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Mesenteric ischemia presentation by Dr.NOSHI Capital Hospital Islamabad Pakistan

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BIO DATA :

MESENTERIC ISCHEMIADR.NOSHISURGERY DEPARTMENTCAPITAL HOSPITAL ISLAMABADPAKISTAN

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BIO DATA : Name : MR.XYZ .Age: 36yrs, male . Religion: Islam , sunni . Marital status: Married . Profession : ex director at NADRA. Address: ISLAMABAD. DOA: 12-12-2015 at 05 PmSOA : ER

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Lower abdominal pain 4 DAYS

Vomiting 1 DAYPRESENTING COMPLAINTS:

HISTORY OF PRESENT ILLNESS :My patient was living a healthy life 4 days back, when he developed Lower Abdominal pain, it wasgradual in onset n later on it was sudden acute excruciating pain localized in lower abdomennon radiating Intermittent initially later on continous, colicky in character, INITIALLY mild in severity LATER on severe constant between meals NO aggravating factors NO relieving factors associated with bloating and vomiting.There is no h/o of Weight loss, retching No relation of posture with pain.

No h/o of haemetmesis, melena, heart burn, large bulky greasy stools and altered bowel habits.He consulted a local doctor on the same day and receive anti pyretics but didnt relieved the pain.

He also developed intractable VomitingCommenced on the day of admissionFrequency was multiple episode of vomitingProjectile in nature, containing mostly semi digested food particals later on it was watery in consistency. Clear with offensive smell. Associated with epigastric pain.anxiety,sweatingAggravated by intake of meal and relieved by limatation of meal.No associated complain of hemetemasis ,RHC pain with or without jaundice, polyuria, polydipsia, unconsciousness, headache or vertigo.

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Past medical HISTORY: pneumonia 2 yr back PAST surgical history : nilPAST allergic history: nilPAST blood transfusion hx: nilPAST drug history :nilDrug addiction history: nilFamily history : Mother k/c cholithiasis & Elder brother newly diagnosed htn

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PERSONAL HISTORY :MARRIED SINCE ONE & HALF YEAR. One baby girl of 3 months old.Bowel habits is normal.Sleep is not disturbed.Appetite is reduced.Living in well constructed home with proper sanitation.Socioeconomic history is good.

GP EXAMINATION :A gentleman of normal built, conscious alert and well oriented in time, space and person lying on the bed with discomfort due to pain GCS 15/15I/V line maintained in left forarm Vitals:Pulse: 141/min .B.P: 100/70.RR: 29/min .BMI: 31.

Systemic Examination:GIT: Abdomen tense , tenderness in lower abdomen with generalized guarding BS +veRespiratory system: Normal B/L vesicular breathing with no added sounds.CVS: S1+S2+0CNS: GCS 15/15, agitated and in agony, well oriented to time space ,person.

PRE OP Base line investigations:

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On chest xray : Normal

On erect xray abdomen: Distended gut loop

On urine R/E: Normal

On u/s ABDOMEN & PELVIS: FATTY LIVER & MILD ASCITES

Per -op findings:DATE: 13/12/16SURGEON: DR TANSEER & DR YASMEENANESTHESIA:GAPROCEDURE: EXPLORATORY LAPAROTOMYPER-OP FINDINGS:INFARCTED SMALL INTESTINE FROM 5 CM FROM DJ JUNCTION TO 2 FEET AWAT FROM ILLEO-CECAL JUNSTIONDOUBLE BARREL STOMA made on left side.

Post op orders:NPO TFO.KEEP THE PATIENT IN ICU.CVP was maintained & start with TPN.STRICT HOURLY MONITORING of vitals .TRANSFUSE BLOOD.I/V ANTIBIOTICS AND I/V PAIN KILLERS.URINE OUT PUT and NG was montiored.Gut viability was visualized through stoma bag.ON HISTOPATHOLOGY REPORT: SHOWING FULL THICKNESS INFARCTIONEXCISION MARGINS ARE VIABLE..

