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| {{CMG}}; {{AE}} {{MKK}}, {{SSW}} | | {{CMG}}; {{AE}} |
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| == Oral Cancer ==
| |
| Oral cancer differential diagnosis
| |
| The table below outlines the different types of tumors/cancers present in the oral cavity and oropharynx and how they can be differentiated from one another.
| |
| {| class="wikitable" | | {| class="wikitable" |
| !Type of cancer | | !Site |
| !Subtype | | !Patient |
| !ICD-O Code | | !AE |
| !Epidemiology | | !Complication |
| !Etiology | | !Event date |
| !Localization | | !AE code |
| !Clinical features
| |
| !Diagnostic procedures
| |
| |-
| |
| |[[Squamous cell carcinoma]]
| |
| * Basaloid squamous cell carcinoma
| |
| * Papillary squamous cell carcinoma
| |
| * Spindle cell carcinoma
| |
| * Acantholytic squamous cell carcinoma
| |
| * Acantholytic squamous cell carcinoma
| |
| * [[Adenosquamous carcinoma]]
| |
| | |
| |[[Verrucous carcinoma]]
| |
| |8051/3
| |
| |
| |
| * Older males
| |
| * 5th and 6th decades of life
| |
| * Males are affected more often than females
| |
| |
| |
| * [[Tobacco smoking]] and [[alcohol]]
| |
| * Chronic smokeless tobacco
| |
| * HPV 16 and 18
| |
| |
| |
| * Lip SCC arise almost exclusively on the lower lip
| |
| * Buccal mucosa
| |
| * Upper and lower gingiva
| |
| | |
| * Hard palate
| |
| * Anterior two-thirds of the tongue, including dorsal, ventral and lateral surfaces, and the floor of mouth
| |
| |
| |
| * Often asymptomatic or may present with vague symptoms and mini- mal physical finding
| |
| |Biopsy shows:
| |
| Thickened club-shaped
| |
| | |
| papillae and blunt stromal invaginations
| |
| | |
| of well-differentiated squamous epitheli-
| |
| um with marked keratinization
| |
| |-
| |
| |Lymphoepithelial carcinoma
| |
| |
| |
| |8082/3
| |
| |0.8-2% of all oral or oropharyngeal cancers
| |
| |EBV
| |
| |
| |
| * Tonsil and tongue(90%)
| |
| * Palate and buccal mucosa(others)
| |
| |
| |
| * Intra-oral mass, which may be ulcerated.
| |
| | |
| * Some tumors can be bilateral
| |
| |Biopsy chows:
| |
| * Syncytial sheets and clusters of carcinoma cells with vesicular nuclei
| |
| | |
| * Prominent nucleoli and ill-defined cell borders
| |
| * A rich lymphoplasmacytic infiltrate is present
| |
| |-
| |
| |Epithelial precursor lesions
| |
| |
| |
| |
| |
| |
| |
| |Smoking
| |
| |Seen in the entire digestive tract
| |
| |
| |
| * White patches (leukoplakia)
| |
| * Red patches (erythroplasia/erythroplakia)
| |
| * Mixed red and white lesions
| |
| |Biopsy shows:
| |
| * Hyperplasia
| |
| * Dysplasia, / squamous intraepithelial neoplasia / atypical hyperplasia
| |
| * Carcinoma in-situ
| |
| |-
| |
| |Proliferative verrucous leukoplakia and precancerous conditions
| |
| |
| |
| |
| |
| |
| |
| * Average age at diagnosis is 62 years
| |
| * Women are more commonly afflicted (ratio, 4:1)
| |
| |Unknown
| |
| |
| |
| * Buccal mucosa in women
| |
| * Tongue in men.
| |
| |An aggressive form of oral leukoplakia with considerable morbidity and
| |
| | |
| strong predilection to malignant transformation
| |
| |Biopsy shows:
| |
| * Extensive, thick, white plaques
| |
| * Hyperplasia and dense hyperkeratosis
| |
| * Verrucous surface with hyperkeratosis, hypergranulosis and a dense inflammatory infiltrate in the corium
| |
| |-
| |
| | rowspan="3" |Papillomas
| |
| |Squamous cell papilloma and
| |
| verruca vulgaris
| |
| |
| |
| |
| |
| * Common in children and in adults in the 3rd to 5th decades
| |
| | |
| * Almost equal sex incidence with a slight male predominance
| |
| |HPV subtype
| |
| 2,4,6,7,10,40.
| |
| |Any oral site may be affected mostly:
| |
| * Hard and soft palate
| |
| | |
| * Labial mucosa
| |
| * Tongue
| |
| * Gingiva
| |
| |
| |
| * Soft, peduncu-
| |
| lated lesions formed by a cluster of finger-like fronds or a sessile, dome-
| |
| | |
| shaped lesion with a nodular, papillary or
| |
| verrucous surface
| |
| |Biopsy shows:
| |
| * Exophytic and comprise folds of hyperplastic stratified epithelium
| |
| * Cluster of finger-like projections
| |
| |-
| |
| |Condyloma acuminatum
| |
| |
| |
| |2nd and 5th decade with a peak in teenagers and young adults
| |
| |
| |
| * HPV, most commonly types 6,11,16 and 18
| |
| |
| |
| * Labial mucosa
| |
| * Tongue
| |
| * Palate
| |
| |
| |
| * Painless, rounded, dome-shaped exophytic nodules
| |
| | |
| * 15mm in diameter
| |
| | |
| * Have a broad base and a nodular or mulberry-like surface that is slightly red, pink or of normal mucosal color.
