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__NOTOC__
__NOTOC__


{{CMG}}; {{AE}} {{MKK}}, {{SSW}}
{{CMG}}; {{AE}}


== Oral Cancer ==
== Demographic / Medical history ==
Oral cancer differential diagnosis
* '''Demographic''': 77, M
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.
* '''Past Medical History:''' HTN, BPH, CAD w CABG, MI, AVR
{| class="wikitable"
* '''Past Surgical History:'''
!Type of cancer
** AVR (#25 magna ease valve) on 12/14/17
!Subtype
** Stent on 10/10/2017
!ICD-O Code
** CABG in 2007
!Epidemiology
** Appendectomy in 1957
!Etiology
!Localization
!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]]
* '''Medications:'''
|8051/3
** Metoprolol
|
** DAPT
* Older males
** Tamsulosin
* 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
== Procedure ==
* Anterior two-thirds  of  the  tongue,  including  dorsal, ventral and lateral surfaces, and the floor of mouth
* '''Index Procedure Date/Time''':
|
** mm/dd/YYYY at xx:xx [insert date and time]
* Often asymptomatic or may  present  with  vague  symptoms  and mini- mal  physical  finding
* '''Index Procedure Detail''': 
|Biopsy shows:
** On mm/dd/YYYY at xx:xx [insert date and time] the subject underwent a [select surgical correction] for [select etiology].
Thickened  club-shaped
** Access site details
** The site reported that there were/were not procedural complication(s).


papillae  and  blunt  stromal  invaginations
== Event(s) ==
'''Event (1):'''
* '''Site Reported Event Onset Date: 12/26/2017'''


of  well-differentiated  squamous  epitheli-
* '''Event summary''':
um with marked keratinization
** Symptoms and sign: Subject presented with
|-
*** Right leg collapse,
|Lymphoepithelial carcinoma
*** Right arm and right leg weakness
|
** Episodes lasted approximately  2 -10 minutes and ranged from 1-4/day
|8082/3
** No visual or speech difficulties, no headache or neck pain
|0.8-2%  of all  oral  or oropharyngeal cancers
** No history of vertigo, syncope, loss of consciousness or seizures
|EBV
** Other important symptoms related to the chief complaint.
|
** Physical assessment:
* Tonsil  and  tongue(90%)
*** Normal neurological exam
* Palate  and  buccal  mucosa(others)
*** BP: 124/66
|
*** HR: 96
* Intra-oral mass,  which  may  be  ulcerated.
== Laboratory data ==
* '''Lab studies list: ('''Date/ name/ value)
** 01/04/2018 / HDLC / 31
** 01/03/2018 / INR / 1.2


* Some tumors  can  be  bilateral
== Diagnostic tests ==
|Biopsy chows:
* 01/03/2018 '''TTE'''
* Syncytial sheets and  clusters  of  carcinoma  cells  with vesicular  nuclei
** Mild left ventricular hypertrophy with normal systolic function and left ventricular diastolic dysfunction
 
** Moderate left atrial enlargement
* Prominent  nucleoli  and ill-defined  cell  borders
** Bioprosthetic aortic valve peak vel 2 m/s and mean grad 6.4 hg, no AI
* A  rich  lymphoplasmacytic infiltrate is present
* 01/03/2018 '''MR Brain'''
|-
** NO evidence of vascular occlusion
|Epithelial precursor lesions
** No evidence of restricted diffusion to suggest infarction
|
* 01/03/2018 '''MRA H/N'''
|
** Eccentric filling defect in the left internal carotid artery just distil to the bifurcation that may be from calcification / nonocclusive thrombus
|
* 01/03/2018 '''Carotid US(Preliminary)'''
|Smoking
** Right: 1-49% stenosis of right internal carotid
|Seen in the entire digestive tract
** Left: 1-49% stenosis of left internal carotid
|
** Bilateral vrtebral arteries patent with antegrade flow
* White  patches  (leukoplakia)
* 01/03/2018 '''EEG'''
* Red patches  (erythroplasia/erythroplakia)
** Normal awake EEG
* Mixed red and white lesions
** No epilitiform discharges, focal changes or other abnormalities
|Biopsy shows:
==Consults==
* Hyperplasia
*Neurology consult : 01/03/2018
* Dysplasia,  / squamous  intraepithelial  neoplasia / atypical hyperplasia
*Recommendations:  
* Carcinoma in-situ
**CBC,CMP
|-
**Admission to neurology service
|Proliferative verrucous leukoplakia and precancerous conditions
**MRI brain with or without contrast
|
**MRA of the extracranial and intracranial circulation
|
**Carotid duplex US
|
**EEG
* Average age at diagnosis is 62 years
*Date and time of consult
* Women are  more  commonly  afflicted  (ratio,  4:1)
*Suggested treatments:  
|Unknown
**Aspirin 81mg chew tab
|
**Clopidogrel 75 mg tab
* Buccal  mucosa in women
**Enoxaparin 40mg inj
* Tongue  in  men.
**Metoprolol succinate 25mg extended release
|An  aggressive  form  of  oral  leukoplakia  with considerable  morbidity  and
==Clinical course==
 