Post op baselines

Pre op optimization for illostomy reversalEncourage the oral intakeCounselling regarding the bowel habits Special care of stoma bag to prevent any complications.(stomal,peri-stomal or metabolic) Proper care of wound Stool softnersEffective antibiotics & pain killersGut preparation prior to surery AT 6PM,12AM,& 6AMPASSED CVP ON 20/1/16 WE PLANNED FOT CT ANGIOGRAPHY BUT NOT POSSIBLE DUE TO derranged LFTS & RFTS.WEIGHT WAS MARKEDLY REDEUCED TO 65 KG

Stoma(necrosis,stenosis,retraction,prolapsePeri stomal(dermatitis,mechanical trauma

Pot op illostomy reversal

Bowel habits1.constipation/diarrhoeaIncreased frequency..increased urgency..or foecal incontinencePersistent bloating sore skin around anal region

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PRE OP investigation for ILLOSTOMY IRREVERSAL

surgeryOPERATED ON 28/1/16SURGEON DR.TANSEER & DR Ruqia &DR NOSHIANESTHESIA:GASTEPS:After Asceptic measure DOUBLE BARREL LUMEN was dissected from surrounding structures.EDGES were refreshed & antimesenteric border of both lumen was stapled from 60mm staple (linear). Later on DOUBLE BARREL LUMEN was closed with 90mm linear stapler.Abdominal wound closed .

Post op illostomy reversalNpo TFOAntibiotics & PAIN KILLERS STRICT MONITORING OF VITALS,NG & UOSTART TPN ENCOURAGE ORAL DIET AFTER NPO IS BREAKIf diet doesnt improve situation then add up anti-dirrhoeal ,softners.COUNSELLING FOR BOWEL HABITS & Skin care( do not use talcum powder or baby wipes instead use sudocrem. Additional counselling of balanced diet & avoid food & vegetables which alter the bowel habits.

Limit food like citrus food..highly spicy foodbig fatty meals..vegetable with flatulence factorbeer or frizzy drinks

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Post op illostomy irreversal

OFFICER SWD

ISCHEMIC BOWEL DISEASE LITERATURE

INTESTINAL ISCHEMIA occurs when mesenteric perfusion is inadequate to meet intestinal metabolic demands for oxygen .IT may affect small or large bowel or both.CAN develop suddenly(acute mesenteric ischemia) or gradually over months( chronic Mesenteric Ischemia.

DEFINITION OF INTESTINAL ISCHEMIA

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BLOOD SUPPLY

The celiac axis, the SMA, and the inferior mesenteric artery (IMA) supply the foregut, midgut, and hindgut, respectively.[15]The celiac axis arises from the ventral surface of the aorta at the T12-L1 vertebral body. It courses anteroinferiorly before branching into the common hepatic, splenic, and left gastric arteries. The hepatic artery gives off the gastroduodenal artery, which branches further to the right gastroepiploic artery and the anterosuperior and posterosuperior pancreaticoduodenal arteries. The right gastroepiploic artery communicates with the left gastroepiploic artery, which is an immediate branch of the splenic artery. The anterosuperior and posterosuperior pancreaticoduodenal arteries communicate with the corresponding inferior branches from the SMA.

The splenic artery gives off the left gastroepiploic artery, as well as the dorsal pancreatic artery, which supplies the body and tail of the pancreas and communicates with the anterosuperior pancreaticoduodenal and gastroduodenal arteries and sometimes with the middle colic artery or SMA.The left gastric artery, the third important branch of the celiac axis, communicates with the right gastric artery along the posterior aspect of the lesser curvature of the stomach. The celiac artery supplies most of the blood to the lower esophagus, stomach, duodenum, liver, pancreas, and spleen.

GIT IS SUPPLIED BY THREE ARTERIES1)COELIAC AXIS supplies liver spleen stomach duodenum & pancrease.2)SM ARTERY supplies duodenum pancrease small bowel & proximal colon(upto splenic flexure)3)INFERIOR MA supplies left colon & rectum. THERE are extensive collaterals and a high flow rate ( approximately 20% of cardiac output)VENOUS drainage is via inferior mesenteric vein(splenic vein) and superior mesenteric vein to portal vein

The SMA comes off the ventral aorta and supplies the midgut by giving off the inferior pancreaticoduodenal artery, middle colic, right colic, and jejunal and ileal branches.The inferior pancreaticoduodenal artery gives rise to the corresponding anteroinferior and posteroinferior branches, which anastomose with their superior counterparts. This communication is an important connection that helps to maintain bowel perfusion in times of atherosclerosis of the mesenteric vessels. (For an illustration of a meandering artery, see the image below.)Meandering artery (radiographic sign of preexisting bowel ischemia).The ileocolic artery supplies the ileum, cecum, and ascending colon, whereas the middle colic supplies the transverse colon and communicates with the IMA. The right colic artery typically branches at the same level as the middle colic artery. The right and middle colic arteries are an important supply of blood to the marginal artery of Drummond and give rise to the terminal vasa recta, which provide blood to the colon.

