COMPLICATIONS OFULCER SURGERY

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COMPLICATIONS OF:

COMPLICATIONS OF PEPTIC ULCER SURGERY

COMPLICATIONS:

COMPLICATIONS RECURRENT ULCERATION SMALL STOMACH SYNDROME BILE VOMITING DUMPING SYNDROMES EARLY LATE POST VAGOTOMY DIARRHOEA MALIGNANT TRANSFORMATION NUTRITIONAL CONSEQUENCES GALLSTONES

RECURRENT ULCERATION:

RECURRENT ULCERATION INCIDENCE OF RECURRENCE OPERATION INCIDENCE GASTRECTOMY 1-4 GASTRECTOMY ALONE 50 TRUNCAL VAGOTOMY+DRAINAGE SELECTIVE VAGOTOMY +DRAINAGE 2-7 5-10 HIGHLY SEL.VAGOTOMY 2-10 T.V&ANTRECTOMY 1

REC. ULCERATION….:

REC. ULCERATION…. SITE HSV - 1 ST PART OF DUODENUM GJ - AT ANASTOMOSIS ON JEJUNAL SIDE (JEJUNAL MUCOSA MORE SENSITIVE TO ACID DIGESTION) GASTRECTOMY - JEJUNAL SIDE OF THE STOMA MC PRESENTING SYMPTOM - PAIN RISK FACTORS TECHNICALLY INADEQUATE OPERATION CIGARATE SMOKING REFRACTORY ULCERS BEFORE OPERATION

REC. ULCERATION…:

REC. ULCERATION … COMLICATIONS BLEEDING PERFORATION GASTROJEJUNOCOLIC FISTULA ANASTOMOTIC ULCER PENETRATES INTO TRANSVERSE COLON SYMPTOMS SEVERE DIARRHOEA AFTER EVERY MEAL FOUL BREATH &MAY VOMIT FORMED FECES NUTRITIONAL DISTUBANCES(DUE TO SEVERE CONTAMINATION OF JEJUNUM WITH COLONIC BACTERIA INVESDTIGATIONS - BARIUM ENEMA,CT SCAN , ENDOSCOPY , BARIUM MEAL TREATEMENT -CORRECTION OF DEHYDRATION & , MALNUTRITION,REVISIONAL SURGERY

SMALL STOMACH SYNDROME:

SMALL STOMACH SYNDROME EARLY SATIETY DUE REDUCTION IN THE SIZE OF STOMACH IN HIGHLY SELECTIVE VAGOTOMY -- LOSS OF RECEPTIVE RELAXATION IMPOOVES WITH TIME NO NEED OF REVISIONAL SURGERY

BILE VOMITING:

BILE VOMITING AFTER ANY FORM OF VAGOTOMY WITH DRAINAGE OR GASTRECTOMY EATING PRECIPITATES PAIN &REFLUX SYMPTOMS VOMITS A MIXTURE OF FOOD & BILE OR SOME TIMES BILE ALONE AFTER MEAL TREATEMENT REVISIONAL SURGERY GASTRECTOMY - ROUX-EN Y DIVERSION GJ – TAKEN DOWN & SMALL PYLOROPLASTY IS DONE PYLOROPLASTY – ANTRECTOMY & ROUX-EN-Y RECONSTRUCTION

EARLY DUMPING:

EARLY DUMPING INCIDENCE IN10% OF PTS. FOLLOWING GASTRECTOMYOR VAGOTOMY&DRAINAGE AND RARELY FOLLOWING HSV SYMPTOMS – ABDOMINAL&VASOMOTOR MECHANISM SMALL BOWEL IS FILLED WITH FOOD STUFFS FROM STOMACH WHICH HAVE HIGH OSMOTIC LOAD LEADS TO SEQUESTRATION OF FLUID FROM CIRCULATION INTO GIT

LATE DUMPING:

LATE DUMPING INCIDENCE 5% REACTIVE HYPOGLYCEMIA MECHANISM - CARBOHYDRATE LOAD IN STOMACH CAUSES HYPERGLYCEMIA WHICH INTURN RISES INSULINLEVELS RESULTING IN SECONDARY HYPOGLYCEMIA

FEATURES OF EARLY&LATE DUMPING:

FEATURES OF EARLY&LATE DUMPING FEATURE EARLY LATE INCIDENCE 5-10% 5% RELATION TO MEALS ALMOST IMMEDIATE SECOND HOUR AFTER MEAL DURATION 30-40 MIN 30-40 MIN RELIEF LYING DOWN FOOD AGGRAVATEDBY MORE FOOD EXCERCISE PRECIPITATING FACTOR FOOD ,ESPECIALLY CARBOHYDRATE RICH&WET AS EARLY DUMPING MAJOR SYMPTOMS EPIGASTRIC FULLNESS, SWETTING, LIGHTHEADEDNESS, TACHYCARDIA,COLIC, SOMETIMES DIARRHOEA TREMOUR,FAINTNESS, PROSTRATION

TREATMENT OF DUMPING SYNDROMES:

TREATMENT OF DUMPING SYNDROMES SAME FOR BOTH EARLY & LATE DIETARY MANIPULATION SMALL DRY MEALS,AVOID FLUIDS WITH HIGH CARBOHYDRATE CONTENT SOMATOSTATIN ANALOGUE OCTREOTIDE BEFORE MEALS REVISIONAL SURGERY GJ – DRAINAGE IS TAKEN DOWN PYLOROPLASTY – REPAIRGASTRECTOMY - ANTRERCTOMY&ROUX-EN-Y RECONSTRUCTION

POST VAGOTOMY DIARHOEA:

POST VAGOTOMY DIARHOEA MOST DEVASTATING SYMPTOM. MOST PTS. HAVE SOME DEGREE OF LOOSENESS OF STOOLS EXCEPT IN HSV IN 5% IT IS INTRACTABLE CAUSE RAPID GASTRIC EMPTYING DENERVATION OF UPPER GIT EXGGERATED GASTROINTESTINAL PEPTIDE RESPONSE SEVERAL FORMS SEVERE & EXPLOSIVE WITH URGENCY FEELING LIKE PASSING OF BOILING WATER MINOR EPISODES OF DIARRHOEA TREATMENT DIFFICULT TO TREAT AS FOR EARLY DUMPING ANTIDIARRHOEALS OCTREOTIDE&REVISIONAL SURGERY ARE NOT EFFECTIVE

MALIGNANT TRANSFORMATION:

MALIGNANT TRANSFORMATION GASTRECTOMY OR VAGOTOMY WITH DRAINAGE ARE INDEPENDENT RISK FACTORS FOR CA.STOMACH BILE REFLUX GASTRITIS - INTESTINAL METAPLASIA - GASTRIC CANCER RISK INCREASES BY FOUR TIMES LAG PHASE 10 YEARS HSV NOT ASSOCIATED WITH CARCINOMA

NUTRITIONAL CONSEQUENCES:

NUTRITIONAL CONSEQUENCES MORE COMMON AFTER GASTRECTOMY THAN AFTER VAGOTOMY &DRAINAGE WEIGHT LOSS ANAEMIA IRON DEFFICIENCY OR B12 DEFFICIENCY IRON DEFFICIENCY AFTER GASTRECTOMY &VAGOTOMY &DRAINAGE CAUSE REDUCED IRON ABSORPTION&LOSS OF BLOOD FROM GASTRIC MUCOSA B12 DEFFICIENCY AFTER TOTAL; GASTRECTOMY CAUSE REDUCED INTRINSIC FACTOR PRODUCTION& BACTERIAL COLANISATION DESTROYS B12 INGUT OSTEOPOROSIS CA. DEFFICIENCY CAUSES OSTEOPOROSIS SEEN AFTER POLYA GASTRECTOMY TREATMENT CA. & VITAMIN D SUPPLEMENTATION,EXCERCISE

GALLSTONES:

GALLSTONES MC AFTER TRUNCAL VAGOTOMY CAUSE BILIARY TRE&STOMACH IS DENERVATED LEEDS TO STASIS & FORMATION OF GALLSTONES TREATEMENT CHOLECYSTECTOMY MAY WORSEN POST CHOLECYSTECTOMY SYNDROMES LIKE BILIOUS VOMITINGS &POSTVAGOTOMY DIARRHOEA

INFANTILE HYPERTROPHIC PYLORIC STENOSIS:

INFANTILE HYPERTROPHIC PYLORIC STENOSIS INCIDENCE 3/1000BIRTHS M:F 4:1 AETIOLOGY UNKNOWN FAILURE OF PYLORUS TO RELAX LEADS TO MUSCULAR HYPERTROPHY FAMILIAL ASSOCIATION PATHOLOGY MUSCULATURE OF PYLORUS ANDADJACENT ANTRUM IS HYPERTROPHIED,MAXIMUM IN PYLORUS COMPRRESSION OF MUCOSA ,ONLY APROBE CAN BE PASSED

