Acute gastrointestinal bleeding

Abstract

Acute gastrointestinal bleeding is a common medical and/or surgical emergency that can be caused by a range of diverse pathologies. Gastrointestinal Bleeding can be divided into upper and lower in nature, presenting in sometimes subtly different fashions, but with differing requirements for investigation and management. Prompt identification, risk stratification and treatment are required in order to minimise the ongoing significant morbidity and mortality rates associated with severe presentations of gastrointestinal bleeding.

Clinical case scenario 1

Peter, a 60-year-old retired engineer, gives a 3-day history of passing tarry, smelly stools that stick to the toilet bowl. He has also had some mild abdominal pain, worse a few hours after eating, and settling slightly with Gaviscon, for the last week. He has a background of cardiovascular disease, and currently takes daily low-dose aspirin and atorvastatin. He drinks five bottles of wine per week with his wife and is an ex-smoker. He is normally active, but has felt breathless on walking upstairs over the last 24 hours. On examination, he has a heart rate of 105 beats per minute and a blood pressure of 132/65 mm Hg. His abdomen is soft, with epigastric tenderness and rectal examination reveals a small amount of melaena.

Classification of gastrointestinal bleeding

Acute gastrointestinal bleeding can be anatomically divided into upper and lower in nature, dependent on its relation to the ligament of Treitz (a double fold of peritoneum that suspends the duodenojejunal flexure from the retroperitoneum). Upper gastrointestinal bleeding (UGIB) occurs proximally; lower gastrointestinal bleeding (LGIB) distally (Fig. 1). This distinction is important, due to the differing investigations and management required, as well as the morbidity and mortality outcomes. Acute UGIB has an estimated incidence of 90–170 per 100 000 head of population in the UK (Button et al., 2011), with approximately a 10% mortality rate, that has remained virtually unchanged over the last 50 years (Hearnshaw et al., 2010). Acute LGIB is less common, with a UK-wide incidence of 33–87 per 100 000 population (Lanas et al., 2009) and a much lower in-hospital mortality rate of 3.4% (Oakland et al., 2018).

Figure 1.

Anatomical division of the upper and lower gastrointestinal tract.

Causes of upper GI bleeding

These can be divided into variceal and non-variceal causes, according to differing management strategies. Variceal bleeding accounts for 8% of all UGIB, a figure that has increased over the last few decades with the rising prevalence of chronic liver disease. Peptic ulcer disease remains the most common cause of non-variceal UGIB. Typically, UGIB presents with frank haematemesis, coffee-ground vomiting, melaena (the passage of dark, tarry, smelly stools) or an unexpected drop in haemoglobin (Fig. 2).

Figure 2.

Causes of UGIB.

Peptic ulcer disease

Gastroduodenal ulcers are the most common cause of UGIB, defined as defects in the gastric or duodenal mucosa that extend through the muscularis mucosae. They occur secondarily to an imbalance in the acid-peptic activity in gastric secretions. The greatest risk factor for their development is the presence of Helicobacter pylori infection, a gram-negative spiral bacterium that colonises the superficial gastric mucosa via production of an alkaline micro-environment and induction of an inflammatory mucosal response (Li et al., 2010).

The use of non-steroidal anti-inflammatory medications (NSAIDs) is also strongly associated with the development of peptic ulcer disease. Damage is mediated by both local effects and the systemic effect of prostaglandin inhibition via blockage of cyclooxygenase enzymes (COX-1 and COX-2). Other implicated factors include physiological stress (such as severe burns (Curling’s ulcer) or head trauma (Cushing’s ulcer) and Zollinger–Ellison syndrome (a rare syndrome consisting of a triad of severe peptic ulcer disease, gastric acid hypersecretion and gastrinoma).

