Автореферат и диссертация по медицине (14.00.27) на тему:Поздние осложнения острого панкреатита: диагностика и лечение

PEOPLE'S FRIENDSHIP UNIVERSITY OF RUSSIA BOMBAY HOSPITAL INSTITUTE OF MEDICAL SCIENCES

LATE COMPLICATIONS OF ACUTE PANCREATITIS: DIAGNOSIS AND MANAGEMENT

DISSERTATION

SCIENTIFIC WORK FOR THE PROCUREMENT OF DOCTOR OF PHILOSOPHY (PhD)

Scientific Guides: ProffVI.Maljarchuk, M.D., DSc.

Proff. V.N.Shrikhande, FRCS.

Written by the right hand of

04.2.00 2 07851 "

TADEPALLI ROW NARESH

14.00. 27 - Surgery

Moscow 2002

INDEX

PAGE

INTRODUCTION

3

CHAPTER 1 : LATE COMPLICATIONS OF ACUTE PANCREATITIS: DIAGNOSIS AND MANAGEMENT (REVIEW OF LITRATURE).

8

CHAPTER 2: MATERIAL AND METHODS

2.1 SELECTION OF PATIENTS.

2.2 INVESTIGATIVE MODALITIES.

41

CHAPTER 3: OBSERVATIONS

55

3.1 CLINICAL MANIFESTATIONS.

3.2 INVESTIGATIONS.

3.3 MANAGEMENT.

3.4 COMPLICATION.

3.5 MORTALITY AND MORBIDITY.

CHAPTER 4: DISCUSSION 95

ALGORITHM 112

SUMMERY 114

CONCLUSION 118

PRACTICAL RECOMMENDATIONS 119

REFERANCES 120

INTRODUCTION:

Pancreatic necrosis is associated with high mortality and morbidity world

over.

The different mortalities of operative procedure have been found to be as follows:

Banks (1971) 54%

Warshaw (1974) 34%

Camer (1975) 28%

Jones et al (1975) 11%

Ranson and Spencer (1977) 26%

Frey et al (1979) 37%

Saxon etal (1981) 5%

Bardley and Fuleninder (1984) 30.5%

Warshaw and Jin (1985) 5%

Hollender etal (1987) 25%

Beger (1989) 10%

Saw etal (1991) 17%

Reber etal (1991) 20%

Rattner et al (1992) 25%

A large amount of research has been done to understand the process of pan-

creatic necrosis , its diagnosis and management.

Different studies have had different observations and given different conclusions.

Blazer, in 1879, made the first recorded observation of pancreatitis with fat necrosis , Reginald Fitz (1889) was the first person to give accurate description and classification of acute pancreatic disease, in which he distinguished three types of inflammation; - haemorrhagic; gangrenous and suppurative pancreatitis, with the different symptoms accompanying each.

Inl925, Lord Moynihan further delineated the surgical approach to pancreatitis, Wherein he out lined the principles of lesser sac drainage and debridment, and these are very nearly followed till date.

The reported incidence of pancreatic necrosis in acute pancreatitis varies from: 1-9%, as evaluated by various authors such as Altemerier(1963); Far-ringed 1966-67); Lukash(1967); Evans(1969); Cogbill(1970); and Grace( 1976).

E.C.P.Shi et al and Warsaw (1984) reported an incidence of about 4% in cases of acute pancreatitis .

Yeo and Cameron(1990) reported an incidence of pancreatic necrosis to be 5% as a complication of acute pancreatitis.

Bardley(1982) reported an incidence of 8.5% in his series.

As per H.G.Beger(1989), necrotising course of acute pancreatitis develops in 8-15% of patients.

E.L.Bradley III (1997), reports an incidence of 19.5%, of pancreo-necrosis, from a prospective study of 194 patients presenting with acute pancreatitis, using dynamic pancreatography as a standard for detection.

Buchler et al, (1999) in a retrospective study have reported to have an incidence of 20% of pancreatic necrosis, in patients admitted for acute pancreatitis.

