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__NOTOC__
Lower GI bleeding is defined as any bleed that occurs distal to the ligament of Treitz.
==Incidence==
*In the United States the incidence of LGIB ranges from 20.5 to 27 per 100,000 persons per year.
==Age==
*There is a greater than 200 fold increase from the third to the ninth decade of life.
==Classification==
*Lower GI bleeding can be classified into 3 groups based on the severity of bleeding:
**Occult lower GI bleeding
**Moderate lower GI bleeding
**Severe lower GI bleeding


{{CMG}}<br>
{| class="wikitable"
{{SK}} sleeping sickness, Human African trypanosomiasis
!
==Overview==
!Severe lower GI bleeding
Human African trypanosomiasis, also known as sleeping sickness, is a vector-borne parasitic disease. It is caused by infection with protozoan parasites belonging to the genus Trypanosoma. They are transmitted to humans by tsetse fly (Glossina genus) bites which have acquired their infection from human beings or from animals harbouring human pathogenic parasites.Tsetse flies are found just in sub-Saharan Africa though only certain species transmit the disease. For reasons that are so far unexplained, in many regions where tsetse flies are found, sleeping sickness is not. Rural populations living in regions where transmission occurs and which depend on agriculture, fishing, animal husbandry or hunting are the most exposed to the tsetse fly and therefore to the disease. The disease develops in areas ranging from a single village to an entire region. Within an infected area, the intensity of the disease can vary from one village to the next.
!Moderate lower GI bleeding
==Overview==
!Occult lower GI bleeding
African trypanosomiasis has been present in Africa since at least the 14th century, and probably for thousands of years before that. The causative agent and vector were not identified until 1902–1903 by [[David Bruce (microbiologist)|Sir David Bruce]], and the differentiation between protozoa was not made until 1910. The first effective treatment, [[Atoxyl]], an [[arsenic]] based drug developed by [[Paul Ehrlich]] and [[Kiyoshi Shiga]] was introduced in 1910 but blindness was a serious side effect. Numerous drugs designed to treat the disease have been introduced since then.
|-
|Age
|> 65 years
|Occur at any age
|Any age
|-
|Presenting symptoms
|Hematochezia or bright red blood per rectum.
|Hematochezia or melena.
|Symptoms of anemia (fatigue, tirdness)
|-
|Hemodynamics
|Unstable
|Stable
|Stable
|-
|Lab findings
|hemoglobin equal to or less than 6 g/dl.
|Microcytic anemia
|Microcytic hypochromic anemia due to chronic blood loss.
|-
|Differential
|Diverticulosis and angiodysplasias
|Neoplastic disease Inflammatory, <nowiki><br></nowiki> infectious, benign anorectal, and congenital diseases.
|Inflammatory, neoplastic and congenital.
|}


There have been three severe epidemics in Africa over the last century: one between 1896 and 1906, mostly in Uganda and the Congo Basin, one in 1920 in several African countries, and one that began in 1970 and is still in progress. The 1920 epidemic was arrested due to mobile teams systematically screening millions of people at risk. The disease had practically disappeared between 1960 and 1965. After that success, screening and effective surveillance were relaxed and the disease has reappeared in endemic form in several foci over the last thirty years.
==Blood supply==
<ref>{{cite paper
* The SMA and IMA are connected by the marginal artery of Drummond.
  |author=WHO Media centre
* This vascular arcade runs in the mesentery close to the bowel.
  |title=Fact sheet N°259: African trypanosomiasis or sleeping sickness
* As patients age, there is increased incidence of occlusion of the IMA.  
  |date=2001
* The left colon stays perfused, primarily because of the marginal artery.
  |url=http://www.who.int/mediacentre/factsheets/fs259/en/index.html
{| border="1" cellpadding="5" cellspacing="0" align="center" |class="wikitable"
}}</ref>
! colspan="2" align="center" style="background:#4479BA; color: #FFFFFF;" |Lower GI Tract
! align="center" style="background:#4479BA; color: #FFFFFF;" | Arterial Supply
! align="center" style="background:#4479BA; color: #FFFFFF;" |Venous Drainage
|-
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |Midgut
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Distal duodenum jejunum
* Ileum
* Appendix
* Cecum
* Ascending colon
* Hepatic flexure
* Proximal transverse colon.
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Superior mesenteric artery (SMA)
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Portal system.
|-
| style="padding: 5px 5px; background: #DCDCDC;" align="center" |Hindgut
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Distal one-third of the transverse colon
* Splenic flexure
* Descending colon,
* Sigmoid colon
* Rectumhu
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Inferior mesenteric artery (IMA)
| style="padding: 5px 5px; background: #F5F5F5;" align="left" |
* Portal system '''<sup>ɸ</sup>'''
|-
| colspan="4" style="padding: 5px 5px; background: #F5F5F5;" align="center" |ɸ -Except lower rectum, which drains into the systemic circulation.
|}


==Historical Perspective==
[[Image: Colonic blood supply1.gif|thumb|center|300px|Blood supply to the intestines includes the celiac artery, superior mesenteric artery (SMA), inferior mesenteric artery (IMA), and branches of the internal iliac artery (IIA). <br>Source: By Anpol42 (Own work) [CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0)], via Wikimedia Commons]]
===Drug Developments===
[[Suramin]] was introduced in 1920 to treat the first stage of the disease.   By 1922, Suramin was generally combined with Tryparsamide (another pentavalent organo-arsenic drug) in the treatment of the second stage of the gambiense form. It was used during the grand epidemic in West and Central Africa in millions of people and was the mainstay of therapy until 1969.  


[[Pentamidine]], a highly effective drug for the first stage of the disease, has been used since 1939. During the fifties, it was widely used as a [[prophylactic]] agent in Western Africa, leading to a sharp decline in infection rates. At the time, it was thought that eradication of the disease was at hand.
===Pathogenesis===
Diverticulosis is the most common etiology of lower GI bleeding accounting for 30% of all cases, followed by anorectal disease, ischemia, inflammatory bowel disease (IBD), neoplasia and arteriovenous (AV) malformations.
*'''<u>Diverticulosis</u>'''
**The colonic wall weakens with age and results in the formation of saclike protrusions known as diverticula.
**These protrusions generally occur at the junction of blood vessel penetrating through the mucosa and circular muscle fibers of the colon.
**Diverticula are most common in the descending and sigmoid colon.
**Despite the majority of diverticula being on the left side of the colon, diverticular bleeding originates from the right side of the colon in 50% to 90% of instances.
**Most of the time bleeding from diverticulosis stops spontaneously, however, in about 5% of patients, the bleeding can be massive and life-threatening.
[[Image:Sigmoid diverticulum (diagram).jpg|thumb|center|400px|Diagram of sigmoid diverticulum<br>Source:By Anpol42 (Own work) [CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0)], via Wikimedia Commons]]
*'''<u>Anorectal disease</u>'''
:*Hemorrhoids and anal fissures are the most common disease under anorectal disease responsible for GI bleeding.
:*Hemorrhoids are engorged vessels in the normal anal cushions. When swollen, this tissue is very friable and susceptible to trauma, which leads to painless, bright red bleeding.
:*Anal fissures are defined as a tear in the anal mucosa. With the passage of stool, the mucosa continues to tear and leads to bright red bleeding.
*'''<u>Mesenteric Ischemia</u>'''
:*Mesenteric ischemia results when there is inadequate blood supply at the level of the small intestine.
:*2 or more vessels (celiac, SMA, or IMA) must be involved for symptoms to occur.
:*Non occlusive mesenetric ischemia affects critically ill patients who are vasopressor-dependent.
:*Venous thrombosis of the visceral vessels can also precipitate an acute ischemic event.
*'''<u>Ischemic Colitis</u>'''
:*Ischemic colitis is caused by poor perfusion of the colon, which results in the inability of that area of the colon to meet its metabolic demands.
:*It can be gangrenous or nongangrenous, acute, transient, or chronic.
:*The left colon is predominantly affected, with the splenic flexure having increased susceptibility.
:*Intraluminal hemorrhage occurs as the mucosa becomes necrotic, sloughs, and bleeds.
:*Damage to the tissue is caused both with the ischemic insult as well as reperfusion injury.
*'''<u>Inflammatory Bowel Disease</u>'''
:*In Crohn's disease T cell activation stimulates interleukin (IL)-12 and tumor necrosis factor (TNF)-a, which causes chronic inflammation and tissue injury.
:*Initially, inflammation starts focally around the crypts, followed by superficial ulceration of the mucosa.
:*The deep mucosal layers are then invaded in a noncontinuous fashion, and noncaseating granulomas form, which can invade through the entire thickness of the bowel and into the mesentery and surrounding structures.
:*In ulcerative colitis T cells cytotoxic to the colonic epithelium accumulate in the lamina propria, accompanied by B cells that secrete immunoglobulin G (IgG) and IgE.
:*This results in inflammation of the crypts of Lieberkuhn, with abscesses and pseudopolyps.
:*Ulcerative colitis generally begins at the rectum and is a continuous process confined exclusively to the colon.
*'''<u>Neoplasia</u>'''
:*Colon carcinoma follows a distinct progression from polyp to cancer.
:*Mutations of multiple genes are required for the formation of adenocarcinoma, including the APC gene, Kras, DCC, and p53.
:*Certain hereditary syndromes are also classified by defects in DNA mismatch repair genes and microsatellite instability.
:*These tumors tend to bleed slowly, and patients present with hemocult positive stools and microcytic anemia.
:*Although cancers of the small bowel are much less common than colorectal cancers, they should be ruled out in cases of lower GI bleeding in which no other source is identified.
*'''<u>AV Malformation/Angiodysplasia</u>'''
:*In AV malformation direct connections between arteries and veins occur in the colonic submucosa.
:*The lack of capillary buffers causes high pressure blood to enter directly into the venous system, making these vessels at high risk of rupture into the bowel lumen.
:*In Angiodysplasia over time, previously healthy blood vessels of the cecum and ascending colon degenerate and become prone to bleeding.
:*Although 75% of angiodysplasia cases involve the right colon, they are a significant cause of obscure bleeding and the most common cause of bleeding from the small bowel in the elderly.
==Epidemiology==
===Prevalence===
*Approximately 20 patients/100,000 population in the U.S.
===Incidence===
*The estimated annual incidence of lower GI bleeding is approximately 0.03% in the adult population as a whole.
==Demographics==
===Gender===
*More common in men than women
===Age===
*Rare in children
*The incidence of lower GI bleeding increases with age with a 200-fold increase from the second to eighth decades of life la.
**Largely due to the increase in the prevalence of diverticular disease and angiodysplasia with age.
==Symptoms==
*Occult LGIB may present with symptoms of iron deficiency anemia such as fatigue, palpitations, and dyspnea.
*Patients with intussusception may present with pallor and vomiting in addition to LGIB
*Associated symptoms, such as abdominal pain or change in bowel habits, may also aide in the diagnosis
*Bloody diarrhea associated with abdominal pain may suggest an infectious cause or IBD in a younger patient and ischemic colitis in an older patient with vascular disease
*Painless bleeding usually suggests angiodysplasia, diverticular disease, or internal hemorrhoids
*Perianal pain suggests a perianal fissure or fistula
==History==
*A detailed description of the nature of the blood loss can help in pinpointing the likely source of bleeding.
===Past Medical History===
*The clinical history should identify whether this is a recurrent bleed.
*Bleeding from angiodysplasia is usually recurrent and chronic, but severe bleeding resulting in hemodynamic instability can occur.
*Associated weight loss suggests malignancy.
*The presence of systemic diseases such as atherosclerotic disease, IBD, coagulopathies, and HIV, and a history of pelvic irradiation for malignancy should be considered
===Past Surgical History===
*A history of recent colonic polypectomy or biopsy indicates iatrogenic bleeding.
**This is usually low grade and limited, although it can be severe if an underlying artery is involved or if there is an inadequate coagulation of the polypectomy stalk.
**In 1.5% of polypectomies bleeding occurs immediately. However, delayed bleeding can occur several hours or days following the procedure
*It is essential to establish the presence of comorbid diseases, as these not only help in diagnosis but may also influence treatment.
===Family history===
*A family history of diseases such as IBD or colorectal malignancy is relevant.
==Symptoms==
*The clinical presentation of LGIB varies with the anatomic source of the bleeding.  
*Commonly, LGIB from the right side of the colon can manifest as maroon stools, whereas a left-sided bleeding source may be evidenced by bright red blood per rectum.
*The presentation of LGIB can also vary depending on the etiology.
**A young patient may present with fever, dehydration, abdominal cramps, and hematochezia caused by infectious or noninfectious (idiopathic) colitis.
**An older patient may present with painless bleeding and minimal symptoms caused by diverticular bleeding or angiodysplasia.
**LGIB can be mild and intermittent, as often is the case with angiodysplasia, or it may be moderate or severe, as may be the situation in diverticula-related bleeding.
**Young patients may present with abdominal pain, rectal bleeding, diarrhea, and mucous discharge that may be associated with IBD.
** Elderly patients presenting with abdominal pain, rectal bleeding, and diarrhea may have ischemic colitis.
** Elderly patients with atherosclerotic heart disease may present with intermittent LGIB and syncope that may be due to angiodysplastic lesions.
** Stools streaked with blood, perianal pain, and blood drops on the toilet paper or in the toilet bowl may be associated with perianal pathology, such as anal fissure or hemorrhoidal bleeding.
** The passage of maroon stools or bright red blood from the rectum is usually indicative of massive lower GI hemorrhage.
* Massive LGIB is a life-threatening condition in which patients present with a systolic blood pressure (SBP) of below 90 mm Hg and a hemoglobin (Hb) level of 6 g/dL or less.  
{| class="wikitable"
! colspan="2" |Disease
!Symptoms
|-
| colspan="2" |Diverticular bleeding
|Painless bleeding
Mild abdominal cramping