The IMA, the smallest mesenteric vessel, also comes off the anterior aorta. It supplies the distal transverse, descending, and sigmoid colon, as well as the rectum. Many communications to the SMA exist within the mesentery, and rectal branches offer communication between the visceral blood supply and the common supply. The watershed area near the splenic flexure was once believed more susceptible to ischemia secondary to poor arterial flow; however, it is now thought that the poor development of this area results in an increased propensity for ischemia.The venous system, for the most part, parallels the arterial system. The superior mesenteric vein (SMV) is formed by the jejunal, ileal, ileocolic, right colic, and middle colic veins, which drain the small intestine, cecum, ascending colon, and transverse colon. The right gastroepiploic vein drains the stomach to the SMV, whereas the inferior pancreaticoduodenal vein drains the pancreas and duodenum.The inferior mesenteric vein (IMV) drains the descending colon, the sigmoid colon, and the rectum through the left colic vein, the sigmoid branches, and the superior rectal vein, respectively. The IMV joins the splenic vein, which then joins the SMV to form the portal vein. The portal vein enters the liver.

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AETIOLOGY OF INTESTINAL ISCHEMIAINADEQUATE INFLOW

OCCLUDED(60%)EmbolismThrombosisVolvulusMesenteric tearAAA surgeryAortic dissectinStrangulated hernia

NON OCCLUSIVECardiogenic shockHypovolumeiaSepsisPancreatitisIntra abdominal hypertensionVasospasm due to drugs

INCREASED WALL TENSION

CLOSED LOOP DESTRUCTION

PSEUDO-OBSTRUCTIONREDUCED VENOUS OUTFLOW

MESENTERIC VEIN THROMBOSIS

MESENTERIC NODAL DISEASES

PANCREATIC NEOPLASM

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CLASSIFICATION OF MIACUTE SUPERIOR MESENTERIC ISCHEMIAEpidemiologyASMI is 1-2 episode/1000Pathogenesis & Associations:SMA Embolism.SMA Thrombosis.Non-Occlusive Mesenteric IschemiaSM Vein Thrombosis.

CHRONIC SUPERIOR MESENTERIC ISCHEMIA

EpidemiologyCSMI is 1/100,000 Pathogenesis & Associations:AtherosclerosisFibrodysplasiaVasculitistakayasus diseaseSM Vein Thrombosis

ASSOCIATED WITH :Acute myocardial InfarctionCardiac ThrombI (48%)Atrial FibrillationSynchoronus EMBOLI(68%)Associated with:SmokingHTN(66%)D.MCoronary artery disease(58%)HyperlipedemiPeripheral vascular disease(72%)Superior Mesenteric Vein Thrombosis: Hypercoguable statesThrombophiliaOcpPrevious ThromboembolismDehydrationObesityInflammatory bowel diseaseLiver cirrhosisIntra-abdominal malignancyPost operatively. Generalized athersclerosisAorticCMI coronary arteryceberovascular diseaseperipheral vascular disease Disseminated Cancer.Critically ill patients.Seen in elderlyPatients with severe cardiac diseasesPost cardiac surgery.Patients who are in sepsisPatients who receive inotropes.Other Drugs(digioxin,amphetaines,cocaine)\Synchronous Infarction in Liver,Spleen & Kidney.

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PATHOGENESIS OF AMI:Superior Mesenteric Artery Embolism: Emboli usually lodge at points of anatomical narrowing & are frequently found 3-10 cm distal to SMA origion (often beyond middle colic artery origion)

Superior Mesenteric Artery Thrombosis : Thrombosis occurs in areas of atherosclerosis near SMA origion or its main branches. Mesenteric atherosclerosis increases in frequency with age. Most patient with one stenotic mesenteric artery is asymptomatic.thrombotic occlusions are ususally more proximally then emboliand as a result infarction is more extensive .