CT-scan offers better visualization of the retroperitoneal structures and better overall visualisation of the pancreas: according to Mender (1980) and Silver-stein (1981). In contrast, Danmann (1980) observed that CT changes do not always correlate with disease severity.

Siler and Wulsin in 1950, pointed out that for pancreatic collection, operation should be sufficient to ensure adequate drainage, but extensive exploration should be avoided.

As stated by Blumenthal et al (1959), while the treatment of acute pancre-atits is largely medical, the treatment of its complications and squeal are largely surgical.

Bradley (1987), in his series of 28 patients managed the infected pancreatic necrosis by extensive de-roofing of the superior retro peritoneum, blunt pancreatic

sequestrectomy, laparotomy and packing of the lesser sac and scheduled reexplorations at intervals of 2-3 days, i.e., by the technique of open drainage.

According to Hancke (1985), there has been a recent interest in percutaneous aspiration of pancreatic collection under Ultrasound or CT-control.

In the experience of M.J.McMohan (1987), this is only successful in about 10% of cases and carries the risk of introduction of infection or precipitating haemorrhage.

Yet another study by Rattner et al (1992), reached to a conclusion that aggressive initial surgical debridment should be the 1st step in managing symptomatic pancreatic necrosis and that the presence of infection should not be the sole determinant of intervention. This is in contrast to the study by Reber (1986) and Bradley (1991), who state that the presence or absence of infection should determine whether or not surgical intervention is undertaken.

Thus, the diagnosis and management of pancreatic necrosis has always been controversial since the first observation made in its history.

The aim of this study is to mark the methods of diagnosis and treatment of late complications of acute pancreatitis, which are used in Bombay Hospital of Medical Sciences (India).

Our tasks to resolve this problem were:

1) To compare diagnostic results of different methods of investigations in patients with complications of acute pancreatitis.

2) To compare different methods of surgical treatment.

3) To work out different indications for surgery.

4) To work out an algorithm of management in destructive form of

pancreatitis.

With these aims and the results gathered, I have presented my work for discussion.

Scientific innovation

Worked out an algorithm for the treatment of patients with late complications of acute pancreatitis.

Demonstrated the need for feeding jejunostomy, for the purpose of enteral feeding in patients with severe late complications of acute pancreatitis.

Important for practise

We have demonstrated that, early operations are indicated for better results in patients with late complications of acute pancreatitis. Wide inscisions, through necrosectomy and dependent drainage through the lumber region. Also, early enteral feeding in the early post-operative period, for the recovery on the patient, through the feeding jejunostomy.

Introduction of these results into practice

The key of this dessertation is being introduced and used in practise in Bombay Hospital Institute of Medical Science (India). The method of diagnosis and treatment have been introduced in the teaching program of the 4th and 5th course, medical students, in General surgery, of Russian Peoples' Friendship University, also, in the training of the post graduate spiciality.

Approbation of work

The result of this work was presented in the conferance of the Department of General Surgery, Russian Peoples" Friendship University and to the doctors of Hospital No.64, Moscow.

The material of this dessertation was discussed in the International conferance on Pancreatis Diseases (Bombay-Jan.2001), International Congress of Surgical Hepatology (Bombay-Nov.2001), in the Third International Scientific and practical conferance ' Health and Education in 21st Centuary" (Moscow-March 2002).

Publication of this work

There were 3 scientific works published. 1. Pancreatic necrosis: standards of diagnosis & management.// Bombay Hospital Journal, Vol.43, Jan/01, /Especial issue on pancreatic diseases. /V.I.Maljarchouk, Naresh Row, et.al.

2. Surgical management in Pancreatic necrosis. // Здоровье и образование в XXI веке : Материалы Третьей международной научно-практической конференции.- М.: Из-во РУДН, 2002 : С. 297.

3. Pancreatic necrosis: Diagnosis: Computer Tomographic Scan. // Здоровье и образование в XXI веке : Материалы Третьей международной научно-практической конференции.- М.: Из-во РУДН, 2002 : С. 297.