The organo-arsenical [[melarsoprol]] (Arsobal) was developed in the 1940s, and is effective for patients with second stage sleeping sickness. However, 3 - 10% of those injected have reactive [[encephalopathy]] (convulsions, progressive coma, or psychotic reactions), and 10 - 70% die; it can cause [[brain damage]] in those that survive the encephalopathy. However, due to its effectiveness, [[melarsoprol]] is still used today.  Resistance to melarsoprol is increasing, and combination therapy with nifurtimox is currently under research.
If the bleeding is brisk and voluminous, patients may be hypotensive and display signs of shock
|-
| colspan="2" |Angiodysplasia
|Painless, hematochezia or melena (slow but repeated bleeding episodes)
Syncope
|-
| rowspan="4" |Colitis
|Ischemic colitis
| rowspan="4" |Fever
Abdominal pain


[[Eflornithine]] (difluoromethylornithine or DFMO), the most modern treatment, was developed in the 1970s by Albert Sjoerdsmanot and underwent clinical trials in the 1980s. The drug was approved by the United States [[Food and Drug Administration]] in 1990, but [[Aventis]], the company responsible for its manufacture, halted production in 1999.  In 2001, however, Aventis, in association with [[Médecins Sans Frontières]] and the [[World Health Organization]], signed a long-term agreement to manufacture and donate the drug.
Bloody diarrhea


===Biological Understanding of African Trypanosomiasis===
Dehydration
The genome of the parasite has been decoded and several proteins have been identified as potential targets for drug treatment. The decoded DNA also revealed the reason why generating a vaccine for this disease has been so difficult. ''T. brucei'' has over 800 genes that manufacture proteins that the disease mixes and matches to evade immune system detection.<ref>{{cite journal |author=Berriman M, Ghedin E, Hertz-Fowler C, ''et al'' |title=The genome of the African trypanosome Trypanosoma brucei |journal=Science |volume=309 |issue=5733 |pages=416-22 |year=2005 |pmid=16020726 |doi=10.1126/science.1112642 |url=http://www.sciencemag.org/cgi/content/full/309/5733/416}}</ref>


Recent findings indicate that the parasite is unable to survive in the bloodstream without its [[flagellum]]. This insight gives researchers a new angle with which to attack the parasite.<ref>{{cite web | title=African Sleeping Sickness Breakthrough | url=http://domino.lancs.ac.uk/info/LUNews.nsf/I/448E635736B6B25A8025714700317FD1 | accessdate=April 7 | accessyear=2006 }}</ref>
Hypotension in severe cases


A new treatment based on a truncated version of the apolipoprotein L-1 of [[high density lipoprotein]] and a nanobody has recently been found to work in mice, but has not been tested in humans.<ref>
Weight loss
[[New Scientist]], [http://www.newscientist.com/channel/health/mg19526181.400-cholesterol-secret-of-our-killer-blood.html 25 Aug. 2007, pp. 35-7]
|-
</ref>
|Infectious colitis
|-
|Radiation-induced colitis
|-
|Ulcerative colitis
|-
| colspan="2" |Colon cancer
|Right-sided bleeding (Maroon stools or melena)
Insidious


===Research===
Patients presents with iron-deficiency anemia and syncope
An international research team working in the Democratic Republic of the Congo, Southern Sudan and Angola involving Immtech International and University of North Carolina at Chapel Hill have completed a [[Phase IIb]] clinical trial and commenced a [[Phase III]] trial in 2005 testing the efficacy of the first oral treatment for Sleeping Sickness, known at this point as "DB289".
<ref>{{cite news
  |first=David
  |last=Williamson
  |title=Compound might defeat African sleeping sickness, clinical trial beginning this month
  |date=August 25, 2005
  |publisher=University of North Carolina
  |url=http://usinfo.state.gov/xarchives/display.html?p=washfile-english&y=2005&m=August&x=20050826160501cmretrop0.7327387&t=livefeeds/wf-latest.html
}}</ref>
<ref>{{cite news
  |author=Staff
  |page=5
  |title=Clinical Trials Update
  |date=September 15, 2005
  |publisher=[[Genetic Engineering News]]
}}</ref>


==Pathophysiology==
Whereas left-sided colonic neoplasms can present as bright red blood per rectum
===Transmission===
|-
*The disease is mostly transmitted through the bite of an infected tsetse fly but there are other ways in which people are infected:
| colspan="2" |Hemorrhoids
*Mother-to-child infection: the trypanosome can cross the placenta and infect the fetus.
|Painless, whereas bleeding secondary to fissures tends to be painful.
*Mechanical transmission through other blood-sucking insects is possible, however, it is difficult to assess its epidemiological impact.
Can also present with strangulation, hematochezia, and pruritus.
*Accidental infections have occurred in laboratories due to pricks with contaminated needles.
|}
*Transmission of the parasite through sexual contact has been documented.
===Common causes===
Human African trypanosomiasis takes 2 forms, depending on the parasite involved:
*Colonic diverticulosis
===Trypanosoma brucei gambiense===
**Colonic diverticulosisis the most common cause of acute LGIB in the western world, accounting for 15% to 55% of all LGIB
*Trypanosoma brucei gambiense is found in 24 countries in west and central Africa.  
**Diverticula can occur anywhere in the gastrointestinal tract, but are most common in the sigmoid colon. However, approximately 60% of diverticular bleeds arise from diverticula in the right colon, highlighting a tendency for right-sided diverticula to bleed
*This form currently accounts for 97% of reported cases of sleeping sickness and causes a chronic infection.  
**Hemorrhage results from rupture of the intramural branches (vasa recta) of the marginal artery at the dome of a diverticulum and can give rise to a massive, life-threatening LGIB
*A person can be infected for months or even years without major signs or symptoms of the disease.
**This is by far the most common cause of bleeding in the elderly, as the prevalence of diverticular disease increases with age, being as high as 85% by the age of 85 years
*When more evident symptoms emerge, the patient is often already in an advanced disease stage where the central nervous system is affected.
 
