37-year-old woman was taken to our hospital after alimentary abuse and with consequent abdominal pain. Examinations proved acute pancreatitis. Despite the appropriate conservative therapy her condition worsened, IAP reached 20 mmHg, respiratory distress and oliguria developed.

Laparotomy, lavage, drainage was performed. To prevent abdominal distension the abdomen was left open and organs were covered with a sterile urinary drainage bag (Bogota Bag). In the ICU 12 operations were performed during 108 nursing days. The IAP was monitored permanently and when it reached the critical value necrectomy and lavage was performed. On the 116th nursing day she was sent home without complaints.

Her abdomen was covered with epithelized omentum which wiIl be solved by a further operation (1-2).

#### **9. Discussion**

176 Pancreatitis – Treatment and Complications

spincterotomy in patients with common bile duct gallstone-induced pancreatitis have

Loosing patients in the early phase is frequently due to not recognised and not treated ACS. The presence of IAH can also be used as a predictor of the severity of acute pancreatitis, because by some clinical trials there is correlation with the increased IAP and severity of pancreatitis, mortality, peripancreatic infection rate, and need for surgical intervention (53). The true prevalence of IAH in patients with severe acute pancreatitis is not known. We can find numerous studies in the bibliography of the prevalence of IAH among the patients treated by severe acute pancreatitis. De Waele and his team described in their study that 44% of the 41 study patients had IAP levels higher than 12 mmHg, and 4 patients (10%) had IAP levels higher than 25 mmHg with severe organ disfunction and undergoing surgical decompression (54). Keskinen treated 37 patients in the ICU for acute pancreatitis and 27% of the patients (n=10) had IAP levels higher than 25 mmHg (55). In a study of 297 patients

Severe acute pancreatitis is one of the most common diseases associated with IAH in the

Thus, it can be estimated that the overall prevalence of IAH in patients with severe acute pancreatitis is about 40%, and the frequency of ACS requiring surgical decompression is

In a study comparing patients with or without ACS (IAP > 25 mmHg) treated in the ICU for severe acute pancreatitis the hospital mortality rate for patients with ACS was 50%

The following case reports from patientes treated in our department are to point out the

33-year-old man was taken to ICU with signs of acute pancreatitis after alcoholic abuse. Conservative treatment was started but on the second day the conditions of the man were getting worse. IAP measurement was started and we found IAP = 12 mmHg which rised to 26 mmHg during the next 3 days and developed MOF. During the intervention we found the tipical clinical picture of acute necrotizing pancreatitis with retroperitoneal necrosis. Although the decompression with Bogota Bag insertion was performed we lost the patient 2 days later. Concluding this case it is very important to pay attention to the early signs of IAP

37-year-old woman was taken to our hospital after alimentary abuse and with consequent abdominal pain. Examinations proved acute pancreatitis. Despite the appropriate conservative therapy her condition worsened, IAP reached 20 mmHg, respiratory distress

Laparotomy, lavage, drainage was performed. To prevent abdominal distension the abdomen was left open and organs were covered with a sterile urinary drainage bag (Bogota Bag). In the ICU 12 operations were performed during 108 nursing days. The IAP was

from China presented that the overall incidence of IAH was 36% (56).

compared with 15% in patients without ACS (55).

/ ACS and the timing of the decompression.

importance of measurement of IAP:

improved survival.

ICU environment.

about 10% (53-56).

*First patient:*

*Second patient:*

and oliguria developed.

IAH and ACS are one of the major causes of organ failure and increased mortality (ACS with extremely high 38-71% mortality) among a wide variety of patient populations.

The pathophysiology of IAH and ACS is based on the chain reaction of physiological processes generated by the increased abdominal pressure which affects almost every organ and it could be fatal without correct diagnosis and treatment. It was originally noticed in traumatological cases (gunshot and stab wounds, intra-abdominal haemorrhage) when the extreme abdominal distension was related with a rapidly worsening condition and ended in ARDS, MOF and toxic shock. The same process is taking place in general surgical patients in spite of the different etiology. The leading etiological factor among general surgical critically ill patients is the acute pancreatitis. The cause of this phenomenon is the extremely increased IAP. The diagnosis was supported by the improved methods of monitoring IAP because the physical examination of the abdomen is far from accurate with a sensitivity of only 40%. The gold standard of the IAP monitoring is the CIAPM ensures diagnosis of ACS and the appropriate indication of the operation. The treatment consists of adequate fluid resuscitation and surgical decompression.

Intra-abdominal hypertension and abdominal compartment syndrome are frequent clinical findings among acute general surgical patients. Patients with comparable demographics and acute severity of illness are more likely to die if intra-abdominal hypertension or abdominal compartment syndrome is present. We conclude that the early recognition and surgical decompression is urgent.

"We must study and learn from the past and, at the same time, proactively "invent" the future. The future of IAH and ACS is in our hands. It is time to pay attention." (Cheatham, Ivatury, Malbrain, Sugrue) (53)

#### **10. References**

Intra-Abdominal Hypertension and Abdominal Compartment Syndrome in

blood flow. Am. Surg. 58:573-575.

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315:1150–1157

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human monocytes. J Immunol 156:4408–4414

open cholecystectomy. Arch Med Sci 3 (3):223-228

hypertension? Acta Clin Belg Suppl 62:119–130

function. Acta Clin Belg 62(Suppl):371–374

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[24] Diebel LN, Dulchavsky SA, Willson RF (1992) Effect ofincreased intra-abdominal

[25] Diebel L, Saxe J, Dulchavsky SA (1992) Effect of intra-abdominal pressure on abdominal

[26] Vegar-Brozovic V, Brezak J, Brozovic I (2008) Intra-abdominal hypertension: pulmonary

[27] Waele JJ, Leppaniemi AK (2009) Intra-abdominal hypertension in acute pancreatitis.

[28] Motew SJ, Mourelatos MG, Miller RN et al (1997) Evidence that adenosine contributes

[29] Eltzschig HK, Thompson LF, Karhausen J, Cotta RJ, Ibla JC, Robson SC, Colgan SP

[30] Housley GD, Bringmann A, Reichenbach A (2009) Purinergic signalling in special

[31] Berne RM, Knabb RM, Ely SW, Rubio R (1983) Adenosine in the local regulation of

[32] McCallion K, Harkin DW, Gardiner KR (2004) Role of adenosine in immunomodulation: review of the literature. Crit Care Med 32:273–277 [33] Sipka S, Kovács I, Szántó S et al (2005) Adenosine inhibits the release of interleukine-1β in activated human peripheral mononuclear cells. Cytokine 31:258–263 [34] Le Moine O, Stordeur P, Schanane L et al (1996) Adenosine enhances IL-10 secretion by

[35] Mosser DM, Zhang X (2008) Interleukin 10: new perspectives on an old cytokine.

[36] Paraskevi M, Sidiropovlov T, Pandazi A, Batistaki C, Matiatov S, Panagiotou GK (2007)

[37] Ozmen MM, Zulfikarogly B, Col C, Cinel I, Isman FK, Cinel L, Besler TH (2009) Effect of

[38] Hansen PB, Hashimoto S, Oppermann M, Huang Y, Briggs JP, Schnermann L (2005)

[39] De Laet I, Malbrain MLNG, Jadoul JL, Rogiers P, Sugrue M (2007) Renal implications of

[40] De Waele JJ, De laet I (2007) Intra-abdominal hypertension and the effect of renal

[41] Vallon V, Mühlbauer B, Osswald H (2006) Adenosine and kidney function. Physiol Rev

Changes of gastric intramucosal pH in obese patients undergoing laparoscopic and

increased abdominal pressure on cytokines (IL-1 β, IL-6, TNFα) C-reactive protein (CRP), free radicals (NO, NDA), and histology. Surg Laparosc Endosc Percutan

Vasoconstrictor and vasodilator effects of adenosine in the mouse kidney due to preferential activation of A1 or A2 adenosine receptors. J Pharmacol Exp Ther

decreased intra-abdominal pressure: are the kidneys the canary for abdominal

to the maintenance of hepatosplanchnic blood flow during peritoneal sepsis in rats.

(2004) Endogenous adenosine produced during hypoxia attenuates neutrophil accumulation: coordination by extracellular nucleotide metabolism. Blood

and cerebral complications. Transplant Proc. 40:1190-1192.

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[7] Iberti TJ, Lieber CE, Benjamin E (1989) Determination of intraabdominal pressure using

[8] Iberti TJ, Kelly KM, Gentili DR, Hirsch S, Benjamin E (1987) A simple technique to accurately determine intra-abdominal pressure. Crit. Care Med. 15:1140-1142.