Clinical features include epigastric or retrosternal pain, nausea, bloating and early satiety. UGIB is the presenting symptom in only 10% of patients with peptic ulcer disease, with duodenal ulcers four times more likely to bleed than gastric ulcers. Duodenal ulcers are also more likely to result in massive haemorrhage, due to their typical location on the posterior wall with proximity to the gastroduodenal artery, although high, lesser curve gastric ulcers involving branches of the left gastric artery can also be severe (Palmer, 2004).

Oesophagitis

Causative factors involved in the development of oesophagitis include reflux disease, medications and infection. Erosive oesophagitis typically occurs in the distal oesophagus, in the context of gastro-oesophageal reflux disease, causing multiple irregular ulcerations. There is often a background history of heartburn, regurgitation, dysphagia and/or odynophagia. Oesophagitis may also be medication-induced; typical culprits include tetracycline, NSAIDs and bisphosphonates. In these cases, a single deep ulcer is normally found on endoscopy, usually in the proximity of the carina. In contrast, infectious oesophagitis typically involves the proximal oesophagus, with multiple circumferential ulcers. Causative organisms include herpes simplex and cytomegalovirus. Bleeding secondary to oesophagitis is unlikely to be life-threatening, typically presenting as ‘coffee-ground’ vomiting, rather than frank haematemesis.

Gastritis and duodenitis

These are inflammatory processes with associated mucosal injury, and although commonly identified at endoscopy, are not typically causative of significant upper gastroentestinal (GI) bleeds, unless associated with coagulopathy or anticoagulation. The apparent presentation of gastritis or duodenitis alone should prompt thorough investigation for missed lesions including ulcers or Dieulafoy lesion (a large, tortuous submucosal arteriole that may erode the overlying epithelium to cause haemorrhage), which may be difficult to identify. Many of the risk factors are shared with peptic ulcer disease, but there is an additional association with excessive alcohol consumption, autoimmune disease, radiation injury, chronic bile reflux and bariatric surgery.

Portal hypertensive gastropathy

Portal hypertensive gastropathy develops secondary to portal hypertension, as a consequence of chronic liver disease. There is congestion and ectasia of the gastric vessels, with friable overlying mucosa, which may lead to haemorrhage secondary to rupture. Bleeding is typically chronic, rarely acute and massive.

Varices

Varices are abnormally dilated veins of the porto-systemic venous anastomotic system, typically located in the distal oesophagus or stomach. These are a consequence of portal hypertension in approximately 50% of patients with liver cirrhosis. Likelihood increases with increasing severity of cirrhosis and haemorrhage is more typical in patients with a Child-Pugh class of B or C, with an average annual rate of up to 15% (Garcia-Tsao et al., 2007). Risk factors are therefore associated with conditions causing liver cirrhosis, including chronic alcohol abuse, chronic viral hepatitis, non-alcoholic fatty liver disease.

Mallory–Weiss syndrome

Mallory–Weiss syndrome is typified by longitudinal intramural dissections at the gastro-oesophageal junction, secondary to sudden increase in intra-abdominal pressure. Trigger factors include forceful retching or vomiting (initially typically non-bloody), straining to pass stool and severe coughing. Patients may complain of epigastric or back pain. Although often minor, with spontaneous resolution in 90% of cases, Mallory–Weiss tears have the propensity to be severe and lead to significant blood loss, which may prove to be fatal (Harris et al., 1993).

Clinical case scenario 2.

Ellie is a usually fit 23-year-old teacher, but reports passing fresh red blood mixed in with her stools and on wiping for 2 days. She has mild anal pain on opening her bowels. She has an aunt with inflammatory bowel disease and is anxious that this is the cause of her symptoms. She is mildly tachycardic, but other observations are normal. Her abdomen is soft and non-tender. She is unable to tolerate a rectal examination due to discomfort.

Causes of lower GI bleeding

These can be divided into anatomic, vascular, inflammatory and neoplastic causes. Anatomic and vascular bleeds are typically large volume and painless, whereas inflammatory causes are associated with abdominal pain and diarrhoea. LGIB typically presents with haematochezia; maroon or bright-red blood, depending on proximity to the rectum. Very rarely, right-sided colonic bleeds may present with melaena. It is also important to note that UGIB may mimic LGIB; they are responsible for up to 13% of presentations with haematochezia (Fig. 3).