===Trypanosoma brucei rhodesiense ===
* Obesity has recently been recognized as a risk factor in the development of diverticular disease, and the risk of diverticular bleeding in this group of patients is higher than that in patients who are not obese
*Trypanosoma brucei rhodesienseis found in 13 countries in eastern and southern Africa.
* Vascular ectasias (angiodysplasias/angioectasias):
*Nowadays, this form represents under 3% of reported cases and causes an acute infection.  
** Tortuous dilated submucosal vessels that account for approximately 10% of LGIB.  
*First signs and symptoms are observed a few months or weeks after infection.
** They appear endoscopically as small, flat lesions (5-10 mm) with ectatic capillaries radiating from a central vessel (Fig. 1)
*The disease develops rapidly and invades the central nervous system. Only Uganda presents both forms of the disease, but in separate zones.
** The prevalence of angiodysplasia in the gastrointestinal tract is not well known, but a pooled analysis of three colonoscopic cancer screening studies detected angiodysplasia in 0.8% of the patients The prevalence of angiodysplasia is higher in older populations and, in the past, has been linked to certain conditions such as end-stage renal disease, Von Willebrand disease , and aortic stenosis In one series, 37% of colonic dysplasias were found in the cecum, 17% in the ascending colon, 7% in the transverse colon, 7% in the descending colon, and 32% in rectosigmoid area
===American trypanosomiasis or Chagas disease===
** Angiodysplasia can also be found throughout the small bowel and is responsible for up to 40% of small intestinal bleeding in patients older than 40 years.
*Another form of trypanosomiasis occurs mainly in Latin America.
** Angiodysplasia of the stomach and duodenum is responsible for up to 7% of UGIB I
*The causal organism belongs to a different Trypanosoma subgenus and is transmitted by a different vector.
* Iatrogenic:
===Animal trypanosomiasis===
** Bleeding is recognized as the most common complication of colonoscopy and polypectomy, occurring in 0.3% to 6.1% of polypectomies
*Other parasite species and sub-species of the Trypanosoma genus are pathogenic to animals and cause animal trypanosomiasis in wild and domestic animals.
** Risk factors for bleeding include polyp size greater than 1 cm, patient age older than 65 years, presence of comorbid disease, and polypectomy using the cutting mode of current
*In cattle the disease is called Nagana.
** The risk is also greater in patients taking anticoagulant or antiplatelet agents
*Trypanosomiasis in domestic animals, particularly in cattle, is a major obstacle to the economic development of affected rural areas.
* Ischemic colitis:
** Ischemic colitis accounts for approximately 20% of LGIB
** Ischemia results from a sudden reduction in blood flow to the mesenteric vessels as a result of hypotension, occlusion, or spasm of the mesenteric vessels
** Nonocclusive disease typically affects the watershed areas of the bowels, such as the splenic flexure and adjacent transverse colon due to the poor blood supply from the marginal artery.
** Occlusive disease is rarer but can occur as a result of thrombus formation or embolus.  
** It is a recognized complication of aortic surgery
** Elderly patients with comorbid disease are at higher risk of developing ischemic colitis.
** There may be a history of ischemic heart disease
** The majority of patients with ischemic colitis improve following conservative management; however, approximately 20% will progress to develop colonic gangrene
** Other complications include chronic colitis and stricture formation
** Diagnosis requires a high index of suspicion
* Colorectal malignancy:
** Colorectal cancer accounts for approximately 10% of bleeds, either as occult bleeding presenting with anemia or as frank blood loss per rectum
** A family history of colorectal cancer is important to establish
* Anorectal abnormalities:
** Hemorrhoids, fissures, fistulae, and polyps can all present with bright red rectal bleeding, which may be intermittent in nature
** Hemorrhoids are the most common cause of rectal bleeding in adults younger than 50 years
** The finding of hemorrhoids in older patients with LGIB should not preclude further investigation, as hemorrhoids are an extremely common finding and may not be the cause of bleeding
* Inflammatory bowel disease (IBD):
** IBD refers to both Crohn disease and ulcerative colitis Accounts for 5% to 10% of bleeds.
** It is by far the most common cause of LGIB in Asian populations in whom the prevalence of diverticular disease is much lower
** A previous history of IBD in patients with LGIB is important, as these patients have a higher risk of developing colorectal malignancy than do the general population
* Infectious colitis:
** The most common organisms in the U.S. are species ofSalmonella,Campylobacter,Shigella, andYersinia
 
=== Rare causes ===
* Colonic polyps:
** These can occur in isolation or as part of an inherited polyposis syndrome
** Can cause occult or overt LGIB
 
* Radiation proctitis:
** This usually occurs a few months following ionizing radiation for pelvic malignancies (Fig. 2). In one study of patients with radiation proctitis following pelvic irradiation, 69% presented with bleeding within 1 year and 96% within 2 years


Animals can host the human pathogen parasites, especially T.b. rhodesiense, of which domestic and wild animals are an important reservoir. Animals can also be infected with T.b. gambiense and act as a reservoir to a lesser extent. However the precise epidemiological role of the animal reservoir in the gambiense form of the disease is not yet well known.
* Rectal varices:
** Associated with portal hypertension; may result in massive bleeding
** Stercoral ulceration:
** Can cause significant fresh rectal bleeding in elderly constipated patients


Major human epidemics
* Meckel diverticulum:
There have been several epidemics in Africa over the last century:
** These small bowel diverticula may contain ectopic gastric mucosa that can ulcerate and cause bleeding
** They are the most common cause of massive LGIB in young children, and can be diagnosed with angiography, Meckel scans, and radionuclide imaging


one between 1896 and 1906, mostly in Uganda and the Congo Basin;
* Intussusception :
one in 1920 in a number of African countries; and
** More common in children, with the highest incidence between the ages of 6 months and 2 years
the most recent epidemic started in 1970 and lasted until the late 1990s.
* Henoch-Schönlein purpura (HSP):
The 1920 epidemic was controlled thanks to mobile teams which carried out the screening of millions of people at risk. By the mid-1960s, the disease was under control with less than 5000 cases reported in the whole continent. After this success, surveillance was relaxed, and the disease reappeared, reaching epidemic proportions in several regions by 1970. The efforts of WHO, national control programmes, bilateral cooperation and nongovernmental organizations (NGOs) during the 1990s and early 21st century reversed the curve.
** Most commonly affects children
** Bleeding may be a direct result of vasculitis or secondary to intussusception, which is associated with HSP
* Aortoenteric fistula:


Since the number of new human African trypanosomiasis cases reported between 2000 and 2012 dropped by 73%, the WHO neglected tropical diseases roadmap targeted its elimination as a public health problem by 2020.
* Abdominal aortic aneurysms, especially those of the inflammatory type, may fistulate into the small bowel, giving rise to a massive, life-threatening hemorrhage


Disease burden
* Peutz-Jeghers syndrome:
** Polyps may give rise to frank or occult bleeding
* Klippel-Trenaunay-Weber syndrome:
** Hemangiomas in the colon can cause significant bleeding


Sleeping sickness threatens millions of people in 36 countries in sub-Saharan Africa. Many of the affected populations live in remote rural areas with limited access to adequate health services, which complicates the surveillance and therefore the diagnosis and treatment of cases. In addition, displacement of populations, war and poverty are important factors that facilitate transmission.
* Hereditary hemorrhagic telangiectasia:
** Blood loss from mucosal telangiectasia can be chronic or acute
* Neurofibromatosis :
** Neurofibromas within the lumen of the bowel can ulcerate, causing bleeding
* Blue rubber bleb syndrome:
** Bleeding can arise from hemangiomas in the bowel Usually occult in nature
**


In 1998, almost 40 000 cases were reported, but estimates were that 300 000 cases were undiagnosed and therefore untreated.
=== Risk factors ===
During the most recent epidemic the prevalence reached 50% in several villages in Angola, the Democratic Republic of the Congo, and South Sudan. Sleeping sickness was the first or second greatest cause of mortality in those communities, even ahead of HIV/AIDS.
Common risk factors in the development of lower GI bleeding include:<ref name="pmid23997409">{{cite journal |vauthors=Navuluri R, Kang L, Patel J, Van Ha T |title=Acute lower gastrointestinal bleeding |journal=Semin Intervent Radiol |volume=29 |issue=3 |pages=178–86 |year=2012 |pmid=23997409 |pmc=3577586 |doi=10.1055/s-0032-1326926 |url=}}</ref><ref name="pmid16303575">{{cite journal |vauthors=Strate LL |title=Lower GI bleeding: epidemiology and diagnosis |journal=Gastroenterol. Clin. North Am. |volume=34 |issue=4 |pages=643–64 |year=2005 |pmid=16303575 |doi=10.1016/j.gtc.2005.08.007 |url=}}</ref><ref name="pmid17131153">{{cite journal |vauthors=Ríos A, Montoya MJ, Rodríguez JM, Serrano A, Molina J, Ramírez P, Parrilla P |title=Severe acute lower gastrointestinal bleeding: risk factors for morbidity and mortality |journal=Langenbecks Arch Surg |volume=392 |issue=2 |pages=165–71 |year=2007 |pmid=17131153 |doi=10.1007/s00423-006-0117-6 |url=}}</ref><ref name="pmid12695275">{{cite journal |vauthors=Strate LL, Orav EJ, Syngal S |title=Early predictors of severity in acute lower intestinal tract bleeding |journal=Arch. Intern. Med. |volume=163 |issue=7 |pages=838–43 |year=2003 |pmid=12695275 |doi=10.1001/archinte.163.7.838 |url=}}</ref>
In 2009, after continued control efforts, the number of cases reported dropped below 10 000 (9878) for the first time in 50 years. This decline in number of cases has continued with 2804 new cases reported in 2015, the lowest level since the start of systematic global data-collection 76 years ago. The estimated number of actual cases is below 20 000 and the estimated population at risk is 65 million people.
* Advancing age
Current disease distribution
* Previous history of gastrointestinal bleed
The disease incidence differs from one country to another as well as in different parts of a single country.
* Chronic constipation
* Hematologic disorders
* Anticoagulants medications
* Nonsteroidal anti-inflammatory drugs
* Human immunodeficiency virus
{| class="wikitable"
|Chronic constipation
|Results in colonic diverticula and predispose patients to anal fissures and hemorrhoid formation
|-
|Hematologic disorders
|Deficiencies in clotting factors, such as factor VII and factor VIII, predispose persons to LGIB
|-
|Anticoagulants medications
|Patients taking warfarin and heparin, aspirin, and platelet inhibitors are at increased risk of bleeding in general
|-
|Nonsteroidal anti-inflammatory drugs
|NSAIDs cause ulceration in the terminal ileum and proximal colon, and can exacerbate IBD
|-
|Human immunodeficiency virus
|In patients with HIV, bleeding is caused by opportunistic infections, cytomegalovirus colitis, Kaposi sarcoma, or lymphoma
|}
==Management==
===Initial Evaluation===
*In patients with acute lower gastrointestinal bleeding who are unstable rapid assessment and resuscitation should be initiated even before diagnostic evaluation.  
*The initial steps in the management of a patient with lower gastrointestinal bleeding are to assess the severity of bleeding, and then institute fluid and blood resuscitation as needed.  
*Once hemodynamic stability is achieved, nasogastric lavage should be performed to rule of upper GI source.  
*Equilibration between the intravascular and extravascular volumes cannot be achieved until 24 to 72 hours after bleeding has occurred.