[10] Malbrain MNLG (1999) Abdominal pressure in the critically ill: measurement and

[11] Balogh Zs, Jones F, D'Amours S, Parr M, Sugrue M (2004) Continuous intra-abdominal

[12] Schein M, Wittmann DH, Aprahamian CC, Condon RE (1995) The abdominal

[13] Burch IM, Moore EE, Moore FA, Franciose R (1996) The abdominal compartment

[14] Malbrain MLNG, Cheatham ML, Kirkpatrick A, Sugrue M, Parr M, De Waele J, Balogh

[16] Malbrain MLNG, Chiumello D, Pelosi P, et al (2005) Incidence and prognosis of

[17] Tóns Ch, Schachtrupp A, Rau M, Mumme Th, Schumpelick V (2000) Abdominelles Kompartment Syndrom: Vermeidung und Behandlung. Chirurg. 71:918-926. [18] Malbrain MNLG, Chiumello D, Pelosi P, Bihari D, Innes R, Ranieri VM et al (2005)

[19] Chen H, Li F, Sun JB, Jia JG (2008) Abdominal compartment syndrome in patients with severe acute pancreatitis in early stage. World J Gastroenterol. 14:3541-3548. [20] Balogh Zs, McKinley BA, Holcomb JB et al (2003) Both primary and secondary

[21] Sugrue M, Balogh Zs, Malbrain M (2004) Intra-abdominal hypertension and renal

[23] Diebel LN, Dulchavsky SA, Brown WJ (1997) Splanchnic ischaemia and bacterial translocation in the abdominal compartment syndrome. J. Trauma. 43:852-855.

multiple-center epidemiological study. Crit Care Med. 33:315-322.

harbingers of multiple organ failure. J. Trauma. 54:848-861.

[22] Jakob SM (2002) Clinical review: Splanchnic ischaemia. Crit. Care 6:306-312.

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compartment syndrome: the physiological and clinical consequences of elevated

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pressure measurement technique. Am. J. Surg. 188:679-684.

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a transurethral bladder catheter: clinical validation of the technique.

**12**

*Japan*

**Traumatic Pancreatitis –**

Hirotaka Okamoto1,2 and Hideki Fujii2 *1Department of Surgery, Tsuru Municipal Hospital,*

*2Department of Gastrointestinal,*

**Endoscopic and Surgical Management**

 *Breast & Endocrine Surgery, Faculty of Medicine, University of Yamanashi*

Acute pancreatitis is inflammation of the pancreas that occurs suddenly and usually resolves in a few days with treatment. Acute pancreatitis can be a life-threatening illness with severe complications. The most common cause of acute pancreatitis is the presence of small gallstones that cause inflammation of the pancreas as they pass through the common bile duct. Chronic heavy alcohol use is also a common cause. Acute pancreatitis can occur within hours or as long as 2 days after consuming alcohol. Other causes of acute pancreatitis include abdominal trauma, medications, infections, tumors, and genetic abnormalities of the

Pancreatic trauma is uncommon, accounting for only 0.2-6% of all injuries resulting from abdominal trauma, and is associated with a high mortality rate of 13.8-31% (Leppäniemi et al., 1988). The high mortality rate is due to the frequent occurrence of associated abdominal injuries. In addition, blunt abdominal trauma is considered to be the cause of one fifth of all cases of traumatic pancreatitis and it may result in contusion, parenchymal fracture, or ductal disruption (Portis et al., 1994). These injuries to the pancreas are typically caused by compression of the organ against the vertebral column, mostly in traffic related-accidents. Blunt trauma to the epigastrium is caused by steering wheels, handlebars, seatbelts, or directly. Other mechanisms of injury include sporting accidents, such as direct hits from a

Therapeutic decisions for pancreatic trauma are based on the injury site and status of the pancreatic ductal system. When pancreatic ductal disruption exists or when duodenal injury cannot be ruled out, surgical exploration is usually required; however, surgery carries considerable morbidity and mortality risks. In this chapter, we discuss the management of pancreatic trauma and acute pancreatitis, including therapeutic endoscopy and surgical

The pancreas grows rapidly during a child's first five years of life with a slower growth rate up to the age of 18 years of age (Spiegel et al., 1997). It is a large complex gland that lies

**1. Introduction**

pancreas.

ball or a blunt blow.

**2. Amatomy and physiology**

exploration.

### **Traumatic Pancreatitis – Endoscopic and Surgical Management**

Hirotaka Okamoto1,2 and Hideki Fujii2

*1Department of Surgery, Tsuru Municipal Hospital, 2Department of Gastrointestinal, Breast & Endocrine Surgery, Faculty of Medicine, University of Yamanashi Japan*

#### **1. Introduction**

180 Pancreatitis – Treatment and Complications

[42] Wauters J, Claus P, Brosens N, McLaughlin MM, Wilmer A (2009) Pathophysiology of

[43] Imai K, Furuya K, Kawada M et al (2006) Human pelvic extramural ganglion cells: a semiquantitative and immunohistochemical study. Surg Radiol Anat 28:596–605 [44] De Laet I, Hoste E, Verholen E, Waele D (2007) The effect of neuromuscular blockers in patients with intra-abdominal hypertension. Intensive Care Med 33:1811–1814 [45] Bodnar Zs, Keresztes T, Kovács I, Hajdu Z, Boissonneault GA, Sipka S (2010) Increased

[46] Bodnar Zs, Szentkereszty Z, Hajdu Z, Boissonneault GA, Sipka S (2011) Beneficial

[48] Davis PJ, Koottayi S, Taylor A, Butt WW, (2005) Comparison of indirect methods of measuring intra-abdominal pressure in children. Int. Care Med. 31:471-475. [49] Balogh Zs, McKinley BA, Cocanour CS et al (2003) Supranormal trauma resuscitation causes more cases of abdominal compartment syndrome. Arch. Surg. 138:637-643. [50] Howdiesholl TR, Proctor CD, Sternberg E, Cué JI, Mondy JS, Hawkins ML (2004)

[51] Vargo D (2004) Component separation in the management of the difficult abdominal

[52] Young SP, Thompson JP (2008) Severe acute pancreatitis. Contin Educ Anaesth Crit

[53] Ivatury RR, Cheatham ML, Malbrain MLN, Sugrue M (2006) Abdominal Compartment

[54] De Waele J, Hoste E, Blot S et al (2004) Intraabdominal hypertension and severe acute

[55] Keskinen P, Leppaniemi A, Pettila V et al (2004) Intra-abdominal pressure in acute

[56] Tao HQ, Zhang JX, Zou SC (2004) Clinical characteristics and management of patients

with early acute severe pancreatitis: Experience from a medical center in China.

necrotizing pancreatitis. Inaugural WCACS, Noosa (Australia)

hypertension. Langenbecks Arch Surg. (Published Online: 03 June 2011) [47] Malbrain MLNG (2004) Different techniques to measure intra-abdominal pressure

elevated intra-abdominal pressure. J Trauma 66:713–719

intra-abdominal pressure. Langenbecks Arch Surg. 395: 969-972.

(IAP): time for a critical re-appraisal. Int. Care Med. 30:357-371.

reconstruction of the abdomen. Am. J. Surg. 188:301-306.

wall. Am. J. Surg. 188:633-637.

Syndrome. Landes Bioscience. Texas (USA)

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pancreatitis. Inaugural WCACS, Noosa (Australia)

Care Pain. 8 (4): 125-128.

renal hemodynamics and renal cortical microcirculation in a porcine model of

serum adenosine and interleukin 10 levels as new laboratory markers of increased

effects of theophylline infusions in surgical patients with intra-abdominal

Temporary abdominal closure followed by definitive abdominal wall

Acute pancreatitis is inflammation of the pancreas that occurs suddenly and usually resolves in a few days with treatment. Acute pancreatitis can be a life-threatening illness with severe complications. The most common cause of acute pancreatitis is the presence of small gallstones that cause inflammation of the pancreas as they pass through the common bile duct. Chronic heavy alcohol use is also a common cause. Acute pancreatitis can occur within hours or as long as 2 days after consuming alcohol. Other causes of acute pancreatitis include abdominal trauma, medications, infections, tumors, and genetic abnormalities of the pancreas.

Pancreatic trauma is uncommon, accounting for only 0.2-6% of all injuries resulting from abdominal trauma, and is associated with a high mortality rate of 13.8-31% (Leppäniemi et al., 1988). The high mortality rate is due to the frequent occurrence of associated abdominal injuries. In addition, blunt abdominal trauma is considered to be the cause of one fifth of all cases of traumatic pancreatitis and it may result in contusion, parenchymal fracture, or ductal disruption (Portis et al., 1994). These injuries to the pancreas are typically caused by compression of the organ against the vertebral column, mostly in traffic related-accidents. Blunt trauma to the epigastrium is caused by steering wheels, handlebars, seatbelts, or directly. Other mechanisms of injury include sporting accidents, such as direct hits from a ball or a blunt blow.