Figure 3.

Causes of LGIB.

Diverticular disease

Colonic diverticular bleeding is the most common cause of brisk haematochezia in the adult population; it accounts for 30 to 50% of massive rectal bleeding. Colonic diverticulae are sac-like protrusions of mucosa and submucosa through the muscular layer of the colon, most commonly affecting the sigmoid. These herniations occur at clear points of weakness, corresponding to the penetration of the circular muscular layer of the colon by the vasa recta. Their aetiology is multi-factorial and not fully understood, although the prevalence of diverticulosis increases significantly with increasing age; from less than 20% at 40 years to 60% at 60 years. It is purported that abnormal colonic motility is the key predisposing factor in the development of diverticulae. Risk factors include low fibre, high fat and red meat diets, obesity and physical inactivity. Diverticular bleeding is an anatomic consequence of the diverticular formation itself with the penetrating vessel responsible for colonic weakness at that point separated from the bowel lumen only by mucosa. It is thus vulnerable to repetitive injury along its luminal aspect. Segmental weakening of the artery thus predisposes to luminal rupture. This typically occurs independently of diverticulitis and is most common in the right colon.

The most common presentation is painless haematochezia (bright red if left-sided, maroon, or rarely melaena, if right-sided). There are typically few additional abdominal symptoms, although some patients may suffer from the urge to defaecate, bloating or cramping. Clinical signs are related to degree of blood loss and subsequent shock with normal abdominal examination and evidence of blood on digital rectal examination. Bleeding stops spontaneously in approximately 75% of patients, although there is a significant risk of re-bleeding (up to 38%) (McGuire, 1994).

Angiodysplasia

Angiodysplasia is due to the formation of arteriovenous malformations, typically occurring in the caecum or ascending colon. It may be congenital (such as hereditary haemorrhagic telangiectasia) or acquired (secondary to chronic venous obstruction, causing dilation of feeding capillaries, loss of precapillary sphincteric competence, and thus, development of small tufts of arterio-venous communications). Incidence increases with age. It is the most common cause of LGIB in those over 65 years of age (Boley et al., 1977). It is associated with conditions, including aortic stenosis, von Willebrand’s disease and chronic renal failure. Unlike diverticular bleeding, angiodysplasia is of venous origin, and thus tends to be less dramatic. It presents with overt painless haematochezia, or more commonly with occult faecal loss and iron deficiency anaemia. These overt bleeding episodes tend to be intermittent and self-limiting.

Colorectal cancer

Adenocarcinomas comprise 90% of colorectal cancer, the fourth most common cancer in the UK, accounting for 11% of all new cancer diagnoses. Change in bowel habit is the most common presenting complaint (trending towards increased stool frequency), followed by rectal bleeding associated with change in bowel habit (Thompson et al., 2017). This haematochezia is typically mixed in with the stools, rather than coating them (as with haemorrhoidal disease). Bleeding occurs in a secondary manner to overlying erosion or ulceration of the carcinoma, and tends to be intermittent, recurrent and low-grade. It is responsible for up to 11% of cases of LGIB and more prevalent over 50 years of age. Other presenting features include iron deficiency anaemia, rectal or abdominal mass or abdominal pain. Patients may present with symptoms or signs of metastatic disease.

Colitis

Colitis is defined broadly as mucosal inflammation of the colon, and can be caused by multiple aetiologies, including infection, ischaemia, radiation and inflammatory bowel disease (IBD). Clinical presentation is similar regardless of underlying cause, although there may be distinguishing factors within the history, endoscopic appearances are often indistinguishable. Patients typically present with abdominal pain, haematochezia (usually mild), diarrhoea, fever and/or dehydration. Diagnosis is important because treatment regimens differ. Diagnosis relies on history, examination and histological assessment.

