Upper Gastrointestinal Bleeding (UGIB)
Definition
Upper gastrointestinal bleeding (UGIB) is a haemorrhage originating from a source proximal to the Ligament of Treitz, the anatomical point marking the duodenojejunal junction (1).
Epidemiology
Upper gastrointestinal bleeding is a significant cause of hospital admission and mortality in Malaysia (1). While precise national incidence figures are not readily available in recent large-scale surveys, a study from a Kuala Lumpur hospital highlighted that peptic ulcer disease (PUD) was the most common cause, with duodenal ulcers accounting for 32% and gastric ulcers for 29.7% of cases (2). A separate analysis of non-variceal UGIB (NVUGIB) patients in a Malaysian hospital found a mean age of 63.9 years, with a male predominance (65.6%) and an ethnic distribution of 76.1% Malays, 13.9% Chinese, and 6.1% Indians; however, this data is from a single centre and may not represent the entire country (3). Globally, UGIB is a common medical emergency with an incidence ranging from 48 to 160 cases per 100,000 people annually and a considerable in-hospital mortality rate of up to 11% (4).
Pathophysiology
The pathophysiology of UGIB diverges into two primary pathways: non-variceal and variceal bleeding (5).
Non-Variceal Upper GI Bleeding (NVUGIB): This is the more frequent type, primarily caused by a breach in the gastroduodenal mucosa (5). The trigger is often peptic ulcer disease, driven by Helicobacter pylori infection or the use of Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) (5). These agents disrupt the protective mucosal barrier, allowing gastric acid and pepsin to cause injury, leading to erosion into an underlying blood vessel and subsequent bleeding (5).
Variceal Upper GI Bleeding: This is a direct consequence of portal hypertension, most commonly stemming from liver cirrhosis (5). Increased pressure in the portal venous system causes the formation of dilated, thin-walled collateral vessels (varices), typically in the oesophagus and stomach. Bleeding occurs when the pressure within these varices exceeds their wall tension, leading to rupture and often catastrophic haemorrhage (5).
Clinical Presentation
Patients with UGIB can present with a spectrum of signs and symptoms (1). The classic presentation involves the vomiting of blood or the passage of altered blood in the stool (1).
Diagnostic Clues
Haematemesis: The vomiting of fresh, bright red blood indicates active and significant bleeding (1). More commonly, patients may present with "coffee-ground" vomit, which is dark, granular material resulting from the conversion of haemoglobin to methaemoglobin by gastric acid (1).
Melaena: The passage of black, tarry, and foul-smelling stools is a strong indicator of an upper GI source, as it results from the digestion of blood as it passes through the intestines (1). This can occur with as little as 50-100 mL of blood loss (1).
Haematochezia: While typically a sign of lower GI bleeding, the passage of bright red blood per rectum can occur in cases of massive UGIB (>1 litre) due to rapid intestinal transit (1).
Common Symptoms
Symptoms of hypovolaemia such as dizziness, weakness, fatigue, or exertional dyspnoea (1).
Epigastric pain, particularly in cases of peptic ulcer disease (6).
⚠️ Red Flag Signs & Symptoms
Syncope (fainting) (1)
Persistent hypotension (Systolic Blood Pressure < 100 mmHg) despite fluid resuscitation (6)
Tachycardia (Pulse > 100 bpm) (6)
Altered mental state (confusion, agitation, drowsiness), a late and ominous sign of poor cerebral perfusion (6).
Ongoing, massive haematemesis (7).
Complications
Cardiovascular: Hypovolaemic shock, myocardial infarction (precipitated by anaemia), arrhythmias (7).
Respiratory: Aspiration pneumonitis from vomited blood (7).
Renal: Acute kidney injury due to hypoperfusion.
Metabolic: Lactic acidosis from tissue hypoperfusion (7).
Hepatic: In patients with cirrhosis, bleeding can precipitate hepatic encephalopathy, hepatorenal syndrome, or bacterial infections like Spontaneous Bacterial Peritonitis (SBP) (8).
Re-bleeding: A major complication associated with significantly increased mortality (8).
Prognosis
The prognosis of UGIB depends on the underlying cause, the severity of the initial bleed, the presence of co-morbidities, and the patient's age (4, 8). The overall mortality rate remains around 10% (4). Variceal bleeding carries a higher mortality than non-variceal bleeding (5). The use of risk stratification scores like the Glasgow-Blatchford Score (GBS) and the post-endoscopy Rockall score helps to predict outcomes and guide the level of care (7, 8). A high Rockall score (>8) indicates a very poor prognosis (8).