Therapeutic decisions for pancreatic trauma are based on the injury site and status of the pancreatic ductal system. When pancreatic ductal disruption exists or when duodenal injury cannot be ruled out, surgical exploration is usually required; however, surgery carries considerable morbidity and mortality risks. In this chapter, we discuss the management of pancreatic trauma and acute pancreatitis, including therapeutic endoscopy and surgical exploration.

#### **2. Amatomy and physiology**

The pancreas grows rapidly during a child's first five years of life with a slower growth rate up to the age of 18 years of age (Spiegel et al., 1997). It is a large complex gland that lies

Traumatic Pancreatitis - Endoscopic and Surgical Management 183

It is generally reported that laboratory findings are relatively insensitive and non-specific in diagnosing pancreatic injury (Arkovitz et al., 1997; Bradley et al., 1998; Jobst et al., 1999). Serum amylase evaluation can suggest pancreatic injury; however, amylase levels have failed to predict or correlate with the degree of injury or disclose potential ductal disruption,

Serum lipase is often based clinically in the setting of acute pancreatitis, but after blunt trauma, elevated serum lipase levels may be nonspecific and a poor indication of injury (Buechter et al., 1990). Because of their low sensitivity and specificity for pancreatic trauma, serum amylase and lipase have limited diagnostic value, but elevated levels may provide a

An ultrasound examination will usually be performed to enable the diagnosis of free abdominal fluid or gross damage to the liver or spleen. The pancreas is not easily identified and examined to its full extent; therefore, pancreatic injuries, parenchymal or ductal, will frequently be missed. However, routine abdominal ultrasound examination in the emergency room will establish the diagnosis of an intra-abdominal injury and therefore establish the need for an urgent explorative laparotomy. To disclose main pancreatic duct injury in blunt and penetration pancreatic trauma, intraoperative ultrasonography has

When initially evaluating for injury, CT scanning is a simple, noninvasive means of evaluating the pancreas. New-generation helical CT scanners quickly enable an overview of abdominal injuries in severely traumatic patients. CT was reported to have 90% sensitivity in detecting pancreatic disruption (Teh et al., 2007). Furthermore, CT allows additional assessment of the severity and extent of pancreatic tissue damage and concomitant injuries

Magnetic resonance cholangiopancreatography (MRCP) is another non-invasive diagnostic tool that allows the evaluation of pancreatic injuries with high sensitivity and specificity. Particularly in stable patients with suspected pancreatic injury, MRCP enables the noninvasive detection or exclusion of pancreatic duct trauma and pancreatic specific complications. It may therefore provide information that can be used to guide management decisions in the further course of pancreatic trauma patients; however, its purely diagnostic nature and its inability to provide real-time visualization of ductal findings and extravasation are two of its disadvantages (Fulcher et al., 2000). Recently, secretinstimulated MRCP was also reported to be a safe, non-invasive test that can provide additional useful information about duct integrity and facilitate management (Gillams AR et

especially when obtained in the early post-trauma period (Simon et al., 1994).

clue to a severe injury requiring further investigation.

**5.4 Magnetic resonance cholangiopancreatography**

proven to be helpful (Hikida et al., 2004).

**5.3 Computed tomography**

(Bigattini et al. 1999).

al., 2006)**.**

**5. Diagnosis**

**5.2 Ultrasound**

**5.1 Laboratory data**

outside the walls of the alimentary tract parallel to the stomach at the level of the first and second lumbar vertebrae. It is surrounded anteriorly by the upper abdominal intraperitoneal organs and posteriorly by the thick paraspinal muscles. The lobules of the pancreas drain into the main pancreatic duct of Wirsungs which traverses the length of the gland and joins the common bile duct, emptying into the duodenum through the ampulla of Vater. The minor duct of Santorini usually branches off from the main pancreatic duct and also empties into the duodenum. The gland is not encapsulated; therefore, tears in pancreatic tissues permit pancreatic digestive enzymes to invade the peripancreatic tissue and leak into the peritoneal cavity.

#### **3. Pathogenesis**

The mechanism of blunt pancreatic trauma usually involves anterior compressive forces applied to the pancreas, which lies over the vertebral column. The pancreas is relatively fixed so that during blunt impact, the pancreas is not displaced and absorbs the full amount of force applied (**Rawls, 2001**).

#### **4. Classification**

Classically, according to Lucas's classification of pancreatic injury, injuries without MPD disruption are designated Class I, while Class II or III injuries involve MPD disruption (Lucas, 1977). The Organ Injury Scaling Committee of the American Association for the Surgery of Trauma has proposed a pancreatic organ injury scale that is widely used and is based on the extent of parenchymal damage as well as the presence or absence of pancreatic duct injury (Moore et al., 1990). Minor contusions or superficial lacerations of the pancreas without duct involvement are classified as grade I injury. Grade II injuries are major contusions or lacerations without duct disruption. Distal transection of the pancreas or major parenchymal injuries with duct injuries is described as grade III. Grade IV injuries are proximal transections or any proximal parenchymal injuries involving the ampulla. Grade V injuries describe massive destructions of the pancreas head (**Table 1**).

Table 1. Pancreatic injury severity scale (Moore et al., 1990)

### **5. Diagnosis**

182 Pancreatitis – Treatment and Complications

outside the walls of the alimentary tract parallel to the stomach at the level of the first and second lumbar vertebrae. It is surrounded anteriorly by the upper abdominal intraperitoneal organs and posteriorly by the thick paraspinal muscles. The lobules of the pancreas drain into the main pancreatic duct of Wirsungs which traverses the length of the gland and joins the common bile duct, emptying into the duodenum through the ampulla of Vater. The minor duct of Santorini usually branches off from the main pancreatic duct and also empties into the duodenum. The gland is not encapsulated; therefore, tears in pancreatic tissues permit pancreatic digestive enzymes to invade the peripancreatic tissue

The mechanism of blunt pancreatic trauma usually involves anterior compressive forces applied to the pancreas, which lies over the vertebral column. The pancreas is relatively fixed so that during blunt impact, the pancreas is not displaced and absorbs the full amount

Classically, according to Lucas's classification of pancreatic injury, injuries without MPD disruption are designated Class I, while Class II or III injuries involve MPD disruption (Lucas, 1977). The Organ Injury Scaling Committee of the American Association for the Surgery of Trauma has proposed a pancreatic organ injury scale that is widely used and is based on the extent of parenchymal damage as well as the presence or absence of pancreatic duct injury (Moore et al., 1990). Minor contusions or superficial lacerations of the pancreas without duct involvement are classified as grade I injury. Grade II injuries are major contusions or lacerations without duct disruption. Distal transection of the pancreas or major parenchymal injuries with duct injuries is described as grade III. Grade IV injuries are proximal transections or any proximal parenchymal injuries involving the ampulla. Grade V

injuries describe massive destructions of the pancreas head (**Table 1**).

Table 1. Pancreatic injury severity scale (Moore et al., 1990)

and leak into the peritoneal cavity.

of force applied (**Rawls, 2001**).

**3. Pathogenesis**

**4. Classification**

#### **5.1 Laboratory data**

It is generally reported that laboratory findings are relatively insensitive and non-specific in diagnosing pancreatic injury (Arkovitz et al., 1997; Bradley et al., 1998; Jobst et al., 1999). Serum amylase evaluation can suggest pancreatic injury; however, amylase levels have failed to predict or correlate with the degree of injury or disclose potential ductal disruption, especially when obtained in the early post-trauma period (Simon et al., 1994).

Serum lipase is often based clinically in the setting of acute pancreatitis, but after blunt trauma, elevated serum lipase levels may be nonspecific and a poor indication of injury (Buechter et al., 1990). Because of their low sensitivity and specificity for pancreatic trauma, serum amylase and lipase have limited diagnostic value, but elevated levels may provide a clue to a severe injury requiring further investigation.

#### **5.2 Ultrasound**

An ultrasound examination will usually be performed to enable the diagnosis of free abdominal fluid or gross damage to the liver or spleen. The pancreas is not easily identified and examined to its full extent; therefore, pancreatic injuries, parenchymal or ductal, will frequently be missed. However, routine abdominal ultrasound examination in the emergency room will establish the diagnosis of an intra-abdominal injury and therefore establish the need for an urgent explorative laparotomy. To disclose main pancreatic duct injury in blunt and penetration pancreatic trauma, intraoperative ultrasonography has proven to be helpful (Hikida et al., 2004).