| |
| | |
| * Lesions may be multiple and are then usually clustered
| |
| |Biopsy shows:
| |
| | |
| Several sessile, cauliflower-like swellings forming a cluster
| |
| |-
| |
| |Focal epithelial hyperplasia
| |
| |
| |
| |Disease of children,adolescents and young adults
| |
| |HPV
| |
| | |
| 13 and 32
| |
| |
| |
| * All areas of the oral cavity
| |
| * Labial
| |
| * Buccal mucosa
| |
| * Tongue
| |
| |
| |
| * Multiple asymptomatic lesions
| |
| | |
| * Soft rounded or flat plaque-like sessile swelling.
| |
| * Usually pink or white in color
| |
| * 2-10mm in diameter
| |
| |Biopsy shows:
| |
| * Rounded sessile swelling formed by a sharply demarcated zone of epithelial acanthosis
| |
| | |
| * Koilocytes similar to those of squamous papilloma are usually present
| |
| | |
| * “Mitosoid bodies”, which are nuclei with coarse clumped heterochromatin resembling a mitotic figure
| |
| |-
| |
| |Granular cell tumour
| |
| |
| |
| |9580/0
| |
| |
| |
| * Arise in all age groups, with a peak between 40 and 60 years
| |
| * Females are affect- ed more often than males with an M/F ratio of 2:1
| |
| |No etiological factors are known
| |
| |
| |
| * Tongue is the most common single site
| |
| * Buccal mucosa
| |
| * Floor of oral cavity
| |
| * Palate
| |
| * Salivary gland
| |
| |
| |
| * Lesion presents as a smooth, sessile mucosal swelling
| |
| * 1-2 cm in diameter with a firm texture.
| |
| | |
| * The overlying epithelium is of normal color or may be slightly pale
| |
| |Biopsy shows:
| |
| * Plump eosinophilic cells with central small dark nuclei and abundant granular cytoplasm
| |
| |-
| |
| |Keratoacanthoma
| |
| |
| |
| |8071/1
| |
| |
| |
| * Occurs more often in
| |
| whites
| |
| * Twice as frequent in
| |
| men as in women
| |
| |Associated with uptake of carcinogens(e.g. via particular smoking habits)
| |
| |
| |
| * Skin of the face,including the lips
| |
| * Mucocutaneous linings may also be involved
| |
| |
| |
| * Verrucous, speckled or ulcerated lesions
| |
| | |
| * Deep projections, which extend through minor salivary glands and underlying bone
| |
| |Biopsy shows:
| |
| * Verrucous surface, keratinized clefts and penetrating squamous rete processes
| |
| * Minimal atypia seen
| |
| |-
| |
| |Papillary hyperplasia
| |
| |
| |
| |
| |
| |Affects all age groups
| |
| |Associated with:
| |
| * Wearing ill-fit- ting dentures
| |
| * Xerostomia
| |
| * Individuals with a high arched palate
| |
| * HIV infection
| |
| |Palate
| |
| |Asymptomatic nodular or papillary mucosal lesion
| |
| |Biopsy shows:
| |
| * Parakeratinisation or less frequently orthokeratinisation
| |
| |-
| |
| |Median rhomboid glossitis
| |
| |
| |
| |
| |
| |
| |
| |Associated with chronic candidal infection
| |
| |Dorsum of the tongue at the junction of the anterior two thirds
| |
| and posterior third
| |
| |Forms a patch of papillary atrophy in the region of the
| |
| embryological foramen caecum
| |
| |Biopsy shows:
| |
| * Psoriasiform hyperplasia
| |
| | |
| * Areas of pseudoepitheliomatous hyperplasia
| |
| * Atypia may be present
| |
| |-
| |
| | rowspan="8" |Salivary gland tumours
| |
| |Acinic cell carcinoma
| |
| |8550/3
| |
| |
| |
| * 2-6.5% of all intraoral salivary gland tumors
| |
| * Age range was from 11-77 years, with a mean of 45 years
| |
| * Male to female ratio of 1.5:1
| |
| |Unknown
| |
| |
| |
| * Buccal mucosa
| |
| * Upper lip and
| |
| * Palate
| |
| |Tumors usually
| |
| | |
| form non-descript swellings
| |
| |Biopsy shows:
| |
| * Solid sheets of epithelium with secretory material
| |
| * Ductal differentiation in tumors
| |
| |-
| |
| |Mucoepidermoid carcinoma
| |
| |8430/3
| |
| |
| |
| * 9.5-23% of all minor gland tumors
| |
| |Unknown
| |
| |
| |
| * Palate (most common site)
| |
| * Buccal mucosa
| |
| * Lips: upper>lower
| |
| * Floor of oral cavity
| |
| * Retromolar pad
| |
| |
| |
| * Asymptomatic
| |
| * Bluish, domed swellings that resemble mucoceles or haemangiomas
| |
| * High-grade tumors result in ulceration, loosening of teeth, paraesthesia or anaesthesia
| |
| |Low power microscopy shows low-grade tumor with both cystic and solid areas and an inflamed, fibrous stroma
| |
| |- | | |- |
| |Adenoid cystic carcinoma | | |xxx |
| |8200/3 | | |xxx |
| | | | |x |
| * 42.5% of minor gland tumors
| |
| *
| |
| |Unknown
| |
| |
| |
| * Tongue
| |
| * Tonsil
| |
| * Oropharynx
| |
| * Cheek
| |
| * Lips
| |
| * Retromolar pad and gingiva
| |
| | | | | |
| * Slow growing submucosal masses and ulceration may be seen, particularly in the palate
| | |mm/dd/YYYY |
| * Pain, or evidence of nerve involvement, is usually only present in advanced tumors
| | |xxx |
| |
| |
| Predominantly solid variant shows peri- and intraneural invasion.