Differential Diagnosis
1. Lower Gastrointestinal Bleeding (LGIB): This is a key differential, especially if the patient presents with haematochezia (1). LGIB originates distal to the Ligament of Treitz. However, in a shocked patient, massive UGIB can present with fresh rectal bleeding due to rapid transit time, making it crucial to first rule out an upper source which is more common and often more severe (1). The absence of haematemesis or melaena may point towards LGIB, but this is not definitive.
2. Oropharyngeal or Nasopharyngeal Bleeding: Bleeding from the nose (epistaxis) or throat can be swallowed and later present as haematemesis or melaena, mimicking UGIB. A focused history on recent nasal trauma or instrumentation and a thorough ear, nose, and throat examination are essential to distinguish this, especially if endoscopic findings in the upper GI tract are negative.
3. Haemoptysis: This is the coughing up of blood from the respiratory tract and can sometimes be confused with haematemesis. A careful history is needed to clarify if the blood was coughed up (often frothy, bright red) versus vomited. A chest X-ray can help identify a pulmonary source, such as a tumour, infection, or bronchiectasis (7).
Investigations
Investigations must be performed simultaneously with resuscitation to guide immediate management and risk stratification (1).
Immediate & Bedside Tests
Bedside ECG: This is mandatory to immediately rule out arrhythmias or signs of cardiac ischaemia (the action), which can be precipitated by the haemodynamic stress and anaemia of a major bleed (the rationale) (7).
Venous/Arterial Blood Gas (VBG/ABG): A VBG provides a rapid point-of-care estimate of haemoglobin and lactate (the action), which is critical for assessing the severity of blood loss and tissue hypoperfusion without waiting for formal lab results (the rationale) (7).
Fingerprick Blood Glucose: This is essential to quickly exclude hypoglycaemia as a cause for an altered mental state (the action), particularly in patients with known liver disease or sepsis who are at high risk (the rationale) (7).
Digital Rectal Examination (DRE): This should be performed to provide objective evidence of bleeding by confirming the presence of melaena or haematochezia (the action), helping to solidify the diagnosis of a significant GI bleed (the rationale) (6).
Diagnostic Workup
First-Line Investigations (STAT Bloods): Bloods must be drawn from a large-bore cannula before fluid infusion to ensure results are not diluted. This panel is crucial for risk stratification using the Glasgow-Blatchford Score (GBS) (the action) and for guiding resuscitation (the rationale) (1, 6). The panel includes:
Full Blood Count (FBC): To establish a baseline haemoglobin for transfusion decisions and to check the platelet count, which is vital for haemostasis (1).
Urea & Electrolytes (U&E): A disproportionately raised urea compared to creatinine is a key biochemical marker of UGIB, resulting from the digestion of blood proteins, and is a core component of the GBS (1).
Liver Function Tests (LFTs): To identify underlying chronic liver disease, which strongly suggests a variceal cause of bleeding (6).
Coagulation Screen (PT/INR, APTT): To detect any underlying or drug-induced coagulopathy that requires urgent reversal (6).
Group & Save / Crossmatch: A Group and Save is mandatory for all patients, while a Crossmatch for a minimum of 2-4 units of packed red cells should be sent for any patient with active bleeding or haemodynamic instability, ensuring blood products are ready for rapid transfusion (6).
Gold Standard:
Oesophago-gastro-duodenoscopy (OGD): This is the definitive investigation for UGIB. It provides direct visualisation to diagnose the source of bleeding (the rationale) and allows for immediate therapeutic intervention to achieve haemostasis in the same procedure (the action) (7, 8).
Monitoring & Staging
Glasgow-Blatchford Score (GBS): This pre-endoscopy score is the recommended tool to stratify the patient's risk of needing an intervention (transfusion, endoscopy) or death (the action), thereby guiding the crucial decision on whether the patient requires hospital admission or can be safely managed as an outpatient (the rationale) (7). A score of >1 indicates the need for admission (7).
Management
Management Principles
The management of acute UGIB is a time-critical process focused on three pillars: immediate haemodynamic resuscitation, risk stratification to guide the urgency of intervention, and targeted endoscopic therapy to control bleeding and prevent recurrence (1).
Acute Stabilisation (The First Hour)
The ABCDE approach must be initiated immediately upon patient arrival (7).