In the last 10 years, over 70% of reported cases occurred in the Democratic Republic of the Congo (DRC).
===Role of Nasogastric tube (NGT)===
The DRC is the only country that currently reports more than 1000 new cases annually and accounts for 84% of the cases reported in 2015.
*Nasogastric tube (NGT) lavage is recommended in all patients with lower gastrointestinal bleeding once the patient is stabilized.
Central African Republic is the only country that declared between 100 and 200 new cases in 2015.
*A carefully placed nasogastric tube (NGT) with irrigation and aspiration of bile is necessary to ensure sampling of duodenal contents.
Countries such as Angola, Burkina Faso, Cameroon, Chad, Congo, Côte d'Ivoire, Equatorial Guinea, Gabon, Gjana, Guinea, Malawi, Nigeria, South Sudan, Uganda, United Republic of Tanzania, Zambia and Zimbabwe are reporting fewer than 100 new cases per year.
*If there is a bloody NGT aspirate then an esophagogastroduodenoscopy (EGD) is warranted (11 to 15% of patients despite “negative” NGT aspirates are due to upper GI bleeding).
Countries like Benin, Botswana, Burundi, Ethiopia, Gambia, Guinea Bissau, Kenya, Liberia, Mali, Mozambique, Namibia, Niger, Rwanda, Senegal, Sierra Leone, Swaziland and Togo have not reported any new cases for over a decade. Transmission of the disease seems to have stopped in some of these countries but there are still some areas where it is difficult to assess the exact situation because the unstable social circumstances and/or difficult accessibility hinder surveillance and diagnostic activities.
*Obtaining clear fluid favors a lower GI source of bleeding.
==Epidemiology and demographics==
{| border="1" cellpadding="5" cellspacing="0" align="center" |class="wikitable"
There are two subspecies of the parasite Trypanosoma brucei that cause disease in humans. The clinical features of the infection depend on the subspecies involved. The two subspecies are found in different regions of Africa. At present, there is no overlap in their geographic distribution.
! colspan="2" style="background:#efefef;" | Workup and Initial Management
|-
|I'''nitial Evaluation'''
|
* Airway Breathing, Circulation
|-
|'''Supportive Therapy'''
|
* Ensure patent and protected airway


T. b. rhodesiense (East African sleeping sickness) is found in focal areas of eastern and southeastern Africa. Each year a few hundred cases are reported to the World Health Organization. Over 95% of the cases of human infection occur in Tanzania, Uganda, Malawi, and Zambia. Animals are the primary reservoir of infection. Cattle have been implicated in the spread of the disease to new areas and in local outbreaks. A wild animal reservoir is thought to be responsible for sporadic transmission to hunters and visitors to game parks. Infection of international travelers is rare, but it occasionally occurs. In the U.S., one case per year, on average, is diagnosed. Most cases of sleeping sickness imported into the U.S. have been in travelers who were on safari in East Africa.
* [[Intubation|Intubate]] if needed
* Consider [[mechanical ventilation]]


T. b. gambiense (West African sleeping sickness) is found predominantly in central Africa and in limited areas of West Africa. Most of the sleeping sickness in Africa is caused by this form of the parasite. Epidemics of sleeping sickness have been a significant public health problem in the past, but the disease is reasonably well-controlled at present, with 7,000-10,000 cases reported annually in recent years. Over 95% of the cases of human infection are found in Democratic Republic of Congo, Angola, Sudan, Central African Republic, Chad, and northern Uganda. Humans are the important reservoir of infection, although the parasite can sometimes be found in domestic animals (e.g., pigs, dogs, goats). Imported infection in the U.S. is extremely rare, and most cases have occurred in African nationals who have immigrated rather than in returning U.S. travelers.
* 2 large-bore, peripheral intravenous lines


* Can consider [[Central venous catheter|large-bore central venous catheter]] or intraosseous line if rapid transfuser will be needed
|-
|'''Blood transfusion'''
|
* Resuscitate with 1:1:1 of packed red blood cells (PRBCs) to fresh frozen plasma (FFP) to platelets.


*=Epidemiology and Demographics==
* Consider massive transfusion protocol
<!-- Image with unknown copyright status removed: [[Image:Sleepinggeographic.jpg|thumb|200px|right|Geographic distribution vector for sleeping sickness cases.]] -->


According to recent estimates, the disability adjusted life years (9 to 10 years) (DALYs) lost due to sleeping sickness are 2.0 million.<ref>{{cite paper
* Res:Low riskto a target hemoglobin of 7 mg/dL.
  |author=World Health Organization (Geneva)
  |title=World Health Report 2000: Health Systems Improving Performance
  |date=2000
  |url=http://www.who.int/tdr/diseases/tryp/direction.htm#Refs
}}</ref>


Recent estimates indicate that over 60 million people living in some 250 foci are at risk of contracting the disease, and there are about 300,000 new cases each year.<ref>{{cite paper
* Consider Sengstaken-Blakemore tube for control of immediately life-threatening upper GI bleeding
  |author=WHO Expert Committee on Control and Surveillance of African trypanosomiasis (Geneva)
|}
  |title=WHO Technical Report Series,No.881
===Assessment of severity of bleeding===
  |date=1998
{| border="1" cellpadding="5" cellspacing="0" align="center" |class="wikitable"
  |url=http://www.who.int/tdr/diseases/tryp/direction.htm#Refs
! colspan="1" style="background:#efefef;" | Bleeding severity
}}</ref>
! colspan="1" style="background:#efefef;" | Vital signs
The disease has been recorded as occurring in 36 countries, all in sub-Saharan Africa.
! colspan="1" style="background:#efefef;" | Blood loss
|-
|Minor
|Normal
|<10%
|-
|Moderate
|Postural hypotension
|10-20%
|-
|Severe
|Shock
|>25%
|}
===Fluid resuscitation===
*Two large caliber (16-gauge) peripheral catheters or a [[Central venous catheter|central venous line]] should be inserted in patients who are [[hemodynamically unstable]].
*The rate of fluid resuscitation is proportional to the severity of [[bleeding]] with the goal of restoring and maintaining the patient’s [[blood pressure]].
*Infusion of 500 mL of [[normal saline]] or lactated [[Ringer's lactate|Ringer's solution]] over 30 minutes is preferred treatment for patients with [[Bleeding|active bleeding]] before [[Blood type|blood type matching]] and blood [[transfusion]].
*Intensive monitoring with a [[pulmonary artery catheter]] is recommended to monitor the response of initial resuscitation efforts and any complications of fluid overload.
*If the blood pressure fails to respond to initial resuscitation, the rate of fluid administration should be increased and urgent intervention (eg, angiography) considered.


Humans are the main reservoir for ''Trypanosoma brucei gambiense'', but this species can also be found in pigs and other animals.  Wild game animals and cattle are the main reservoir of ''T. b. rhodesiense''.
===Blood transfusion===
*Patients with severe [[bleeding]] need to be transfused.<ref name="pmid24063362">{{cite journal |vauthors=Al-Jaghbeer M, Yende S |title=Blood transfusion for upper gastrointestinal bleeding: is less more again? |journal=Crit Care |volume=17 |issue=5 |pages=325 |year=2013 |pmid=24063362 |pmc=4056793 |doi=10.1186/cc13020 |url=}}</ref><ref name="pmid23281973">{{cite journal |vauthors=Villanueva C, Colomo A, Bosch A, Concepción M, Hernandez-Gea V, Aracil C, Graupera I, Poca M, Alvarez-Urturi C, Gordillo J, Guarner-Argente C, Santaló M, Muñiz E, Guarner C |title=Transfusion strategies for acute upper gastrointestinal bleeding |journal=N. Engl. J. Med. |volume=368 |issue=1 |pages=11–21 |year=2013 |pmid=23281973 |doi=10.1056/NEJMoa1211801 |url=}}</ref>
*[[Fresh frozen plasma|Fresh frozen plasma,]] [[platelets]], or both should be given to patients with [[coagulopathy]] who are actively bleeding and to those who have received more than 10 units of packed [[erythrocytes]].


Horse-flies (Tabanidae) and Stomoxydinae possibly could play a role by mechanical transmission (in special situations) not only of [[Nagana]] (the animal form of sleeping sickness) but also of the human disease form.<ref>{{cite journal
{| border="1" cellpadding="5" cellspacing="0" align="center" |class="wikitable"
  |author=Cherenet T, Sani RA, Panandam JM, Nadzr S, Speybroeck N, van den Bossche P
! colspan="2" style="background:#efefef;" |Indications for transfusion
  |title=Seasonal prevalence of bovine trypanosomosis in a tsetse-infested zone and a tsetse-free zone of the Amhara Region, north-west Ethiopia
|-
  |journal=[[The Onderstepoort journal of veterinary research]]
! colspan="1" style="background:#efefef;" |Age
  |year=2004 |volume=71 | issue=4 | pages= 307&ndash;312
! colspan="1" style="background:#efefef;" |Target Hematocrit
  |url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15732457&query_hl=1
|-
}}</ref>
|Elderly patient ( >45)
|30%
|-
|Younger patient (<45)
|25%
|-
|Patients with portal hypertension
|28%
|}


===East African Trypanosomiasis===
===Triage and consultations ===
Worldwide, approximately 40,000 new cases of both East and West African trypanosomiasis are reported to the [[World Health Organization]] each year. However, many cases are not reported due to a lack of infrastructure and the true number of new cases is undoubtedly much higher. Since 1967, thirty-six cases of East African trypanosomiasis have been reported within the United States, all among individuals who had traveled to Africa.
*All patients with visible rectal bleeding warrants an immediate evaluation in all cases. The timing and setting of the evaluation depends upon the severity of bleeding and the patient's comorbid illnesses.
*A gastroenterology consultation should be obtained early in the hospital course of patients with acute lower GI bleeding.
{| border="1" cellpadding="5" cellspacing="0" align="center" |class="wikitable"
! colspan="1" style="background:#efefef;" |Evaluation setting
! colspan="1" style="background:#efefef;" |Patient catagories
|-
|ICU
|Patients with high-risk features.
|-
|Outpatient
|Patients with low-risk features.<sup>†</sup> 
|-
|Regular Ward
|Most other patients can be admitted to a regular medical ward.<sup>♦</sup>


East African trypanosomiasis is found in parts of Eastern and Central Africa, including Uganda, Kenya, Tanzania, Malawi, Ethiopia, Zaire, Zimbabwe, and Botswana. Areas where infection is spread are largely determined by the location of the infected [[tsetse fly]] and wild animal population.
|-
| colspan="2" style="background:#efefef;" |
* '''†''': Low-risk features include a young, otherwise healthy patient with minor, self-limited rectal bleeding suspected to be from an anal source)