| |
| | |
| |-
| |
| |Epithelial-myoepithelial
| |
| carcinoma
| |
| |8562/3
| |
| |
| |
| |Unknown
| |
| |
| |
| |
| |
| |
| |
| |-
| |
| |Clear cell carcinoma,
| |
| NOS
| |
| |8310/3
| |
| |
| |
| |Unknown
| |
| |
| |
| |
| |
| |
| |
| |-
| |
| |Basal cell
| |
| adenocarcinoma
| |
| |8147/3
| |
| |Rare in minor glands
| |
| |Unknown
| |
| |
| |
| * Palate
| |
| * Buccal mucosa
| |
| * Lip
| |
| |Asymptomatic, smooth or lobulated sub-mucosal masses
| |
| |Microscopically similar to basal
| |
| | |
| cell adenocarcinomas of the major
| |
| gland
| |
| |-
| |
| |Cystadenocarcinoma
| |
| |8450/3
| |
| |32% developed in the minor glands
| |
| |Unknown
| |
| |
| |
| * Palate
| |
| * Lips
| |
| * Buccal mucosa
| |
| * Tongue and retromolar regions.
| |
| |Slow growing and painless but
| |
| | |
| some palatal tumors may erode the
| |
| | |
| underlying bone causing
| |
| sinonasal complex.
| |
| |
| |
| |-
| |
| |Salivary duct carcinoma
| |
| |8500/3
| |
| |
| |
| * Rare in minor salivary glands
| |
| * Age range was 23-80 years (mean 56 years)
| |
| |Unknown
| |
| |
| |
| * Palate (65%)
| |
| * Buccal mucosa and vestibule (19%)
| |
| | |
| * Tongue (8%)
| |
| * Retromolar pad (4%) and upper lip (4%)
| |
| |Tumours formed painless swellings but many in the palate can be painful and ulcerated or fungated with metastases to regional lymph nodes.
| |
| |The range of
| |
| | |
| microscopical appearances os similar
| |
| | |
| to that seen in the major glands.
| |
| |-
| |
| | rowspan="4" |Salivary gland adenomas
| |
| |Pleomorphic adenoma
| |
| |8940/0
| |
| |40-70% of minor gland tumors
| |
| |Unknown
| |
| |
| |
| * Palate
| |
| * Lips and
| |
| * Buccal mucosa
| |
| |Painless, slow growing, submucosal masses, but when
| |
| | |
| traumatized may bleed or ulcerate.
| |
| |Biopsy shows cellular, and hyaline or plasmacytoid cell
| |
| |-
| |
| |Myoepithelioma
| |
| |8982/0
| |
| |42% of minor gland tumors
| |
| |Unknown
| |
| |
| |
| * Palate of younger individuals
| |
| |
| |
| |
| |
| |-
| |
| |Basal cell adenoma
| |
| |8147/0
| |
| |20% of minor gland tumors
| |
| |Unknown
| |
| |
| |
| * Upper lip
| |
| * Buccal mucosa
| |
| |
| |
| |They are histologically
| |
| | |
| similar to those in major glands.
| |
| |-
| |
| |Cystadenoma
| |
| |8149/0
| |
| |7% of benign minor gland tumors
| |
| |Uknown
| |
| |
| |
| * Lips
| |
| * Cheek
| |
| * Palate
| |
| |
| |
| |
| |
| |-
| |
| |Kaposi sarcoma
| |
| |
| |
| |
| |
| |
| |
| * Classic (elderly men of Mediterranean/EastEuropean descent)
| |
| * Endemic ( middle-aged adults and children in Equatorial Africa who are not HIV infected)
| |
| * Iatrogenic (Immunosuppressed, post-transplant)
| |
| * AIDS associated (HIV-1 infected individuals)
| |
| |
| |
| * HHV-8
| |
| * Immunologic, genetic, and environmental factors
| |
| |
| |
| * Skin ( most common)
| |
| * Mucosal mem- branes such as oral mucosa, lymph nodes and visceral organs
| |
| |
| |
| * Purplish, reddish blue or dark brown macules
| |
| * Plaques and nodules that may ulcerate
| |
| |Biopsy of all 4 types show:
| |
| * Vascular slits and sparsely distributed lymphocytes.
| |
| |-
| |
| |Lymphangioma
| |
| |
| |
| |9170/0
| |
| |
| |
| * Pediatric lesions
| |
| * Present at birth or during the first years of life.
| |
| | |
| * Appear mostly in the head and neck area but may be found in any other part of the body
| |
| |
| |
| * Developmental malformation
| |
| * Genetic abnormalities
| |
| * Turner's syndrome
| |
| |Tongue
| |
| |
| |
| * Circumscribed painless swelling
| |
| * Soft and fluctuant on palpation
| |
| * Irregular nodularity of the dorsum of the tongue
| |
| |Biopsy shows:
| |
| * Thin-walled, dilated lymphatic vessels of different size, which are lined by a flattened endothelium
| |
| |-
| |
| |Ectomesenchymal chondromyxoid
| |
| tumour of the anterior tongue
| |
| |
| |
| |
| |
| |
| |
| * Age range varies from 9-78 years
| |
| * No distinct sex predilection.