Structure of the thesis

Dessertation has been written in the english language. It has 134 pages, consisting of Introduction, 4 Chapters of own investigations, Conclusion, Summary, Practical recommendation, Algorithm and referances.

CHAPTER 1: LATE COMPLICATIONS OF ACUTE

PANCREATITIS: DIAGNOSIS AND MANAGEMENT:-

(REVIEW OF LITRATURE).

Blazer made the first recorded observation of pancreatitis with fat necrosis

in 1879, Reginald Fitz (1889) was the first person to give accurate description and classification of acute pancreatic disease, in which he distinguished three types of inflammation; - haemorrhagic; gangrenous and suppurative pancreatitis, with the different symptoms accompanying each. It is now recognised that these differences, are dependent upon the physiologic peculiarities of the pancreas and which make necrosis and haemorrhage such an important component of acute pancreatitis.

A determination of the frequency of pancreatitis and pancreatic necrosis remains extremely uncertain, as evaluated by McWhorter in 1952. The definition of a ratio acute pancre: titis and pancreatic necrosis remains rather various and changes from 1 % up to 2C % Altemerier (1963); Farringer (1966-67); Lukash (1967); Evans (1969); Cogbill (1970); and Grace (1976) Bardley (1982) Becker both al (1984) E.C.P.Shi and al (1984) Warsaw (1985) Bruse Allardyce (1987) H.G.Beger (1989), Yeo and Cameron (1990) E.L.Bradley III (1997), Buchler and al(1999). Definitions:

Focal or diffuse areas of devitalised pancreatic parenchyma and peripancre-atic fatty tissue necrosis involving different retroperitoneal areas microscopically characterize necrotising pancreatitis. Microscopically, there is extensive interstitial tissue necrosis with vessel damage. The necrotic process affects both the aciner and ductal cells as well as the islet cell component. Pancreatic and peripancreatic necrosis are believed to be the product of combined injury by activated proteases and other pancreatic enzymes, which eventually cause thrombosis of the microcirculation of pancreas. Pancreatic necrosis has been reported in 1% to 20% of patients with acute pancreatitis. (A.Choudhary,2000-As defined by the Atlanta classification).

Pancreatic necrosis is defined as one or more areas of non-viable pancreatic parenchyma and is usually associated with peripancreatic fat necrosis. Approximately 20% of patients with acute pancreatitis have necrotising pancreatitis, the remainder have interstitial pancreatitis.(Peter A.Banks,Harvard Medical School,US A, 1999).

Etio-pathogenesis and Classification:

The need to know the etiopathogenisis is essential for:

1. To treat the primary cause of pancreatitis, e.g. gallstones.

2. To prevent further attacks of pancreatitis.

Pathogenesis:

The basic process of pancreatitis is that the pancreatic secretions gain access to the interstitium of the gland, resulting in the catalytic and auto digestion through enzymatic changes. The early changes are seen as interaciner oedema and this stage of disease is defined as acute oedematous pancreatitis. The theory of 'Cri-nophagy' has been explained in an article by Mike Larvin (1999), which says that the damage to tissue is caused by certain enzymes, notably the proteases, but remarkable safeguard exist. Within aciner cell, inactive proteases are 'packaged' in zymogen granules containing trypsin inhibitors, Intracellular traffic directs zymogens to the apical margin and into the duct. Activation normally occurs only when duodenal enteropeptidase cleaves a small activation peptide. While most attacks are attributed to alcohol or gall stones, a variety of uncommon association exists. Electron microscopy in experimental pancreatitis implicates this common pathogenic pathway, whereby intracellular traffic chaos permits lysosomes to merge with zymogens and trigger activation.

In a small group of patients the disease progression is more fulminant and develop into a necrotizing pancreatitis.

This may occur by way of canalicular, lymphatic or vascular system or by

direct action upon the pancreatic parenchyma.

Almost all the pancreatic enzymes produced by the pancreas have been found to cause damaging pancreatitis. The most important of them is the proteolytic enzyme, trypsin.