#### **5.3 Computed tomography**

When initially evaluating for injury, CT scanning is a simple, noninvasive means of evaluating the pancreas. New-generation helical CT scanners quickly enable an overview of abdominal injuries in severely traumatic patients. CT was reported to have 90% sensitivity in detecting pancreatic disruption (Teh et al., 2007). Furthermore, CT allows additional assessment of the severity and extent of pancreatic tissue damage and concomitant injuries (Bigattini et al. 1999).

#### **5.4 Magnetic resonance cholangiopancreatography**

Magnetic resonance cholangiopancreatography (MRCP) is another non-invasive diagnostic tool that allows the evaluation of pancreatic injuries with high sensitivity and specificity. Particularly in stable patients with suspected pancreatic injury, MRCP enables the noninvasive detection or exclusion of pancreatic duct trauma and pancreatic specific complications. It may therefore provide information that can be used to guide management decisions in the further course of pancreatic trauma patients; however, its purely diagnostic nature and its inability to provide real-time visualization of ductal findings and extravasation are two of its disadvantages (Fulcher et al., 2000). Recently, secretinstimulated MRCP was also reported to be a safe, non-invasive test that can provide additional useful information about duct integrity and facilitate management (Gillams AR et al., 2006)**.**

Traumatic Pancreatitis - Endoscopic and Surgical Management 185

pancreatic fluid was increasing (**Fig. 1**); furthermore, serum amylase and elastase levels were elevated. ERP (endoscopic retrograde pancreatography) revealed that contrast medium in the main pancreatic duct (MPD) had leaked into the parenchyma, indicating MPD injury (**Fig. 2**). To prevent the traumatic pancreatitis from worsening, a stent was inserted endoscopically at a site distal to the injured portion of the MPD (**Fig. 3**). Thereafter, the patient's complaint was markedly reduced, and his serum amylase levels returned to normal. In addition, the apparent pancreatic edema and peripheral fluid were decreased on

Fig. 2. Endoscopic pancreatography (ERP) revealed leakage of contrast medium.(white

Fig. 3.  ERCP was also reported to be the definitive test for pancreatic duct injury, particularly, to demonstrate clearly the site of duct disruption and the grade of duct injury, whether the branch or main duct and partial or complete disruption of the main pancreatic duct MPD (Kim et al., 2001).

Recently, ERCP has been shown not only to provide sufficient information for conclusive diagnosis but also to be an effective and safe non-operative treatment tool (Bendahan et al., 1995; Huckfeldt et al., 1996; Kim et al., 2001; Cay et al., 2005; Houben et al., 2007). In certain cases of leakages of the pancreatic duct, transpapillary stent insertion might seal the injury and stabilize it in a way that eventually leads to resolution of the leakage

#### **6. Therapy**

Isolated pancreatic trauma is rare and usually results from direct trauma to the epigastrium, for example from the handle bars in bicycle accidents or in sports, typically in children or adolescents. Most patients with pancreatic lesions will present with multiple injuries, some of them hemodynamically unstable, and concomitant abdominal injuries; therefore, unstable patients may require initial damage control and correct assessment of the extent of pancreatic injury. On the other hand, in stable patients, ERCP plays an important role in the diagnosis, but also in the treatment of pancreatic duct injuries. Reports on the transpapillary stenting of duct lesions are very encouraging and justify the extensive use of ERCP (Canty et al., 2001).

#### **6.1 Case of endoscopic treatment**

A 17-year-old man was brought to the emergency department of our hospital with severe upper abdominal pain following a blow received in a rugby game. Emergency computed tomography (CT) revealed severe pancreatic neck injury. Forty-eight hours later, follow-up enhanced CT revealed that the pancreas was clearly lacerated and that the amount of peri-

Fig. 1.  ERCP was also reported to be the definitive test for pancreatic duct injury, particularly, to demonstrate clearly the site of duct disruption and the grade of duct injury, whether the branch or main duct and partial or complete

Recently, ERCP has been shown not only to provide sufficient information for conclusive diagnosis but also to be an effective and safe non-operative treatment tool (Bendahan et al., 1995; Huckfeldt et al., 1996; Kim et al., 2001; Cay et al., 2005; Houben et al., 2007). In certain cases of leakages of the pancreatic duct, transpapillary stent insertion might seal the injury

Isolated pancreatic trauma is rare and usually results from direct trauma to the epigastrium, for example from the handle bars in bicycle accidents or in sports, typically in children or adolescents. Most patients with pancreatic lesions will present with multiple injuries, some of them hemodynamically unstable, and concomitant abdominal injuries; therefore, unstable patients may require initial damage control and correct assessment of the extent of pancreatic injury. On the other hand, in stable patients, ERCP plays an important role in the diagnosis, but also in the treatment of pancreatic duct injuries. Reports on the transpapillary stenting of duct lesions are very encouraging and justify the extensive use of ERCP (Canty et al., 2001).

A 17-year-old man was brought to the emergency department of our hospital with severe upper abdominal pain following a blow received in a rugby game. Emergency computed tomography (CT) revealed severe pancreatic neck injury. Forty-eight hours later, follow-up enhanced CT revealed that the pancreas was clearly lacerated and that the amount of peri-

Fig. 1. Enhanced CT revealed an obvious laceration of the pancreas neck. (white arrow)

**5.5 Endoscopic retrograde cholangiopancreatography**

disruption of the main pancreatic duct MPD (Kim et al., 2001).

**6. Therapy**

**6.1 Case of endoscopic treatment**

and stabilize it in a way that eventually leads to resolution of the leakage

pancreatic fluid was increasing (**Fig. 1**); furthermore, serum amylase and elastase levels were elevated. ERP (endoscopic retrograde pancreatography) revealed that contrast medium in the main pancreatic duct (MPD) had leaked into the parenchyma, indicating MPD injury (**Fig. 2**). To prevent the traumatic pancreatitis from worsening, a stent was inserted endoscopically at a site distal to the injured portion of the MPD (**Fig. 3**). Thereafter, the patient's complaint was markedly reduced, and his serum amylase levels returned to normal. In addition, the apparent pancreatic edema and peripheral fluid were decreased on CT (Okamoto et al., 2010).

Fig. 2. Endoscopic pancreatography (ERP) revealed leakage of contrast medium.(white arrow)

Fig. 3. Enhanced CT revealed the inserted pancreatic stent and disappearance of pancreas peripheral fluid.(white arrow)

Traumatic Pancreatitis - Endoscopic and Surgical Management 187

Because stenosis of the main pancreatic duct was predicted as a complication, cholecystectomy, external drainage of the common bile duct, and external abdominal drainage were carried out. He was discharged with a pancreatic fistula 4 months postoperatively. Three months later, pancreatic juice output through the drainage tube decreased, and patient developed acute pancreatitis. CT revealed dilatation of the main pancreatic duct and atrophy of the pancreas distal to the site of injury (**Fig. 4**). A second operation was planed to perform to preserve pancreatic function after the patient's general condition improved. ERP demonstrated ductal stricture of the main pancreatic duct in the head of the pancreas and upstream dilatation of the pancreatic duct. A diagnosis of chronic obstructive pancreatitis was made, and in order to preserve the function of the distal pancreas, longitudinal pancreatojejunostomy with Roux-en-Y anastomosis was performed 10 months after the initial operation. After the second operation, the patient's pancreatic

function and pancreatic atrophy improved (Matsuda et al., 1999).

hematoma near pancreas head (right, white arrow).

**6.2.2 Surgical treatment**

**6.3 Nonoperative management**

to follow injury resolution.

injuries.