Ischaemic colitis is most prevalent in older adults with a specific set of cardiovascular risk factors. These include previous myocardial infarction, haemodialysis, aortic instrumentation (e.g. repair of abdominal aortic aneurysm), atrial fibrillation, heart failure and valvular disease. However, often there are no clear precipitating factors and it may occur in younger patients in a hypercoagulable state. It may be occlusive or non-occlusive in nature. It occurs as a result of transient reduction in blood flow, typically at ‘watershed’ colonic regions with reduced collateral circulation such as the splenic flexure and rectosigmoid junction. Non-occlusive ischaemia occurs in a secondary manner to hypotension, or primary mesenteric arterial vasoconstriction. Occlusive ischaemia is typically secondary to thrombo-embolic disease. In most cases bleeding is limited and stops with fluid resuscitation and treatment of the underlying cause.

Infective colitis may be attributable to numerous pathogens, with Shigella, Salmonella and Campylobacter the most common causative organisms (Talan et al., 2001). These can be isolated on routine stool culture. The history usually gives clues to the diagnosis.

IBD is an umbrella term that encompasses ulcerative colitis and Crohn’s disease. Ulcerative colitis (UC) is inflammation limited to the bowel mucosa, typically progressing in an ascending continuous fashion from the rectum. Crohn’s disease, by contrast, is typified by transmural inflammation affecting any part of the gastrointestinal tract, from the oral cavity to the peri-anal area. Haematochezia is far more common in UC but may also be present in Crohn’s disease. Extra-intestinal manifestations, including musculoskeletal, ocular and pulmonary disease also occur during an initial attack. Management for either subtype of IBD is aimed at induction and maintenance of remission.

Anal fissure

Anal fissures are small tears in the mucosa of the anus, characteristically occurring at the 6 o’clock position. They are typically due to constipation or the passage of hard stools. The majority heal within 1 to 2 weeks, but healing may be delayed by spasm of the anal sphincter muscles. Anal fissure is a relatively common with an incidence of 1 in 350 per head of population per year and typically affects 15 to 40 year olds, especially during pregnancy or in the early post-partum period. Presenting features include anal pain when passing stools and for approximately an hour afterwards (this can range from mild to severe) and bright red rectal bleeding during defaecation.

Haemorrhoids

Haemorrhoids (known colloquially as piles) are abnormal swellings or enlargements of the anal vascular cushions. These are located at the 3, 7 and 11 o’clock positions and normally assist the anal sphincter in maintenance of continence. However, if enlarged they can become pathological and symptomatic. Risk factors for their development include excessive straining (i.e. secondary to chronic constipation), increasing age, obesity and elevated intra-abdominal pressure (due to pregnancy, persistent cough or heavy lifting). Haemorrhoids can be distinguished according to anatomical position. Internal haemorrhoids originate above the dentate line (2 cm above the anal verge), whereas external haemorrhoids originate below. Piles can also be graded from first to fourth degree ranging from retention within the rectum (first) to persistent prolapse (fourth). This is a common pathology, affecting between 13 and 36% of the population, and is the most common cause of LGIB in patients less than 50 years old (Korkis et al., 1995). Haemorrhoids typically present with bright red painless rectal bleeding on defaecation. Blood characteristically coats the stools (not mixed with stools) or is found on the toilet paper with wiping. Other symptoms include a feeling of rectal fullness or tenesmus, awareness of a lump at the anal verge or anal itching secondary to chronic mucosal discharge. Rarely, haemorrhoids may prolapse and then strangulate and thrombose, causing severe pain.

Primary care assessment of GI bleeding

Patients should be evaluated with a full history and ABCDE approach to examination (Box 1). Although community-based assessment may be challenging, the focus should be on identifying those patients with evidence of haemodynamic compromise and/or risk factors for adverse outcomes. It is important to recognise that up to 15% of patients with signs and symptoms suggestive of LGIB, e.g. haematochezia are later determined to be of upper GI origin.