Non- Occlusive Mesenteric Ischemia: Ischemia occurs despite patent mesenteric arteries due to mesenteric artery vasospasm (vasopressin-angiotensin) & low blood flow.

CLINICAL PRESENTATIONSACUTE MESENTERIC ISCHEMIAIt presents with sudden,severe abdominal pain becoming progressively worse associated with vomiting(70%) & diarrhoea (40-50%)Elderly presents with tachypnoea & confusionPain seeming out of keeping ith physical finding.By the time b.s disappear,the abdomen distends & there is guarding & rigidity ischemia will usually have progressed to transmural infarction.

CHRONIC MESENTERIC ISCHEMIAPatients are usually in their 60s & 70s with a colicky,psot-prandial epigastric pain(mesenteric angina) & unintentional weight loss( 10-15 kg)

O/E they may reveal cachexia,smoke-related chest disease,scahphoid abdomen scarred by erythema abigne,abdominal bruit or reduced/absent peripheral pulses.

D/D include biliary disease & peptic ulcer

DIFFERNTIAL DIAGNOSIS:INTESTESTINAL OBSTRUCTIONPERFORATED VISCUSPANCREATITISAPPENDICITISDIVERTICULITISCHOLECYSTITIS DIAGNOSIS

IT should be CONSIDERED & INVESTIGATED in any patient with ACUTE Severe Abdominal pain lasting longer then 2 hours ,out of keeping with physical signs and without obvious cause should be investigated for ASMITYPICAL SYMPTOMSDUPLEX ULTRASONOGRAPHIC evidence of occlusion or HIGH GRADE STENOSIS of SMA & COELIAC ARTERY(peak systolic velocity of more then 275 & 200 cm/s respectively.

SUPERIOR MESENTERIC VEIN THROMBOSIS AND NOMI MAY PRESENT VAGUE ABDOMINAL PAIN , ABDOMINAL DISTENSION AND DOARROHEA.DIAGNOSIS IS OFTEN DELAYED DUE TO NON SPECIFIF PRESENTATION AND EXTENSIVE INFARCTION MAY DEVELOPTHERFORE THIS DIAGNOSIS SHOULD BE CONSIDERED AND INVESTIGATED IN ANY PATIENT WITH ACUTE SEVERE PERSISTEN MORE THEN 2 HOURS AND UNEXPLAINED ABDOMINAL PAIN27

INVESTIGATIONSACUTE MESENTERIC ISCHEMIABLOOD CPWBC is raisedMETABOLIC ACIDOSISELEVATION IN PHOSPHATE (80%)ELEVATION OF AMYLASE (50%)ELEVATION OF LACTATE (100%S)ELEVATED @glutathione s-transferase(72%sen & 77% specf)PLAIN RADIOGRAPHY.Duplex scanning of mesenteric VesselsCT ANGIOGRAPHY.

CHRONIC MESENTERIC ISCHEMIADUPLEX ULTRASONOGRAPGHNon invasiveCriteria are PEAK SYSTOLIC-FLOW,END-DIASTOLIC VELOCITY & RETRO-GRADE FLOW IN HEPATIC ARTERY.(COLIAC STENOSIS)MESENTERIC ANGIOGRAPHYTherapeutic( stent insertion)Indicated to assess the significant disease identified on DUPLEX & in obese patientsCT ANGIOGRAPHY

MAGNETIC RESONANCE ANGIOGRAPHYNON-INVASIVEEVALUATES PROXIMAL COLIAC & SMAMESENTERIC ANGIOGRAPHYSensitivity of 90-100%Range of therapeutic optionsIntra-arterial vasodilators,thrombolysis, angioplasty & stentingDIAGNOSTIC LAPROSCOPYLess invasive then laprotomyUnable to assess mucosal ischemia

MAGNETIC RESONANCE ANGIOGRAPHY e GADOLINIUMHAS high sensitivity & specificity but there is gadolinium associated systemic fibrosis & renal failure