===West African Trypanosomiasis===
* ♦: Requires continuous electrocardiogram monitoring and pulse oximetry.
West African trypanosomiasis can be contracted in parts of Western and Central Africa. The tsetse fly lives only in Africa; areas where infection is spread are largely determined by where the infected tsetse fly is found.<ref>
|}
http://www.cdc.gov/ncidod/dpd/parasites/trypanosomiasis/factsht_ea_trypanosomiasis.htm#what
http://www.cdc.gov/ncidod/dpd/parasites/trypanosomiasis/factsht_wa_trypanosomiasis.htm</ref>


==History and symptoms==
===Risk stratification===
Clinical features can predict the risk of complications in patients with presumed acute lower GI bleeding. These features can also be used to categorize patients as either low or high risk. The number of high-risk features present correlates with the likelihood of a poor outcome.
High-risk features include:
{| border="1" cellpadding="5" cellspacing="0" align="center" |class="wikitable"
! colspan="1" style="background:#efefef;" |High-risk features
|-
|
*Hemodynamic instability (hypotension, tachycardia, orthostasis, syncope)
*Persistent bleeding
*Significant comorbid illnesses
*Advanced age
*Bleeding that occurs in a patient who is hospitalized for another reason
*A prior history of bleeding from diverticulosis or angiodysplasia
*Current aspirin use
*Prolonged prothrombin time
*A non-tender abdomen
*Anemia
*An elevated blood urea nitrogen level
*An abnormal white blood cell count
|}
==Pharmacotherapy==
Epinephrine is used alone or in conjunction with other surgical techniques to treat a variety of causes of LGIB. Local injection of epinephrine stops bleeding by both pressure tamponade and the vasoconstrictor effect.  In patients with rebleeding, surgery should be considered. Pharmacotherapy is only used as an adjuvant therapy for all patients with LGIB.
:*Preferred regimen (1): Local injection of 1:10,000 to 20,000 solution (Intra-arterial vasopressin infusions begin at a rate of 0.2 U/min. If the bleeding persists, the rate of the infusion is increased to 0.4-0.6 U/min).
:*Note:- The bleeding stops in about 91% of patients receiving intra-arterial vasopressin but recurs in up to 50% of patients when the infusion is stopped.
===Major contraindications===
*Closed-angle glaucoma
*Labor
*Shock
*Sulfite hypersensitivity
*CAD, PAD
===Complications===
During vasopressin infusion, monitor patients for:
*Recurrent hemorrhage
*Myocardial ischemia (Nitroglycerine drip can be used to overcome cardiac complications).
*Arrhythmias
*Hypertension
*Volume overload with hyponatremia.
==Colonoscopy==
*Colonoscopy is considered as the initial diagnostic modality of choice in patients presenting with lower GI bleeding. Colonoscopy can identify the origin of severe LGI bleeding in 74% to 82% of patients.
*As long as patients remain stable during the bowel preparation and sedation, colonoscopy has the advantage of not only localizing the source of bleeding, but also allowing intervention via clips, epinephrine injection, thermoregulation, or laser photocoagulation.
*In patients with massive lower GI bleeding, colonoscopic hemostasis is an effective means of controlling bleeding from a diverticular source when appropriately skilled providers are available.
*In cases in which no source of bleeding is seen on colonoscopy, esophagogastroduodenoscopy should be undertaken, as occasionally, brisk UGIB increases transit time and presents as blood per rectum.
*If a patient has pain associated with bleeding, ischemic bowel disease should be considered. CTA may be a more appropriate first-line investigation in patients with abdominal pain or suspected peritonitis.
===Timing of colonoscopy===
*In patients with ongoing bleeding or high-risk clinical features, a colonoscopy should be performed within 24 hours of presentation after adequate colon preparation to potentially improve diagnostic and therapeutic yield.
===Bowel preparation===
*In a patient who is not actively bleeding, rapid bowel preparation can be administered with 3 to 4 L of polyethylene glycol.
*This can be administered orally or via a nasogastric tube to avoid nausea and reduce the potential risk of aspiration.
*However, there is the potential risk of fluid overload in the acutely ill patient receiving rapid bowel preparation this way.
*Metoclopramide, 10 to 20 mg, can be administered with the bowel preparation as a prokinetic agent to facilitate gastric emptying and reduce the risk of vomiting.
*Some have advocated colonoscopy following limited bowel preparation using polyethylene glycol purges supplemented with rectal enemas.
*Blood is cathartic to the colon and tends to facilitate the emptying of colonic residue.
===Complications===
*Perforation of the luminal wall, resulting in peritonitis and sepsis.
*Poor visualization in an unprepared colon.


In the first stage, the trypanosomes multiply in subcutaneous tissues, blood and lymph. This is also called haemo-lymphatic stage, which entails bouts of fever, headaches, joint pains and itching
===Non surgical options===
*Once the bleeding site is localized, therapeutic options include coagulation and injection with vasoconstrictors or sclerosing agents.
*In cases of diverticular bleeding, bipolar probe coagulation, epinephrine injection, and metallic clips may be used.
*If recurrent bleeding is present, the affected bowel segment can be resected.
*In cases of angiodysplasia, thermal therapy, such as electrocoagulation or argon plasma coagulation, is generally successful.
*Angiodysplastic lesions may be missed at colonoscopy if the lesions are small or covered with blood clots.
*Endoscopic hemostasis therapy is a safe and effective method to control high-risk indications of hemorrhage: active bleeding, nonbleeding visible vessel, or adherent clot.
*It is also effective for diverticular bleeding, angioectasia bleeding, and post-polypectomy bleeding.
*In patients with brisk, active lower gastrointestinal bleeding, obtain a surgical consultation.


In the second stage the parasites cross the blood-brain barrier to infect the central nervous system. This is known as the neurological or meningo-encephalic stage. In general this is when more obvious signs and symptoms of the disease appear: changes of behaviour, confusion, sensory disturbances and poor coordination. Disturbance of the sleep cycle, which gives the disease its name, is an important feature. Without treatment, sleeping sickness is considered fatal although cases of healthy carriers have been reported.
{| class="wikitable"
{| class="wikitable"
!
!
!Symptoms
!
!
!
|-
|Diverticulosis
|
|
|
|-
|Angiodysplasia
|
|
|
|-
|Hemmrohoids
|
|
|
|-
|-
|First stage (hemo-lyphatic stage)
|
|
* Fever
|
* Headaches
|
* Joint pains and itching
|
|-
|-
|Second stage (neurological or meningo-encephalic stage)
|
|
* Changes of behaviour
|
* Confusion
|
* Sensory disturbances 
|
* Poor coordination
* Disturbance of the sleep cycle,
|}
|}
===CXXX===
*Diverticula are most common in the descending and sigmoid colon.
*Most of the time bleeding from diverticulosis stops spontaneously, however, in about 5% of patients, the bleeding can be massive and life-threatening.


==Diagnosis==
==References==
*Definitive diagnosis rests on the observation of trypanosomes by microscopy.
{{reflist|2}}
*In T. b. rhodesiense infection, the identification of suspected cases relies on the clinical presentation and a history of exposure. The level of parasitemia is relatively high, particularly in the first stage of disease, and trypanosomes can be found in blood.
*In centrifuged blood, the parasite sediments just above the white cells, and examination of buffy coat will increase sensitivity. Slides stained with Giemsa can be used, but it is easiest to find the parasite by microscopic examination of fresh wet preparations, because the trypanosomes are motile and attract the eye. Delay between sampling and microscopy should be minimized, because trypanosomes will lose motility within a few hours. Parasites can also be found in fluid expressed in trypanosomal chancres and in lymph node aspirates. Serologic testing is not used for the diagnosis of T. b. rhodesiense infection.
Detecting trypanosomes in T. b. gambiense infection is more difficult.
==Serology==
*The card agglutination test for trypanosomiasis/T. b. gambiense is a serologic screening test used for mass population screening in endemic areas of Africa. It is not available in the U.S.
*The test is not specific enough for confirmation of infection, but it is helpful in identifying suspect cases.
*For parasitologic confirmation, a posterior cervical lymph node (if present) is punctured and the fluid examined. The yield in lymph node examination varies from about 40% to 80%.
*Trypanosomes can also be found in blood, however, the yield is low, and concentration techniques (e.g. buffy coat examination, miniature anion-exchange centrifugation technique) are helpful. Serial examinations on consecutive days may be needed.
*Treatment decisions are based on the stage of the disease. Every patient diagnosed with African trypanosomiasis must undergo a lumbar puncture for the examination of CSF. *The most widely used criteria for defining second stage disease are the observation of trypanosomes in CSF or a white cell count of 6 or higher. Other indications of second stage disease include elevated protein and an increase in nonspecific IgM in CSF.
Disease management is made in 3 steps:
*Screening for potential infection. This involves using serological tests (only available for T.b.gambiense) and checking for clinical signs - especially swollen cervical lymph nodes.
*Diagnosing by establishing whether the parasite is present in body fluids.
*Staging to determine the state of disease progression. This entails examining the cerebrospinal fluid obtained by lumbar puncture.
Diagnosis must be made as early as possible to avoid progressing to the neurological stage in order to elude complicated and risky treatment procedures
 
==Treatment==
The type of treatment depends on the disease stage. The drugs used in the first stage are safer and easier to administer than those for second stage. Also, the earlier the disease is identified, the better the prospect of a cure. The assessment of treatment outcome requires follow up of the patient up to 24 months and entails laboratory exams of body fluids including cerebrospinal fluid obtained by lumbar puncture, as parasites may remain viable for long periods and reproduce the disease months after treatment. Treatment success in the second stage depends on drugs that cross the blood-brain barrier to reach the parasite. Such drugs are toxic and complicated to administer. In total five different drugs are used for the treatment of sleeping sickness. These drugs are donated to WHO by manufacturers and distributed free of charge to disease endemic countries.
Medical treatment of African trypanosomiasis should begin as soon as possible and is based on the infected person’s symptoms and laboratory results.  Medication for the treatment of African trypanosomiasis is available through the [[CDC]].  Pentamidine isethionate and suramin (under an investigational New Drug Protocol from the CDC Drug Service) are the drugs of choice to treat the hemolymphatic stage of West and East African Trypanosomiasis, respectively.  Melarsoprol is the drug of choice for late disease with central nervous system involvement (infections by T.b. gambiense or T. b. rhodiense).
 
Hospitalization for treatment is necessary.  Periodic follow-up exams that include a [[spinal tap]] are required for 2 years.  If a person fails to receive medical treatment for African trypanosomiasis, death will occur within several weeks to months.
 