| |
| |Unknown
| |
| |
| |
| |Asymptomatic, slow growing solitary nodule in the anterior dorsal tongue
| |
| |Biopsy shows:
| |
| * Round, cup-shaped, fusiform, or polygonal cells with uniform small nuclei and moderate amounts of faintly basophilic cytoplasm
| |
| * Some tumors may show nuclear pleomorphism, hyperchromatism, and multinucleation
| |
| |-
| |
| |Focal oral mucinosis (FOM)
| |
| |
| |
| |
| |
| |
| |
| * The lesion affects all ages
| |
| * Rare in children
| |
| * There is no distinct sex predilection.
| |
| |Unknown
| |
| |
| |
| * Gingiva( most common site)
| |
| * Palate
| |
| * Cheek mucosa and
| |
| * Tongue
| |
| |Asymptomatic fibrous or cystic-like lesion
| |
| |Histopathology is characterized by:
| |
| * Well-circumscribed area of myxomatous
| |
| tissue
| |
| * Fusiform or stellate fibroblasts
| |
| | |
| * Absent or sparse reticular fibres
| |
| | |
| * Mucinous material shows alcianophilia at pH 2.5
| |
| |-
| |
| |Congenital granular cell epuli
| |
| |
| |
| |
| |
| |
| |
| * Affects newborns
| |
| * Females are affected ten times more often than males
| |
| |Etiology uncertain
| |
| |
| |
| * Maxilla
| |
| | |
| * Mandible
| |
| |Solitary, somewhat pedunculated fibroma-like lesion attached to the alveolar
| |
| ridge near the midline
| |
| |
| |
| * Ultrasound for prenatal diagnosis
| |
| * Immuno histochemically, the tumor cells are positive for vimentin and neuron specific enolase
| |
| * No reactivity with cytokeratin, CEA, desmin, hormone receptors or S-100
| |
| |-
| |
| | rowspan="5" |Haematolymphoid tumours
| |
| |Non-Hodgkin lymphoma
| |
| |
| |
| |Second most com-
| |
| mon cancer of the oral cavity
| |
| | |
| |
| |
| * There is no known etiology in most patients.
| |
| | |
| * Underlying immunodeficiency state (e.g. HIV Infection)
| |
| * Strong association with EBV
| |
| |
| |
| * Palate,
| |
| | |
| * Tongue
| |
| | |
| * Floor of mouth
| |
| * Gingiva
| |
| * Buccal mucosa
| |
| * Lips
| |
| * Palatine tonsils
| |
| * Lingual tonsils or
| |
| * Oropharynx
| |
| |NHL of the lip presents with:
| |
| * Ulcer
| |
| * Swelling,
| |
| * Discoloration
| |
| * Pain
| |
| * Paraesthesia
| |
| * Anaesthesia, or
| |
| * Loose teeth
| |
| |
| |
| Biopsy shows:
| |
| * Large cells with predominantly round nuclei and membrane-bound nucleoli, consistent with centroblastic morphology.
| |
| | |
| * Predominantly medium-sized cells with abundant pale cytoplasm.
| |
| * Large cells with round or multilobated nuclei
| |
| |-
| |
| |Langerhans cell histiocytosis
| |
| |9751/1
| |
| |
| |
| |Associated with:
| |
| * Eosinophilic granulomas
| |
| * Multifocal multisystem disease
| |
| |
| |
| * Jaw bone
| |
| * Intraoral soft tissues
| |
| * Gingiva
| |
| | |
| * Palate
| |
| * Floor of mouth
| |
| * Buccal mucosa
| |
| and
| |
| * Tonsil
| |
| |Common oral symptoms
| |
| | |
| include:
| |
| * Swelling
| |
| * Pain
| |
| * Gingivitis
| |
| * Loose teeth and
| |
| * Ulceration
| |
| |Biopsy shows ovoid Langerhans cells
| |
| | |
| with deeply grooved nuclei, thin nuclear membranes and abundant eosinophilic cytoplasm
| |
| |-
| |
| |Hodgkin lymphoma
| |
| |
| |
| |
| |
| |Strongly associated with Epstein- Barr Virus
| |
| |
| |
| * Waldeyer ring, particularly the pala-tine tonsil
| |
| * Oropharynx
| |
| * Alveolar crest of mandible
| |
| * Maxillary gingiva
| |
| |Most patients present with localized disease (stage I/II), with
| |
| * Chronic tonsillitis or tonsillar enlargement with or without enlarged cervical lymph nodes
| |
| |
| |
| |-
| |
| |Extramedullary myeloid
| |
| sarcoma
| |
| |9930/3
| |
| |
| |
| |History of acute myeloid leukaemia,
| |
| | |
| predominantly in the monocytic or
| |
| myelomonocytic subtypes
| |
| |
| |
| * Palate
| |
| | |
| * Gingiva
| |
| |Isolated tumor-forming intraoral mass
| |
| |Biopsy shows an Indian-file pattern of infiltration
| |
| |-
| |
| |Follicular dendritic cell
| |
| sarcoma / tumour
| |
| |9758/3
| |
| |
| |
| * Tumor of adulthood
| |
| | |
| * Affects wide age range
| |
| |History of underlying hya-line-vascular Castleman disease
| |
| |
| |
| * Tonsil
| |
| * Palate or
| |
| * Oropharynx.