Fig. 4. Enhanced CT revealed a laceration of pancreatic head (left, white arrow) and a

Isolated pancreatic injuries are rare and most patients will present with multiple injuries, some of them hemodynamically unstable, and concomitant abdominal injuries; therefore, unstable patients may require initial damage control and correct assessment of the extent of pancreatic injury. This usually allows delayed definitive treatment of complex injuries, especially of the head of the pancreas. With regard to treatment, external drainage alone has been proposed for grade I and II injuries, while surgical intervention, including distal pancreatectomy or pancreaticojejunostomy, is usually performed for grade III, IV, and V

Conservative management of pancreatic trauma in the absence of a ductal injury (grade I and II) is widely accepted and practiced as the majority are contusions that usually resolve spontaneously after conservative treatment (Rescorla et al., 1995; Keller et al., 1997; Meier et al., 2001; Canty et al., 2001). Nonoperative management of a pancreatic injury consists of bowel arrest, total parental nutrition, and serial imaging with either CT scans or ultrasound

#### **6.2 Endoscopic pancreatic duct stent treatment**

Endoscopic transpapillary stent insertion by literature review is summarized in **Table 2**.

n.d.: not determined, h: hour, d: day, m: month, L: lipase

Table 2. Summary of reported pancreatic duct stent treatment cases

This summary indicates that endoscopic transpapillary stent insertion is an effective technique for managing certain pancreatic traumatic injuries. A significant improvement in outcome was found for patients with stent therapy. Pancreatic stents are known to be associated with minor damage to the duct including ductal irregularity, stenosis, and side branch ectasia (Kozarek et al., 1991). These changes can occur even if the stent is patent, and they can persist or resolve after stent removal (Huckfeldt et al., 1996). A long-term study of a small group showed that 4 of 6 cases were complicated by ductal stricture, although stent therapy could avoid surgery in the acute trauma stage (Lin et al., 2006). Endo- and exocrine function were not examined. Further accumulated experiences are needed to clarify the significance of stent therapy.

#### **6.2.1 Case of surgical treatment**

A 34-year-old man was transferred to our hospital 18 hours after blunt abdominal trauma caused by impact against an automobile steering wheel. Emergent CT showed laceration of the pancreatic head and surrounding hematoma. Emergent laparotomy was carried out. Intraoperative pancreatography revealed injury of the proximal main pancreatic duct.

Endoscopic transpapillary stent insertion by literature review is summarized in **Table 2**.

Age Gender Trauma Initial S-Amy(IU/L CT findings Time to ERCP ERCP findings Disrupted portion Outcome References 1 22 M Stabbed injury n.d. (Emergent operation) 3d Duct disruption Proximal Recoverd Bendahan J., et al., 1995 2 27 F Car accident 127 Irregular order of the pancreas tail 3-4hr Extravasation of the contrast from MPD Neck (isthmus) Recovered Huckfeldt R, et al. 1996 3 9 F Bike fall 436 Partial disruption of pancreatic parenchyma 1d Extravasation of the contrast from MPD Body Recovered Cantly T.G., et al., 2001 4 8 M Traffic accident 126 Disruption of the distal pancreas 1d Extravasation of the contrast from MPD Tail Recovered, mild MPD stricture Cantly T.G., et al., 2001 5 46 M n.d. 234 Head swelling 1d Extravasation from tail of MPD Head Recovered Kim HS, et al., 20001 6 35 M n.d. 390 Pancreas fracture 4d Intracapsular leakage from MPD n.d. Recovered, pseudocyst Kim HS, et al., 20001 7 40 F n.d. 742 Body swelling 1d Intracapsular leakage from MPD Body Recovered, pseudocyst Kim HS, et al., 20001 8 60 M Car accident 536 Pancreas disruption and pseudocyst 5d Extravasation of the contrast from MPD Proximal Recovered Hashimoto A., et al., 2003 9 37 F Steering wheel 2467 Hematoma over pancreatic head 22d Stricture at the head with contrast extravasation Head Recovered, stent migration Lin B.C., et al.,2006 10 35 M Steering wheel 435 n.d. 19d Stricture at the head with contrast extravasation Head Recovered, MPD stricture Lin B.C., et al.,2006 11 36 M Steering wheel 417 Pancreatic neck laceration 8d Contrast extravasation at the body and tail Body Recovered, MPD stricture Lin B.C., et al.,2006 12 61 F Steering wheel 2270 Pancreatic body laceration 1d Contrast extravasation at the body with retroperiton Body Sepsis, Death Lin B.C., et al.,2006 13 18 M Steering wheel 366 Pancreatic body laceration 8h Contrast extravasation at the body Body Recovered, MPD stricture Lin B.C., et al.,2006 14 28 M Steering wheel 231 Pancreatic head laceration 16h Contrast extravasation at the head Head Recovered, mild MPD stricture Lin B.C., et al.,2006 15 8 M Handlebar n.d. n.d. 28d Incomplete disruption Body Recovered Houben C.H., et al., 2007 16 11 M Hit lamppost n.d. n.d. 4d Transection of MPD Neck Recovered Houben C.H., et al., 2007 17 10 F Handlebar n.d. n.d. 2d Incomplete disruption Body Recovered Houben C.H., et al., 2007 18 11 M Handlebar n.d. n.d. 2d Transection of MPD Neck Recovered Houben C.H., et al., 2007 19 11 F Fall from seesaw n.d. n.d. 2d Transection of MPD Body Recovered Houben C.H., et al., 2007 20 7 M Handlebar n.d. n.d. 9d Transection of MPD Neck Recovered Houben C.H., et al., 2007 21 10 M Handlebar n.d. n.d. 7d Transection of MPD Neck Recovered Houben C.H., et al., 2007 22 12 M Trivial fall n.d. n.d. 3d Transection of MPD Neck Recovered Houben C.H., et al., 2007 23 9 M Trivial fall n.d. n.d. 4d Transection of MPD Neck Recevered Houben C.H., et al., 2007 24 28 M Gun shot 406 Pancreatic injuruy involving the head, neck 1m Leakage of the contrast Head Recovered Rastogi M, et al., 2009 25 31 F Bicycle accident 406 Pancreatic edema 0d Disrupted unicinate branch Unicinate process Recovered Rogers S.J., et al., 2009 26 49 M Car accident L 7121 Pancreatic edema 0d Disrupted MPD Body Recovered Rogers S.J., et al., 2009 27 41 F Car accident L 480 Pancreatc edema 15d Disrupted unicinate branch Unicinate process Recovered Rogers S.J., et al., 2009 28 41 F Car accident 235 Distal pancreatic tear 10d Disrupted unicinate branch Unicinate process Recovered Rogers S.J., et al., 2009 29 18 F Skiing fall L 844 Peripancreatic edema, possible laceration 2d Transection of MPD Tail Recovered Rogers S.J., et al., 2009 30 54 M Gun shot L 583 IVC laceration, retroperitoneal fluid 1d Extravasation MPD Head Recovered Rogers S.J., et al., 2009 31 17 M Sport 437 Pancreas disruption and pseudocyst 2d Leakage from MPD Neck Recovered Okamoto H., et al., 2010

**6.2 Endoscopic pancreatic duct stent treatment**

n.d.: not determined, h: hour, d: day, m: month, L: lipase

significance of stent therapy.

**6.2.1 Case of surgical treatment**

Table 2. Summary of reported pancreatic duct stent treatment cases

This summary indicates that endoscopic transpapillary stent insertion is an effective technique for managing certain pancreatic traumatic injuries. A significant improvement in outcome was found for patients with stent therapy. Pancreatic stents are known to be associated with minor damage to the duct including ductal irregularity, stenosis, and side branch ectasia (Kozarek et al., 1991). These changes can occur even if the stent is patent, and they can persist or resolve after stent removal (Huckfeldt et al., 1996). A long-term study of a small group showed that 4 of 6 cases were complicated by ductal stricture, although stent therapy could avoid surgery in the acute trauma stage (Lin et al., 2006). Endo- and exocrine function were not examined. Further accumulated experiences are needed to clarify the

A 34-year-old man was transferred to our hospital 18 hours after blunt abdominal trauma caused by impact against an automobile steering wheel. Emergent CT showed laceration of the pancreatic head and surrounding hematoma. Emergent laparotomy was carried out. Intraoperative pancreatography revealed injury of the proximal main pancreatic duct. Because stenosis of the main pancreatic duct was predicted as a complication, cholecystectomy, external drainage of the common bile duct, and external abdominal drainage were carried out. He was discharged with a pancreatic fistula 4 months postoperatively. Three months later, pancreatic juice output through the drainage tube decreased, and patient developed acute pancreatitis. CT revealed dilatation of the main pancreatic duct and atrophy of the pancreas distal to the site of injury (**Fig. 4**). A second operation was planed to perform to preserve pancreatic function after the patient's general condition improved. ERP demonstrated ductal stricture of the main pancreatic duct in the head of the pancreas and upstream dilatation of the pancreatic duct. A diagnosis of chronic obstructive pancreatitis was made, and in order to preserve the function of the distal pancreas, longitudinal pancreatojejunostomy with Roux-en-Y anastomosis was performed 10 months after the initial operation. After the second operation, the patient's pancreatic function and pancreatic atrophy improved (Matsuda et al., 1999).

Fig. 4. Enhanced CT revealed a laceration of pancreatic head (left, white arrow) and a hematoma near pancreas head (right, white arrow).