Wbs is usually raised 10 -14 thousand in 25%patients 15-30 in 50 $ patients and moe then 30 thousand in 25% patientsELEVATION OF LACTATE is 100 % sensitive but only 46% specific for intestinal ischemia/infarction

PLAIN RADIOGRAPHS are mostly useful to exclude other causes of abdominal pain ( obstruction,perforation) as findings in mesenteric ischemia are non specific( bowel distension or wall thickening).IN ADVANCED ischemia there may be air in the bowel ( pneumatosis intestinalis) or air in portal vein (pneumatosis portalis)

DUPLEX SCANNING OF MESENTERIC VESSELS :It has low sensitivity in acute ischemia due to over lying bowel gas and low blood flow in acutely ill patients thus it is not recommended.DUPLEX scanning only assess proximal SAM but emboli tend to lodge more distally

CT ANGIOGRAPHY: CT ANGIOGRAPHY using multi slice scanners can demonstrate mesenteric arterial stenosis or occlusion ,venous thrombosis,bowel wall thickening ,mucosal enhancment ,pneumatosis (intestinalis & portalis) and infarction of other organs and can exclude other causes of abdominal pain.High positive and negative predative values of 100% & 96% reported.

MESENTERIC ANGIOGRAPHY: angiography offers a sensitivity of 90 100 % and a range of therapeutic options ( intra-arterial vasodilators ,thrombolytics,angiplasty and stenting.disadvantages are invasive procedure ,limited emergency avalability ,contast associated nephrotoxicity and inability to assess intestinal infarction.

MESENTERIC RESONANACE ANGIOGRAPHY:MRA is a non invasive ( avoid risk of contast associated allergic reactions and nephrotoxity ) ,mainly evaluates proximal coeliac ans SMAA ( missing distal emboli) and may not identify low flow states or secondary signs of acute ischemia( bowel wall thickening)

DIAGNOSTIC LAPROSCOPY: IT IS less invasive then laprotomy .However laproscopy is unable to assess mucosal ischemia may have difficulty in assessing areasof doubtful bowel viability and may miss segmental ischemia CHROMIC MESENTERIC ISCHEMIA

DUPLEX ULTRASONOGRAPHY:: NON- INVASIVE 7 NNOT CONTRAINDICATED IN RENAl diseasw( avoids intravenous contrast) but obesity & bowel gas can inhibits its accuracy.CRITERIA FOR CSMI ARE *PEAK SYSTOLIC FLOW*END DIASTOLIC VELOCITYRETRO GRADE FLOW IN HEAPTIC ARTERY( COELIAC STENOSIS)

MESENTERIC ANGIOGRAPHY:IT is a femoral & brachial approach to demonstrate arterial stenosis or anatomical variations, distal flow & collateralisation ADVANTAGS:THERAPEUTIC POTENTIAL(stent insertion DISADVANTAGES: arterial dissection, bleeding or contrast related nephropathyContrast angiography is used to assess significant disease identified on duplex or in patients too obese to permit reliable duplex assessment. ANGIOGRAPHY:CT

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PRE-OPERATIVE PROCEDURE: GIVE 100 %OXYGENI/V ANTIBIOTICS & PAIN KILLERS.HEMODYNAMIC & FLUID/ELECTROLYTES/ACID-BASE DISTURBANCES are CORRECTED.ASSOCIATED CONDITIONS are TREATED.HEPARIN is ADMINISTERED EARLY unless ACTIVE BLEEDING.INVASIVE MONITORING in CRITICAL CARE is ADVISEDPATIENT need INOTROPES if fluid rususcitation fails to correct hemodynamic disturbances,although VASOPRESSORS may exacerbate MI.Start with TPN

CONDITIONS(CARDIAC FAILURE OR ARRYTHMIA ) ARE TREATED

INVASIVE MONITORING IN CRITICAL CARE IS ADVISED(HOURLY URINE VOLUME CVP AND ARRTERIAL PRESSURE)

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COMPLICATION OF PARENTERAL NUTRITION