| |
| |The patients usually
| |
| | |
| present with a painless mass
| |
| |Biopsy usually exhibits
| |
| | |
| borders and comprises:
| |
| * Fascicles
| |
| * Whorls
| |
| | |
| * Nodules,
| |
| | |
| * Storiform arrays or
| |
| * Diffuse sheets of spindly to ovoid tumour cells sprinkled with small lymphocytes
| |
| |-
| |
| |Mucosal malignant melanoma
| |
| |
| |
| |8720/3
| |
| |
| |
| * 0.5% of oral malignancies
| |
| * Incidence 0.02 per 100,000
| |
| |No known etiological factors associated with oral melanoma
| |
| |80% arise:
| |
| * Palate
| |
| * Maxillary alveolus or gingivae
| |
| * Mandibular
| |
| gingivae
| |
| | |
| Others:
| |
| * Buccal mucosa
| |
| | |
| * Floor of mouth
| |
| | |
| * Tongue
| |
| |
| |
| * Asymmetric with irregular outlines
| |
| * Macular pigmentation
| |
| * Nodular growth
| |
| * Ulceration
| |
| * Melanosis
| |
| |
| |
| * Biopsy:
| |
| * S100 positive
| |
| * Negative for cytokeratins
| |
| | |
| * More specific markers include:
| |
| * HMB45,
| |
| | |
| * Melan-A or anti-tyrosinase
| |
| |}
| |
| | |
| ==2017 ACG Guidelines for first-line treatment strategies of peptic ulcer disease for providers in North America==
| |
| {| class="wikitable"
| |
| |-
| |
| | colspan="1" style="text-align:center; background:LightGreen" |Strong recommendation
| |
| |-
| |
| | bgcolor="LightGreen" |In patients with persistent H. pylori infection, every effort should be made to avoid antibiotics that have been previously taken by the patient.
| |
| | |
| |-
| |
| | bgcolor="LightGreen" |The following regimens can be considered for use as salvage treatment:
| |
| 1.Bismuth quadruple therapy for 14 days is a recommended salvage regimen.
| |
| | |
| 2.Levofloxacin triple regimen for 14 days is a recommended salvage regimen.
| |
| |-
| |
| |-
| |
| |-
| |
| |-
| |
| |}
| |
| | |
| {| class="wikitable"
| |
| |-
| |
| | colspan="1" style="text-align:center; background:LemonChiffon" |Conditional recommendation
| |
| |-
| |
| | bgcolor="LemonChiffon" |Bismuth quadruple therapy or levofloxacin salvage regimens are the preferred treatment options if a patient received a first-line treatment containing
| |
| clarithromycin. Selection of best salvage regimen should be directed by local antimicrobial resistance data and the patient’s previous exposure to antibiotics.
| |
| |-
| |
| | bgcolor="LemonChiffon" |Clarithromycin or levofloxacin-containing salvage regimens are the preferred treatment options, if a patient received first-line bismuth quadruple therapy.
| |
| Selection of best salvage regimen should be directed by local antimicrobial resistance data and the patient’s previous exposure to antibiotics.
| |
| |-
| |
| | bgcolor="LemonChiffon" |The following regimens can be considered for use as salvage treatment:
| |
| 1.Concomitant therapy for 10–14 days is a suggested salvage regimen.
| |
| | |
| 2.Clarithromycin triple therapy should be avoided as a salvage regimen.
| |
| | |
| 3.Rifabutin triple regimen consisting of a PPI, amoxicillin, and rifabutin for 10 days is a suggested salvage regimen.
| |
| | |
| 4.High-dose dual therapy consisting of a PPI and amoxicillin for 14 days is a suggested salvage regimen.
| |
| | |
| |-
| |
| |}
| |
| | |
| ==2017 ACG Guidelines for first-line treatment strategies of peptic ulcer disease for providers in North America==
| |
| {| class="wikitable"
| |
| |-
| |
| | colspan="1" style="text-align:center; background:LightGreen" |Strong recommendation
| |
| |-
| |
| | bgcolor="LightGreen" |1.Bismuth quadruple therapy consisting of a PPI, bismuth, tetracycline, and a nitroimidazole for 10–14 days is a recommended fi rst-line treatment option.
| |
| Bismuth quadruple therapy is particularly attractive in patients with any previous macrolide exposure or who are allergic to penicillin
| |
| | |
| |-
| |
| | bgcolor="LightGreen" |2.Concomitant therapy consisting of a PPI, clarithromycin, amoxicillin and a nitroimidazole for 10–14 days is a recommended first-line treatment option
| |
| |-
| |
| |}
| |
| | |
| {| class="wikitable"
| |
| |-
| |
| | colspan="1" style="text-align:center; background:LemonChiffon" |Conditional recommendation
| |
| |-
| |
| | bgcolor="LemonChiffon" |'''1.'''Patients should be asked about any previous antibiotic exposure(s) and this information should be taken into consideration when choosing an H. pylori
| |
| treatment regimen '''.'''
| |
| |-
| |
| | bgcolor="LemonChiffon" |2.Clarithromycin triple therapy consisting of a PPI, clarithromycin, and amoxicillin or metronidazole for 14 days remains a recommended treatment in regions
| |
| where H. pylori clarithromycin resistance is known to be <15% and in patients with no previous history of macrolide exposure for any reason.
| |
| |-
| |
| | bgcolor="LemonChiffon" |3.Sequential therapy consisting of a PPI and amoxicillin for 5–7 days followed by a PPI, clarithromycin, and a nitroimidazole for 5–7 days is a suggested first line
| |
| | |
| treatment option.
| |
| | |
| |-
| |
| |-
| |
| | bgcolor="LemonChiffon" |4.Hybrid therapy consisting of a PPI and amoxicillin for 7 days followed by a PPI, amoxicillin, clarithromycin and a nitroimidazole for 7 days is a suggested
| |
| | |
| first-line treatment option.
| |
| |-
| |
| | bgcolor="LemonChiffon" |5.Levofloxacin triple therapy consisting of a PPI, levofloxacin, and amoxicillin for 10–14 days is a suggested first-line treatment option.
