Transfusion for Massive Blood Loss
Transfusion for Massive Blood Loss
Presented below is a description of massive blood loss and the inherent problems associated with large volume blood transfusions. Following this is a suggested protocol for guiding management of the patient receiving a massive transfusion for haemorrhage.
Massive transfusion is arbitrarily definied as the replacement of a patient's total blood volume in less than 24 hours, or as the acute administration of more than half the patient's estimated blood volume per hour.
Aim of Treatment
The aim of treatment is the rapid and effective restoration of an adequate blood volume and to maintain blood composition within safe limits with regard to haemostasis, oxygen carrying capacity, oncotic pressure and biochemistry.
Complications of Massive Transfusion
The complications of massive transfusion are those of any blood transfusion plus :
Blood Volume ReplacementThe complications of massive transfusion are exacerbated by inadequate or excessive transfusion. Traditionally transfusion of hypovolaemic patients has been directed towards maintaining a haemoglobin concentration of 10g/dl. The use of haemoglobin as the only indicator (or 'transfusion trigger') may result in unnecessary administration of blood products, with their concommittant risks.
Transfusion requirements should be based on the patient's physiologic needs, defined by their oxygen demand (consumption).
The most appropriate monitor of tissue oxygen supply is the tissue oxygen tension, reflected by the PvO2, or mixed venous partial pressure of oxygen (normally 6 kPa, 45mmHg). Patients with a low PvO2 can be classed as stable or unstable depending on haemodynamics, ventilation, acid base status and urine output. If they are stable, no therapy is indicated until a true critical level is reached (PvO2 around 3 kPa, 23mmHg). If unstable, treatment must be intituted.
Thus transfusion should be guided by haemodynamic stability, PvO2 and ER. Obviously during trauma resuscitation, haemodynamic stability is the key indicator.
In summary :
If Hb > 10g/dl transfusion is rarely indicated.
If Hb < 7g/dl transfusion is usually necessary.
With Hbs between 7 and 10 g/dl, clinical status, PvO2 and ER are helpful in defining transfusion requirements.
ThrombocytopeniaDilutional thrombocytopenia is inevitable following massive transfusion as platelet function declines to zero after only a few days of storage. It has been shown that at least 1.5 times blood volume must be replaced for this to become a clinical problem. However, thrombocytopenia can occur following smaller transfusions if disseminated intravascular coagulation (DIC) occurs or there is pre-existing thrombocytopenia.
Coagulation Factor DepletionStored blood contains all coagulation factors except V and VIII. Production of these factos is increased by the stress response to trauma. Therefore only mild changes in coagulation are due to the transfusion per se, and supervening DIC is more likely to be responsible for disordered haemostasis. DIC is a consequence of delayed or inadequate resuscitation, and the usual explanation for abnormal coagulation indices out of proportion to the volume of blood transfused.
Oxygen Affinity ChangesMassive transfusion of stored blood with high oxygen affinity adversely affects oxygen delivery to the tissues. Evidence for this is as yet not forthcoming, but it would seem wise to use fairly fresh red cell transfusions (<1 week old). Use of fresh (<24 hours) blood is not indicated. 2,3 DPG levels rise rapidly following transfusion and normal oxygen affinity is usually restored in a few hours.
HypocalcaemiaEach unit of blood contains approximately 3g citrate, which binds ionized calcium. The healthy adult liver will metabolise 3g citrate every 5 minutes. Transfusion at rates higher than one unit every five minutes or impaired liver function may thus lead to citrate toxicity and hypocalcaemia. Hypocalcaemia does not have a clinically apparent effect on coagulation, but patients may exhibit transient tetany and hypotension. Calcium should only be given if there is biochemical, clinical or electrocardiographic evidence of hypocalcaemia.
HyperkalaemiaThe plasma potassium concentration of stored blood increases during storage and may be over 30mmol/l. Hyperkalaemia is generally not a problem unless very large amounts of blood are given quickly. On the contrary, hypokalaemia is more common as red cells begin active metabolism and intracellular uptake of potassium restarts.
Acid/Base DisturbancesLactic acid levels in the blood pack give stored blood an acid load of up to 30-40mmol/l. This, along with citric acid is usually metabolised rapidly. Indeed, citrate is metabolised to bicarbonate, and a profound metabolic alkalosis may ensue. The acid-base status of the recipient is usually of more importance, final acid/base status being dependent on tissue perfusion, rate of administration amd citrate metabolism.
HypothermiaHypothermia leads to reduction in citrate and lactate metabolism (leading to hypocalcaemia and metabolic acidosis), increase in affinity of haemoglobin for oxygen, impairment of red cell deformability, platelet dysfunction and an increased tendency to cardiac dysrhythmias.
Acute Respiratory Distress Syndrome (ARDS)The aetiology of ARDS is as yet not fully understood, but various risk factors have been identified. Both under- and over-transfusion are associated with an increased risk of ARDS, as is albumin < 30g/l. Microaggregate filters should be used during massive transfusion except when giving fresh whole blood or platelets.
Protocol for Management of Massive Transfusion
Sequence of ComponentsProfound hypotension should be treated speedily. Administer crystalloid or colloid infusions rather than delay fluid administration. Initial red cell replacement is in the form of packed red cells.
Laboratory SamplesAt the start of resuscitation, blood should be taken for group and crossmatch, coagulation tests, full blood count and biochemistry. These must be properly labelled and identified in all situations.
Blood Bank ArrangementsRoutine procedures should be followed until it becomes obvious that massive transfusion is likely. The blood bank should be informed as soon as possible that a major trauma is arriving or in the building.
For extreme emergencies group O blood should be supplied first. Rhesus D negative blood should be supplied to all women of childbearing age. Type specific (ABO Rh D matched) blood should be available in 5 minutes and the switch should be made promptly so as not to deplete stores of group O blood. Continue transfusing blood on this basis until time is available to crossmatch on the original serum sample. If an antibody screen is negative and more than one blood volume has been administered there is no point attempting compatibility tests except to exclude ABO mismatches.
MonitoringDuring massive transfusion, regular monitoring of haemoglobin, platelet count, prothrombin time (PT), partial thromboplastin time (PTT) and fibrinogen levels should take place and be used to guide component replacement.
ComponentsComponent replacement should occur only in the presence of active bleeding or if interventional procedures are to be undertaken.
Platelet concentrates (1 pack/10kg) are given if platelet count falls below 50. Each platelet concentrate also provides around 50ml of fresh plasma.
Fresh frozen plasma (12ml/kg)is administered if PT or PTT are running higher than 1.5 times control levels.
Cryoprecipitate (1-1.5 packs/10kg) is given for Fibrinogen levels < 0.8g/l.