Although the exact mechanism of alcohol related injury to the pancreas in not fully understood, but the association is well known. Theories put forward by Sarles and Sahel (1976) have documented that chronic alcohol administration leads to changes in the pancreatic exocrine secretion and the earliest changes occurring in the pancreas due to alcohol ingestion is the precipitation of the enzymatic proteins which subsequently block the secondary and the tertiary pancreatic ductules and even the bigger ducts, leading to inflammation.

The etiologic role of gallstone pancreatitis was first suggested by Opie and Halstead (1901), showed in experimental canine pancreatic duct, that the migration of the gallstone or sludge through the ampulla of Vater, causing a transient blockage and leading to the diversion of the bile into the pancreatic duct and causing bile induced pancreatic parenchymal injury. Which is now a well-established cause.

Classification based on etiological factors are:

1.Metabolic. 5.Genetic.

2.Mechanical 6.Autoimmune.

3. Vascular 7.Structural

4.Infection 8.Idiopathic.

9.Drug induced

Classification based on different Clinical presentations:

1.Cambridge classification (1983).

2.Marseilles Classification (1984).

3 .Atlanta classification (1992).

4.B.C. Савельев с соавт. (1978-83) classification: based on Clinico-morphological features.

5." Working" classification : (used in the Russian Federation) 1 .Interstitial-oedematous pancreatitis.

2.Necrotic pancreatitis.

3.Purulent pancreatitis.

The most common etiologic factors are Alcohol and Gallstones, which are seen in about 80% of patients.

In about 20% of the patients no identifiable cause are found and they are labelled as 'Idiopathic'.

Post ERCP pancreatitis is an entitity now seen very commonly as a cause of acute pancreatitis.

Etiological Distribution:

There are various etiological factors, the frequency of which has been evaluated by various authors.

The association between gallstone and acute haemorrhagic pancreatitis was beautifully illustrated by Opie and Halstead (1901), who described a case of fatal pancreatitis with a small stone impacted in the Ampulla of Vater and intense bile staining of pancreatic parenchyma.

Bell (1946) stated that gallstone is 6 times more common in patients with pancreatitis than in the population at large.

According to Howard J.M. (1962), of all pancreatitis syndromes, gallstone pancreatitis perhaps rests on the most solid factual basis. It is the most frequently recognised form, since it is found in about half of the patients with acute pancreatitis. It occurs in female three times more commonly that the males.

Over the intervening 85 years, the association between gallstones and pancreatitis has been convincingly documented as reported by Taylor et al (1983) and Frei et al (1986) Ю.В. Заблоцкий, 1990; A.B. Березин, 1997; E.A. Решетников и соавт., 1998; C.M. Дыньков с соавт.,2000).

Abuse of alcohol is becoming increasingly important in the aetiology of acute pancreatitis in many countries. This has been shown by Wilson and Bernstein (1985), where he has established a definite relationship of diet and drinking habits with the development of alcoholic pancreatitis.

Fink et al (1988) reported that most cases of pancreatic necrosis follow alcoholic pancreatitis and men outnumbered women by approximately 4:1.

As reported by M.J.McMohan (1987), most cases of acute pancreatitis occur in association with gallstones or alcohol abuse. However an identified cause could not be established in up to 30% of patients.

Bermann, Dunn, Strachley(1961) used the term 'indeterminate' rather than 'idiopathic' pancreatitis.Incidence found was 16% among 644 patients with pancreatitis.

Efron (1966), described and reported idiopathic pancreatitis in 49 patients, i.e. 24% among 204 patients seen at St.George Hospital, London.

These findings agree with those of most other reports of pancreatic necrosis by Alexander(1968), Bolooki et al (1968), Holden et al (1976), Ranson and Spencer (1977), Donahue,Nupus, Baker(1980), Aranha et al(1982), Stone et al (1984), Shi and Yoe(1984), Warshaw and Jin(1985), Maroske and Roher (9185), Pemberton et al(1986) and Bardley (1987).