| |
| |-
| |
| | bgcolor="LemonChiffon" |6.Fluoroquinolone sequential therapy consisting of a PPI and amoxicillin for 5–7 days followed by a PPI, fluoroquinolone, and nitroimidazole for 5–7 days is a
| |
| suggested first-line treatment option.
| |
| |}
| |
| | |
| == Initial assessment and risk stratification ==
| |
| {| class="wikitable"
| |
| |-
| |
| | colspan="1" style="text-align:center; background:LightGreen" |'''Strong recommendation'''
| |
| |-
| |
| | bgcolor="LightGreen" |1. Hemodynamic status should be assessed immediately upon presentation and resuscitative measures begun as needed. | |
| |-
| |
| |}
| |
| | |
| {| class="wikitable"
| |
| |-
| |
| | colspan="1" style="text-align:center; background:LemonChiffon" |'''Conditional recommendation'''
| |
| |-
| |
| | bgcolor="LemonChiffon" |1.Blood transfusions should target hemoglobin ≥ 7 g / dl, with higher hemoglobins targeted in patients with clinical evidence of intravascular volume depletion or comorbidities, such as coronary artery disease.
| |
| 2. Risk assessment should be performed to stratify patients into higher and lower risk categories and may assist in initial decisions such as the timing of endoscopy, time of discharge, and level of care.
| |
| | |
| 3. Discharge from the emergency department without inpatient endoscopy may be considered in patients with urea nitrogen < 18.2 mg / dl; hemoglobin ≥ 13.0 g / dl for men (12.0 g / dl for women), systolic blood pressure ≥ 110 mm Hg; pulse 100 beats / min; and absence of melena, syncope, cardiac failure, and liver disease, as they have <1 % chance of requiring intervention.
| |
| | |
| |-
| |
| |}
| |
| == Pre-endoscopic medical therapy ==
| |
| {| class="wikitable" style="width:82%"
| |
| |-
| |
| | colspan="1" style="text-align:center; background:LemonChiffon" |'''Conditional recommendation'''
| |
| |-
| |
| | bgcolor="LemonChiffon" |1. Intravenous infusion of erythromycin (250 mg ~ 30 min before endoscopy) should be considered to improve diagnostic yield and decrease the need for
| |
| | |
| repeat endoscopy. However, erythromycin has not consistently been shown to improve clinical outcomes
| |
| | |
| |-
| |
| | bgcolor="LemonChiffon" |2. Pre-endoscopic intravenous PPI (e.g., 80 mg bolus followed by 8 mg / h infusion) may be considered to decrease the proportion of patients who have
| |
| | |
| higher risk stigmata of hemorrhage at endoscopy and who receive endoscopic therapy. However, PPIs do not improve clinical outcomes such as further
| |
| | |
| bleeding, surgery, or death
| |
| |-
| |
| | bgcolor="LemonChiffon" |3. If endoscopy will be delayed or cannot be performed, intravenous PPI is recommended to reduce further bleeding.
| |
| |-
| |
| |}
| |
| | |
| == Gastric lavage ==
| |
| {| class="wikitable"
| |
| |-
| |
| | colspan="1" style="text-align:center; background:LemonChiffon" |'''Conditional recommendation'''
| |
| |-
| |
| | bgcolor="LemonChiffon" |1. Nasogastric or orogastric lavage is not required in patients with UGIB for diagnosis, prognosis, visualization, or therapeutic effect
| |
| |-
| |
| |}
| |
| | |
| == Timing of endoscopy ==
| |
| {| class="wikitable" style="width:82%"
| |
| |-
| |
| | colspan="1" style="text-align:center; background:LemonChiffon" |'''Conditional recommendation'''
| |
| |-
| |
| | bgcolor="LemonChiffon" |Timing of endoscopy
| |
| 1. Patients with UGIB should generally undergo endoscopy within 24 h of admission, following resuscitative efforts to optimize hemodynamic parameters and
| |
| | |
| other medical problems.
| |
| |-
| |
| | bgcolor="LemonChiffon" |2. In patients who are hemodynamically stable and without serious comorbidities endoscopy should be performed as soon as possible in a non-emergent
| |
| setting to identify the substantial proportion of patients with low-risk endoscopic fi ndings who can be safely discharged.
| |
| |-
| |
| | bgcolor="LemonChiffon" |3. In patients with higher risk clinical features (e.g., tachycardia, hypotension, bloody emesis or nasogastric aspirate in hospital) endoscopy within 12 h may
| |
| | |
| be considered to potentially improve clinical outcomes.
| |
| |- | |
| |} | | |} |
|
| |
|
| ==Endoscopic diagnosis== | | == Demographic / Medical history == |
| | * '''Demographic''': [age] year old [gender] |
| | * '''Past Medical History:''' [eg. VHD, diabetes, and CAD,.../ including date] |
| | * '''Past Surgical History:''' [including date] |
| | * '''Medications:''' [relevant to the event not all] |
|
| |
|
| {| class="wikitable"
| | == Procedure == |
| |-
| | * '''Index Procedure Date/Time''': |
| | colspan="1" style="text-align:center; background:LightGreen" |'''Strong recommendation'''
| | ** mm/dd/YYYY at xx:xx [insert date and time] |
| |-
| | * '''Index Procedure Detail''': |
| | bgcolor="LightGreen" |1. Stigmata of recent hemorrhage should be recorded as they predict risk of further bleeding and guide management decisions. The stigmata, in descending
| | ** On mm/dd/YYYY at xx:xx [insert date and time] the subject underwent a [select surgical correction] for [select etiology]. |
| risk of further bleeding, are active spurting, non-bleeding visible vessel, active oozing, adherent clot, fl at pigmented spot, and clean base .