Box 1.

Pertinent questions to consider when taking a history.

Type of bleeding:

• Frank haematemesis: Suggestive of moderate to severe UGIB that may be ongoing

• Coffee ground vomiting: Suggestive of more limited UGIB

• Melaena: Typically indicative of UGIB, although may be associated with right-sided colonic bleeds

• Haematochezia: Suggestive of LGIB, although may be seen in massive upper GI bleeds

• Frank clots passed per rectum: Suggestive of LGIB

Associated symptoms:

• Epigastric pain: Peptic ulceration

• Odynophagia, dysphagia and/or reflux: Oesophagitis

• Prolonged retching or bloodless emesis: Mallory–Weiss tear

• Jaundice, ascites, peripheral stigmata of chronic liver disease:Variceal haemorrhage or portal hypertension

• Dysphagia, early satiety, cachexia, weight loss: Upper GI malignancy

• Painless haematochezia: Diverticular bleed or angiodysplasia

• Peri-anal pain: Anal fissure, solitary rectal ulcer or haemorrhoids

• Cramping lower abdominal pain and diarrhoea: Infectious, ischaemic or inflammatory colitis

• Change in bowel habit, cachexia, weight loss: Lower GI malignancy

Assessment of severity:

• Symptoms of anaemia/significant blood loss: Dyspnoea, pre-syncope or syncope, fatigue, palpitations, chest pain

• Estimated volume of blood loss: Often hard for patients to quantify

Past medical history suggestive of causative lesion:

• History of previous GI bleed (up to 60% of re-bleeds occur from the same lesion)

• Known chronic liver disease or alcohol excess: Variceal haemorrhage or portal hypertension

• Haemodialysis, aortic stenosis or hereditary haemorrhagic telangiectasia (HHT): angiodysplasia

• Known H.pylori infection: Peptic ulcer disease

• Gastro-oesophageal reflux disease: Oesophagitis

• Known diverticular disease/previous episodes of diverticulitis: Diverticular bleed

• Constipation: Diverticular disease, haemorrhoids, anal fissure

Past medical history affecting physiological response to haemorrhage:

• Increased sensitivity to anaemia: Coronary artery disease, pulmonary disease, cardiac failure

• Increased risk of aspiration: Dementia, hepatic encephalopathy

• Coagulopathies: Hepatic dysfunction, congenital disease e.g. von Willebrand’s disease, thrombocytopaenia

Medication history:

• NSAID (including aspirin) use: Predisposes to peptic ulcer disease

• Bisphosphonate, tetracycline or doxycycline use: Risk of medication-induced oesophagitis

• Anti-platelet (e.g. aspirin, clopidogrel) or anti-coagulant (e.g. rivaroxaban, warfarin) agents: Promotion of haemorrhage

• Bismuth or iron preparations: Can be confounding as turn stools black

A thorough ABCDE examination, including observations, abdominal and digital rectal examination should be undertaken. An estimation of the degree of blood loss can be made using the so called ‘Tennis’ staging of hypovolaemic shock (Table 1).

Table 1.

The ‘Tennis’ staging of hypovolaemic shock.

	Class of haemorrhagic shock
	I	II	III	IV
Blood loss (ml)	<750	750–1500	1500–2000	>2000
Blood loss (% blood volume)	<15%	15–30%	30–40%	>40%
Pulse rate (beats per minute)	<100	100–120	120–140	>140
Blood pressure	Normal	Normal	Decreased	Decreased
Pulse pressure	Normal or increased	Decreased	Decreased	Decreased
Capillary refill	Normal	Delayed	Delayed	Delayed
Respiratory rate (respirations per minute)	14–20	20–30	30–40	>35
Mental status	Slightly anxious	Anxious	Anxious and confused	Confused and lethargic

NB: Urine output is ml/hr also normally used as an indicator of shock, but this is difficult to assess in the primary care setting.