#### **6.2.2 Surgical treatment**

Isolated pancreatic injuries are rare and most patients will present with multiple injuries, some of them hemodynamically unstable, and concomitant abdominal injuries; therefore, unstable patients may require initial damage control and correct assessment of the extent of pancreatic injury. This usually allows delayed definitive treatment of complex injuries, especially of the head of the pancreas. With regard to treatment, external drainage alone has been proposed for grade I and II injuries, while surgical intervention, including distal pancreatectomy or pancreaticojejunostomy, is usually performed for grade III, IV, and V injuries.

#### **6.3 Nonoperative management**

Conservative management of pancreatic trauma in the absence of a ductal injury (grade I and II) is widely accepted and practiced as the majority are contusions that usually resolve spontaneously after conservative treatment (Rescorla et al., 1995; Keller et al., 1997; Meier et al., 2001; Canty et al., 2001). Nonoperative management of a pancreatic injury consists of bowel arrest, total parental nutrition, and serial imaging with either CT scans or ultrasound to follow injury resolution.

Traumatic Pancreatitis - Endoscopic and Surgical Management 189

Incomplete disruption of the MPD or complete disruption of the MPD without duct obstruction is the best candidate for the pancreatic duct stent therapy. Transductal pancreatic stent allows internal drainage of the pancreatic secretion and re-establishment of duct continuity (Bendahan et al., 1995; Huckfeldt et al., 1996; Cantly et al., 2001; Kim et al.,

Complete disruption of the MPD with duct obstruction increases the difficulty of stent placement beyond the fracture site. Disruption or complex injuries of the pancreatic head involving the ampulla, or devitalizing injuries of the pancreas head and duodenum usually are non-reconstructable injuries. In stable patients, pancreaticoduodenectomy is the best definite treatment for grade IV injuries. In unstable patients, exploration and placing of external drainage may be the best choice for damage control. Definitive treatment of the

Distal pancreatic injury with duct involvement include major or stab wounds in the body or tail of the pancreas with an obvious duct injury or transection of more than half the width of the pancreas. If the clinical condition of the patient allows it, these grade III injuries are best treated by distal pancreatectomy even in emergency situations. In some cases, such as complete transection of the pancreatic body from the head, a distal pancreaticojejunostomy and closure of the proximal end of the pancreas rupture as in the Letton & Wilson procedure, may even become necessary if an organ-preserving approach is attempted (Letton et al., 1959). It has been documented that 19 patients were treated by distal pancreatectomy with splenectomy, 8 by pancreatectomy with preserving the spleen, and 2 by placing a pancreatic duct stent in a series of 32 grade III patients (Lin et al., 2004). Major

The complication rate of any pancreatic injury is not only associated with concomitant injuries, but also with the severity of the pancreatic injury. As is widely accepted, the grade of pancreatic injury is an independent predictor of both pancreas-associated morbidity and mortality. Complications following pancreatic trauma include fistula, pancreatic abscess, pseudocyst formation, and sepsis. The American Association for the Surgery Trauma Organ Injury Score has been shown to predict the development of complications and mortality

Pancreatic abscesses have been treated interventionally by percutaneous drainage, but are frequently infected by multiple resistant bacteria, leading to sepsis. The treatment of pancreatic pseudocysts is interventional drainage and sealing, endoscopic gastrocystostomy,

Endoscopic transpapillary pancreatic duct stent is effective and safe management for pancreatic duct disruption, especially for proximal duct injury in selected patients. It may

2001; Lin et al., 2006; Houben et al., 2007; Rogers et al., 2009).

lesion can be achieved later, after the patient has been stabilized.

distal duct injuries have been managed mainly by surgical exploration.

**7.1 Proximal duct injury**

**7.2 Distal duct injury**

**8. Complications and outcome**

after pancreatic injury (Kao et al., 2003).

and operative enteric drainage.

**9. Conclusion**

Octreotide, a synthetic somatostatin analogue that inhibits pancreatic secretions has been shown in adults to reduce the incidence of postsurgical pancreatitis after pancreatic surgery. The benefits of octreotide in pancreatic trauma are controversial, and in particular its role in pediatric trauma is still undefined (Amirara et al., 1994; Nwariaku et al., 1995; Mulligan et al., 1995; Cavallini et al., 2001), however, there are few reported cases of octreotide administration being effective for traumatic pancreatic injury (Morali et al.,1991; Shan et al., 2002). Further accumulated evidence is required to prove this effect.

#### **7. Treatment algorithm**

We proposed an early treatment algorithm for endoscopic and surgical therapy, based on the presence or absence of a major pancreatic duct lesion.

Fig. 4. Proposed early treatment algorithm for endoscopic and/or surgical therapy.

#### **7.1 Proximal duct injury**

188 Pancreatitis – Treatment and Complications

Octreotide, a synthetic somatostatin analogue that inhibits pancreatic secretions has been shown in adults to reduce the incidence of postsurgical pancreatitis after pancreatic surgery. The benefits of octreotide in pancreatic trauma are controversial, and in particular its role in pediatric trauma is still undefined (Amirara et al., 1994; Nwariaku et al., 1995; Mulligan et al., 1995; Cavallini et al., 2001), however, there are few reported cases of octreotide administration being effective for traumatic pancreatic injury (Morali et al.,1991; Shan et al.,

We proposed an early treatment algorithm for endoscopic and surgical therapy, based on

Fig. 4. Proposed early treatment algorithm for endoscopic and/or surgical therapy.

2002). Further accumulated evidence is required to prove this effect.

the presence or absence of a major pancreatic duct lesion.

**7. Treatment algorithm**

Incomplete disruption of the MPD or complete disruption of the MPD without duct obstruction is the best candidate for the pancreatic duct stent therapy. Transductal pancreatic stent allows internal drainage of the pancreatic secretion and re-establishment of duct continuity (Bendahan et al., 1995; Huckfeldt et al., 1996; Cantly et al., 2001; Kim et al., 2001; Lin et al., 2006; Houben et al., 2007; Rogers et al., 2009).

Complete disruption of the MPD with duct obstruction increases the difficulty of stent placement beyond the fracture site. Disruption or complex injuries of the pancreatic head involving the ampulla, or devitalizing injuries of the pancreas head and duodenum usually are non-reconstructable injuries. In stable patients, pancreaticoduodenectomy is the best definite treatment for grade IV injuries. In unstable patients, exploration and placing of external drainage may be the best choice for damage control. Definitive treatment of the lesion can be achieved later, after the patient has been stabilized.

#### **7.2 Distal duct injury**

Distal pancreatic injury with duct involvement include major or stab wounds in the body or tail of the pancreas with an obvious duct injury or transection of more than half the width of the pancreas. If the clinical condition of the patient allows it, these grade III injuries are best treated by distal pancreatectomy even in emergency situations. In some cases, such as complete transection of the pancreatic body from the head, a distal pancreaticojejunostomy and closure of the proximal end of the pancreas rupture as in the Letton & Wilson procedure, may even become necessary if an organ-preserving approach is attempted (Letton et al., 1959). It has been documented that 19 patients were treated by distal pancreatectomy with splenectomy, 8 by pancreatectomy with preserving the spleen, and 2 by placing a pancreatic duct stent in a series of 32 grade III patients (Lin et al., 2004). Major distal duct injuries have been managed mainly by surgical exploration.

#### **8. Complications and outcome**

The complication rate of any pancreatic injury is not only associated with concomitant injuries, but also with the severity of the pancreatic injury. As is widely accepted, the grade of pancreatic injury is an independent predictor of both pancreas-associated morbidity and mortality. Complications following pancreatic trauma include fistula, pancreatic abscess, pseudocyst formation, and sepsis. The American Association for the Surgery Trauma Organ Injury Score has been shown to predict the development of complications and mortality after pancreatic injury (Kao et al., 2003).

Pancreatic abscesses have been treated interventionally by percutaneous drainage, but are frequently infected by multiple resistant bacteria, leading to sepsis. The treatment of pancreatic pseudocysts is interventional drainage and sealing, endoscopic gastrocystostomy, and operative enteric drainage.