| | ** Access site details |
| |-
| | ** The site reported that there were/were not procedural complication(s). |
| |}
| |
| | |
| == Endoscopic therapy ==
| |
| {| class="wikitable"
| |
| |-
| |
| | colspan="1" style="text-align:center; background:LightGreen" |'''Strong recommendation'''
| |
| |-
| |
| | bgcolor="LightGreen" |1. Endoscopic therapy should be provided to patients with active spurting or oozing bleeding or a non-bleeding visible vessel.
| |
| |-
| |
| | bgcolor="LightGreen" |2. Endoscopic therapy should not be provided to patients who have an ulcer with a clean base or a fl at pigmented spot .
| |
| |-
| |
| | bgcolor="LightGreen" |3. Epinephrine therapy should not be used alone. If used, it should be combined with a second modality.
| |
| |-
| |
| | bgcolor="LightGreen" |4. Thermal therapy with bipolar electrocoagulation or heater probe and injection of sclerosant (e.g., absolute alcohol) are recommended because they
| |
| reduce further bleeding, need for surgery, and mortality.
| |
| |-
| |
| |}
| |
|
| |
| {| class="wikitable" style="width:82%"
| |
| |-
| |
| | colspan="1" style="text-align:center; background:LemonChiffon" |'''Conditional recommendation'''
| |
| |-
| |
| | bgcolor="LemonChiffon" |1. Endoscopic therapy may be considered for patients with an adherent clot resistant to vigorous irrigation. Benefi t may be greater in patients with clinical features
| |
| potentially associated with a higher risk of rebleeding (e.g., older age, concurrent illness, inpatient at time bleeding began).
| |
| |-
| |
| | bgcolor="LemonChiffon" |2. Clips are recommended because they appear to decrease further bleeding and need for surgery. However, comparisons of clips vs. other therapies yield
| |
| variable results and currently used clips have not been well studied .
| |
| |-
| |
| | bgcolor="LemonChiffon" |3. For the subset of patients with actively bleeding ulcers, thermal therapy or epinephrine plus a second modality may be preferred over clips or sclerosant
| |
|
| |
|
| alone to achieve initial hemostasis .
| | == Event(s) == |
| |-
| | '''Event (1):''' |
| |}
| | * '''Site Reported Event Onset Date:''' mm/dd/YYYY |
|
| |
|
| == Medical therapy after endoscopy ==
| | * '''Event summary''': |
| {| class="wikitable"
| | ** Symptoms and sign: Subject presented with [sign and symptom] on mm/dd/YYYY. |
| |-
| | ** Important characteristics of the chief complaint such as severity, site, and duration. |
| | colspan="1" style="text-align:center; background:LightGreen" |'''Strong recommendation'''
| | ** Other important symptoms related to the chief complaint. |
| |-
| | ** Physical assessment: |
| | bgcolor="LightGreen" |1. After successful endoscopic hemostasis, intravenous PPI therapy with 80 mg bolus followed by 8 mg/h continuous infusion for 72 h should be given to
| | *** Vital signs |
| patients who have an ulcer with active bleeding, a non-bleeding visible vessel, or an adherent clot.
| | *** Positive physical examinations or related negative examinations. |
| |-
| | '''Event (2):''' |
| | bgcolor="LightGreen" |2. Patients with ulcers that have fl at pigmented spots or clean bases can receive standard PPI therapy (e.g., oral PPI once daily).
| | *'''Site Reported Event Onset Date:''' mm/dd/YYYY |
| |-
| | * '''Event summary''': |
| |}
| | ** Symptoms and sign: Subject presented with [sign and symptom] on mm/dd/YYYY. |
| | ** Important characteristics of the chief complaint such as severity, site, and duration. |
| | ** Other important symptoms related to the chief compliant. |
| | ** Physical assessment: |
| | *** Vital signs |
| | *** Positive physical examinations or related negative examinations. |
|
| |
|
| == Repeat endoscopy == | | == Laboratory data == |
| {| class="wikitable"
| | * '''Lab studies list: ('''Date/ name/ value) |
| |-
| |
| | colspan="1" style="text-align:center; background:LemonChiffon" |'''Conditional recommendation'''
| |
| |-
| |
| | bgcolor="LemonChiffon" |1. Routine second-look endoscopy, in which repeat endoscopy is performed 24 h after initial endoscopic hemostatic therapy, is not recommended.
| |
| |-
| |
| | bgcolor="LemonChiffon" |2.If further bleeding occurs after a second endoscopic therapeutic session, surgery or interventional radiology with transcathether arterial embolization is
| |
| generally employed
| |
| |-
| |
| |}
| |
|
| |
|
| == Hospitalization == | | == Diagnostic tests == |
| {| class="wikitable"
| | * mm/dd/YYYY at xx:xx on brain MRI |
| |-
| | * mm/dd/YYYY at xx:xx on MRA |
| | colspan="1" style="text-align:center; background:LemonChiffon" |'''Conditional recommendation'''
| | * mm/dd/YYYY at xx:xx on CT |
| |-
| | * mm/dd/YYYY at xx:xx on EEG |
| | bgcolor="LemonChiffon" |1.Patients with high-risk stigmata (active bleeding, visible vessels, clots) should generally be hospitalized for 3 days assuming no rebleeding and no other
| | * mm/dd/YYYY at xx:xx on Carotid US |
| reason for hospitalization. They may be fed clear liquids soon after endoscopy.