==Medical Therapy==
===Antimicrobial Regimen===
:* ''' Sleeping sickness'''<ref>{{cite web|title=African Trypanosomiasis| url=  http://www.cdc.gov/parasites/sleepingsickness/health_professionals/index.html}}</ref> 
::* 1. '''East african trypanosomiasis'''
:::* 1.1 '''T. b. rhodesiense, hemolymphatic stage'''
::::* 1.1.1 '''Adult '''
:::::* Preferred regimen: [[Suramin]] 1 gm IV on days 1,3,5,14, and 21
::::* 1.1.2 '''Pediatric'''
:::::* Preferred regimen: [[Suramin]] 20 mg/kg IV on days 1, 3, 5, 14, and 21
:::* 1.2 '''T. b. rhodesiense, CNS involvement'''
::::* 1.2.1 '''Adult'''
:::::* Preferred regimen: [[Melarsoprol]] 2-3.6 mg/kg/day IV for 3 days. After 7 days, 3.6 mg/kg/day for 3 days. Give a 3rd series of 3.6 mg/kg/d after 7 days.
::::* 1.2.2 '''Pediatric'''
:::::* Preferred regimen: [[Melarsoprol]] 2-3.6 mg/kg/day IV for 3 days. After 7 days, 3.6 mg/kg/day for 3 days. Give a 3rd series of 3.6 mg/kg/d after 7 days
::* 2. '''West african trypanosomiasis'''
:::* 2.1 '''T. b. gambiense, hemolymphatic stage'''
::::* 2.1.1 '''Adult'''
:::::* Preferred regimen: [[Pentamidine]] 4 mg/kg/day IM/ IV for 7-10 days
::::* 2.1.2 '''Pediatric'''
:::::* Preferred regimen: [[Pentamidine]] 4 mg/kg/day IM/IV for 7-10 days
:::::* Note (1): Pentamidine should be used during pregnancy and lacation  only if the potential benefit justifies the potential risk
:::::* Note (2): IM/IV Pentamidine have a similar safety profile in children age 4 months and older as in adults. Pentamidine is listed as a medicine for the treatment of 1st stage African trypanosomiasis infection (Trypanosoma brucei gambiense) on the WHO Model List of Essential Medicines for Children, intended for the use of children up to 12 years of age.
:::* 2.2  '''T. b. gambiense, CNS involvement'''
::::* 2.2.1 '''Adult'''
:::::* Preferred regimen: [[Eflornithine]] 400 mg/kg/day  IV qid for 14 days
::::* 2.2.2 '''Pediatric'''
:::::* Preferred regimen: [[Eflornithine]] 400 mg/kg/day IV  qid for 14 days
:::::* Note (1): [[Eflornithine]] should be used during pregnancy and lactation, only if the potential benefit justifies the potential risk
:::::* Note (2): The safety of [[Eflornithine]] in children has not been established. Eflornithine is not approved by the Food and Drug Administration (FDA) for use in pediatric patients. [[Eflornithine]] is listed for the treatment of 1st stage African trypanosomiasis inTrypanosoma brucei gambiense infection on the WHO Model List of Essential Medicines for Children, intended for the use of children up to 12 years of age.
 
==Prevention==
Wear protective clothing, including long-sleeved shirts and pants. The tsetse fly can bite through thin fabrics, so clothing should be made of medium-weight material.
Wear neutral-colored clothing. The tsetse fly is attracted to bright colors and very dark colors.
Inspect vehicles for tsetse flies before entering. The flies are attracted to moving vehicles.
Avoid bushes. The tsetse fly is less active during the hottest period of the day. It rests in bushes but will bite if disturbed.
Use insect repellant. Though insect repellants have not proven effective in preventing tsetse fly bites, they are effective in preventing other insects from biting and causing illness.
==Screening==
*Instances of sleeping sickness are being reduced by the use of the [[sterile insect technique]].
*Systematic [[Screening (medicine)|screening]] of communities in identified foci is the best approach as case-by-case screening is not practically possible in highly endemic regions.
*Systematic screening may be in the form of mobile clinics or fixed screening centres where teams travel daily to the foci.
*The nature of gambiense disease is such that patients don't seek treatment early enough because the symptoms at that stage are not evident or serious enough to warrant seeking medical attention, considering the remoteness of some affected areas. Also, diagnosis of the disease is difficult and most health workers may not be able to detect it.
*Systematic screening allows early-stage disease to be detected and treated before the disease progresses, and removes the potential human reservoir.<ref>{{cite web
  |title=Strategic Direction for African Trypanosomiasis Research
  |work=Special Programme for Research and Training in Tropical Diseases
  |url=http://www.who.int/tdr/diseases/tryp/direction.htm
  |accessdate=2006-03-01
}}</ref>

Latest revision as of 19:13, 13 December 2017

Lower GI bleeding is defined as any bleed that occurs distal to the ligament of Treitz.

Incidence

  • In the United States the incidence of LGIB ranges from 20.5 to 27 per 100,000 persons per year.

Age

  • There is a greater than 200 fold increase from the third to the ninth decade of life.

Classification

  • Lower GI bleeding can be classified into 3 groups based on the severity of bleeding:
    • Occult lower GI bleeding
    • Moderate lower GI bleeding
    • Severe lower GI bleeding
Severe lower GI bleeding Moderate lower GI bleeding Occult lower GI bleeding
Age > 65 years Occur at any age Any age
Presenting symptoms Hematochezia or bright red blood per rectum. Hematochezia or melena. Symptoms of anemia (fatigue, tirdness)
Hemodynamics Unstable Stable Stable
Lab findings hemoglobin equal to or less than 6 g/dl. Microcytic anemia Microcytic hypochromic anemia due to chronic blood loss.
Differential Diverticulosis and angiodysplasias Neoplastic disease Inflammatory, <br> infectious, benign anorectal, and congenital diseases. Inflammatory, neoplastic and congenital.

Blood supply

  • The SMA and IMA are connected by the marginal artery of Drummond.
  • This vascular arcade runs in the mesentery close to the bowel.
  • As patients age, there is increased incidence of occlusion of the IMA.
  • The left colon stays perfused, primarily because of the marginal artery.
Lower GI Tract Arterial Supply Venous Drainage
Midgut
  • Distal duodenum jejunum
  • Ileum
  • Appendix
  • Cecum
  • Ascending colon
  • Hepatic flexure
  • Proximal transverse colon.
  • Superior mesenteric artery (SMA)
  • Portal system.
Hindgut
  • Distal one-third of the transverse colon
  • Splenic flexure
  • Descending colon,
  • Sigmoid colon
  • Rectumhu
  • Inferior mesenteric artery (IMA)
  • Portal system ɸ
ɸ -Except lower rectum, which drains into the systemic circulation.
Blood supply to the intestines includes the celiac artery, superior mesenteric artery (SMA), inferior mesenteric artery (IMA), and branches of the internal iliac artery (IIA).
Source: By Anpol42 (Own work) [CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0)], via Wikimedia Commons

Pathogenesis

Diverticulosis is the most common etiology of lower GI bleeding accounting for 30% of all cases, followed by anorectal disease, ischemia, inflammatory bowel disease (IBD), neoplasia and arteriovenous (AV) malformations.

  • Diverticulosis
    • The colonic wall weakens with age and results in the formation of saclike protrusions known as diverticula.
    • These protrusions generally occur at the junction of blood vessel penetrating through the mucosa and circular muscle fibers of the colon.
    • Diverticula are most common in the descending and sigmoid colon.
    • Despite the majority of diverticula being on the left side of the colon, diverticular bleeding originates from the right side of the colon in 50% to 90% of instances.
    • Most of the time bleeding from diverticulosis stops spontaneously, however, in about 5% of patients, the bleeding can be massive and life-threatening.
Diagram of sigmoid diverticulum
Source:By Anpol42 (Own work) [CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0)], via Wikimedia Commons
  • Anorectal disease
  • Hemorrhoids and anal fissures are the most common disease under anorectal disease responsible for GI bleeding.
  • Hemorrhoids are engorged vessels in the normal anal cushions. When swollen, this tissue is very friable and susceptible to trauma, which leads to painless, bright red bleeding.
  • Anal fissures are defined as a tear in the anal mucosa. With the passage of stool, the mucosa continues to tear and leads to bright red bleeding.
  • Mesenteric Ischemia
  • Mesenteric ischemia results when there is inadequate blood supply at the level of the small intestine.
  • 2 or more vessels (celiac, SMA, or IMA) must be involved for symptoms to occur.
  • Non occlusive mesenetric ischemia affects critically ill patients who are vasopressor-dependent.
  • Venous thrombosis of the visceral vessels can also precipitate an acute ischemic event.
  • Ischemic Colitis
  • Ischemic colitis is caused by poor perfusion of the colon, which results in the inability of that area of the colon to meet its metabolic demands.
  • It can be gangrenous or nongangrenous, acute, transient, or chronic.
  • The left colon is predominantly affected, with the splenic flexure having increased susceptibility.
  • Intraluminal hemorrhage occurs as the mucosa becomes necrotic, sloughs, and bleeds.
  • Damage to the tissue is caused both with the ischemic insult as well as reperfusion injury.
  • Inflammatory Bowel Disease
  • In Crohn's disease T cell activation stimulates interleukin (IL)-12 and tumor necrosis factor (TNF)-a, which causes chronic inflammation and tissue injury.
  • Initially, inflammation starts focally around the crypts, followed by superficial ulceration of the mucosa.
  • The deep mucosal layers are then invaded in a noncontinuous fashion, and noncaseating granulomas form, which can invade through the entire thickness of the bowel and into the mesentery and surrounding structures.
  • In ulcerative colitis T cells cytotoxic to the colonic epithelium accumulate in the lamina propria, accompanied by B cells that secrete immunoglobulin G (IgG) and IgE.
  • This results in inflammation of the crypts of Lieberkuhn, with abscesses and pseudopolyps.
  • Ulcerative colitis generally begins at the rectum and is a continuous process confined exclusively to the colon.
  • Neoplasia
  • Colon carcinoma follows a distinct progression from polyp to cancer.
  • Mutations of multiple genes are required for the formation of adenocarcinoma, including the APC gene, Kras, DCC, and p53.
  • Certain hereditary syndromes are also classified by defects in DNA mismatch repair genes and microsatellite instability.
  • These tumors tend to bleed slowly, and patients present with hemocult positive stools and microcytic anemia.
  • Although cancers of the small bowel are much less common than colorectal cancers, they should be ruled out in cases of lower GI bleeding in which no other source is identified.
  • AV Malformation/Angiodysplasia
  • In AV malformation direct connections between arteries and veins occur in the colonic submucosa.
  • The lack of capillary buffers causes high pressure blood to enter directly into the venous system, making these vessels at high risk of rupture into the bowel lumen.
  • In Angiodysplasia over time, previously healthy blood vessels of the cecum and ascending colon degenerate and become prone to bleeding.
  • Although 75% of angiodysplasia cases involve the right colon, they are a significant cause of obscure bleeding and the most common cause of bleeding from the small bowel in the elderly.

