MESENTERIC ISCHAEMIA(ACUTE&CHRONIC)

Mesenteric ischaemia as such is not uncommon in any clinical setting.Unfortunately it goes unnoticed largely because of the symptoms with which the patient first presents to the clinician or else because of the clinical acumen of the physician .But clinicians are not to be blamed for this in totality for the simple reason that we really don’t have proper diagnostic facilities around to be sure what the patient is going through.Added to this is the disparity in the symptomotology and the signs with which the patient presents.By the time the diagnosis is made (generally on the operation table during laprotomy),the patient is already on death bed waiting for the final call.Acute mesenteric ischaemias generally present with severe pain abdomen which is “OUT OF PROPORTION TO CLINICAL FINDINGS”.Abdomen is generally soft and the pain the patient complains of is unexplainable .This delays the diagnosis and by the third or the forth day of presentation patient develops peritonitis and gangrene of the gut.The prognosis is dismal in such cases.Situation is no better in chronic mesenteric ischaemic patients.These patients are generally thin built for they have “FOOD FEAR”.Any small intake of food leads to pain abdomen and therefore these patients largely keep themselves fasting.The basic thing is to be strongly suspicious of a clinicopathological entity like this and when ever you come across a patient with unexplained pain abdomen with lean and thin built suspect mesenteric ischaemia and refer the patient to a vascular surgeon before its too late.

I present to you a similar case which we operated upon recently.This patient who was lean and thin came to us with unexplained pain abdomen,uncontrolled hypertension inspite of taking four antihypertensives and bilateral lower limb claudication.It was the strong clinical suspicion of chronic mesenteric ischaemia in him that clinched the diagnosis and probably saved him from an impending disaster.We got a conventional angio done in him which was suggestive of aorto-iliac block with ostial near total occlusions of the cealic axis,superior mesenteric artery and right renal artery.

We did an aorto-bifemoral bypass along with conventional “TRANSAORTIC ENDARTRECTOMY OF THE CAELIAC,SMA AND RIGHT RENAL VESSELS”.Patient did fine postoperatively and was discharged on the fifth post operative day.Presently he is on just one antihypertensive.

The plaque that has been removed has been displayed .Hope you can make out and appreciate the plaque extensions going into the caeliac,sma and renal arteries.

The carry home message is”BE STRONGLY SUSPICIOUS OF UNEXPLAINED PAIN ABDOMEN AND CONSIDER MESENTERIC ISCHAEMIA IN SUCH CASES UNLESS PROVED OTHERWISE”.

IVC THROMBECTOMY AS A LIFE SAVING SURGERY

ACUTE VENOUS THROMBOSIS IS VERY COMMON IN INDIAN SCENARIO.
WE AS DOCTORS COME ACROSS SUCH PATIENTS IN OUR DAILY ROUTINE.THERE CAN BE DIFFERENT CAUSES FOR ACUTE THROMBOSIS.IT CAN EITHER BE DUE TO INBORN ERRORS IN THE BLOOD OR ELSE IT CAN BE ACQUIRED.GENERALLY IT INVOLVES THE LOWER LIMB VENOUS SYSTEM BUT UPPER LIMB DVT IS NOT UNCOMMON.INFERIOR VENA CAVA THROMBOSIS PER SE IS NOT VERY COMMON TO COME ACROSS IN DAILY PRACTICE.GENERALLY IT IS ASSOCIATED WITH THROMBUS ANYWHERE ELSE WHICH GETS PROPAGATED TO INVOLVE THE IVC.THE OTHER USUAL CAUSE IS RENAL CELL CARCINOMA WHICH PROGRESSES TO INVOLVE THE IVC. THE TREATMENT OF IVC THROMBOSIS IS ALL THE MORE CONTROVERSIAL BECAUSE OF ITS RARITY.WHETHER TO GO AHEAD WITH INTERVENSION OR TO FOLLOW CONSERVATIVE MANAGEMENT IN PATIENTS WITH ACUTE PRESENTATION IS STILL UNCLEAR.