For massive uncontrolled traumative haemorrhage, maintenance of full haeostatic ability is usually unrealistic. The priority is for definitive surgical arrest of haemorrhage from major vessels. Combinations of stored whole blood, packed cells, colloids & crystalloids are given to maintain blood volume or pressure at adequate levels and haemoglobin at around 7g/dl or haematocrit at 0.25. Conserve limited supplies of fresh blood, plasma or platelets until the bleeding is controlled.
When blood loss has lessened (0.5l/hour) and major vessels have been controlled, it becomes worthwhile correcting haemostasis.
Damage Control Surgery
Damage control surgery is one of the major advances in surgical technique in the past 20 years. The principles of damage control have been slow to be accepted by surgeons around the world, as they contravene most standard surgical teaching practices - that the best operation for a patient is one, definitive procedure.
However it is now well recognized that multiple trauma patients are more likely to die from their intra-operative metabolic failure that from a failure to complete operative repairs. Patients with major exsanguinating injuries will not survive complex procedures such as formal hepatic resection or pancreaticoduodenectomy. The operating team must undergo a paradigm shift in their 'mindset' if the patient is to survive such devastating injuries.
The central tenet of damage control surgery is that patients die from a triad of coagulopathy, hypothermia and metabolic acidosis. Once this metabolic failure has become established it is extremely difficult to control haemorrhage and correct the derangements. If the patient is to survive the operation must be foreshortened so that they can be transferred to a critical care facility where they can be warmed and the hypothermia and acidosis is corrected. Once this is achieved the definitive surgical procedure can be carried out as necessary - the 'staged procedure'.
The principles of the first 'damage control' procedure then are control of haemorrhage, prevention of contamination and protection from further injury. Damage control surgery is the most technically demanding and challenging surgery a trauma surgeon can perform. There is no margin for error and no place for careless surgery.
Hypothermia. Acidosis. Coagulopathy. These three derangements become established quickly in the exsanguinating trauma patient and, once established, form a vicious circle which may be impossible to overcome.
HypothermiaThe majority of major trauma patients are hypothermic on arrival in the emergency department due to environmental conditions at the scene. Inadequate protection, intravenous fluid administration and ongoing blood loss will worsen the hypothermic state. Haemorrhagic shock leads to decreased cellular perfusion and oxygenation and so inadequate heat production. Hypothermia has dramatic systemic effects on the bodies functions but most importantly in this context exacerbates coagulopathy and interferes with blood homeostatic mechanisms.
AcidosisUncorrected haemorrhagic shock will lead into inadequate cellular perfusion, anaerobic metabolism and the production of lactic acid. This leads to profound metabolic acidosis which also interferes with blood clotting mechanisms and promotes coagulopathy and blood loss.
CoagulopathyHypothermia, acidosis and the consequences of massive blood transfusion
all lead to the development of a coagulopathy. Even if control of mechanical bleeding is achievable, patients may continue to bleed from all cut surfaces. This leads to a worsening of haemorrhagic shock and so a worsening of hypothermia and acidosis, prolonging the vicious cycle.
Some studies have attempted to place threshold levels on these parameters. Some state that conversion to a damage control procedure should take place if the pH is below 7.2, core temperature is below 32C or the patient has received more than one blood volume transfusion. However, once these levels are reached, it is already too late.
The trauma surgeon must make the decision to convert to a limited procedure within 5 minutes of starting the operative procedure. This decision is made on the initial physiological state of the patient and the rapid initial assessment of internal injuries. Do not wait for metabolic failure to set in. This early decision is imperative to the patients survival.
Damage Control Laparotomy
The principles of damage control surgery are:
1. Control haemorrhage
2. Prevention contamination
3. Avoid further injury
PreparationPrehospital and emergency department times should be minimized in these patients. All unnecessary and superfluous investigations that will not immediately affect patient management should be deferred. Cyclic fluid resuscitation prior to surgery is futile and will worsen hypothermia and coagulopathy. Colloid solutions will also interfere with clot quality.
These patients should be transferred rapidly to the operating room without repeated attempts to restore circulating volume. They require operative control of haemorrhage and simultaneous vigorous resuscitation with blood and clotting factors.
Anaesthesia should be induced on the operating table once the patient is prepped and draped and the surgeons ready. The shocked patient usually requires minimal anaesthesia and a careful, haemodynamically-neutral induction method should be used. An arterial line is valuable for patient monitoring peroperatively but small-calibre central venous access is of limited use. Blood, fresh frozen plasma, cryoprecipitate and platelet transfusions should be available but clotting factor therapy should be administered rapidly only once control of major vascular haemorrhage has been achieved. All fluids should be warmed and as much of the patient covered and actively warmed as possible.
General Conduct and PhilosophyThe patient should be rapidly prepped from neck to knees with large abdominal packs soaked in antiseptic skin preparation solution. The incision should be made from the xiphisternum to the pubis. This incision may require extension into the right chest or as a median sternotomy depending on the injury pattern.
Relief of intraperitoneal pressure with muscle paralysis and opening of the abdominal wall may result in dramatic haemorrhage and hypotension. Immediate control is necessary and this is initially achieved with four quadrant packing with multiple large abdominal packs.
Aortic control may be necessary at this stage. This is generally best achieved at the diaphragmatic hiatus with blunt finger dissection and finger pressure by an assistant followed by aortic cross-clamping. The aorta may be difficult to identify in the severely hypovolaemic patient and direct visualization by division of the right crus of the diaphragm may be necessary. Some surgeons prefer to perform a left anterolateral thoracotomy to control the descending thoracic aorta in the chest. However this requires the opening of a second body cavity and further heat loss and is rarely necessary.
The next step is to identify the main source of bleeding. Careful inspection of the four quadrants of the abdomen is necessary. A moment of silence may allow the bleeding to be heard. Immediate control of haemorrhage is with direct, blunt pressure using the surgeons hands, swabs on sticks or abdominal packs. Proximal and distal control techniques are rarely useful in the acute stage. Bleeding from the liver, spleen or kidney can generally be achieved by applying pressure with several large abdominal packs.
Examination of the abdomen must be complete. This includes, where necessary, mobilization and delivery of retroperitoneal structures using several medial visceral rotation manoeuvers. All intraabdominal and most retroperitoneal haematomas require exploration and evacuation. Even a small perienteric or peripancreatic haematoma may mask a serious vascular or enteric injury. Exploration should proceed regardless of whether the haematoma is pulsatile, expanding or stable or due to blunt or penetrating trauma. Nonexpanding perirenal haematomas, retrohepatic haematomas or blunt pelvic haematomas should not be explored and may be treated with abdominal packing. Subsequent angiographic embolization may be required.