#### **9. Conclusion**

Endoscopic transpapillary pancreatic duct stent is effective and safe management for pancreatic duct disruption, especially for proximal duct injury in selected patients. It may

Traumatic Pancreatitis - Endoscopic and Surgical Management 191

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**10. References**

**Part 5**

 **Complications**

## **Part 5**

 **Complications**

192 Pancreatitis – Treatment and Complications

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**13**

K. Prakash

*India*

*PVS Memorial Hospital, Kaloor, Kochi, Kerala,*

**Pancreatic Ascites**

**and Pleural Effusion**

Pancreatic ascites or internal pancreatic fistulae and pancreatic pleural effusion are rare complications of pancreatitis. This can occur in the clinical setting of an acute pancreatitis and more commonly as a complication of chronic pancreatitis1. This is an uncommon clinical condition; often the patients are sick and nutritionally compromised. Pancreatic ascites was first reported in the literature in 1953 when Smith described two cases of ascites

Exact definition to diagnose this condition is not clear in the literature. Pancreatic ascites /pleural effusion is characterised by accumulation of high amylase fluid in the peritoneal cavity/pleural cavity due to leakage of pancreatic juice from a disrupted pancreatic duct and a diagnosis is usually made once the aspirated fluid is high in protein (>3g/dl) and high

Pancreatic ascites/pleural effusion can occur due to a) rupture of a pseudocyst into peritoneal cavity or to mediastinum and pleura or b) due to the disruption of a main pancreatic duct during the natural course of chronic pancreatitis3. Pancreatic leak occurs in 3.5% of patients with chronic pancreatitis and 6% to 14% of patients with pancreatic pseudocyst 4, 5. The pathogenesis of the serous cavity effusion is different in acute and chronic pancreatitis setting. In acute pancreatitis, mostly in alcoholic pancreatitis, there is enough inflammatory reaction around the pancreas with neighbouring structures like stomach and transverse colon to form a pseudocyst. This can rupture into peritoneal cavity or mediastinum and to pleural cavity subsequently to produce ascites or pleural effusion respectively. Similar type of duct disruptions may also occur in acute setting in blunt abdominal trauma, biliary pancreatitis, and rupture of duplication cyst and rarely after

In the setting of chronic pancreatitis, leakage is seen in up to 80% of cases from a communicating pseudocyst due to ductal stricture and less commonly (20%) due to duct

**1. Introduction**

**2. Definition**

in amylase (>1000 IU/L)3.

associated with chronic pancreatitis2.

**3. Aetiology and pathogenesis**

pancreatic surgery or splenectomy1, 6.

### **Pancreatic Ascites and Pleural Effusion**

K. Prakash *PVS Memorial Hospital, Kaloor, Kochi, Kerala, India*

#### **1. Introduction**

Pancreatic ascites or internal pancreatic fistulae and pancreatic pleural effusion are rare complications of pancreatitis. This can occur in the clinical setting of an acute pancreatitis and more commonly as a complication of chronic pancreatitis1. This is an uncommon clinical condition; often the patients are sick and nutritionally compromised. Pancreatic ascites was first reported in the literature in 1953 when Smith described two cases of ascites associated with chronic pancreatitis2.

#### **2. Definition**

Exact definition to diagnose this condition is not clear in the literature. Pancreatic ascites /pleural effusion is characterised by accumulation of high amylase fluid in the peritoneal cavity/pleural cavity due to leakage of pancreatic juice from a disrupted pancreatic duct and a diagnosis is usually made once the aspirated fluid is high in protein (>3g/dl) and high in amylase (>1000 IU/L)3.

#### **3. Aetiology and pathogenesis**

Pancreatic ascites/pleural effusion can occur due to a) rupture of a pseudocyst into peritoneal cavity or to mediastinum and pleura or b) due to the disruption of a main pancreatic duct during the natural course of chronic pancreatitis3. Pancreatic leak occurs in 3.5% of patients with chronic pancreatitis and 6% to 14% of patients with pancreatic pseudocyst 4, 5. The pathogenesis of the serous cavity effusion is different in acute and chronic pancreatitis setting. In acute pancreatitis, mostly in alcoholic pancreatitis, there is enough inflammatory reaction around the pancreas with neighbouring structures like stomach and transverse colon to form a pseudocyst. This can rupture into peritoneal cavity or mediastinum and to pleural cavity subsequently to produce ascites or pleural effusion respectively. Similar type of duct disruptions may also occur in acute setting in blunt abdominal trauma, biliary pancreatitis, and rupture of duplication cyst and rarely after pancreatic surgery or splenectomy1, 6.

In the setting of chronic pancreatitis, leakage is seen in up to 80% of cases from a communicating pseudocyst due to ductal stricture and less commonly (20%) due to duct

Pancreatic Ascites and Pleural Effusion 197

Management of these patients are challenging due to the compromised nutritional state, generalized weakness, diabetes mellitus and disease related factors like multiple strictures, large stones and inflammatory mass. All patients with a diagnosis of pancreatic ascites or pleural effusion should be assessed for their nutritional status. This is important as the morbidity and mortality of the various modes of treatment is related to the patient's general condition. These patients may be managed by conservative approach, endoscopic therapy and by surgical therapy. This may be done in using an algorithm depending upon patient's

**Algorithmic approach to the management of Pancreatic ascites**

Failed Cannulation / stenting

> Persistent ascites, pain

> > Follow up

**Surgery**

**Pancreatic Ascites**

Assessment CT scan ± MRI

**ERCP**

Control of ascites, pain

Table 1. Algorithmic approach to the management of pancreatic ascites.

Initial trial of conservative treatment is indicated in almost all patients. It was generally believed that there is high risk for mortality while the patients are on conservative therapy, which is due to poor nutritional management and assessment in the initial reports. Though an old series14 had reported high mortality with conservative therapy, the progress of the patient can be safely monitored on conservative therapy in current daily practice. The key steps in the conservative management of the pancreatic ascites or pleural effusion are a). Rest to the pancreas and to limit pancreatic exocrine stimulation by keeping the patients nil orally, b). Nutritional support by means of nasojejunal feeds or by Total Parenteral Nutrition (TPN), c). Use of drugs likes to decrease pancreatic secretion d). Drainage of fluid by aspiration, drainage of ascites or by tube thoracocentesis. So patients are kept nil per oral and nutritional support should be planned on case to case basis. There is no significant difference between enteral or parenteral feeds on pancreatic exocrine secretion clinically15. However, these patients are often nutritionally compromised and have nausea, anorexia and

Pancreatic stenting

**5. Management**

clinical condition8. (Table 1)

Poor nutrition

Nasojejunal feeds Aspiration, Octreotide

**6. Conservative treatment**

disruption itself3, 7. This has also been described in the setting of tropical calcific pancreatitis as well from duct disruptions and leaking pseudocyst8. Once the amylase rich fluid enters serous cavity, since the enzymes are not activated it does not produce digestion, instead it produces irritation resulting in outpouring of albumin resulting in high-albumin ascites. This accumulation of amylase rich fluid is usually massive before it produces symptoms due to its pressure effects. The amylase in the fluid can get reabsorbed into the blood stream and produce elevation of serum amylase as well. It has been also reported in one series that pancreatic ascites or effusions may present with indolent symptoms and up to 42% of patients gave no history of pancreatic disease9.

#### **4. Diagnosis and evaluation**

Aim of the investigations in patients with pancreatic ascites are a). Overall assessment of patient's general and nutritional status and b). To delineate the pancreatic ductal anatomy and to locate the possible site of leak. These patients should have a haemogram, serum protein, and albumin and amylase value and coagulation profile. Upper GI endoscopy to rule out peptic ulcer or periampullary malignant disease and ultrasonography should be done. The diagnosis is usually confirmed with ascitic fluid assay. Usually the ascitic/pleural fluid contains high protein >3g/dl and high amylase >1000 IU/ml. Ascitic fluid assay should also be done to rule out other differential diagnosis like cirrhosis of liver or disseminated malignancy.

The localization of site of rupture or leak of main pancreatic duct is essential for planning therapy. Earlier, intraoperative pancreatography was the mainstay of localisation which is superseded largely by Endoscopic Retrograde Pancreatography (ERP) in recent years. However, these procedures are invasive and correct delineation of the duct anatomy and leak may not be feasible in all cases due to strictures or due to technical reasons. Demonstration of pancreatic duct leak by non invasive methods offer advantages like avoiding a sedation or anaesthesia, avoiding risk of introducing infection during injection of dye to the pancreatic duct. Non invasive investigations like CT scan helps in indentifying peripancreatic collections and details of the parenchyma of the pancreas. The details of pancreatic parenchyma, duct size, stones, strictures and psuedocysts are well displayed in a CT scan. The identification of site of leak from the pancreatic duct is possible in nearly half of the patients10. Magnetic Resonance Imaging (MRI) has also been reported to give good details of pancreatic parenchyma, details of the duct and details of the fistula11, 12. In MRP, high signal intensity of static or slowly flowing liquids is observed in T2 weighted images. Hence the pancreatic duct and the fistulous tract is displayed as high-signal intensity structure which helps in identifying the communication like pancreaticopleural fistula. The details of the pancreatic parenchyma and duct structural changes are also well displayed in MRI. Moreover, in MRI no contrast material is injected and there is no risk of infection in comparison with ERP. In a recent study13, the ability of helical CT scan and Magnetic Resonance Pancreatography (MRP) when performed alone in identifying the site of duct disruption were 50 and 67% respectively. When these two modalities were combined the exact site of rupture of duct was observed in 94% of cases. Hence, a combination of imaging modalities helps to improve the details of the duct disruption,the site of leak and the details of the pancreatic parenchyma which is essential in planning of therapy.