Epidemiology

Prevalence

  • Approximately 20 patients/100,000 population in the U.S.

Incidence

  • The estimated annual incidence of lower GI bleeding is approximately 0.03% in the adult population as a whole.

Demographics

Gender

  • More common in men than women

Age

  • Rare in children
  • The incidence of lower GI bleeding increases with age with a 200-fold increase from the second to eighth decades of life la.
    • Largely due to the increase in the prevalence of diverticular disease and angiodysplasia with age.

Symptoms

  • Occult LGIB may present with symptoms of iron deficiency anemia such as fatigue, palpitations, and dyspnea.
  • Patients with intussusception may present with pallor and vomiting in addition to LGIB
  • Associated symptoms, such as abdominal pain or change in bowel habits, may also aide in the diagnosis
  • Bloody diarrhea associated with abdominal pain may suggest an infectious cause or IBD in a younger patient and ischemic colitis in an older patient with vascular disease
  • Painless bleeding usually suggests angiodysplasia, diverticular disease, or internal hemorrhoids
  • Perianal pain suggests a perianal fissure or fistula

History

  • A detailed description of the nature of the blood loss can help in pinpointing the likely source of bleeding.

Past Medical History

  • The clinical history should identify whether this is a recurrent bleed.
  • Bleeding from angiodysplasia is usually recurrent and chronic, but severe bleeding resulting in hemodynamic instability can occur.
  • Associated weight loss suggests malignancy.
  • The presence of systemic diseases such as atherosclerotic disease, IBD, coagulopathies, and HIV, and a history of pelvic irradiation for malignancy should be considered

Past Surgical History

  • A history of recent colonic polypectomy or biopsy indicates iatrogenic bleeding.
    • This is usually low grade and limited, although it can be severe if an underlying artery is involved or if there is an inadequate coagulation of the polypectomy stalk.
    • In 1.5% of polypectomies bleeding occurs immediately. However, delayed bleeding can occur several hours or days following the procedure
  • It is essential to establish the presence of comorbid diseases, as these not only help in diagnosis but may also influence treatment.

Family history

  • A family history of diseases such as IBD or colorectal malignancy is relevant.

Symptoms

  • The clinical presentation of LGIB varies with the anatomic source of the bleeding.
  • Commonly, LGIB from the right side of the colon can manifest as maroon stools, whereas a left-sided bleeding source may be evidenced by bright red blood per rectum.
  • The presentation of LGIB can also vary depending on the etiology.
    • A young patient may present with fever, dehydration, abdominal cramps, and hematochezia caused by infectious or noninfectious (idiopathic) colitis.
    • An older patient may present with painless bleeding and minimal symptoms caused by diverticular bleeding or angiodysplasia.
    • LGIB can be mild and intermittent, as often is the case with angiodysplasia, or it may be moderate or severe, as may be the situation in diverticula-related bleeding.
    • Young patients may present with abdominal pain, rectal bleeding, diarrhea, and mucous discharge that may be associated with IBD.
    • Elderly patients presenting with abdominal pain, rectal bleeding, and diarrhea may have ischemic colitis.
    • Elderly patients with atherosclerotic heart disease may present with intermittent LGIB and syncope that may be due to angiodysplastic lesions.
    • Stools streaked with blood, perianal pain, and blood drops on the toilet paper or in the toilet bowl may be associated with perianal pathology, such as anal fissure or hemorrhoidal bleeding.
    • The passage of maroon stools or bright red blood from the rectum is usually indicative of massive lower GI hemorrhage.
  • Massive LGIB is a life-threatening condition in which patients present with a systolic blood pressure (SBP) of below 90 mm Hg and a hemoglobin (Hb) level of 6 g/dL or less.
Disease Symptoms
Diverticular bleeding Painless bleeding

Mild abdominal cramping

If the bleeding is brisk and voluminous, patients may be hypotensive and display signs of shock

Angiodysplasia Painless, hematochezia or melena (slow but repeated bleeding episodes)

Syncope

Colitis Ischemic colitis Fever

Abdominal pain

Bloody diarrhea

Dehydration

Hypotension in severe cases

Weight loss

Infectious colitis
Radiation-induced colitis
Ulcerative colitis
Colon cancer Right-sided bleeding (Maroon stools or melena)

Insidious

Patients presents with iron-deficiency anemia and syncope

Whereas left-sided colonic neoplasms can present as bright red blood per rectum

Hemorrhoids Painless, whereas bleeding secondary to fissures tends to be painful.

Can also present with strangulation, hematochezia, and pruritus.

Common causes

  • Colonic diverticulosis
    • Colonic diverticulosisis the most common cause of acute LGIB in the western world, accounting for 15% to 55% of all LGIB
    • Diverticula can occur anywhere in the gastrointestinal tract, but are most common in the sigmoid colon. However, approximately 60% of diverticular bleeds arise from diverticula in the right colon, highlighting a tendency for right-sided diverticula to bleed
    • Hemorrhage results from rupture of the intramural branches (vasa recta) of the marginal artery at the dome of a diverticulum and can give rise to a massive, life-threatening LGIB
    • This is by far the most common cause of bleeding in the elderly, as the prevalence of diverticular disease increases with age, being as high as 85% by the age of 85 years
  • Obesity has recently been recognized as a risk factor in the development of diverticular disease, and the risk of diverticular bleeding in this group of patients is higher than that in patients who are not obese
  • Vascular ectasias (angiodysplasias/angioectasias):
    • Tortuous dilated submucosal vessels that account for approximately 10% of LGIB.
    • They appear endoscopically as small, flat lesions (5-10 mm) with ectatic capillaries radiating from a central vessel (Fig. 1)
    • The prevalence of angiodysplasia in the gastrointestinal tract is not well known, but a pooled analysis of three colonoscopic cancer screening studies detected angiodysplasia in 0.8% of the patients The prevalence of angiodysplasia is higher in older populations and, in the past, has been linked to certain conditions such as end-stage renal disease, Von Willebrand disease , and aortic stenosis In one series, 37% of colonic dysplasias were found in the cecum, 17% in the ascending colon, 7% in the transverse colon, 7% in the descending colon, and 32% in rectosigmoid area
    • Angiodysplasia can also be found throughout the small bowel and is responsible for up to 40% of small intestinal bleeding in patients older than 40 years.
    • Angiodysplasia of the stomach and duodenum is responsible for up to 7% of UGIB I
  • Iatrogenic:
    • Bleeding is recognized as the most common complication of colonoscopy and polypectomy, occurring in 0.3% to 6.1% of polypectomies
    • Risk factors for bleeding include polyp size greater than 1 cm, patient age older than 65 years, presence of comorbid disease, and polypectomy using the cutting mode of current
    • The risk is also greater in patients taking anticoagulant or antiplatelet agents
  • Ischemic colitis:
    • Ischemic colitis accounts for approximately 20% of LGIB
    • Ischemia results from a sudden reduction in blood flow to the mesenteric vessels as a result of hypotension, occlusion, or spasm of the mesenteric vessels
    • Nonocclusive disease typically affects the watershed areas of the bowels, such as the splenic flexure and adjacent transverse colon due to the poor blood supply from the marginal artery.
    • Occlusive disease is rarer but can occur as a result of thrombus formation or embolus.
    • It is a recognized complication of aortic surgery
    • Elderly patients with comorbid disease are at higher risk of developing ischemic colitis.
    • There may be a history of ischemic heart disease
    • The majority of patients with ischemic colitis improve following conservative management; however, approximately 20% will progress to develop colonic gangrene
    • Other complications include chronic colitis and stricture formation
    • Diagnosis requires a high index of suspicion
  • Colorectal malignancy:
    • Colorectal cancer accounts for approximately 10% of bleeds, either as occult bleeding presenting with anemia or as frank blood loss per rectum
    • A family history of colorectal cancer is important to establish
  • Anorectal abnormalities:
    • Hemorrhoids, fissures, fistulae, and polyps can all present with bright red rectal bleeding, which may be intermittent in nature
    • Hemorrhoids are the most common cause of rectal bleeding in adults younger than 50 years
    • The finding of hemorrhoids in older patients with LGIB should not preclude further investigation, as hemorrhoids are an extremely common finding and may not be the cause of bleeding
  • Inflammatory bowel disease (IBD):
    • IBD refers to both Crohn disease and ulcerative colitis Accounts for 5% to 10% of bleeds.
    • It is by far the most common cause of LGIB in Asian populations in whom the prevalence of diverticular disease is much lower
    • A previous history of IBD in patients with LGIB is important, as these patients have a higher risk of developing colorectal malignancy than do the general population
  • Infectious colitis:
    • The most common organisms in the U.S. are species ofSalmonella,Campylobacter,Shigella, andYersinia

Rare causes

  • Colonic polyps:
    • These can occur in isolation or as part of an inherited polyposis syndrome
    • Can cause occult or overt LGIB
  • Radiation proctitis:
    • This usually occurs a few months following ionizing radiation for pelvic malignancies (Fig. 2). In one study of patients with radiation proctitis following pelvic irradiation, 69% presented with bleeding within 1 year and 96% within 2 years
  • Rectal varices:
    • Associated with portal hypertension; may result in massive bleeding
    • Stercoral ulceration:
    • Can cause significant fresh rectal bleeding in elderly constipated patients
  • Meckel diverticulum:
    • These small bowel diverticula may contain ectopic gastric mucosa that can ulcerate and cause bleeding
    • They are the most common cause of massive LGIB in young children, and can be diagnosed with angiography, Meckel scans, and radionuclide imaging
  • Intussusception :
    • More common in children, with the highest incidence between the ages of 6 months and 2 years
  • Henoch-Schönlein purpura (HSP):
    • Most commonly affects children
    • Bleeding may be a direct result of vasculitis or secondary to intussusception, which is associated with HSP
  • Aortoenteric fistula:
  • Abdominal aortic aneurysms, especially those of the inflammatory type, may fistulate into the small bowel, giving rise to a massive, life-threatening hemorrhage
  • Peutz-Jeghers syndrome:
    • Polyps may give rise to frank or occult bleeding
  • Klippel-Trenaunay-Weber syndrome:
    • Hemangiomas in the colon can cause significant bleeding
  • Hereditary hemorrhagic telangiectasia:
    • Blood loss from mucosal telangiectasia can be chronic or acute
  • Neurofibromatosis :
    • Neurofibromas within the lumen of the bowel can ulcerate, causing bleeding
  • Blue rubber bleb syndrome:
    • Bleeding can arise from hemangiomas in the bowel Usually occult in nature