Moberg et al (1968), in an autopsy series reported the incidence of idiopathic pancreatitis to be 11%. According to 1968 Literature Review, the incidence varied between 12% to 35%, Edlund et al and Blumenthal et al.

Reid and Kune (1980) could ascertain no etiologic antecedent in 35 patients, i.e. 37%. They determined that, with the acute attack, the mortality rate in the idiopathic group was twice as high as in the alcoholic group and four times as high as in the gallstone. Bennet and Jepson (1966) had made a similar observation.

In the experience of John M.Howard (1987), approximately 25% of patients fall into the idiopathic group. This incidence is gradually diminishing, but still remains a significant group.

Trapnell and Duncan (1975) described the incidence as 34%. As observed by Ranson (1977), necrosis was most common in the post-operative pancreatitis: 39%, in comparison to alcoholic: 6.6%, billiary: 3.6% and miscellaneous: 15%.

Traumatic pancreatitis is associated with a geographic variation. Blunt trauma from traffic accident is the dominant cause in Europe while penetrating in-

jury is more common in North America. The type and extent of the damage depends on the presence of other associated injuries, which have been studied by Jones R.C. (1985) and Wynn et al (1985).

ERCP can also cause acute pancreatitis.

Hyperamylaseamia is common after ERCP in 10% of patients, but severe pancreatitis only follows approximately 1% of patients as studied by M.J.McMohan (1987).

Age and Sex distribution:

In 1959, Blumenthal et al, said that the information regarding the age and sex distribution is quite meagre and varies in different population series.

In 1982, Bardley observed that pancreatitis has been reported in patients over the entire spectrum of age, ranging from a newborn to more than 100 years.

In 1987, M.J.McMohan, reported that aetiology played a major role in the distribution factor, in his study he found that the peak incidence of alcoholic pancreatitis was found to be in the fifth decade, where as pancreatitis associated with gallstone and others causes peaks in the seventh decade.

In 1983,Mitchell et al, reported from a multi-centre study of acute pancreatitis in the United Kingdom, that 57% of the patients were over 60 years.

In 1978, Ranson, reported the age trends from North America, where the peak age incidence of alcoholic pancreatitis was 44 years.

In 1980,Stone reported in Atlanta, the age incidence for alcoholic pancreatitis to be 38 years.

The male to female ratio as studied by M.J.McMohan (1987) were 1: 1.5, for gallstone pancreatitis; and 1:1.3 for alcoholic pancreatitis.

Imrie et al (1978), studied that although alcohol induced pancreatitis was probably commoner in Glasgow than in England, 60% of attacks were associated with gallstone disease with a ratio of 1: 1.5, with male preponderance.

In a number of reported series the development of a necrosis may be almost coincidental with an acute haemorrhagic attack of pancreatitis that leads to massive pancreatic necrosis. In such cases (50% or more) diagnosis of necrosis formation

may not be difficult. In the delayed form of abscess development, occurring up to several weeks following an attack of pancreatitis, diagnosis may be difficult to make, Donahue (1980) and Frey (1979).

As described by Hanscan (1968), Acute pancreatitis has a wide gamut of manifestation and often the diagnosis is not considered. Most pancreatitis seen by physician presents a problem in differential diagnosis of abdominal pain. If the pain happens to be rather mild and tolerable, the patient is likely to be dismissed. Blumenthal et al (1959), found that in true abscess formation as a sequel to acute pancreatitis occurred in 17% in his series. 14 of these were in patients who gave no antecedent history of attack of pancreatitis while the remaining three were in patients with known pervious acute bouts. Whenever a temperature above 101 F is encountered, this complication should be suspected.

Hardy and Bowlin (1957), point out that the alert and persistent examiner will occasionally be rewarded by palpating a mass in the left flank region, which appears to be the most common site of abscess formation, after long standing necrosis of the pancreas.

Most Commonly seen:

With the unmistakable type of epigastric pain radiating to the back, comfort in the bent forward position, painkillers giving minimal relief; vomiting; fever, gets you working towards the possibility of acute pancreatitis and you turn to the investigative modalities for confirmation.