Adapted from the American College of Surgeons Advanced Trauma Life Support classification of haemorrhage severity.

Severity of GI bleeding

The severity of UGIB is usually with scoring systems. The Glasgow–Blatchford score and the Rockall score are most often used. Unlike the Rockall score, the Glasgow–Blatchford score does not take endoscopic findings into account and is used in the initial triage of severity. It requires blood tests and is not suitable for use in primary care where same-day blood results are not usually available.

There are no widely adopted scoring systems to predict the severity of LGIB. However, the Oakland score (Table 2) has been validated to determine whether bleeding is major or minor. Minor bleeds (score less than eight), have a 95% chance of safe discharge from the emergency department and are suitable for outpatient follow up (Oakland et al., 2017). This also requires blood tests, and again is not suitable for use in primary care. The shock index (heart rate/systolic blood pressure) is an additional tool used to identify unstable patients with either UGIB or LGIB.

Table 2.

Scoring systems used to predict severity of acute GI bleeding.

Glasgow-Blatchford Score		Rockall Score		Oakland Score
Variable	Score	Variable	Score	Variable	Score
Blood urea (mmol/L)		Age (years)		Age (years)
6.5–8	2	<60	0	<40	0
8–10	3	60–79	1	40–69	1
10–25	4	>80	2	>70	2
>25	6	Shock		Gender
Hb (g/L)		No evidence	0	Female	0
Men:		HR >100, SBP >100 mmHg	1	Male	1
120–130	1	HR >100, SBP <100 mmHg	2	Previous lower GI bleed
100–120	3	Comorbidity		No	0
<100	6	None	0	Yes	1
Women: 100–120	1	Cardiac failure, IHD, other major	2	Digital rectal examination findings
<100 Systolic BP (mmHg)	6	Renal or liver failure, metastatic malignancy	3	No blood Blood	0 1
100–109 90–99	1 2	Diagnosis (post-endoscopy)		Heart rate (bpm) <70	0
<90	3	Mallory–Weiss tears	0	70–89	1
Pulse >100/min	1	Other diagnoses	1	90–109	2
Hx and comorbidities Melaena	1	Malignancy of UGI tract	2	>110 Systolic blood pressure (mmHg)	3
Syncope	2			<90	5
Hepatic disease	2			90–119	4
Cardiac failure	2			120–129	3
				130–159	2
				>160	0
				Haemoglobin (g/L)
				<70	22
				70–89	17
				90–109	13
				110–129	8
				130–159	4
				>160	0

Source: Blatchford et al., (2000), Rockall et al. (1996) and Oakland et al. (2017).

Primary care management of GI bleeding

All patients with evidence of upper GI bleed should be transferred to hospital for oesophagogastroduodenoscopy (OGD). The timing of this (either within 24 hours, or urgently as an outpatient), will be determined by the secondary care team dependent on the patient’s clinical and biochemical parameters and risk-stratification scores.

Patients presenting with evidence of lower GI bleeding should be transferred to hospital for assessment, with a few important exceptions. Otherwise, healthy, haemodynamically stable patients with minimal self-terminating haematochezia and no red flag features may be suitable for urgent or 2-week-wait outpatient assessment. In patients less than 40 years of age, digital rectal examination and sigmoidoscopy may be sufficient evaluation (Pasha et al., 2014). However, guidelines suggest that colonoscopy is appropriate for all patients without an anorectal source of bleeding at initial evaluation and for those over 50 years of age with alarm symptoms or risk factors for colorectal cancer. It is important to note that the presence of anorectal disease, for example, fissure or haemorrhoids, does not preclude additional pathology. Any underlying suspicion of an alternative diagnosis must be investigated. In this patient cohort, it is imperative that appropriate safety netting advice is given.

