Mallory weiss syndrome

MALLORY-WEISS SYNDROMEMALLORY-WEISS SYNDROME
 Vigorous vomiting-vert split in the gastricVigorous vomiting-vert split in the gastric
mucosa (below sc jn at the cardia)- 90%mucosa (below sc jn at the cardia)- 90%
 Tear in the oesophagus-10%Tear in the oesophagus-10%
 Presents with hematemesisPresents with hematemesis
 endoscopic injection therapy requird 4 severeendoscopic injection therapy requird 4 severe
casescases

CORROSIVE INJURYCORROSIVE INJURY
 Corrosive-sod hydroxide,sulphuric acidCorrosive-sod hydroxide,sulphuric acid
 Accidental ingestion-damageAccidental ingestion-damage
2nouth,pharynx,larynx,oeso,stomach2nouth,pharynx,larynx,oeso,stomach
 Alkalies causeliquifaction,saponification ofAlkalies causeliquifaction,saponification of
fat,dehydration and thrombosis of bv- fibrousfat,dehydration and thrombosis of bv- fibrous
scarringscarring
 Acids-coagulative necrosis with eschar formationAcids-coagulative necrosis with eschar formation
-causes intense pylorospasm with pooling-causes intense pylorospasm with pooling
in the antrum(more gastric damage)in the antrum(more gastric damage)

Investigaion- endoscopy
-deep ulcers n black eschars-greatest
risk of perforation
Managemnt-minor injury- pt safely fed
sev injury-feeding jejunostomy
Complication-stricture formation-50%
(oeso resection)

GORDGORD
 Loss of competence of LOSLoss of competence of LOS
 Competence affected-obesity,smoking nCompetence affected-obesity,smoking n
excissive eatingexcissive eating
 Gastric acid reflux- extensive inflammmation ofGastric acid reflux- extensive inflammmation of
lower oeso- oesophagitislower oeso- oesophagitis
 Types-a/c – alcohol,burns,stressTypes-a/c – alcohol,burns,stress
c/c – hitus hernia,oesophagojejunostomyc/c – hitus hernia,oesophagojejunostomy

PRECIPITATING FACTORS-
 1.structurally defective LOS
 2.short length of oesophagus
 3.ineffective oesophageal
pump(influenced by gravity,oeso motility,salivation)
 4.increased gastric pressure

overeating/ingestion of irritants
gasrtic distension
unfolding of sphincter
terminal s epi of oeso exposed to acid
erosion,ulceration,fibrosis,metaplasia
barret”s oeso
AdenoCa

AetiopathogenesisAetiopathogenesis
 Acid reflux to LOS – diffuse inflmn withAcid reflux to LOS – diffuse inflmn with
multiple ulcersmultiple ulcers
 Symptoms worse when patient lies downSymptoms worse when patient lies down
 Vicious cycleVicious cycle
 vagal hypersensitivity – oesophagitis –vagal hypersensitivity – oesophagitis –
long muscle spasm – displacement oflong muscle spasm – displacement of
oesophagus – increased regurgitationoesophagus – increased regurgitation

CLINICAL FEATURESCLINICAL FEATURES
 Retrosternal painRetrosternal pain
 Epigastric painEpigastric pain
 RegurgitationRegurgitation
 Occult blood in stoolsOccult blood in stools
 Anaemia & weaknessAnaemia & weakness
 Dysphagia(sricture)Dysphagia(sricture)
 Atypical symp – Angina like chest pain , pulm orAtypical symp – Angina like chest pain , pulm or
laryngeal symplaryngeal symp

DIAGNOSISDIAGNOSIS
 Assume rather than prevent – Rx isAssume rather than prevent – Rx is
empericalemperical
 Investigations – when patient does notInvestigations – when patient does not
respond to ppirespond to ppi
 24 hr ph recording – gold std24 hr ph recording – gold std
 TLOSR – manometric findingTLOSR – manometric finding
 Ba swallow( in trendelenburg position)Ba swallow( in trendelenburg position)
 OesophagoscopyOesophagoscopy

MEDICAL MANAGEMENTMEDICAL MANAGEMENT
 Alcohol minimisedAlcohol minimised
 Loose weightLoose weight
 Coffee & tea minimisedCoffee & tea minimised
 Oeso mucosal protecters(Antacids,H2 blockers)Oeso mucosal protecters(Antacids,H2 blockers)
 Head up tiltHead up tilt
 Oily& spicy food avoidedOily& spicy food avoided
 Large meal avoided at nightLarge meal avoided at night
 PPI most effective drug Rx (8 wks)PPI most effective drug Rx (8 wks)

SURGERYSURGERY
 Endoscopic treatmentsEndoscopic treatments
 Surgical treatments –Surgical treatments –
uncomplicated gord –pt”s choiceuncomplicated gord –pt”s choice
Symptomatic on PPI(volume reflux ,Symptomatic on PPI(volume reflux ,
hermit lifestyle , poor compliance)hermit lifestyle , poor compliance)
Laproscopic fundoplicationLaproscopic fundoplication

COMPLICATIONSCOMPLICATIONS
 Barret”s oesophagusBarret”s oesophagus
 StrictureStricture
 Oesophageal shorteningOesophageal shortening

HIATUS HERNIAHIATUS HERNIA
 Abnormal protrusion of abdominal viscusAbnormal protrusion of abdominal viscus
through oesophageal hiatus into chest.through oesophageal hiatus into chest.
 TYPESTYPES
 1.Sliding hernia(oesophageo gastric1.Sliding hernia(oesophageo gastric
hernia) – 80%hernia) – 80%
 2.Rolling or paraoesophageal hernia2.Rolling or paraoesophageal hernia
 3.Mixed hernia3.Mixed hernia
 4.Massive herniation4.Massive herniation