The development of pancreatic necrosis in patients with acute pancreatitis results in a dramatic increase in local and systemic organ complications. Most patient who develop organ system failure with acute pancreatitis have pancreatic necrosis, autopsy studies have shown that >80% of deaths with acute pancreatitis are associated with presence of pancreatic necrosis.(Beger HG, Rau B, Mayer J-1997)

Investigative modalities to diagnose pancreatic collections:

Laboratory Investigations: Blumenthal et al (1959) had reported a number of laboratory investigations, which along with clinical findings were suggestive of

pancreatic collections e.g.: Demonstration of elevated enzyme levels in the blood and / or urine, i.e. S.lipase and S.amylase.

Elman (1955), had questioned the specificity of S.amylase tests as high amylase values had been reported in other conditions like perforated DU, renal insufficiency, cerebral trauma, ectopic pregnancy, which stand true till toe1 ay.

Also, the other tests reported were serum electrolytes, S.calicium, E.C.G for electrical changes and to rule out myocardial infarction. Reece and Burrows (1950) had stressed that transitory S-T segment and T wave changes were found in ECG's of patients with acute pancreatitis.

Radiological Investigation: X-ray abdomen findings were found particularly significant if they revealed secondary ileus.

Bockus et al (1955) had suggested the following criteria for establishing this event:

1. Presence of air in a few loops of small bowel adjacent to each other and in the absence of significant air in other small intestinal loops.

2. Small amounts of air in the stomach and /or colon.

3. A calibre of air filled loop of at least 2.5 to 3 cm.

4. A stiffened appearance of gas-filled loops and a space between the adjacent loop wider then normal.

These and some other x-ray manifestations have been well illustrated by Grollman et al, as early as 1950.

The Colon cut-off' sign, reflects large intestinal involvement with peri-pancreatic inflammation, Price (1956).

The Abdominal fat necrosis' sign is more specific for acute pancreatitis, Berenson (1971).

The presence of intra pancreatic gas in the setting of pancreatitis with abscess formation may also be visible on the plain X-ray film, J.M.Howard (1987).

Ultrasonography: The introduction of the grey scale technique in the mid 1970's offer significant technological advances over the older biphasic equip-

merit, prompting some enthusiasts to claim that ultrasonography should be the first test performed in the patients with suspected pancreatic disease (В.Н.Полищук,1989; И.И. Затевахин с соавт.,1991; В.И. Филин с соавт., 1994; К.В.Лапкин, В.А. Иванов, 1995, 1996; Н.Л. Травникова с соавт., 1996; Filly et al, 1970).

Pancreatic necrosis, which appears as irregular, sonolucent areas in the region of pancreas, is not so well visualised as with CT scan, it is often difficult to distinguish from fibrosis except by serial examinations, which show a return to normal over time in the case of inflammation, as said by Beger and Blauenstein (1974).

USG can detect cholelithiasis with 96% accuracy when the gall bladder is visualised, McKay (1982).

Since it can detect cysts as small as 2 cm, it is the method of choice for detection of pancreatic abscess, and collections. Editorial (1977); Duncan (1976); Sigel (1982).

CT-scan: According to Mender (1980) and Silverstein (1981), CT-scan offers better visualization of the retroperitoneal structures and better overall visualisation of the pancreas.

The examination is more accurate regardless of the presence of abdominal gas or the patient's size or clinical status.

In contrast, Danmann (1980) observed that CT changes do not always correlate with disease severity.

The CT-scan is most useful in diagnosing later complications of acute necrotic pancreatitis, such as pseudocyst, abscess or peri-pancreatic fluid collections, in providing a baseline for serial examinations when technical difficulties preclude the use of USG and in showing the extent of inflammatory changes beyond the pancreas, А.Н.Лищенко, В.В.Лаптев (1995), Siegelmann et al (1980), Silverstein (1981), Hill et al (1982), Lawson (1983).