RELATED TO OVER FEEDINGExcess glucose: Hyperglycemia,hyperosmolar dehdration, hepatis steatosis , hypercapnia,increased sympathetic activity , fluid retention ,electrolyte abnormalitiesEXCESS FAT: Hypercholesterolemia & formation of lipo protein X, hypertriglyceridemiaEXCESS AMINOACIDS: Hypercholerimc metabolic acidosis ,hypercalcemia, aminoacedmia,uremiaRELATED TO SEPSIS:Catheter related sepsisIncreased pre disposition to synthetic sepsisRELATED TO LINEON INSERTION: pneumothorax, damage to adjacent artery,air embolism, thoracic duct damage,cardiac perforation,or tamponade ,pleural effusion Long term occlusion, venous thrombosis

Clinical suspicion of ASMI

NO PERITONEAL SIGNSPERITONITISINVES FORTHROMBO-PHILIASMVTNOMIOCCLUSIONSMAE/SMATLAPROTOMY/LAPROSCOPYNO IMPROVEMENTPAPAVERINETHROMBOLYSISCT ANGIOGRAPHYDETERIOATIONHEPARIN & THEN WARFARINLAPAROTOMY

TREATMENT DEPENDS ON CLINICAL FINDINGS AND undrlying causePeritonitis needs urgent laprotomy but in its absence medical and cardiovascular options can be considered.

MEDICAL AND ENDOVASCULAR TREATMENTS: IT depnds upon under lying aetiology1.SMAT/SAME:end0 vascular manaGment alone does not allow assessment for intestinal necrosis and should not be used if there is hemodynamic instability or peritonitis.Arterial access is gained by FEMORAL OR BRACHIAL arteries,an aortagram defines anatomy and mesenteric arteries are selectively cannulated.OPTIONS includeaspiration embolectomy(for proximal SAME)*CATHETER DIRECTED THROMBOLYSIS( use of plasminogen activator to remove residual clot after embolectomy),mechanical thrombus fragmentationStent insertion

ANGIOPLASTY AND STENT INSERTION involves dilating a stenosis with an angioplasty ballon and insertion of a ballon expendable stent.repeat angiography and pressure gradient measurments confirms a satisfactory result. AFTER endovascular procedures,patient require s critical care monitoring and a serial abdominal examinations

NOMI: TX IS RESUSCIATION,improvement of cardiac output and administration of intra- arterial vasodilators at the time of angiography(60mg of papaverine bolus followed by infusion 30-60mg/hr) angiography is repeated after 24 hr to document improvement in vaso spasm.paaverine can be continued for upto 5 days if vaso spasm persists.

SMVT: AIMS of tx are to stop extension of thrombosis and facilitate fibrinolysis.Rapid anti coagulation with heparin is necessary but risks intestinal bleeding wih necrotic mucosa sloughs.ANTICOAGULATION is successsful in upto 90% althpugh 32& patients may require small bowel resection..Patient requires investigation of under lying causes( hyper coaguable state ,liver cirrhosis).warfarin is recommended for 3-6bmonths but it is necesssary life long foor associated thrombophilia.SURGERY may be necessary subsequently due to stricture formation

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surgeryPLAN URGENT EXPOLARTORY LAPRATOMYOPTIMIZE THE PATIENT CONDITION DURING & AFTER SURGERYSTOMA CARECOUNSELLING REGARDING HIGH PROTIEN DIETMONITOR ELECTROLYE IMBALANCE & BSRCORRECT THE ABNORMALITIES BECAUSE OF SHORT BOWEL SYNDROME

About 50% of small intestine can be surgically removed or bypassed without permanent detoriation effect.With extensive resection(less then 150 to 100 cm of remaining small intestine) leads to metabolic & nutritional defeciencies resulting in disease known as bowel syndrome

Adult bowel receives 5 to 6 liters of endogenous fluid per day where 2 to 3 liters of exogenous fluid per dayJejunum mucosa is leaky so contents are isotonicIlleum is critical in the conservation of fluid & electrolytes & its only site of absorption of vitamin b12 & bile salts. bile salts are essential for the absorption of fats & fat-soluble vitamins.entero-hepatic circulations of bile-salts is critical to maintain the bile salt pool. following resection of the illeum the loss of bile salts increases & is not met by an increase in synthesis .depletion of bile salts results on fat malabsorption. In addition loss of bile salts into the colon affects colonic mucosa,causing a reduction in salt & water absorption which increases stool losses.