Risk factors

Common risk factors in the development of lower GI bleeding include:[1][2][3][4]

  • Advancing age
  • Previous history of gastrointestinal bleed
  • Chronic constipation
  • Hematologic disorders
  • Anticoagulants medications
  • Nonsteroidal anti-inflammatory drugs
  • Human immunodeficiency virus
Chronic constipation Results in colonic diverticula and predispose patients to anal fissures and hemorrhoid formation
Hematologic disorders Deficiencies in clotting factors, such as factor VII and factor VIII, predispose persons to LGIB
Anticoagulants medications Patients taking warfarin and heparin, aspirin, and platelet inhibitors are at increased risk of bleeding in general
Nonsteroidal anti-inflammatory drugs NSAIDs cause ulceration in the terminal ileum and proximal colon, and can exacerbate IBD
Human immunodeficiency virus In patients with HIV, bleeding is caused by opportunistic infections, cytomegalovirus colitis, Kaposi sarcoma, or lymphoma

Management

Initial Evaluation

  • In patients with acute lower gastrointestinal bleeding who are unstable rapid assessment and resuscitation should be initiated even before diagnostic evaluation.
  • The initial steps in the management of a patient with lower gastrointestinal bleeding are to assess the severity of bleeding, and then institute fluid and blood resuscitation as needed.
  • Once hemodynamic stability is achieved, nasogastric lavage should be performed to rule of upper GI source.
  • Equilibration between the intravascular and extravascular volumes cannot be achieved until 24 to 72 hours after bleeding has occurred.

Role of Nasogastric tube (NGT)

  • Nasogastric tube (NGT) lavage is recommended in all patients with lower gastrointestinal bleeding once the patient is stabilized.
  • A carefully placed nasogastric tube (NGT) with irrigation and aspiration of bile is necessary to ensure sampling of duodenal contents.
  • If there is a bloody NGT aspirate then an esophagogastroduodenoscopy (EGD) is warranted (11 to 15% of patients despite “negative” NGT aspirates are due to upper GI bleeding).
  • Obtaining clear fluid favors a lower GI source of bleeding.
Workup and Initial Management
Initial Evaluation
  • Airway Breathing, Circulation
Supportive Therapy
  • Ensure patent and protected airway
  • 2 large-bore, peripheral intravenous lines
Blood transfusion
  • Resuscitate with 1:1:1 of packed red blood cells (PRBCs) to fresh frozen plasma (FFP) to platelets.
  • Consider massive transfusion protocol
  • Res:Low riskto a target hemoglobin of 7 mg/dL.
  • Consider Sengstaken-Blakemore tube for control of immediately life-threatening upper GI bleeding

Assessment of severity of bleeding

Bleeding severity Vital signs Blood loss
Minor Normal <10%
Moderate Postural hypotension 10-20%
Severe Shock >25%

Fluid resuscitation

Blood transfusion

Indications for transfusion
Age Target Hematocrit
Elderly patient ( >45) 30%
Younger patient (<45) 25%
Patients with portal hypertension 28%

Triage and consultations

  • All patients with visible rectal bleeding warrants an immediate evaluation in all cases. The timing and setting of the evaluation depends upon the severity of bleeding and the patient's comorbid illnesses.
  • A gastroenterology consultation should be obtained early in the hospital course of patients with acute lower GI bleeding.
Evaluation setting Patient catagories
ICU Patients with high-risk features.
Outpatient Patients with low-risk features.
Regular Ward Most other patients can be admitted to a regular medical ward.
  • : Low-risk features include a young, otherwise healthy patient with minor, self-limited rectal bleeding suspected to be from an anal source)
  • ♦: Requires continuous electrocardiogram monitoring and pulse oximetry.

Risk stratification

Clinical features can predict the risk of complications in patients with presumed acute lower GI bleeding. These features can also be used to categorize patients as either low or high risk. The number of high-risk features present correlates with the likelihood of a poor outcome. High-risk features include:

High-risk features
  • Hemodynamic instability (hypotension, tachycardia, orthostasis, syncope)
  • Persistent bleeding
  • Significant comorbid illnesses
  • Advanced age
  • Bleeding that occurs in a patient who is hospitalized for another reason
  • A prior history of bleeding from diverticulosis or angiodysplasia
  • Current aspirin use
  • Prolonged prothrombin time
  • A non-tender abdomen
  • Anemia
  • An elevated blood urea nitrogen level
  • An abnormal white blood cell count

Pharmacotherapy

Epinephrine is used alone or in conjunction with other surgical techniques to treat a variety of causes of LGIB. Local injection of epinephrine stops bleeding by both pressure tamponade and the vasoconstrictor effect. In patients with rebleeding, surgery should be considered. Pharmacotherapy is only used as an adjuvant therapy for all patients with LGIB.

  • Preferred regimen (1): Local injection of 1:10,000 to 20,000 solution (Intra-arterial vasopressin infusions begin at a rate of 0.2 U/min. If the bleeding persists, the rate of the infusion is increased to 0.4-0.6 U/min).
  • Note:- The bleeding stops in about 91% of patients receiving intra-arterial vasopressin but recurs in up to 50% of patients when the infusion is stopped.

Major contraindications

  • Closed-angle glaucoma
  • Labor
  • Shock
  • Sulfite hypersensitivity
  • CAD, PAD

Complications

During vasopressin infusion, monitor patients for:

  • Recurrent hemorrhage
  • Myocardial ischemia (Nitroglycerine drip can be used to overcome cardiac complications).
  • Arrhythmias
  • Hypertension
  • Volume overload with hyponatremia.

Colonoscopy

  • Colonoscopy is considered as the initial diagnostic modality of choice in patients presenting with lower GI bleeding. Colonoscopy can identify the origin of severe LGI bleeding in 74% to 82% of patients.
  • As long as patients remain stable during the bowel preparation and sedation, colonoscopy has the advantage of not only localizing the source of bleeding, but also allowing intervention via clips, epinephrine injection, thermoregulation, or laser photocoagulation.
  • In patients with massive lower GI bleeding, colonoscopic hemostasis is an effective means of controlling bleeding from a diverticular source when appropriately skilled providers are available.
  • In cases in which no source of bleeding is seen on colonoscopy, esophagogastroduodenoscopy should be undertaken, as occasionally, brisk UGIB increases transit time and presents as blood per rectum.
  • If a patient has pain associated with bleeding, ischemic bowel disease should be considered. CTA may be a more appropriate first-line investigation in patients with abdominal pain or suspected peritonitis.

Timing of colonoscopy

  • In patients with ongoing bleeding or high-risk clinical features, a colonoscopy should be performed within 24 hours of presentation after adequate colon preparation to potentially improve diagnostic and therapeutic yield.

Bowel preparation

  • In a patient who is not actively bleeding, rapid bowel preparation can be administered with 3 to 4 L of polyethylene glycol.
  • This can be administered orally or via a nasogastric tube to avoid nausea and reduce the potential risk of aspiration.
  • However, there is the potential risk of fluid overload in the acutely ill patient receiving rapid bowel preparation this way.
  • Metoclopramide, 10 to 20 mg, can be administered with the bowel preparation as a prokinetic agent to facilitate gastric emptying and reduce the risk of vomiting.
  • Some have advocated colonoscopy following limited bowel preparation using polyethylene glycol purges supplemented with rectal enemas.
  • Blood is cathartic to the colon and tends to facilitate the emptying of colonic residue.

Complications

  • Perforation of the luminal wall, resulting in peritonitis and sepsis.
  • Poor visualization in an unprepared colon.

Non surgical options

  • Once the bleeding site is localized, therapeutic options include coagulation and injection with vasoconstrictors or sclerosing agents.
  • In cases of diverticular bleeding, bipolar probe coagulation, epinephrine injection, and metallic clips may be used.
  • If recurrent bleeding is present, the affected bowel segment can be resected.
  • In cases of angiodysplasia, thermal therapy, such as electrocoagulation or argon plasma coagulation, is generally successful.
  • Angiodysplastic lesions may be missed at colonoscopy if the lesions are small or covered with blood clots.
  • Endoscopic hemostasis therapy is a safe and effective method to control high-risk indications of hemorrhage: active bleeding, nonbleeding visible vessel, or adherent clot.
  • It is also effective for diverticular bleeding, angioectasia bleeding, and post-polypectomy bleeding.
  • In patients with brisk, active lower gastrointestinal bleeding, obtain a surgical consultation.
Diverticulosis
Angiodysplasia
Hemmrohoids

CXXX

  • Diverticula are most common in the descending and sigmoid colon.
  • Most of the time bleeding from diverticulosis stops spontaneously, however, in about 5% of patients, the bleeding can be massive and life-threatening.

References

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  2. Strate LL (2005). "Lower GI bleeding: epidemiology and diagnosis". Gastroenterol. Clin. North Am. 34 (4): 643–64. doi:10.1016/j.gtc.2005.08.007. PMID 16303575.
  3. Ríos A, Montoya MJ, Rodríguez JM, Serrano A, Molina J, Ramírez P, Parrilla P (2007). "Severe acute lower gastrointestinal bleeding: risk factors for morbidity and mortality". Langenbecks Arch Surg. 392 (2): 165–71. doi:10.1007/s00423-006-0117-6. PMID 17131153.
  4. Strate LL, Orav EJ, Syngal S (2003). "Early predictors of severity in acute lower intestinal tract bleeding". Arch. Intern. Med. 163 (7): 838–43. doi:10.1001/archinte.163.7.838. PMID 12695275.
  5. Al-Jaghbeer M, Yende S (2013). "Blood transfusion for upper gastrointestinal bleeding: is less more again?". Crit Care. 17 (5): 325. doi:10.1186/cc13020. PMC 4056793. PMID 24063362.
  6. Villanueva C, Colomo A, Bosch A, Concepción M, Hernandez-Gea V, Aracil C, Graupera I, Poca M, Alvarez-Urturi C, Gordillo J, Guarner-Argente C, Santaló M, Muñiz E, Guarner C (2013). "Transfusion strategies for acute upper gastrointestinal bleeding". N. Engl. J. Med. 368 (1): 11–21. doi:10.1056/NEJMoa1211801. PMID 23281973.