Prevention of contamination is achieved by the rapid closure of hollow viscus injury. This may be definitive if there are only a few enterotomies requiring primary suture, but more complex techniques such as resection and primary anastomosis should be avoided and bowel ends stapled, sewn or tied off. Inspection of the ends and reanastomosis is performed at the second procedure.
Abdominal closureAbdominal closure is rapid and temporary. If possible, the skin only is closed with a rapid continuous suture or even multiple towel clips. Abdominal compartment syndrome
is common in these patients and if there is any doubt the abdomen should be left open as a laparostomy with a silo-bag or vacuum-pack technique.
LiverThe basic damage control technique for control of hepatic haemorrhage is peri-hepatic packing. This manoeuver, when performed properly, will arrest most haemorrhage except for major arterial bleeding.
Major hepatic bleeding may be partially controlled with a soft vascular clamp on the portal triad (Pringle's manoeuver). Further vascular isolation (inferior vena cava above and below the liver) may be hazardous and is generally unnecessary in a damage control setting. Full hepatic mobilization and extension into the chest either through a median sternotomy or left thoracotomy may be required to achieve this.
The liver parenchyma can be compressed manually initially, followed by ordered packing. To adequately pack the liver requires compression in the antero-posterior plane. This can only be achieved by mobilization of the right hepatic ligament and systematic placement of packs posterior and anterior to this, as well as one or two in the hepato-renal space. Even retrohepatic venous and inferior vena cava injuries may be controlled in this manner.
Only major arterial bleeds from the liver parenchyma will require further attention. In this case the liver injury can be extended using a finger-fracture technique and the bleeding vessels identified and tied or clipped. In some cases, where the injury is not deep and easily accessible, rapid resectional debridement may be possible by placing large clamps along the wound edges, performing a rapid debridement and the underrunning the clamp with suture to include all the raw surface.
The patient who undergoes hepatic packing should be transferred to the angiography suite immediately after the operation to identify any ongoing arterial haemorrhage which may be controlled with selective angiographic embolization.
The priority of the critical care phase of treatment is rapid and complete reversal of metabolic failure. The damage control procedure has controlled life-threatening injury, but the patient requires further surgery to remove packs and/or definitively complete the repairs. The next 24 to 48 hours are crucial if the patient is to be fit for a second procedure. After this time multiple organ dysfunction, especially acute respiratory distress syndrome (ARDS), and cardiovascular failure may render re-operation inadequate.
The intensive care unit must act aggressive to reverse the metabolic failure. The patient must be actively warmed, with blankets, air-warming devices or even continuous arteriovenous warming techniques. This is vital to allow correction of coagulopathy and acidosis.
Acidosis is a reflection of impaired oxygen delivery and utilization. Perfusion must be restored to body tissues by warmed intravenous crystalloid and blood administration as necessary. Massive tissue and bowel oedema may ensue due to the activation and release of inflammatory mediators and large volumes of fluid are required. Right heart catheters should be employed as necessary to monitor cardiac filling pressures and determine oxygen delivery. Vasodilating agents such as dobutamine or the phsophodiesterase inhibitors may be necessary to help open up vascular beds. In the absence of technology that can monitor muscle and gut perfusion, the base deficit or lactate levels should be used to guide resuscitation.
Coagulopathy is treated by the administration of fresh frozen plasma, cryoprecipitate and platelets as necessary, and correcting the hypothermia and acidosis. If correction of metabolic failure is to succeed, all three derangements must be treated simultaneously and aggressively. Take care not to miss the patient who has started to actively bleed again. Large losses from thoracostomy tubes, abdominal distention or loss of control of an open abdomen, or repeated episodes of hypotension all suggest that mechanical bleeding is occurring that will require surgical control.
Abdominal Compartment Syndrome
Massive intestinal oedema often follows laparotomy for major tra uma where there has been prolonged shock. Crystalloid resuscitation, capillary leakage due to activated inflammatory mediators and reperfusion injury all contribute to this tissue swelling. Combined with intra-abdominal packing or retroperitoneal haematomas this may render the abdomen difficult or impossible to close. If the abdomen is closed, intra-abdominal pressure may rise to a level (>25 cmH2O) where it leads to significant cardiovascular, respiratory, renal and cerebral dysfunction.
CardiovascularA rise in the intra-abdominal pressure leads to a fall in cardiac output, due mainly to compression of the inferior vena cava and reduction in venous return to the heart. Cardiac output is reduced despite apparent rises in central venous pressure, pulmonary artery occlusion pressure and systemic vascular resistance. This distortion of standard monitoring modalities makes adequate and appropriate resuscitation difficult.
RespiratoryRaised intra-abdominal pressure will effectively splint the diaphragm and lead to a rise in peak airway pressure and intra-thoracic pressure and subsequently a reduced venous return to the heart. The increase in airway pressures may also exacerbate barotrauma and contribute to the development of acute respiratory distress syndrome.
RenalAn acute increase in intra-abdominal pressure leads to oliguria and anuria probably due to compression of the renal vein and renal parenchyma. Renal blood flow, glomerular filtration are decreased with a corresponding increase in renal vascular resistance.
CerebralThe rise in intra-abdominal pressure, intrathoracic pressure leads to a rise in central venous pressure which prevents adequate venous drainage from the brain, leading to a rise in intracranial pressure and worsening of intracerebral oedema.
Diagnosis of Abdominal Compartment SyndromeThe abdominal compartment should be suspected and sought for in any multiple trauma patient who has undergone a period of profound shock. Clinically it is characterized by a fall in urine output associated with an elevated central venous pressure. The diagnosis can be confirmed by the measurement of intra-abdominal pressure. This may be done either through a foley catheter in the bladder or a nasogastric tube in the stomach. Simple water-column manometry is used at 2 to 4 hourly intervals, although it is possible to connect a pressure transducer to a foley catheter.
Normal intra-abdominal pressure is zero or subatmospheric. A pressure of over 25cmH2O is suggestive, and over 30cmH2O diagnostic, of the abdominal compartment syndrome.
ManagementIt is better to anticipate the development of abdominal compartment syndrome and use an alternate wound closure technique to prevent its occurrence. If the abdomen is at all difficult to close, this procedure should be abandoned at alternative techniques applied. A good rule of thumb is that if, when looking at the abdomen horizontally, the guts can be seen above the level of the wound, the abdomen should be left open and temporary closure utilized.
The easiest method to control the open abdomen is to use a silo-bag closure. A 3 litre plastic irrigation bag is emptied and cut open so it lies flat. The edges are trimmed and sutured to the skin, away from the skin edges, using a continuous 1 silk suture. It is useful to place a sterile absorbent drape inside the abdomen to soak up some of the fluid and ease control of the laparostomy.