Resection of illeum in a significant enhancment of gastric motility and acceleration intestinal transit .following resection colon recieves a much larger volume of fluid and electrolytes and it recieves bile salts which reduce its ability to absorb salt and water

Tx: restricting the total amount of hypotonic fluids(tea water juice) to less thann a liter per daypatient should be encouraged to take gliucose & saline replacment solutions whch hv na concentraion of 90mmol/l& anti secretory drugs ..anti motility drugsComplication bowel syndrome include peptioc ulcer cholithiasis & hyper oxalouria( absorption of oxalate in colon predisposing to renal stones?)32

TREATMENT OF CSMIAIM OF TREATMENTTo relieve SYMPTOMSTO restore WEIGHTTO prevent INTESTINAL INFARCTIONDECISION to TREAT depends uponSymptom severityPresence of MULTI-VESSEL DISEASESeverity of STENOSIS

INVASIVE TREATMENT FOR CSMITX OPTIONS FOR CSMIENDOVASCULAR MESENTERIC ANGIOPLASTY & STENTING 90-95%(OPEN SMA REVASCULARISATION)OPEN MESENTERIC BYPASSANGIOPLASTY alone for short,non-ostial,focal stenosis

ANGIOPLASTY & a ballon expandable STENT are deployed for long occlusions flush with the aorta

STENTING has higher technical success then angioplasty & used in 70% of CSMI PATIENTDone when two or more vessels are critically stenosed.

IF ITS NOT TECHNICALLY POSSIBLE ,ANGIOPLASTY OR STENTING OF COLIAC AXIS OR IMA MAY BENEFIT.ANTEGRADE/RETEROGRADESINGLE/MULTIPLE VESSELSWITH AN AORTIC/ILLIAC BASED ORIGION

IT IS reserved for failed PERCUTANEOUS INTERVENTION,OCCLUDED OR STENOSD STENTS.

IT has lower restenosis & symmtomatic recurrence then angioplasty & stentingTRANSAORTIC ENDARTERECTOMY

MESENTEERIC ANGIOPLASTY (VIA FEMORAL OR BRACHIAL APPROACH) stenting has high technical success then angioplasty but symmtomatic relief ,morbidity & mortality restenosis rates are similar

OPEN BYPASS: supra coeliac bifurcated,polyester graft from aorta to the coeliac axis and SMA was the choice in 80% if open mesenteric reconstructions.THE ILLIAC ARTERY IS A BETTER CHOICE IN ELDERLY DUE TO CALCIFIED OR DISEASED AORTAS.

RETEROGRADE SMA STENTS AVOIDS THE NEED FOR EXTENSIVE DISSECTION ,VEIN HARVESTING AND THE USE OF PROSTHETIC GRAFT IN THOSE WITH EXTENSIVE AORTOILLIAC DISEASE34

OUTCOMEACUTE MESENTERIC ISCHEMIAIT has high peri-operative mortality rate 32-69% & 5 year survival rate.MORATLITY depends upon cause,speed of diagnosis & intervention.HIGHEST IS NOMI.(70%)LOWER FOR SMA OCCLUSIONLOWEST FOR SMVT (20%)MORTALITY is higher for SMAT then SAME,possibly due to more proximal SMA OCCLUSION with SMAT(more extensive infarction)Short bowel syndome may result in 23% of patients

CHRONIC MESENTERIC ISCHEMIAENDOVASCULAR SUCCESS IS 90-95 %.PERI-PROCEDURE MORTALITY IS 3-5% & MORBIDITY IS 20%.RISKS:PUNCTURE-SITE PROBLEMS.CONTRAST-INDUCED NEPHROTOXITY.ARTERIAL DISSECTION(or rupture can be manges using covered stent.)DISTAL EMBOLISATION.(may respond to thrombolysis or thromboaspiration.OPEN MESENTERIC BYPASS has a high mortality (0-15%) & morbidity (10-38%) due to cardiac & pulmonary complications.

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KEY POINTS OF MANAGMENTRECOGNITION(high index of suspicion)RESUSCITATIONREVASCULARISATIONRESECTION of intestine(limited initially to necrotic & perforated bowel)REASSESSMENT(after revascularisation & a second look laprotomy)REDUCTION of recurrence( critical care post operatively to prevent secondary ischemia;long term anticoagulation)