answer.

References

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