An alternative technique is the 'vacuum-pack' technique. Here the 3 litre bag is opened and placed into the abdomen to protect the gut contents, under the sheath. Two large calibre suction drains are placed over this, and a large adherent steridrape placed over the whole abdomen. The suction catheters are connected to high-displacement suction to provide control of fluid losses and create the 'vacuum-pack' effect.
Do not suture material to the sheath. Repeated suturing of the sheath damages it and makes definitive closure impossible. If the sheath cannot be closed at a subsequent operation, the defect may be closed with an absorbable mesh system.
Sudden release of the abdominal compartment syndrome may lead to an ischaemia-reperfusion injury causing acidosis, vasodilatation, cardiac dysfunction and arrest. Prior to release the patient should be pre-loaded with crystalloid solution. Mannitol and vasodilators such as dobutamine or the phosphodiesterase inhibitors may have a place here.
The principles of reoperation are removal of clots and abdominal packs, complete inspection of the abdomen to detect missed injuries, haemostasis and restoration of intestinal integrity and abdominal wound closure.
Timing of reoperation is critical. There is usually a window of opportunity between correction of metabolic failure and the onset of the systemic inflammatory response syndrome and multiple organ failure. This window usually occurs at 24-48 hours after the first procedure. There is a tradeoff between earlier re-operation, when the patient may be less stable and bowel-well oedema marked, and delaying the procedure to a point where cardiovascular, respiratory and renal failure make the procedure hazardous. Vascular shunts should be removed and grafts inserted at the earliest opportunity as these may dislodge or clot once coagulopathy is corrected. If packs are left in the abdomen it is generally recommended that these are removed at 48-72 hours, although there is little evidence to suggest that leaving them longer is detrimental.
Abdominal packs, especially around the liver or spleen should be removed cautiously as they may be stuck to the parenchyma and removal may lead to further bleeding. Soaking the swabs may aid this process. The bleeding is rarely dramatic however and may be controlled with argon-beam diathermy or fibrin glue. Occasionally repacking will be necessary.
Any intestinal repairs carried out at the first procedure should be inspected to determine their continued integrity. Bowel ends that were stapled or tied off should be inspected, necrotic tissue debrided and primary repair with end-to-end anastomosis undertaken. With a haemodynamically stable, warm patient, colostomy is rarely necessary.
Copious washout should be performed and the abdomen closed with standard mass closure to the sheath and routine skin closure. If the sheath cannot be re-approximated temporary silo closure can be reinstated or an absorbable PDS or vicryl mesh applied which can be skin grafted at a later stage. The resulting incisional hernia can be closed at a later procedure.
Obstructive jaundice which can be either due to intra-hepatic cholestasis or extra-hepatic biliary obstruction is amenable to surgical treatment. Hence, it is also called surgical jaundice.
It is difficult to diagnose the type and cause of obstruction on clinical grounds alone. But there are certain clinical criterion’s associated with it.
In calculus disease of biliary tract, intermittent or fluctuating jaundice can be seen with chills and rigors. It is progressive and painless and is associated with weight loss and anorexia in malignant obstruction.
In cases of infra-cystic obstruction due to malignant neoplasms, gall bladder may be palpable while in calculus diseases it is not palpable as it gets shrunken because of previous attacks of cholecystitis. This is Courvoisier’s law.
Causes of obstructive jaundice can be broadly classified into benign and malignant diseases.
Diseases causing obstructive jaundice include:
Common bile duct stone
Primary sclerosing cholangitis
Stenosis of papilla
Extra-hepatic biliary atresia
· Klatskin tumor
· Carcinoma of the head of the pancreas
· Carcinoma of the duodenum
· Carcinoma of the ampulla of Vater
· Carcinoma of the gall bladder
2) Secondary- lymph nodes at the porta.
Amongst these the commonest causes include CBD stones and peri-ampullary malignancies.
Common bile duct stones:
Common bile duct stones are usually secondary stones that have migrated into the biliary system and the gall bladder. Common duct stones are known to occur in around 15% of patients undergoing standard open cholecystectomy (Mitchell ’93).
Approximately 11% of patients with gall bladder stones will have CBD stones at the time of operation. This incidence may climb to 18% in older patients who have had gallstones for a longer period of time. Between 5%-7% of CBD stones found at operation may be unsuspected by pre-operative evaluation and are discovered by cystic duct cholangiography during the cholecystectomy (Maingot’s ’01)1
Primary duct stones may be encountered in tropics secondary to infestation of biliary tree due to worms. Incidence is around 4 %( Blumgart’s ’88). Primary CBD stones occur in any situation causing prolonged biliary stasis and infection.2, 3
The natural history of choledocholithiasis is varied and unpredictable.
Most frequently CBD stones are an unanticipated finding during routine cholecystectomy. Small stones usually pass on to the duodenum spontaneously. They may induce and episode of pancreatitis by temporarily obstructing the pancreatic duct.
If stones obstruct the CBD in the presence of infected bile, cholangitis ensues. Classic triad of fever, chills and jaundice should always raise a suspicion of CBD stone. If stones obstruct the CBD in absence of infected bile, asymptomatic jaundice that is classically fluctuating ensues. Fluctuation is due to duct dilatation and floating back of the stone into the dilated CBD and reduction in the edema.
Pancreatitis is the second most common complication of a CBD stone. Other complications include choledochoenteric fistula and biliary stricture.
Diagnostic ultrasound, especially the real-time mode, has become the single most valuable screening test in case of jaundiced patients. It is a non-invasive procedure and can detect up to 50% of stones. Plain abdominal films are of very limited value as <15% of stones are radio-opaque. Either percutaneous transhepatic cholangiograms (PTC) or endoscopic retrograde cholangiograms (ERCP) can be asked for depending upon previous ultrasound findings and availability if more precise information is needed. CT or MRI usually is not of any help in the diagnosis or management of patients with cholelithiasis, with or without cholangitis.
Cholecystectomy is accompanied by exploration of common bile duct in 13-26 % of cases (Sheridan ’87).
Exploration of CBD with cholecystectomy raises the mortality of patients operated upon from 1% if the gall bladder alone is removed to 4.5% (Payne’86). Hence, routine CBD exploration has been condemned. Traditional indications for CBD exploration have given way to following absolute indications:
Palpable stones in the CBD
Jaundice with cholangitis
Stone demonstrable in intra-operative cholangiography
Pre-operative radiological demonstration of calculi in CBD.
Hence, routine intra-operative cholangiography4, 5, 6 is strongly recommended whenever choledochoscopy is not available. Intra-operative cholangiography7 is 85-95% sensitive in recognizing CBD stones (Blumgart’s ’88). Its advantages include –
Exclusion of CBD exploration in patients who have dilated CBD don’t have stones
During routine cystic duct cholangiography while doing cholecystectomy, approximately 5-7% of patients will be found to have unsuspected stones in the CBD
Pre-exploratory size and location of stones
To study the anatomy of the biliary tree and ampulla.