| | * mm/dd/YYYY at xx:xx on ECG: |
| |-
| |
| |}
| |
| | |
| {| class="wikitable"
| |
| |-
| |
| | colspan="1" style="text-align:center; background:LightGreen" |'''Strong recommendation'''
| |
| |-
| |
| | bgcolor="LightGreen" |1.Patients with clean-based ulcers may receive a regular diet and be discharged after endoscopy assuming they are hemodynamically stable, their hemoglobin
| |
| is stable, they have no other medical problems, and they have a residence where they can be observed by a responsible adult.
| |
| |-
| |
| |}
| |
| | |
| == Long-term prevention of recurrent bleeding ulcers ==
| |
| {| class="wikitable"
| |
| |-
| |
| | colspan="1" style="text-align:center; background:LightGreen" |'''Strong recommendation'''
| |
| |-
| |
| | bgcolor="LightGreen" |1.Patients with H. pylori -associated bleeding ulcers should receive H. pylori therapy. After documentation of eradication, maintenance antisecretory
| |
| therapy is not needed unless the patient also requires NSAIDs or antithrombotics.
| |
| |-
| |
| | bgcolor="LightGreen" |2. In patients with NSAID-associated bleeding ulcers, the need for NSAIDs should be carefully assessed and NSAIDs should not be resumed if possible. In
| |
| patients who must resume NSAIDs, a COX-2 selective NSAID at the lowest effective dose plus daily PPI is recommended.
| |
| |-
| |
| |}
| |
| | |
| {| class="wikitable"
| |
| |-
| |
| | colspan="1" style="text-align:center; background:LemonChiffon" |'''Conditional recommendation'''
| |
| |-
| |
| | bgcolor="LemonChiffon" |1.In patients with low-dose aspirin-associated bleeding ulcers, the need for aspirin should be assessed. If given for secondary prevention (i.e., established
| |
| cardiovascular disease) then aspirin should be resumed as soon as possible after bleeding ceases in most patients: ideally within 1 – 3 days and certainly
| |
| | |
| within 7 days. Long-term daily PPI therapy should also be provided. If given for primary prevention (i.e., no established cardiovascular disease), anti-platelet
| |
| | |
| therapy likely should not be resumed in most patients.
| |
| |-
| |
| | bgcolor="LemonChiffon" |2. In patients with idiopathic (non- H. pylori , non-NSAID) ulcers, long-term antiulcer therapy (e.g., daily PPI) is recommended.
| |
| |-
| |
| |}
| |
| | |
| __NOTOC__
| |
| | |
| {{CMG}}; {{AE}} {{MKK}}, {{SSW}}
| |
| ==2017 ACG Guidelines for first-line treatment strategies of peptic ulcer disease for providers in North America==
| |
| {| class="wikitable"
| |
| |-
| |
| | colspan="1" style="text-align:center; background:LightGreen" |Strong recommendation
| |
| |-
| |
| | bgcolor="LightGreen" |In patients with persistent H. pylori infection, every effort should be made to avoid antibiotics that have been previously taken by the patient.
| |
| | |
| |-
| |
| | bgcolor="LightGreen" |The following regimens can be considered for use as salvage treatment:
| |
| 1.Bismuth quadruple therapy for 14 days is a recommended salvage regimen.
| |
| | |
| 2.Levofloxacin triple regimen for 14 days is a recommended salvage regimen.
| |
| |-
| |
| |-
| |
| |-
| |
| |-
| |
| |}
| |
| | |
| {| class="wikitable"
| |
| |-
| |
| | colspan="1" style="text-align:center; background:LemonChiffon" |Conditional recommendation
| |
| |-
| |
| | bgcolor="LemonChiffon" |Bismuth quadruple therapy or levofloxacin salvage regimens are the preferred treatment options if a patient received a first-line treatment containing
| |
| clarithromycin. Selection of best salvage regimen should be directed by local antimicrobial resistance data and the patient’s previous exposure to antibiotics.
| |
| |-
| |
| | bgcolor="LemonChiffon" |Clarithromycin or levofloxacin-containing salvage regimens are the preferred treatment options, if a patient received first-line bismuth quadruple therapy.
| |
| Selection of best salvage regimen should be directed by local antimicrobial resistance data and the patient’s previous exposure to antibiotics.
| |
| |-
| |
| | bgcolor="LemonChiffon" |The following regimens can be considered for use as salvage treatment:
| |
| 1.Concomitant therapy for 10–14 days is a suggested salvage regimen.
| |
| | |
| 2.Clarithromycin triple therapy should be avoided as a salvage regimen.
| |
| | |
| 3.Rifabutin triple regimen consisting of a PPI, amoxicillin, and rifabutin for 10 days is a suggested salvage regimen.
| |
| | |
| 4.High-dose dual therapy consisting of a PPI and amoxicillin for 14 days is a suggested salvage regimen.
| |
| | |
| |-
| |
| |}
| |
|
| |
|
| ===References=== | | * mm/dd/YYYY at xx:xx on ECHO: |
| {{Reflist|1}}
| | * mm/dd/YYYY at xx:xx on Ultrasound: |
| | * mm/dd/YYYY at xx:xx on Endoscopy: |
| | * mm/dd/YYYY at xx:xx ... (Other relevant imaging and diagnostic tests) |
| | ==Consults== |
| | *Date and time of consult |
| | *Suggested treatments |
| | ==Clinical course== |
| | *Date and time of events, |
| | *Patient condition got worse or better. |
| | ==Treatment and outcome== |
| | *List of relevant medical treatments |
| | *Out come [Discharge / Hospice / Death] |