811), Heyde's syndrome, Gastric antral vascular ectasia (GAVE) syndrome (ICD-10 K31.
ICD-10 code K92. 2 for Gastrointestinal hemorrhage, unspecified is a medical classification as listed by WHO under the range - Diseases of the digestive system .
609, Unspecified intestinal obstruction, unspecified as to partial versus complete obstruction is assigned.
ICD-10 code: K92. 2 Gastrointestinal haemorrhage, unspecified.
Angiodysplasia of the colon is swollen, fragile blood vessels in the colon. These can result in bleeding and blood loss from the gastrointestinal (GI) tract.
Upper gastrointestinal hemorrhage is a medical condition in which heavy bleeding occurs in the upper parts of the digestive tract: the esophagus (tube between the mouth and stomach), the stomach or the small intestine. This is often a medical emergency.
An obstruction in which two points along the course of a bowel are obstructed at a single location thus forming a closed loop. Patients present clinically with signs of obstruction: abdominal pain, nausea/vomiting, abdominal distension.
The bowel is part of the digestive system. It is made up of the small bowel (small intestine) and the large bowel (colon and rectum). The small bowel is longer than the large bowel but it gets its name from the fact it is much narrower than the large bowel.
ICD-10 code: K57. 92 Diverticulitis of intestine, part unspecified, without perforation, abscess or bleeding.
Melena refers to black stools that occur as a result of gastrointestinal bleeding. This bleeding typically originates from the upper gastrointestinal (GI) tract, which includes the mouth, esophagus, stomach, and the first part of the small intestine.
Melena is the passage of black, tarry stools. Hematochezia is the passage of fresh blood per anus, usually in or with stools.
Angiectoasias are often located in the colon , and are less often located in the upper gastrointestinal tract and small bowel. Small bowel angioectasias have been reported to be the source of obscure gastrointestinal bleeding.
K55.32 Angiodysplaysia of small intestine, with haemorrhage as appropriate.
VICC sought clinical advice which indicated that angioectasia and angiodysplasia can be considered as synonymous terms. Therefore, in answer to the specific questions in the query, in Eleventh Edition, follow the Index lead term Angiodysplasia (caecum) (colon) (intestine) and:
Small bowel angioectasias have been reported to be the source of obscure gastrointestinal bleeding. Research online also indicates the term angiodysplasia has been used interchangeably with angioectasia, though there has been debate over these terms equivalence. There is no specific index pathway for ‘angioectasia’.
The 2022 edition of ICD-10-CM K55.21 became effective on October 1, 2021.
certain conditions originating in the perinatal period ( P04 - P96) certain infectious and parasitic diseases ( A00-B99) complications of pregnancy, childbirth and the puerperium ( O00-O9A)
Fibrosis of the wall of a segment of the intestine that leads to intestinal lumen narrowing.
The 2022 edition of ICD-10-CM K56.69 became effective on October 1, 2021.
It often requires surgery. Any impairment, arrest, or reversal of the normal flow of intestinal contents toward the anal canal. Any impairment, arrest, or reversal of the normal flow of intestinal contents toward the anus.
Angioectasia is a collection of abnormal blood vessels composed of thin tortuous capillaries without an internal elastic membrane. Yano-Yamamoto’s [7] accepted endoscopic classification of small-bowel vascular lesions classifies small-bowel angioectasia as a type 1 lesion (Fig. 1). These lesions are further subclassified, as follows: type 1a lesions are characterized by punctate erythema (<1 mm) with or without oozing, and type 1b lesions are characterized by patchy erythema (2–3 mm) with or without oozing. Fan et al. reported the use of argon plasma coagulation (APC) for the endoscopic treatment of small-bowel angioectasia [8]. However, there is no consensus on the optimal endoscopic treatment of small-bowel angioectasia.
Cardiovascular disease and liver cirrhosis were significant independent major predictors of small-bowel angioectasia. Type 1a angioectasias with oozing are indicated for PDI and type 1b angioectasias are indicated for PDI with APC or clipping.
Small-bowel angioectasias comprise the majority of small-bowel vascular lesions and are found in 30–40 % of OGIB cases [6]. Despite these facts, the major predictors for small-bowel angioectasia have not been determined.
suggested that a neurohormonal abnormality, in which sympathetic nerve stimulation occurs in response to chronic hypoperfusion, leads to relaxation of intestinal vascular smooth muscle, causing local vascular overload, dilation, and eventually, permanent angioectasia [10]. Junquera et al. reported that the overexpression of angiogenic factors, such as basic fibroblast growth factor and vascular endothelial growth factor, seems to play a pathogenic role in the development of angioectasia [11, 12].
Small-bowel angioectasias are frequently diagnosed with capsule endoscopy (CE) or balloon endoscopy however, major predictors have not been defined and the indications for en doscopic treatment have not been standardized . The aim of this study was to evaluate the predictors and management of small-bowel angioectasia.
In this study, cardiovascular disease and liver cirrhosis were independent predictors of small-bowel angioectasia. Aortic stenosis [13], chronic renal failure [14], and von Willebrand disease [15] have all been associated with gastrointestinal angioectasia. Hemorrhagic gastrointestinal angioectasia associated with aortic stenosis has been reported as Heyde’s syndrome [13]. In the present study, there were four patients in the angioectasia group (6 %) who had aortic stenosis. Additionally, portal hypertensive enteropathy (PHE) associated with portal hypertension in patients with liver cirrhosis has been reported to be a major cause of gastrointestinal bleeding [16]. The endoscopic findings for PHE have been described as red spots, erosions, angioectasia, villous edema, and varices. The presumed cause is blood-flow stasis associated with portal hypertension however, the pathogenesis remains unknown. De Palma et al. conducted a CE-based study and found PHE in 67 % of patients with liver cirrhosis [17]. We previously reported the use of CE to diagnose PHE, especially in patients with Child-Pugh class B or C, ascites, and portal hypertensive gastropathy in patients with compensated liver cirrhosis and portal hypertension [18]. In addition, previously reported major predictors of PHE were the presence of a left gastric vein and splenorenal shunts [19]. Therefore, we believe that patients with OGIB with cardiovascular disease and/or liver cirrhosis should undergo CE and/or DBE to evaluate possible bleeding from small-bowel angioectasia.