The commonest method of approach is supra-duodenal vertical incision (Tompkins ’90).
One of the most controversial aspects of choledocholithotomy is how to conclude the operation. There are three possibilities:
A) Simple closure-
It can only be attempted when one is sure about the patency of the distal duct system as evidenced by passing of dye into duodenum in a post procedure cholangiogram.
B) T-Tube drainage-
Most surgeons will still prefer chledochorraphy to a T-Tube8 in spite of a high incidence of cholangitis and biliary peritonitis. Hence, antibiotic prophylaxis is strongly recommended when T-Tube is in-situ9.
C) Biliary enteric procedures-
There are specific indications for biliary-enteric anastomosis (Blumgart’s ’88). They include-
Multiple primary duct stones with dilated ducts particularly in elderly
Multiple stones in a dilated duct
Irretrievable intrahepatic stones
Proven papillary stenosis
Impacted ampullary stone
Terminal CBD stricture.
Three procedures are in vogue:
It is mainly indicated when CBD is more than 1.5 cms, patient is elderly and high risk. The supra-duodenal choledochoduodenostomy uses vertical CBD and horizontal duodenal incision.
Complications of this procedure include-
Sump syndrome11- the cause of this is accumulation of stones, undigested food matter, or both in the segment of the distal bile duct, which obstructs the anastomotic opening and causes cholangitis and pain.
Retained or recurrent stones
2) TRANS-DUODENAL SPHINCTEROPLASTY12:
It is indicated in a patient of impacted stone in ampulla or a very low CBD stricture (duct is dilated down to terminal few mms). Though an advantage to examine ampulla directly is got, disadvantages are too many. The complications include pancreatitis and duodenal leak.
This is done when CBD can be mobilized completely. A roux-en-y loop or a simple loop is used with a entero-enterostomy below. Its advantages are low incidence of cholangitis and reflux of indigestible intestinal contents into the biliary tree. The drawback is that there is increased incidence of post-operative peptic ulcer disease13.
ADVANCES IN BILIARY CALCULOUS DISEASE
1) THERAPEUTIC ENDOSCOPY-
Endoscopic sphincterotomy (EP)
Classen and Demling first did it in 1974. it was first used only in selected patients. Now it is widely used in a variety of situations. It is the procedure of choice for recurrent or retained stones after cholecystectomy (Miller ’87)14, 15. It is also used in older and high-risk patients who wish to avoid surgery. After papillotomy stones can be either retrieved by a dormia basket or allowed to pass spontaneously. Success rates of between 85-95% have been reported. The complication rate ranges from 6.5-8.7% and mortality rate ranges from 0.1-3%. Long term follow up studies have shown that re-stenosis and/or recurrent stones occurred in 7% of patients, usually within 2 years.
Endoscopic retrograde cholangiography (ERC)
This procedure involves cannulation of the ampulla. A cholangiogram will show the exact number, size and location of the stones. Stone extraction can be done with balloon dilatation and basket extraction or they can be crushed using a mechanical lithotripter (Martin ’93). Endoscopic infusion of monooctanoin has been tried recently to dissolve stones and duct clearance of 18-55% have been reported (Stock ’92)16.
A combination of EP and ERC has achieved a duct clearance of 85-90% in a single procedure.
2) LAPAROSCOPIC APPROACH-
Laparoscopic cholecystectomy and trans-cystic CBD exploration17, 18
After cholecystectomy, cystic duct can be dilated laparoscopically and stones can be retrieved using baskets.
It is an approach in patients with dilated CBD, calculi 1 cm or more in diameter, multiple calculi or those who require lithotripsy for impacted stones.
3) EXTRA-CORPOREAL SHOCK WAVE LITHOTRIPSY (ESWL) 19, 20, 21-
In patients in whom endoscopic sphincterotomy and stone extraction proved to be unsuccessful, the use of ESWL has been proved successful. A multi-institutional study of 42 patients treated at 11 institutions showed that stone fragmentation can be obtained in 95% of the patients. However, 50% of the patients required adjunctive procedures to clear the bile duct stones, including endoscopic extraction, biliary lavage and stenting. Only 2 patients required operation to clear the bile duct stones (Maingot’s 01).
4) PERCUTANEOUS TRANS-HEPATIC ROUTE-
Using a modified dormia basket inserted through a percutaneous trans-hepatic catheter, a Boston group reported successful clearance of CBD stones in 93% of 50 patients treated. All of these patients had contraindications to surgery or had undergone unsuccessful endoscopic attempts at removal. 29 patients in this group required either monooctanoin or methyl-tert-butyl ether infusions to reduce stone size or remove residual debris. The authors reported a 13% morbidity and 4% mortality rate.
The percutaneous transhepatic route has also been used s a method of passing a cholangioscope to visualize and remove the biliary stones.
5) DRUG TREATMENT-
Various drugs like methyl tert-butyl ether, chenodeoxycholic acid and monooctanoin have been used to dissolve stones with variable results.
Many investigative reports on innovative techniques are available22. These include endoscopic introduction of electro hydraulic lithotripters by use of “mother-daughter” endoscopic techniques, endoscopic introduction of intra-corporeal shock-wave lithotripters into the bile duct, percutaneous transhepatic insertion of electro hydraulic lithotripters, and insertion of laser lithotripters via T tube tracts. While these technologic advances are interesting, they remain to be proven effective and economical.
Based on present data, when a patient is less than 65 years of age, open CBD exploration is safer than EP. Patient more then 65 years of age is a candidate for laparoscopic or endoscopic approach23.
Extra hepatic biliary atresia
The incidence throughout the world is approximately 1 in 14,000 live births. The occlusion of the bile ducts is accompanied by a variable degree of intrahepatic damage that can progress to cirrhosis and liver failure, in untreated cases. Historically, cases were classified as correctable or non-correctable, depending on the presence or absence of residual proximal duct segments of bile duct. The introduction of new surgical technique, in the 1960s, invalidated the traditional classification.
The first major review of 49 cases was published by Thompson24 in 1891 and 1892 and concluded that, whatever the etiology of biliary atresia, a progressive, destructive inflammatory lesion of the bile ducts characterized it. Holmes analyzed more than 100 case reports and first suggested that surgical treatment might be effective in biliary atresia. Ladd described 20 more cases. Hays and Synder reported, in 1963, that in most American series, <5% of patients survived beyond early childhood25. In 1959, Kasai and Suzuki described a new radical operation for non-correctable atresia based on the histologic observation that remnants of the extra-hepatic ducts at the porta hepatis frequently contained ductules measuring up to 300 micrometers in diameter26. Approximately 85% of extra-hepatic biliary atresia cases classified as non-correctable now are treated routinely with the Kasai’s portoenterostomy procedure.