I REMEMBER A PHRASE FROM A REPUTED VASCULAR SURGEON WHICH SAYS”ITS CHALLENGING TO DO SOMETHING NEW IN AN INSTITUTION WHERE EVERYONE HAS AN OPINION BUT NO ONE THE EXPERIENCE”.

THIS PATIENT 50 YEARS OLD A CASE OF NEPHROTIC SYNDROME CAME WITH ACUTE RENAL FAILURE TO OUR HOSPITAL.HE HAD MASSIVE SWELLING OF BOTH HIS LEGS AND SCROTUM AND HAD GENERALISED ANASARCA..SUBSEQUENTLY HE WAS FOUND TO HAVE BILATERAL RENAL VEIN THROMBOSIS AND ACUTE THROMBOSIS OF BILATERAL LOWER LIMB VENOUS SYSTEM INVOLVONG THE IVC TILL THE HEPATIC VEINS.THE LIKELY CAUSE FOR ACUTE THROMBOSIS IN THIS PATIENT WAS PROTEIN LOSSING NEPHROPATHY. THE EXCESSIVE URINARY PROTEIN LOSS IS ASSOCIATED WITH DECREASED ANTITHROMBIN III, A RELATIVE EXCESS OF FIBRINOGEN, AND CHANGES IN OTHER CLOTTING FACTORS; ALL LEAD TO PROPENSITY TO CLOT. NUMEROUS STUDIES DEMONSTRATED A DIRECT RELATIONSHIP BETWEEN NEPHROTIC SYNDROME AND BOTH ARTERIAL AND VENOUS THROMBOSIS.THIS CLOT CAN DAMAGE THE KIDNEYS,CAN BREAK AND TRAVEL THROUGH THE BLOOD STREAM TO THE LUNGS A CONDITION CALLED AS PULMONARY THROMBOEMBOLISM WHICH MAY PROVE TO BE FATAL. THIS PATIENT WAS SUBJECTED TO DIALYSIS.AND DIFFERENT OPTIONS WERE THOUGHT OF REGARDING THE FURTHER COURSE OF TREATMENT.CONSERVATIVE TREATMENT WAS VIRTUALLY RULED OUT AS THIS WOULD HAVE LED TO SEVERE MORBIDITY HAD THE PATIENT SURVIVED.THROMBOLYSIS WAS ALSO RULED OUT BECAUSE OF THE EXTENSIVE THROMBUS LOAD.IT WAS AGREED UNANIMOUSLY BETWEEN THE NEPHROLOGY TEAM AND MYSELF TO GO AHEAD WITH IVC THROMBECTOMY THINKING THAT IT WOULD REVERT HIS RENAL STATUS TO NORMAL,WOULD PREVENT THROMBOEMBOLISM,PREVENT LIMB LOSS FROM VENOUS IMPEDIMENT AND PREVENTCHRONIC VENOUS INSUFFICIENCY IN THE LONG RUN.IVC THROMBECTOMY THROUGH MIDLINE LAPROTOMY INCISION WAS DONE .TOTAL IVC CLEARANCE WITH BILATERAL COMMON FEMORAL VEIN THROMBECTOMY WAS DONE. THIS PATIENT HAD MIDGUT MALROTATION WHICH WAS FOUND INTRAOPERATIVELY MAKING IT ALL THE MORE UNIQUE.POSTOPERATIVELY PATIENT DID FINE AND WAS DISCHARGED FROM THE HOSPITAL ON ORAL ANTICOAGULANTS ON THE TENTH POSTOPERATIVE DAY.PRESENTLY HE IS OFF DIALYSIS AS HIS RENAL PARAMETERS HAVE COME TO NORMAL.


THE IMPORTANCE OF THIS CASE LIES IN THE SPEEDY RECOVERY THE PATIENT MADE WHEN IT SEEMED HE IS A HIGH RISK CASE FOR SURGERY. HE IS NOW LEADING A NEAR NORMAL LIFE.HIS LOWER LIMB SWELLING HAS DECREASED REMARKABLY. HIS RENAL PARAMETERS ARE WITHIN NORMAL RANGE..THIS PATIENT NEEDS TO BE IN REGULAR FOLLOWUP OF HIS NEPHROLOGIST AND MY OWNSELF.