Common symptomsCommon symptoms
 1.Symptoms due to reflux(reflux &heart1.Symptoms due to reflux(reflux &heart
burn)burn)
 2.Symptoms due to2.Symptoms due to
complications(dysphagia,complications(dysphagia,
odynophagia,hematemesis, melaena)odynophagia,hematemesis, melaena)
 3.Nonoesophageal synp(asthma & chest3.Nonoesophageal synp(asthma & chest
pain )pain )

SLIDING HERNIASLIDING HERNIA
 Anatomical factors which prevent slidingAnatomical factors which prevent sliding
herniahernia
 1.Presence of 2 cm of intraabd1.Presence of 2 cm of intraabd
oesophagusoesophagus
 2.The angle of His2.The angle of His
 3.Mucosal folds at oesophageocardial jn3.Mucosal folds at oesophageocardial jn
 4.+ intraabd pressure4.+ intraabd pressure
 5.LOS5.LOS

CausesCauses
 1.The position of fatty tissue in the hiatus1.The position of fatty tissue in the hiatus
 2.Advancing age – mus degeneration2.Advancing age – mus degeneration
 3.Lower abd trs , preg – raised intraabd3.Lower abd trs , preg – raised intraabd
pressurepressure
 4.Saint”s triad- Gallstone , diverticulosis,4.Saint”s triad- Gallstone , diverticulosis,
hiatus herniahiatus hernia

CF
like reflux oesophagitis
commom in women,obese
INVESTIATIONS
Oesophagoscopy- reflux of the gastric acd –
most valuable sign.
Ba meal- gord in trendelemburg

TREATMENT
 1.Conservative treatment
Principles:
1.Lifestyle changes
-decrease in wt
-Diet cntrol
-decreasd alcohol n tobecco consumption
2.Oesophageal mucosa protection
-Antacids
-H2 blockers
-PPI

SurgerySurgery
 IndicationsIndications
-Intractable pain-Intractable pain
-Complication –hge or stricture-Complication –hge or stricture
Types of surgeryTypes of surgery
1.Nissen”s total fundoplication1.Nissen”s total fundoplication
2.Partial fundplication(Tupet)2.Partial fundplication(Tupet)
3.Belsey mark IV operation3.Belsey mark IV operation
4.Hill”s repair4.Hill”s repair

ROLLING HERNIAROLLING HERNIA
 Cardio –oeso jn is normal.Cardio –oeso jn is normal.
 Greater curvature of stomach ascends intoGreater curvature of stomach ascends into
a preformed sac in mediastinum.a preformed sac in mediastinum.
 Compression of heart & lung.Compression of heart & lung.

Clinical FeaturesClinical Features
 No retrosternal burning painNo retrosternal burning pain
 Discomfort after a small mealDiscomfort after a small meal
 Feeling of fullness after meal or dysphagiaFeeling of fullness after meal or dysphagia
 PalpitationsPalpitations
 RTI or hiccough (phrenic nerve irritation)RTI or hiccough (phrenic nerve irritation)

InvestigationInvestigation
Ba mealBa meal
RxRx
 Reduction of sac &repair of hiatusReduction of sac &repair of hiatus
MIXED HERNIAMIXED HERNIA
Both rolling & sliding hernia +Both rolling & sliding hernia +
Symptoms & Rx - mixedSymptoms & Rx - mixed

BARRET”S OESOPHAGUSBARRET”S OESOPHAGUS
 When columnar mucosa extends at least 3When columnar mucosa extends at least 3
cm into oesophaguscm into oesophagus
 Intestinal metaplasiaIntestinal metaplasia
PathogenesisPathogenesis
 Rptd reflux –Shifting of oesogastric jnRptd reflux –Shifting of oesogastric jn
upwards – Further increase in reflux –upwards – Further increase in reflux –
Intestinal metaplasia of middle & lowerIntestinal metaplasia of middle & lower
oesooeso

PATHOLOGICAL TYPESPATHOLOGICAL TYPES
 1.Gastric type – Chief & parietal cells1.Gastric type – Chief & parietal cells
 2.Intestinal type – Goblet cells2.Intestinal type – Goblet cells
 3. junctional type – Mucous glands3. junctional type – Mucous glands
CLINICAL TYPESCLINICAL TYPES
-Long segment : Metaplastic changes more-Long segment : Metaplastic changes more
than 3cmthan 3cm
-Short segment:Changes less than 3 cm-Short segment:Changes less than 3 cm

Incidence of malignancyIncidence of malignancy
 Lower &Midle oeso more prone to developLower &Midle oeso more prone to develop
CACA
 CA will be invasive & more proximalCA will be invasive & more proximal
TYPES OF DYSPLASIATYPES OF DYSPLASIA
-Low grade : negligible risk for ca-Low grade : negligible risk for ca
-High grade :very high risk for ca-High grade :very high risk for ca

RxRx
 Laser photodynamic therapyLaser photodynamic therapy
 Argon beam plasma coaulationArgon beam plasma coaulation
 Lap antireflux surgeryLap antireflux surgery
 High dose PPIHigh dose PPI
 Oesophagectomy(High grade dysplasia)Oesophagectomy(High grade dysplasia)
ComplicationsComplications
 1. Oesophageal ulcers1. Oesophageal ulcers
 2.Oesophageal strictures2.Oesophageal strictures
 3.Dysplasia & adenoca3.Dysplasia & adenoca

Mallory weiss syndrome

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