The 4-year survival rate in untreated cases of biliary atresia is approximately 2%, but portoenterostomy performed before the age of 7 weeks has resulted in early jaundice-free survival in more than 90% of the cases. Past 7 weeks of life, the long-term results of surgery are very poor.
Although morphology of the extra-hepatic bile ducts varies widely in biliary atresia, the Japanese Society of Pediatric Surgeons identified three principal types, which form the basis of the classification now in general use-
Type 1: atresia of the CBD
Type 2: atresia of the common hepatic duct
Type 3: atresia of the right and left ducts.
In a Japanese survey of 643 cases, 566 (88%) were type 3, 64(10%) were type 1, and only 13(2%) were type 2 lesions.
Surgical treatment consists of pre-operative percutaneous liver biopsy, followed by radical resection of the occluded biliary tract and reconstruction with a Roux-en-y loop of jejunum.
The results of portoenterostomy has gradually improved as illustrated in a report that showed that the number of jaundice-free children rose from 7.6% in the period 1953-1961 to 85% in 1987-8827. The current probability of 5-year survival after portoenterostomy in specialized unit is around 60%.
A choledochal cyst is defined as an isolated or combined congenital dilation of the extra hepatic or intrahepatic biliary tree.
In 1723, Vater and Ezler described the anatomic details of a choledochal cyst, but Douglas is credited with the final description of a case of a choledochal cyst.
McWhorter reported the first excision of a choledochal cyst
Alonso-Lej et al reviewed the literature in 1959 and proposed an early classification system for choledochal cysts. Todani et al modified the Alonso-Lej classification in 1977, to account for the combination of intra and extra hepatic cystic dilation28.
Type I- dilation of extra hepatic biliary tree: Ia-cystic, Ib-focal, and Ic-fusiform
Type II- saccular diverticulum of extra hepatic bile duct
Type III- biliary tree dilation within the duodenum, choledochocele
Type IV a- dilation of intrahepatic and extrahepatic biliary tree
b- multiple extrahepatic cysts
Type V- dilation confined to the intrahepatic ducts (Caroli’s disease)
Once considered a rare congenital lesion of children, choledochal cysts have been reported in over 3300 patients, with many recent repots including adults. More than 2/3rd of all cases have originated in Asia.
Carcinoma of the head of the pancreas
Carcinoma of the pancreas is a disease with poor prognosis considered by many to be one of the deadliest malignancies. Less than 20 % of affected patients survive one year after diagnosis. (Lilimoe 95)
Pancreatic cancer, by far the most common periampullary malignancy, is the ninth most common cancer and is the fourth and fifth leading cause of death in men and women, respectively, in the United States29. The lowest incidence is seen in India and parts of the Middle East. There is a slight male predilection; however the incidence and mortality rate in women has increased. In the last two decades while remaining constant in men. Blacks are more commonly affected than whites.
Approximately 95 % of malignancies arise from exocrine pancreas; of them 75% occur in the head. Carcinoma head of the pancreas presents early due to development of jaundice. Jaundice is progressive and often associated with significant pruritus. Pain of moderate intensity may be present as a result of obstruction of the biliary or pancreatic ducts. Recent studies suggest that less than one third of patients presenting with pancreatic carcinoma describe moderate to severe pain. Duodenal obstruction, with nausea and vomiting, is usually late manifestation of peri-ampullary carcinomas. Duodenal and periampullary carcinomas may bleed intermittently. In many patients physical findings are absent, especially early in the course. The development of jaundice is often the first physical finding that is apparent as the tumor obstructs the biliary tree. An enlarged liver or palpable gallbladder is present in 25 to 30 % of patients.
Both USG and CT scan are useful in diagnosing carcinoma pancreas. Currently the use of intravenous and oral contrast enhanced spiral CT scan offers the best form of imaging of the pancreas. It also provides information about liver metastases and major vascular involvement30. Once biliary obstruction has been confirmed by imaging studies, the next step in the evaluation of a jaundiced patient is cholangiography. Either the endoscopic or percutaneous approach is appropriate with the choice of technique depending on local expertise30.
During ERCP stent can be placed through tumor for biliary drainage. Preoperative biliary drainage is shown to reduce operative mortality and morbidity. (Lygidakis 87)
Percutaneous transhepatic biliary drainage can also be used for the same purpose.
Biopsy of a periampullary mass can be obtained by endoscopic or percutaneous route. The primary indication for percutaneous biopsy is in patients who would appear not to be surgical candidates because of either extent of disease or medical contraindications. Percutaneous biopsy may be useful if the CT picture suggests pancreatic lymphoma, which is best managed non operatively.
In cases of doubt, pre operative visceral angiography with arteries of the celiac and mesenteric arteries with venous phase studies provide the best demonstration of vascular anatomy and major vessel encasement or occlusion.
Endoscopic ultrasonography is a minimally invasive technique to image pancreas. It can detect small pancreatic lesions (< 2 cm) and also lymph node and vascular involvement.
Liver metastases and peritoneal implants are the most common sites of distant spread of pancreatic carcinoma. Several groups, before the patient is subjected to laprotomy, have used the technique of diagnostic laparoscopy, as an additional staging modality for the evaluation of patients with pancreatic and periampullary malignancies.
TREATMENT OF PANCREATIC AND PERIAMPULLARY CARCINOMA
In 1899 Halstead described the local resection of an ampullary carcinoma. Whipple in 1935 first described the technique for excision of periampullary carcinoma, which was done in two stages. He improved upon it and did a one-stage procedure in 1941. However 60 to 80% of these tumors proved unresectable at the time of exploration. The procedure involves two components of exploration: exploration with assessment of tumor respectability and resection followed by reconstruction if tumor is found resectable. Involvement of portal vein and superior mesenteric vessels is the most common cause of unresectability. Head of pancreas, entire duodenum, distal part of stomach and distal end of CBD are removed followed by reconstruction.
Traverse and Longmire modified the procedure by preserving the pylorus in 197831. Currently in most series, pylorus preserving pancreatico-duodenectomy (PPPD) is the procedure of choice32. PPPD shortens operative time, retains entire stomach as reservoir, maintains a more normal gastrointestinal hormonal milieu and decreases post gastrectomy symptoms (Lilimoe).
Another modification has been added by Fortener, which includes regional pancreatectomy. Complications after pancreatico-duodenectomy remain high usually in the excess of 25 to 35 %. Pancreatic fistula remains the most serious complication after the operation, with its incidence ranging from 5 to 20 %.
The most frequent complication following PPPD is delayed gastric emptying with an incidence in the 20 to 50 % range33.
Although a number of factors appear to contribute to the overall improvement in results following pancreatico-duodenectomy, a high volume of procedures concentrated in the hand of experienced surgeons seems to be of primary importance34.