*
strong  predilection  to  malignant  transformation
*Date and time of events,
|Biopsy shows:
*Patient condition got worse or better.
* Extensive, thick, white plaques
==Treatment and outcome==
* Hyperplasia and dense hyperkeratosis
*List of relevant medical treatments
* Verrucous surface with hyperkeratosis, hypergranulosis and a dense inflammatory infiltrate in the corium
**Aspirin 81mg chew tab
|-
**Clopidogrel 75 mg tab
| rowspan="3" |Papillomas
**Enoxaparin 40mg inj
|Squamous cell papilloma and
**Metoprolol succinate 25mg extended release
verruca vulgaris
*Out come - Discharged home
|
|
* 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
|8200/3
|
* 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
* Pain,  or  evidence  of  nerve  involvement,  is  usually  only  present  in advanced  tumors
|
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==
 
{| class="wikitable"
|-
| colspan="1" style="text-align:center; background:LightGreen" |'''Strong recommendation'''
|-
| 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
risk of further bleeding, are active spurting, non-bleeding visible vessel, active oozing, adherent clot, fl at pigmented spot, and clean base .
|-
|}
 
== 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 .
|-
|}
 
== Medical therapy after endoscopy ==
{| class="wikitable"
|-
| colspan="1" style="text-align:center; background:LightGreen" |'''Strong recommendation'''
|-
| 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
patients who have an ulcer with active bleeding, a non-bleeding visible vessel, or an adherent clot.
|-
| 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).
|-
|}
 
== Repeat endoscopy ==
{| class="wikitable"
|-
| 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 ==
{| class="wikitable"
|-
| colspan="1" style="text-align:center; background:LemonChiffon" |'''Conditional recommendation'''
|-
| 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
reason for hospitalization. They may be fed clear liquids soon after endoscopy.
|-
|}
 
{| 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===
{{Reflist|1}}

Latest revision as of 16:44, 18 June 2018


Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Demographic / Medical history

  • Demographic: 77, M
  • Past Medical History: HTN, BPH, CAD w CABG, MI, AVR
  • Past Surgical History:
    • AVR (#25 magna ease valve) on 12/14/17
    • Stent on 10/10/2017
    • CABG in 2007
    • Appendectomy in 1957
  • Medications:
    • Metoprolol
    • DAPT
    • Tamsulosin

Procedure

  • Index Procedure Date/Time:
    • mm/dd/YYYY at xx:xx [insert date and time]
  • Index Procedure Detail:
    • On mm/dd/YYYY at xx:xx [insert date and time] the subject underwent a [select surgical correction] for [select etiology].
    • Access site details
    • The site reported that there were/were not procedural complication(s).

Event(s)

Event (1):

  • Site Reported Event Onset Date: 12/26/2017
  • Event summary:
    • Symptoms and sign: Subject presented with
      • Right leg collapse,
      • Right arm and right leg weakness
    • Episodes lasted approximately 2 -10 minutes and ranged from 1-4/day
    • No visual or speech difficulties, no headache or neck pain
    • No history of vertigo, syncope, loss of consciousness or seizures
    • Other important symptoms related to the chief complaint.
    • Physical assessment:
      • Normal neurological exam
      • BP: 124/66
      • HR: 96

Laboratory data

  • Lab studies list: (Date/ name/ value)
    • 01/04/2018 / HDLC / 31
    • 01/03/2018 / INR / 1.2

Diagnostic tests

  • 01/03/2018 TTE
    • Mild left ventricular hypertrophy with normal systolic function and left ventricular diastolic dysfunction
    • Moderate left atrial enlargement
    • Bioprosthetic aortic valve peak vel 2 m/s and mean grad 6.4 hg, no AI
  • 01/03/2018 MR Brain
    • NO evidence of vascular occlusion
    • No evidence of restricted diffusion to suggest infarction
  • 01/03/2018 MRA H/N
    • Eccentric filling defect in the left internal carotid artery just distil to the bifurcation that may be from calcification / nonocclusive thrombus
  • 01/03/2018 Carotid US(Preliminary)
    • Right: 1-49% stenosis of right internal carotid
    • Left: 1-49% stenosis of left internal carotid
    • Bilateral vrtebral arteries patent with antegrade flow
  • 01/03/2018 EEG
    • Normal awake EEG
    • No epilitiform discharges, focal changes or other abnormalities

Consults

  • Neurology consult : 01/03/2018
  • Recommendations:
    • CBC,CMP
    • Admission to neurology service
    • MRI brain with or without contrast
    • MRA of the extracranial and intracranial circulation
    • Carotid duplex US
    • EEG
  • Date and time of consult
  • Suggested treatments:
    • Aspirin 81mg chew tab
    • Clopidogrel 75 mg tab
    • Enoxaparin 40mg inj
    • Metoprolol succinate 25mg extended release

Clinical course

  • Date and time of events,
  • Patient condition got worse or better.

Treatment and outcome

  • List of relevant medical treatments
    • Aspirin 81mg chew tab
    • Clopidogrel 75 mg tab
    • Enoxaparin 40mg inj
    • Metoprolol succinate 25mg extended release
  • Out come - Discharged home
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