Airway: Assess airway patency. In a patient with a reduced level of consciousness (GCS ≤ 8) or massive haematemesis, call for senior anaesthetic help early for endotracheal intubation (the action) to prevent aspiration of blood and secure the airway for a safe subsequent endoscopy (the rationale) (7).
Breathing: Administer high-flow oxygen via a non-rebreather mask to maintain SpO2 between 94-98% (the action), which is vital to maximise arterial oxygen content and prevent tissue hypoxia resulting from blood loss (the rationale) (7).
Circulation:
Secure two large-bore (16G or 18G) IV cannulas (the action) to enable rapid administration of fluids and blood products to treat hypovolaemic shock (the rationale) (6).
If hypotensive (SBP < 100 mmHg), administer a STAT fluid bolus of warmed crystalloid (e.g., Normal Saline or Hartmann's solution) 500 mL over <15 minutes, reassessing after each bolus (the action) to restore tissue perfusion while avoiding aggressive over-resuscitation, which can dislodge clots or increase portal pressure (the rationale) (6). The target is a systolic BP > 100 mmHg (6).
Employ a restrictive transfusion strategy. For most patients, initiate transfusion of packed red blood cells only when haemoglobin falls below 7 g/dL (the action), as evidence shows this reduces re-bleeding and mortality compared to more liberal strategies (the rationale) (4, 6).
Definitive Therapy
The choice of therapy depends on whether the bleeding is suspected to be variceal or non-variceal.
Suspected Non-Variceal Bleeding
First-Line Treatment (Endoscopy): For high-risk lesions identified during OGD (e.g., active bleeding, non-bleeding visible vessel - Forrest Ia, Ib, IIa), the standard of care is dual endoscopic therapy (7). This involves the initial injection of dilute epinephrine (1:10,000) to achieve temporary vasoconstriction and allow for a clearer view (the action), followed immediately by a second, more durable modality like thermal coagulation (e.g., Gold Probe) or mechanical clipping (the action) to definitively seal the vessel and prevent re-bleeding (the rationale) (7).
Post-Endoscopy Medical Therapy: For patients who received endoscopic therapy for a high-risk ulcer, administer a high-dose intravenous proton-pump inhibitor (PPI), such as IV Pantoprazole 80mg bolus followed by an 8mg/hour infusion or 40-80mg IV twice daily for 72 hours (the action). This maintains a high intragastric pH (>6), which stabilises the clot and significantly reduces the risk of re-bleeding (the rationale) (7, 8).
Suspected Variceal Bleeding
Vasoactive Drugs: As soon as a variceal bleed is suspected, start a vasoactive agent like Terlipressin (2mg IV bolus, then 1-2mg every 4-6 hours) or Octreotide (50mcg IV bolus, then 50mcg/hour infusion) without waiting for endoscopy (9). These drugs cause splanchnic vasoconstriction (the rationale), which reduces blood flow to the portal system, thereby lowering variceal pressure and helping to control the bleeding (the action) (9).
Prophylactic Antibiotics: All patients with cirrhosis and UGIB should receive prophylactic IV antibiotics, such as Ceftriaxone 1g once daily for up to 7 days (9). This is a critical, life-saving intervention to prevent bacterial infections (like SBP) (the action), which are a major trigger for re-bleeding and mortality in this immunocompromised population (the rationale) (8, 9).
Endoscopic Therapy: For oesophageal varices, Endoscopic Variceal Ligation (EVL) is the treatment of choice (8). For gastric varices, injection of a tissue adhesive like N-butyl-2-cyanoacrylate is preferred (8).
Supportive & Symptomatic Care
Analgesia: Provide pain relief as needed, but strictly avoid NSAIDs (8). Paracetamol is generally safe if there is no severe liver dysfunction.
Antiemetics: Administer antiemetics (e.g., IV Metoclopramide 10mg) to control nausea and vomiting, which can be distressing and increase the risk of re-bleeding from Mallory-Weiss tears.
Coagulopathy Reversal: For patients on Warfarin with major bleeding, reversal with Prothrombin Complex Concentrate (PCC) and IV Vitamin K is preferred over FFP for faster, more effective correction of the INR (6). For actively bleeding patients with thrombocytopenia, transfuse platelets to maintain a count >50 x 10⁹/L (6).
Key Nursing & Monitoring Instructions
Strict hourly monitoring of vital signs (BP, HR, RR, SpO2).
Maintain a strict input/output chart to guide fluid resuscitation.
Hourly neurological observations (GCS) for the first 6 hours.