Survival rate of patients with carcinoma pancreas who have undergone resection remains low35. Five-year survival rate is usually between 18 to 21 %. Survival following resection of distal bile duct, ampullary, and duodenal carcinoma has always been significantly longer than that for pancreatic carcinoma, with some series reporting a five-year survival in the range of 30 to 60 %.
The role of adjuvant radiation therapy is emphasized by the pattern of relapse after surgical excision, since over half of the patients resected developed local regional recurrence without evidence of distant metastases.
Many palliative procedures have been devised for the treatment of unresectable malignancies. Non-operative palliation appears to be associated with lower complication rates, lower procedure related mortality rates, and shorter periods of hospitalization. There appears to be no advantage with respect to long-term survival. Advocates of surgical palliation however criticize non-operative palliation in that it is frequently associated with late complications of gastric outlet obstruction and recurrent jaundice, resulting in the need for rehospitalization.surgical palliation offers the only chance for long term palliation of all three major symptoms of pancreatic carcinoma: obstructive jaundice, duodenal obstruction and pain. Biliary bypass can be performed as either cholecystojejunostomy or choledochohepaticojejunostomy. The ability to perform a gastrojejunostomy to treat or prevent gastric outlet obstruction is currently the only palliative procedure that cannot be performed non-operatively. The final major advantage of operative palliation is in the management of pain. Intraoperative celiac axis injection with 50 % alcohol can both successfully relieve pain in patients, and prevent the development of pain in patients without pain at the time of exploration36. The use of percutaneous neurolytic block of the celiac axis, either using fluoroscopic or CT guidance is also successful, in the vast majority of patients, at eliminating pain37. In those rare patients in whom percutaneous techniques are not possible, thoracoscopic splanchnicectomy has been shown to effectively relieve pain38. Finally, although not well demonstrated by objective measures, it appears that external beam radiation therapy has a beneficial effect on pancreatic cancer pain.
Recently endoprostheses have given a chance of non-surgical palliation39.
Although, traditionally pancreatic cancer has been associated with a dismal prognosis, recent advances in diagnosis and management, both surgical and non-surgical, have led to overall improvement in the management of these conditions.
All the other periampullary malignancies, like carcinoma of the ampulla, distal bile duct and duodenum present with the same clinical pattern. Methods of diagnosis and management remain the same. But these tumors are less lethal and give an excellent survival rates.
Carcinoma of the gall bladder
DeStoll first described gall bladder carcinoma in 1977. The first hepatic resection for gall bladder cancer was performed by Keen in 1891, and Mayo made the association between gall bladder cancer and gallstones in 1903. The incidence of carcinoma of the gall bladder increases in frequency throughout life. In autopsy series, gall bladder carcinomas account for up to 5 % of all malignancies with many of these tumors being asymptomatic at the time of demise of the patient. Autopsy data from Chile have suggested that the risk of gall bladder carcinoma is 7 times greater in presence of cholecystitis and cholelithiasis40.
Obstructive jaundice in case of GB carcinoma can be managed with either percutaneous transhepatic biliary stents or biliary endoprostheses. Appropriate narcotic therapy may provide adequate pain control in many patients. In those patients with disabling pain, either external beam radiation therapy or percutaneous celiac ganglion nerve block may be helpful in reducing the need for narcotics. The mean survival for the subset of patients who undergo non-operative palliation for symptomatic GB carcinoma is less than 6 months.
The operative palliation of jaundice is dependent upon the extent of final disease. Various procedures like Roux-en-Y choledochojejunostomy, segment III bypass, intraoperative celiac splanchnicectomy and gastrojejunostomy can be performed.
Current recommendations for surgical therapy for GB carcinoma41 are based on the pathologic staging of the tumor and the historical survival rates for the different tumor stages42.
Chemotherapy and radiation therapy43 in postoperative adjuvant setting has not produced any survival advantage.
Primary carcinoma of the biliary tract is an uncommon cause of obstructive jaundice, but carries a very poor prognosis and majority of patients die within 6 to 12 months of diagnosis.
Like GB cancer, the incidence of bile duct cancer increases with age. Bile duct malignancies have a more even distribution between men and women than do GB malignancies.
Cancer of the bile ducts has been recognized for more than a century. Musser reported 18 cases of primary extrahepatic bile duct cancer in literature in 1889. In 1940, Stewart and associates reviewed 306 cases of extra hepatic bile duct cancer reported in the literature, and two decades later Sako and associates reviewed the literature from 1935 to 1954, ad found 570 additional cases of extra hepatic bile duct cancer. Malignancies of the intra hepatic and peri-hilar bile ducts have been described more recently, with Altemeier and associates reporting 3 cases of primary adenocarcinoma of the major intrahepatic bile ducts in 1957, and Klatskin reporting 13 patients with cancer of hepatic duct bifurcation in 1965.
Two types of cholangiocarcinoma have been described
(A.) Hilar cholangiocarcinoma (Klatskin tumor)
In most series, the overall resectability rate for hilar bile duct cancer averages between 40 and 60 %. Data from selected recent series reviewing potentially curative resection of hilar bile duct carcinoma reveal a mean survival of 22 months44 .The addition of major liver resection to surgery for hilar bile duct cancer des not show any survival advantage. Reconstruction is done by hepaticojejunostomy. Palliative procedures include trans-tubal drainage using U tube and biliary enteric anastomosis. PTC is usually necessary to delineate the duct system45. Segment III is commonly used for bypass. The duct is approached by ligamentum teres approach, and is anastomosed side to side to a Roux-en-Y loop of jejunum.
(B.) Cholangiocarcinoma of the distal CBD
This has been grouped under periampullary tumors and requires pancreatico-duodenectomy. USG is the preferred investigation but PTC or ERC gets precise information. In most series, the resectability rate of distal CBD cancer exceeds 60 %. Data from more than 221 patients reveal an average mean survival of 39 months; nearly double the mean survival following potentially curative resection of hilar bile duct cancer44
Local excision is suitable treatment for certain small tumors (less than 2 cm) arising from the ampulla of Vater or in the pancreatic or biliary duct within 2 cm of the ampulla, if there is suspicion of malignancy frozen section evaluation of the resected specimen is done and if it confirms malignancy pancreatico-duodenectomy should be done46. After local resection of ampullary tumors, follow up endoscopy is performed 6 to 12 months postoperatively to assess local recurrence. Patient who develop pancreatitis or jaundice months to years following local resection of ampullary tumors must be suspected of having local recurrence and should undergo repeat endoscopy with ERCP.
Surgery for choledocholithiasis:
Cholecystectomy + choledocholithotomy + T tube drainage
Various incisions are used but we prefer midline or long right para median incision.