IHPS….:

IHPS…. CLINICAL FEATURES 1 ST BORN MALE CHILD IS MOST COMMONLY AFFECTED MOST CMMONLY SEEN AT 4 WEEKS AFTER BIRTH ,RANGES FROM 3 RD TO SEVENTH WEEK VOMITINGS FORCIBLE&PROJECTILE VOMITING NONBILIOUS VOMITINGS IMMEDIATELY AFTER VOMITING THE CHILD IS HUNGRY WEIGHT LOSS&EMACIATION DEHYDRATION VGP AFTER A TEST FEED PALPABLE LUMP INVESTIGATION U/S

IHPS…:

IHPS … DIFFERENTIAL DIAGNOSIS GASTRO-OESOPHAGEAL REFLUX FEEDING PROBLEMS UTI RAISED ICT DISTINGUISHED FROM INTESTINAL OBSTRUCTION AS THE CHARACTER OF VOMITUS IS NON BILIOUS

IHPS…:

IHPS… TREATMENT CORRECTION OF METABOLIC ABNORMALITIES FOLLOWED BY SURGERY HYPONATREMIA,HYPOCHLOREMIA,HYPOKALEMIA&METABOLIC ALKALOSIS ARE CORRECTED CORRECTION OF DEHYDRATION 2.5%DEXTROSE .45%NaCl 1gm OF KCL PER 500ml OF FLUID

IHPS…:

IHPS … SURGERY RAMSTED’S OPERATION STOMACH WASH AVOID HYPOTHERMIA GENERAL ANAESTHESIA/LOCAL INCISION TRANSVERSE INCISION IN UPPER ABD. OVER RT. RECTUS INCISION IS MADE THROUGH THE SEROSA ONLY ON PYLORUS &DISTAL ANTRUMMUSCLE COATS ARE SPLITT BY BLUNT DISSECTION MUCOSA SHOULD NOT BE PENETRATED IF PERFORATION OCCURS .CLOSURE WITH OMENTAL PATCH COMLICATIONS POSTOPERATIVE PYREXIA WOUND DISRUPTION1% WOUND INFECTION 5%

GASTRITIS:

GASTRITIS HISTOLOGICALLY DOCUMENTED INFLAMMATION OF THE GASTRIC MUCOSA 2 TYPES ACUTE GASTRITIS – caused mc by infectious agents, sudden onset of epigastric pain, N/V CHRONIC GASTRITIS – identified histologically by an inflammatory cell infiltrate consisting primarily of lymphocytes and plasma cells, with scant neutrophil involvement 2 Forms : Type A Gastritis – LC and involves primarily the fundus and body AUTOIMMUNE Type B Gastritis – mc and antral predominant caused by H. pylori infection

CLASSIFICATION OF GASTRITIS:

CLASSIFICATION OF GASTRITIS

TYPE A GASTRITIS:

TYPE A GASTRITIS AUTOIMMUNE CONDITION ANTIBODIES TO PARIETAL CELL RESULTS IN ATROPHY OF PARIETAL CELL MASS , HYPOCHLORHYDRIA AND ULTIMATELY ACHLORHYDRIA INTRINSIC FACTOR DEF. LEADS TO PERNICIOUS ANAEMIA FUNDUS AND BODY INVOLVED,ANTRUM SPARED ACHLORHYDRIA – CHRONIC HYPERGASTRINEMIA – HYPERTROPHY OF ECL CELLS OF BODY MICRO/MACRO ADENOMAS OF ECL CELLS PREMALIGNANT

TYPE A GASTRITIS:

TYPE A GASTRITIS INTRINSIC FACTOR DEF. &PERNICIOUS ANAEMIA CARCINOMA

TYPE B GASTRITIS:

TYPE B GASTRITIS ASSOCITED WITH H.PYLORI COMMONLY AFFECTS ANTRUM,PRONE FOR PEPTIC ULCERATION MAY ALSO CAUSE PANGASTRITIS,PRONE FOR CARCINOMA INTESTINAL METAPLASIA WITH ATROPHY INTESTINAL METAPLASIA WITH DYSPLASIA HAS SIGNIFICANT MALIGNANT POTENTIAL

TREATMENT OF CHRONIC GASTRITIS :

TREATMENT OF CHRONIC GASTRITIS

MENETRIER’S DISEASE:

MENETRIER’S DISEASE UNUSUAL CONDITION CHARACTERISED BY GROSS HYPERTROPHY OF GASTRIC MUCOSAL FOLDS,MUCUS PRODUCTION & HYPO CHLORHYDRIA PRESENTS WITH HYPOPROTIENAEMIA&ANAEMIA PREMALIGNANT CONDITION CAUSE OVER EXPRESSION OF TRANSFORMING GROWTH FACTOR ALPHA WHICH BINDS TO EGF RECEPTOR TREATMENT GASTRECTOMY

ZOLLINGER ELLISON SYNDROME:

ZOLLINGER ELLISON SYNDROME PEPTIC ULCERATION DUE TO GASTRIN PRODUCING NEUROENDOCRINE TUMOURS ALSO KNOWN AS GASTRINOMAS , HYPER SECRETION OF GASTRIN CAUSES INCREASED ACID SECRETION AND PEPTIC ULCERATION MOST CASES ARE SPORADIC ,25%ARE ASS. WITH MEN 1 SITE DUODENAL WALL 45%(G CELLS IN BRUNNERS GLANDS) PANCREAS 25% LYMPH NODES 5-15% 80% IN GASTRINOMA TRIANGLEOF PASSARO DESCRIBED BY STABILE ET AL SUP JN. OF CYSTIC DUCT & CBD INF JN OF 2 ND & 3 RD PARTS OF DUODENUM MED JN OF NECK &BODY OF PANCREAS(SMA) OUT SIDE TRIANGLE WORST PROGNOSIS 2/3RD ARE MALIGNANT

Z E SYNDROME:

Z E SYNDROME SYMPTOMS&SIGNS 90% HAVE PEPTIC ULCERS USUALLY SOLITARY AND OCCUR IN DUODENAL BULB BUT MAY BE MULTIPLE OR OCCUR IN MORE DISTAL UODENUM 1/3 RD PTS. HAVE DIARRHOEA INT. MUCOSAL INJURY – INACTIVATION OF PANCREATIC ENZYMES – STEATORRHOEA,WT.LOSS

FACTORS FOR SCREENING:

FACTORS FOR SCREENING REFRACTORY ULCERS GIANT ULCERS(>2cms) DISTAL TO DUODENAL BULB MULTIPLE D.U FREQUENT RECURRENCES DIARRHOEA POST ULCER SURGERY ULCER COMLICATIONS HYPERCALCEMIA FAMILY HISTORY H.PYLORI NEGATIVE NOT TAKING NSAIDS

LABORATORY FINDINGS:

LABORATORY FINDINGS FASTING SERUM GASTRIN LEVEL > 1000pg/ml WITH ACID HYPER SECRETION WITH LOWER GASTRIN LEVELS 150-1000pg/ml AND ACID SECRETION SECRETIN STIMULATION SHOULD BE PERFORMED I.V SECRETIN 2UNITS/KG PRODUCES ARISE IN S.GASTRIN OF OVER 200pg/ml WITHIN 2-30 MINUTES IN 85% OF GASTRINOMA PATIENTS S.CALCIUM,PTH,PROLACTIN,LH-FSH&GH TO EXCLUDE MEN1

IMAGING STUDIES FOR ZES:

IMAGING STUDIES FOR ZES CT MRI U/S(TRANSABDOMINAL) SRS(SOMATOSTATIN RECEPTOR SCINTIGRAPHY) EUS(ENDOSCOPIC ULTRASONOGRAPHY) DIFFERENTIAL DIAGNOSIS ATROPHIC GASTRITIS GOO VAGOTOMY CRF

TREATMENT OF ZES:

TREATMENT OF ZES 1.METASTATIC DISEASE MULTIPLE METS. INITIALLY PPI THERAPY TO ACHIEVE A BASAL ACID OUT PUT OF <10meq/hr SOMATOSTATIN ANALOGUE OCTREEOTIDE ISOLATED METS. HEPATIC RESECTION 2.LOCALIZED DISEASE SINGLE TUMOUR WITHOUT METASTASIS RESECTION IS CURATIVE LYMPH NODE METASTASIS DO NOT ADVERSELY AFFECT PRIGNOSIS NO METS. AT INITIAL PRESENTATION 15 YEAR SURVIVAL RATE IS OVER 80%

OPEN SURGERY & LAPAROSCOPIC SURGERY:

OPEN SURGERY & LAPAROSCOPIC SURGERY WE ARE LOOKING AT A GLASS OF BEER OPEN SURGERY IS THE BEER LAPAROSCOPY IS THE FOAM

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