In patients with evidence of peri-anal disease, conservative management in primary care is appropriate. Management of anal fissures aims to limit pain and keep stools soft during the healing process with fibre supplements (such as ispaghula or methylcellulose), dietary advice, adequate fluid intake, analgesia (avoiding opioids) and adjuncts such as lidocaine ointment. In chronic cases glyceryl trinitrate or diltiazem ointment may be used. Haemorrhoidal disease can also be managed conservatively with constipation relief and analgesics if required.

If there is a failure of conservative management, secondary care options include sphincterotomy (for chronic, non-healing fissures) and a variety of surgical and non-surgical options for haemorrhoidal disease, including rubber band ligation, injection sclerotherapy and haemorrhoidectomy.

Secondary care management of GI bleeding

Management in secondary care includes ABCDE assessment and resuscitation to achieve haemodynamic stability. This may involve fluid resuscitation with crystalloids, blood transfusion, correction of underlying coagulopathy and management specific for the suspected cause of bleeding.

Patients with suspected variceal bleeds may receive terlipressin and antibiotics (Tripathi et al., 2015). Terlipressin is an analogue to vasopressin, causing an increase in systemic vascular resistance, reduction in cardiac output and reduction of portal pressures by approximately 20%. Cirrhotic patients presenting with acute upper GI bleed often have concurrent bacterial infections, which increase the risk of re-bleeding. There is evidence that the use of prokinetics (e.g. erythromycin infusion) may improve mucosal visualisation at endoscopy (Rahman et al., 2016). Evidence for use of proton pump inhibitors (PPIs) prior to endoscopy is conflicting in suspected peptic ulcer or erosive disease. The European Society of Gastrointestinal Endoscopy recommends use of PPIs (Gralnek et al., 2015). The National Institute for Health and Care Excellence (NICE) does not because of concerns that it may mask stigmata of haemorrhage and therefore therapeutic targets (NICE, 2012).

Endoscopic management of non-variceal UGIB may involve localised adrenaline injections, thermal haemostasis (using monopolar diathermy or argon plasma coagulation), endoclips or topical haemostatic agents such as hemospray. For variceal UGIB, endoscopic options include band ligation, sclerotherapy and Sengstaken tube insertion.

Patients with LGIB are managed according to their stability. For unstable bleeding (shock index greater than one) the first line investigation is computerised tomography angiogram, followed by treatment with interventional radiography or endoscopy. If stable (shock index less than one) the first line investigation is colonoscopy (with OGD if there is any suspicion of upper GI bleed). Termination of bleeding may be achieved with endoscopic intervention, transcatheter mesenteric embolization and surgery (for example segmental or subtotal colectomy). However, the vast majority of lower GI bleeds will resolve spontaneously (Oakland et al., 2018).

Following investigation and/or primary intervention, further management depends on the underlying diagnosis. Examples of treatment include H.pylori eradication (where appropriate for peptic ulcer disease), long term use of PPIs (for example, omeprazole in gastritis or oesophagitis), secondary prophylaxis using beta blockers (for example, propranolol or carvedilol if varices present) and treatment of underlying liver disease.

There may be a requirement for induction and maintenance of remission in a new diagnosis of IBD, treatment of infective colitis (with appropriately targeted antibiotics) and modification of cardiovascular risk factors in ischaemic colitis.

KEY POINTS

Acute gastrointestinal bleeding can be divided anatomically dependent on the location relative to the ligament of Treitz (upper GI bleeds are proximal, lower GI bleeds are distal)

Upper GI bleeds typically present with haematemesis, coffee-ground vomiting and/or melaena

Lower GI bleeds typically present with haematochezia (frank bright red or maroon blood passed per rectum)

A thorough history and ABCDE assessment (including digital rectal examination) in primary care is an essential component of management and enables recognition of signs and symptoms indicative of haemodynamic instability

Most patients will require same-day referral to secondary care, for risk-stratification and intervention as required

A small cohort of haemodynamically stable, otherwise healthy patients with minimal self-limited LGIB may be suitable for outpatient investigation and management

Footnotes

ORCID iD

Victoria Evans

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