Endoscopic laser treatment of vascular anomalies of the upper gastrointestinal tract.

Bown, Stephen G.; Swain, C. Paul; Storey, David; Collins, Clyde; Matthewson, K; Salmon, P. R.; Clark, C. G.

doi:10.1136/gut.26.12.1338

Cited by 81 publications

(37 citation statements)

References 13 publications

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“…Conventional management of iron deficiency anaemia leads to referral to gastroenterologists for endoscopic therapy, and this is also encouraged with HHT 110 , noting the limitations of endoscopic treatments 218 , and recommendations for a limited number of therapy sessions. 32 Before referring to a gastroenterologist, however, a careful history of nose bleeds is warranted:…”

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confidence: 99%

Hereditary haemorrhagic telangiectasia: Pathophysiology, diagnosis and treatment

2010

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Hereditary haemorrhagic telangiectasia, inherited as an autosomal dominant trait, affects approximately 1 in 5,000 people. The abnormal vascular structures in HHT result from mutations in genes (most commonly endoglin or ACVRL1) whose protein products influence TGF-ß superfamily signalling in vascular endothelial cells. The cellular mechanisms underlying the generation of HHT telangiectasia and arteriovenous malformations are being unravelled, with recent data focussing on a defective response to angiogenic stimuli in particular settings. For affected individuals, there is often substantial morbidity due to sustained and repeated haemorrhages from telangiectasia in the nose and gut. Particular haematological clinical challenges include the management of severe iron deficiency anaemia; handling the intricate balance of antiplatelet or anticoagulants for HHT patients in whom there are often compelling clinical reasons to use such agents; and evaluation of apparently attractive experimental therapies promoted in high profile publications when guidelines and reviews are quickly superseded. There is also a need for sound screening programmes for silent arteriovenous malformations. These occur commonly in the pulmonary, cerebral, and hepatic circulations, may haemorrhage, but predominantly result in more complex pathophysiology due to consequences of defective endothelium, or shunts that bypass specific capillary beds. This review will focus on the new evidence and concepts in this complex and fascinating condition, placing these in context for both clinicians and scientists, with a particular emphasis on haematological settings. Blood Reviews _ HHT 2010_ Shovlin 3 Overview of HHTHHT, also known as Osler Weber Rendu syndrome [1][2][3] , is one of the most common disorders to be inherited as an autosomal dominant trait. Careful epidemiological studies reveal that it affects approximately 1 in 5,000 individuals, 4,5 with regional differences, 6 and isolated communities displaying higher prevalences due to founder effects. 7 8 HHT was first described as a familial disease characterised by severe recurrent nasal and gastrointestinal bleeding with associated anaemia, and visible dilated blood vessels (telangiectasia) on the lips and finger tips. The majority of HHT patients are also affected by larger arteriovenous malformations (AVMs) in the pulmonary, hepatic, cerebral, pancreatic, spinal and other circulations. 1,2,9 These features, presented in more detail within Table 1, are used as criteria to diagnose HHT. 2 The spectrum of disease within the HHT umbrella has extended beyond the telangiectatic/AVM HHT pathology delineated by the Curaçao criteria. 2 More recently recognised features include pulmonary arterial hypertension 10 ; juvenile polyposis 11 ; pulmonary hypertension in the context of high output cardiac failure secondary to hepatic AVMs, when PH may be reversible after hepatic AVM treatment [12][13][14][15][16] ; a prothrombotic state associated with elevated plasma levels of factor VIII 17 , and poten...

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confidence: 99%

Hereditary haemorrhagic telangiectasia: Pathophysiology, diagnosis and treatment

2010

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“…However it is technically difficult, expensive, time-consuming and associated with high risk of perforation (frequency not less than 5-15%). [56][57][58] Other complications include tenesmus, abdominal pain, rectal stenosis, prostatitis, and recto-vaginal fistula. 59,60 Advocates of Nd:YAG laser point to its greater depth of penetration (0.8 vs 1.5 mm for APC vs 0.5 mm for CO 2 ), ability to coagulate larger vessels (5 mm diameter vs 1.5 mm for APC vs 0.5 mm for CO 2 ) and ability to produce more homogenous coagulation.…”

Section: Nd:yag Lasermentioning

confidence: 99%

Management of chronic hemorrhagic radiation proctitis

Agrawal

Bansal

Bahadur

et al. 2007

Asia-Pac J Clncl Oncology

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Rectal bleeding secondary to radiation proctitis is the most dreaded complication of pelvic radiotherapy. Its management remains a perplexing problem despite the availability of multiple treatment modalities. Patients are usually managed on a "hit and miss" basis at most centers. Steroid, 5-aminosalicylic acid, short chain fatty acids and sucralfate enemas, hyperbaric oxygen therapy, and topical application of 4% formaldehyde all have been used with varying results. Surgical procedures such diversion colostomy or resection of involved segment have been proposed for refractory bleeding. Endoscopic methods are being increasingly adopted in the form of bipolar electrocoagulation, heat probe coagulation, photoablation, Nd:YAG laser and preferably argon plasma coagulation. The utility of conservative approaches remains far below desirable levels. Onset of hemorrhagic recurrence represents a major obstacle that leads to a need for repeated therapeutic sessions and sometimes invocation of radical techniques. This review discusses various treatment modalities and aims to identify their efficacy and limitations. A critical review was conducted of published reports regarding management of chronic hemorrhagic radiation proctitis (CHRP). Although there are few prospective randomized trials, enough evidence is available to conclude that argon plasma coagulation represents the current treatment of choice.

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“…By a similar mechanism of trauma, linear erosions may occur in the herniated gastric mucosa of patients with large hiatal hernias, resulting in the anaemia of chronic blood loss. 61 Suction through nasogastric tubes, the ingestion of foreign bodies, and endoscopic procedures such as diathermy 62,63 are common causes of subepithelial haemorrhage and focal erosion. The metal in ingested foreign bodies may occasionally cause gastritis.…”

Section: Traumatic Gastropathymentioning

confidence: 99%