CT-scan and USG can also be used to guide needle aspiration of peri-pancreatic fluid collection to obtain samples for bacterial culture, К.В.Лапкин, B.A. Иванов, (1995, 1996), John M. Howard (1987).

According to Buchler et al (1986), USG is much less useful in the staging of the severity of acute pancreatitis because at least 1 /3 rd of patients with acute pancreatitis, demonstrate paralytic ileus with bowel distension and gas.

Also, 90% of cases with massive and 79% of those with minor necrosis of the pancreas had been demonstrated with contrast enhanced CT-scan.

The overall accuracy rate for dynamic pancreatography, by CT scan, in detecting pancreatic necrosis has been shown to exceed 90%, and easier to gather information regarding the natural history of untreated pancreatic necro-sis.(Beger et al-1987; Bardley EL et al-1989; Larvin M et al-1990).

To differentiate between oedematous interstitial and necrotisisng pancreatitis, H.G.Beger (1989), reported various investigative features:-

1. Serum markers:- S.Anti-protease and C-reactive protein,- 80% reliable.

2. Contrast enhanced CT-scan.

It should be emphasised that the technique of contrast enhancement of the upper Gastrointestinal tract and the vascular system by bolus Intravenous injection plays a decisive role, CT without contrast medium does not provide any information about the viability of the pancreatic gland. This has been reported by Block et al (1986).

The diagnosis of necrosis is based on the perfusion status of the pancreas and areas with low or no contrast enhancement, represent necrotic tissue.

Peter A Banks, in the ACG Draft guidelines for acute pancreatitis, has recommended: Contrast-enhanced CT scan should be performed among patients demonstrated to have severe pancreatitis on the basis of a high APACHE II score and /or evidence of organ failure.

Dynamic contrast-enhanced CT scan is the best available test to distinguish interstitial from necrotizing pancreatitis. Interstitial pancreatitis is char-

acterized by an intact microcirculation and uniform enhancement of the gland. Necrotizing pancreatitis is characterized by disruption of the microcirculation such that large areas do not enhance. Whereas small areas of non-enhancement could represent the presence of intraparenchymal fluid, large areas of nonenhancement indicate the presence of a disrupted microcirculation and pancreatic necrosis. It is also recommended when pancreatic infection is suspected clinically. When there is suspicion of infection, guided percutaneous aspiration with Gram stain and culture should be performed. Infected necrosis requires surgical debridment. Patients with sterile necrosis can be usually managed medically. A subset of patients with sterile necrosis may require surgical debridment after 4-6 weeks.

When the creatinine is in the 1.5-2mg% range, intravenous contrast should not be used or non-ionic contrast should be substituted. While a CT scan without intravenous contrast cannot define the presence of pancreatic necrosis, it nevertheless provides important information pertaining to severity in accordance with a Balthazar-Ranson A-E grading system.

CT severity index: developed by Balthazar and Ranson shows:

CT Grade Score Necrosis Score

A 0 None 0

B 1 One third 2

C 2 One half 4

D 3 > One half 6

E 4 Total 7

CT grade + Necrosis = Total score. Grading System: A: Normal pancreas.

B: Focal or diffuse enlargement of the pancreas.

C: Pancreatic gland abnormalities associated with peripancreatic inflammation.

D: Enlarged pancreas with fluid collection in anterior pararenal space. E: Enlarged pancreas, with two or more fluid collection and/or the presence of gas in or adjacent to the pancreas.

In general, the most severe pancreatitis in term of organ failure and the presence of pancreatic necrosis occur in Grade D or E pancreatitis.

(Balthazar EJ, Ranson JHC 1990).

MRI: Magnetic resonance imaging is the latest of the non-invasive of the imaging modalities used for pancreatitis. It is only a shade better than CT-scan, but when the MR Cholangio-pancreaticogram is used for the detection of the biliary as well as the pancreatic duct, then it becomes a valuable tool in the hands of the radiologist. And offers an insight into the insides of the patient, non-invasively.

ERCP: Endoscopic Retrograde Cholangio-Pancreatography, plays an important role in the determination whether there is a pre-existing or residual structural