After peritoneum is opened any adhesions if present are divided.
Liver is retracted upwards while small bowel, colon and duodenum are covered with moist towels and retracted downwards
An atraumatic Babcock’s forceps is applied to Hartman’s pouch and pulled to right.
Peritoneal fold over Calot’s triangle is incised. Blunt dissection is done to define the CBD and cystic duct. Cystic and right hepatic arteries are defined. Cystic artery is ligated near gall bladder and cut. (Various anatomical variations should always be kept in mind)
Cystic duct is identified up to the neck of the gall bladder. Intraoperative cholangiography is done through the cystic duct. Then the cystic duct is ligated and cut. GB is dissected from GB fossa and removed.
Recent data suggest that selective cholangiography4 is appropriate with indications of a history of jaundice or biliary pancreatititis, abnormal liver function tests suggestive of extra hepatic obstruction, a dilated CBD., or palpable stones
After the exposure of cystic duct, a nick is taken on it and a canula is introduced. It is tied both proximally and distally to prevent leakage of dye and introduction of air bubble which appear as stones.
Dilute 1:1 dye is used as stronger dye may obscure stones.
One film is taken immediately after pushing the dye and one may be repeated after 5 minutes.
Exploration of CBD is done after the cholangiogram confirms presence of stones.
CBD is cleared.
2 stay sutures are taken on the anterior surface of duodenum 2 cms above duodenum.
Duct is opened longitudinally between the stays. Bile is sucked away to avoid contamination.
The duct is explored using Desjardin’s forceps and calculi are removed.
Then CBD is irrigate with normal saline and patency of ampulla ensured.
A T Tube is now kept in the CBD and duct is closed around the tube with 3-0 vicryl or 3-0 catgut.
The T Tube should be brought out at the lower end of CBD to avoid pulling on the suture line.
Incision is closed with a drain in Morison’s pouch.
Postoperative T Tube cholangiogram is taken.
Duodenum should be kocherised and 2nd part mobilized completely and thoroughly.
Transverse or longitudinal incision can be taken on the CBD. We prefer longitudinal incision.
Longitudinal incision is taken on the duodenum.
A single layer anastomosis is done with 3-0 vicryl. All sutures are interrupted and on atraumatic needle.
A stent can be kept across the anastomosis, which is brought out of the duodenum to the outside.
Duodenum is opened longitudinally.
Ampulla is visualized.
An incision is taken at 10’0 clock to avoid injury to the pancreatic duct.
Sutures are taken taking care to include the apex after division by serial clamping.
Duodenum is closed longitudinally.
Surgery for extrahepatic biliary atresia:
A right subcostal or a transverse abdominal incision across the right rectus sheath is taken. In the latter, if atresia is confirmed, the incision is extended across the left rectus muscle.
The GB in EHBA is often thick walled, contracted, and hidden within a cleft in the liver parenchyma. In these circumstances, operative cholangiography is usually impossible and aspiration of the GB should produce reveal “Limey (whitish) bile”. However, operative cholangiography is mandatory whenever bile is found in the gall bladder.
Liver is fully mobilized and Cholecystectomy is done.
Dissection of extrahepatic bile duct remnants is performed towards the porta hepatis and CBD remnants up to the duodenum are excised.
Rarely, a long patent segment of proximal duct (correctable atresia) that can be used for a hepaticojejunostomy is discovered. In the majority of cases, however, the dissection proceeds above and behind the bifurcation of the portal vein and hepatic artery, and the tissue is transected at its junction with, and parallel to, the capsule of liver.
A Roux-en-Y loop of jejunum is prepared. One end is closed, a side opening is made and portoenterostomy is performed with interrupted 5-0 or 6-0 vicryl sutures. Jejunojejunostomy is done to establish intestinal continuity. A drain is placed in the supraduodenal area before closure of the abdomen.
Surgery for peri-ampullary malignancies:
They are divided into
A) Radical resection
B) Palliative bypass
Whipple’s procedure (pancreatico-duodenectomy) was the most common radical procedure performed. Traverso Longmire’s PPPD was done in few cases.
An adequate exploration of the pancreas requires good access and exposure. We preferred a long midline or a long right para-median incision.
On opening the abdomen, metastases, portal vein involvement, and extent of tumor beyond the normal limits of resection should be assessed, all of which indicate inoperability. Hepatic, omental, and peritoneal seedlings also contraindicate resection. Fixity around ligament of Treitz and extension of tumor around superior mesenteric vessels also are contraindications for resection.
A) Mobilization of duodenum and the head of the pancreas
This is called kocherisation of duodenum. The colon is dissected from the hepatic bed and off duodenum. The peritoneal reflection lateral to the 2nd part of the duodenum is incised. The duodenum and the head of the pancreas are mobilized anteriorly and towards the midline. The dissection is continued till aorta and IVC are displayed. The posterior pancreatic and aortocaval group of lymph nodes are mobilized anteriorly with the specimen.
B) Dividing the gastro-colic omentum opens lesser sac and the entire pancreas is examined.
C) Dissection of superior mesenteric vein
Middle colic vein is traced upwards to it’s point of entry into the superior mesenteric vein. There is a safe plane anterior to the portal vein as all the tributaries of portal vein enter it from the lateral aspect.
D) CBD is dissected and hooked out. The left gastric vessels are identified and ligated. The fundus and greater curvature are mobilized.
We prefer cholecystectomy if cholecystostomy has been done previously.
CBD is transected. The neck of the pancreas is then carefully transected to the left of the portal vein. The bleeding vessels are ligated with 4-0 silk sutures. Portal vein tributaries need to be ligated carefully. The stomach is divided between non-crushing clamps at the selected site.
The specimen now remains attached by only uncinate process and the small bowel. The duodenum and the DJ flexure are freed from the transverse mesocolon by dividing the peritoneum around the duodenum. Ligament of Treitz is divided and small bowel transected a small distance away from the DJ flexure.
The uncinate process is then freed. Vessels need careful ligation because troublesome can take place here.
The first anastomosis is the pancreaticojejunal anastomosis. It can be done by the invagination method when the pancreatic duct is smaller or by duct to mucosa anastomosis when the duct is bigger. A stent is kept in the duct, which is brought across the anastomosis out of the jejunum on to the abdominal wall. Then bile duct is anastomosed end to side of jejunum10 cms distal to the first anastomosis. Lastly, gastrojejunostomy is done 25 cms from the first anastomosis in 2 layers.
Tube drain is kept in Morrison’s pouch and the abdomen closed in layers.
These are advised when resection is contraindicated due to advanced disease. Various procedures can be done depending on the level of obstruction. The procedures include-
Gastrojejunostomy is done if there is duodenal obstruction.
Chemical splanchinectomy is done to reduce pain.