Inform the medical officer immediately if systolic BP drops below 100 mmHg, heart rate rises above 120 bpm, or urine output is <0.5mL/kg/hr.
Keep the patient nil-by-mouth (NBM) in preparation for potential emergency endoscopy.
Long-Term Plan & Patient Education
Non-Variceal (PUD): Test all patients for H. pylori. If positive, prescribe eradication therapy (e.g., a PPI plus two antibiotics) (8). Crucially, schedule a follow-up Urea Breath Test or Stool Antigen Test at least 4 weeks after treatment to confirm eradication (8). Patients must be educated to avoid all NSAIDs indefinitely (8). If long-term antiplatelet or anticoagulant therapy is required, it must be co-prescribed with a daily PPI for gastroprotection (8).
Variceal: These patients require secondary prophylaxis, which is a combination of a non-selective beta-blocker (e.g., Propranolol, Carvedilol) to lower portal pressure and enrolment in a serial endoscopic variceal ligation (EVL) programme every 2-4 weeks until the varices are obliterated (9).
When to Escalate
A house officer must be vigilant for signs of deterioration and escalate to a senior colleague promptly.
Call Your Senior (MO/Specialist) if:
The patient remains haemodynamically unstable (hypotensive, tachycardic) despite initial fluid boluses (8).
There is massive or continuous haematemesis (7).
The patient develops any new neurological signs or a drop in GCS (7).
The initial haemoglobin is < 7g/dL or there is a need to activate the Major Haemorrhage Protocol (6).
The patient has known liver disease or stigmata of chronic liver disease are present on examination (a variceal bleed is likely) (6).
You are considering reversal of anticoagulation (8).
Referral Criteria
Refer to Gastroenterology for urgent endoscopy for all admitted patients (8).
Refer to Anaesthetics/ICU for any patient with a compromised airway, persistent haemodynamic instability requiring vasopressors, or the need for multi-organ support (7, 8).
Refer to General Surgery if endoscopic therapy fails to control bleeding, as the patient may require emergency surgery (8).
Refer to Interventional Radiology for consideration of Transjugular Intrahepatic Portosystemic Shunt (TIPS) in refractory variceal bleeding or angiographic embolisation in selected cases of failed endoscopic therapy for non-variceal bleeding (9).
References
Ministry of Health Malaysia. (2004). Clinical Practice Guidelines on the Management of Non-Variceal Upper Gastrointestinal Bleeding. https://www.moh.gov.my/moh/attachments/3966.pdf
Goh, K. L. (2000). Upper gastrointestinal bleeding in a Kuala Lumpur Hospital, Malaysia. Medical Journal of Malaysia, 55(4), 498-504. https://www.e-mjm.org/2000/v55n4/Upper_Gastrointestinal_Bleeding.pdf
Razlan, H., et al. (2021). Haematochezia and Higher Glasgow-Blatchford Score are Predictive Factors for Higher Red Blood Cells Transfusion Units in a Hospital-based Retrospective Study. Malaysian Journal of Medicine and Health Sciences, 17(4), 109-115. https://medic.upm.edu.my/upload/dokumen/2021100809453916_MJMHS_0862.pdf
Jairath, V., & Barkun, A. N. (2018). Management of acute upper gastrointestinal bleeding. The BMJ, 364, l536. https://www.bmj.com/content/364/bmj.1536
Gralnek, I. M., et al. (2021). Diagnosis and management of nonvariceal upper gastrointestinal hemorrhage: European Society of Gastrointestinal Endoscopy (ESGE) Guideline. Endoscopy, 53(10), 1073-1087. (Note: Updated reference)
National Institute for Health and Care Excellence. (2012). Acute upper gastrointestinal bleeding in over 16s: management. (Clinical guideline CG141). https://www.nice.org.uk/guidance/cg141
Laine, L., et al. (2021). ACG Clinical Guideline: Upper Gastrointestinal and Ulcer Bleeding. The American Journal of Gastroenterology, 116(5), 899-917. https://www.darmzentrum-bern.ch/fileadmin/darmzentrum/Education/Bible_Class/2022/upper_GI_bleeding/ACG_-_Upper_Gl_Bleed_2021.pdf
Stanley, A. J., & Laine, L. (2019). Management of acute upper gastrointestinal bleeding. BMJ, 364, l536.
Garcia-Tsao, G., et al. (2017). Prevention and Management of Gastroesophageal Varices and Variceal Hemorrhage in Cirrhosis. Hepatology, 65(1), 310-335. (Note: Updated reference)