#### **5. Management**

196 Pancreatitis – Treatment and Complications

disruption itself3, 7. This has also been described in the setting of tropical calcific pancreatitis as well from duct disruptions and leaking pseudocyst8. Once the amylase rich fluid enters serous cavity, since the enzymes are not activated it does not produce digestion, instead it produces irritation resulting in outpouring of albumin resulting in high-albumin ascites. This accumulation of amylase rich fluid is usually massive before it produces symptoms due to its pressure effects. The amylase in the fluid can get reabsorbed into the blood stream and produce elevation of serum amylase as well. It has been also reported in one series that pancreatic ascites or effusions may present with indolent symptoms and up to 42% of

Aim of the investigations in patients with pancreatic ascites are a). Overall assessment of patient's general and nutritional status and b). To delineate the pancreatic ductal anatomy and to locate the possible site of leak. These patients should have a haemogram, serum protein, and albumin and amylase value and coagulation profile. Upper GI endoscopy to rule out peptic ulcer or periampullary malignant disease and ultrasonography should be done. The diagnosis is usually confirmed with ascitic fluid assay. Usually the ascitic/pleural fluid contains high protein >3g/dl and high amylase >1000 IU/ml. Ascitic fluid assay should also be done to rule out other differential diagnosis like cirrhosis of liver or

The localization of site of rupture or leak of main pancreatic duct is essential for planning therapy. Earlier, intraoperative pancreatography was the mainstay of localisation which is superseded largely by Endoscopic Retrograde Pancreatography (ERP) in recent years. However, these procedures are invasive and correct delineation of the duct anatomy and leak may not be feasible in all cases due to strictures or due to technical reasons. Demonstration of pancreatic duct leak by non invasive methods offer advantages like avoiding a sedation or anaesthesia, avoiding risk of introducing infection during injection of dye to the pancreatic duct. Non invasive investigations like CT scan helps in indentifying peripancreatic collections and details of the parenchyma of the pancreas. The details of pancreatic parenchyma, duct size, stones, strictures and psuedocysts are well displayed in a CT scan. The identification of site of leak from the pancreatic duct is possible in nearly half of the patients10. Magnetic Resonance Imaging (MRI) has also been reported to give good details of pancreatic parenchyma, details of the duct and details of the fistula11, 12. In MRP, high signal intensity of static or slowly flowing liquids is observed in T2 weighted images. Hence the pancreatic duct and the fistulous tract is displayed as high-signal intensity structure which helps in identifying the communication like pancreaticopleural fistula. The details of the pancreatic parenchyma and duct structural changes are also well displayed in MRI. Moreover, in MRI no contrast material is injected and there is no risk of infection in comparison with ERP. In a recent study13, the ability of helical CT scan and Magnetic Resonance Pancreatography (MRP) when performed alone in identifying the site of duct disruption were 50 and 67% respectively. When these two modalities were combined the exact site of rupture of duct was observed in 94% of cases. Hence, a combination of imaging modalities helps to improve the details of the duct disruption,the site of leak and the details of the pancreatic parenchyma which is essential

patients gave no history of pancreatic disease9.

**4. Diagnosis and evaluation**

disseminated malignancy.

in planning of therapy.

Management of these patients are challenging due to the compromised nutritional state, generalized weakness, diabetes mellitus and disease related factors like multiple strictures, large stones and inflammatory mass. All patients with a diagnosis of pancreatic ascites or pleural effusion should be assessed for their nutritional status. This is important as the morbidity and mortality of the various modes of treatment is related to the patient's general condition. These patients may be managed by conservative approach, endoscopic therapy and by surgical therapy. This may be done in using an algorithm depending upon patient's clinical condition8. (Table 1)

#### **Algorithmic approach to the management of Pancreatic ascites**

Table 1. Algorithmic approach to the management of pancreatic ascites.

#### **6. Conservative treatment**

Initial trial of conservative treatment is indicated in almost all patients. It was generally believed that there is high risk for mortality while the patients are on conservative therapy, which is due to poor nutritional management and assessment in the initial reports. Though an old series14 had reported high mortality with conservative therapy, the progress of the patient can be safely monitored on conservative therapy in current daily practice. The key steps in the conservative management of the pancreatic ascites or pleural effusion are a). Rest to the pancreas and to limit pancreatic exocrine stimulation by keeping the patients nil orally, b). Nutritional support by means of nasojejunal feeds or by Total Parenteral Nutrition (TPN), c). Use of drugs likes to decrease pancreatic secretion d). Drainage of fluid by aspiration, drainage of ascites or by tube thoracocentesis. So patients are kept nil per oral and nutritional support should be planned on case to case basis. There is no significant difference between enteral or parenteral feeds on pancreatic exocrine secretion clinically15. However, these patients are often nutritionally compromised and have nausea, anorexia and

Pancreatic Ascites and Pleural Effusion 199

Fig. 1. Endoscopic retrograde pancreatography showing leak of dye from tail duct.

The surgical intervention is planned according to the ductal anatomy and site of leak (figure 2). Aims of the surgery in patients with chronic pancreatitis with pancreatic ascites are to a) wide drainage of pancreatic duct, often with a Lateral Pancreatojejunostomy (LPJ) b) removal of pancreatic stones and ductal strictures and c) drainage of the cysts and external

Patients with chronic pancreatitis with large duct (>7mm) should undergo wide drainage of pancreatic duct often with a lateral panctreatojejunostomy and removal of pancreatic stones and ductal strictures5, 7, 8. Specific repair of the site or disruption is often unnecessary; however the area of disruption should be included in the anastomosis. Similarly, a mature pseudocyst also can be incorporated in the anastomosis. In patients with normal sized duct, identification of the site of leak is very important. In those with distal leak, a distal pancreatectomy with or without splenectomy is a good option. Spleen preservation is often difficult in these patients due to dense adhesions and inflammatory process. If the inflammation and fibrosis is significant a medial to lateral approach in distal

pancreatectomy may be used to avoid excessive bleeding.

**8. Surgery**

drainage of abscess.

poor tolerance to feeds due to exocrine insufficiency. Enteral nutritional support should be attempted whenever possible as it maintains mucosal integrity and prevents bacterial translocation. Nasojejunal feeds have a theoretic benefit as it prevents stimulation of pancreas and minimises fistula output. In patients who do not tolerate enteral feeds well or those with catabolic response TPN should be used either alone or along with enteral feeds.

Serous cavities should be emptied to promote approximation of serosal surfaces by drainage of ascitic/pleural fluid. Repeated aspiration of ascites or drainage of the ascites with the tube near the pseudocyst helps to drain the fluid by a controlled fistula. Similarly, aspiration or tube drainage should be done according to be patient's symptoms. Along with above measures, use of drugs with the aim to decrease the pancreatic exocrine secretion like somatostatin or octreotide also have a role in improving the pancreatic leak15-17. These drugs have been noted to decrease the fistula output (often within 24 hours of treatment) and accelerate the fistula closure. Depending upon the clinical situation a conservative therapy with above measures for 3-4 weeks helps in resolution of pancreatic leak in 25 – 60% of cases17,18. Patients with low sodium levels, albumin levels and those with a high fluid to serum protein levels had high chance for treatment failure18. Other agents attempted in closure of pancreatic leak are fibrin glue and nafamostat mesilate with variable results. Patients those who fails to respond to conservative measures or those patients who are symptomatic should undergo endotherapy or surgery.

#### **7. Endotherapy**

Endoscopic Retrograde Pancreatography (ERP) is the key step in planning of endoscopic treatment. ERP helps to delineate the anatomy of the duct, presence of strictures and site pancreatic leak (Figure 1). The principles of endotherapy include pancreatic sphincterotomy and placement of a transduodenal pancreatic stent across the site of ductal leak. This helps to obliterate the high-pressure gradient at the pancreatic sphincter, allowing preferential flow of pancreatic secretions along a low resistance path to the duodenum, thereby allowing the site of leak to heal. This has been reported in many series6, 8,13,19,20. It has been observed that a sphincterotomy and placement of stent close to the fistula, even if the stent could not be advance beyond the site of leak helps to heal the fistula or stabilizes patients clinical condition8. Other endoscopic approaches which are practised are endoscopic placement of nasopancreatic drainage21 and endosonography guided pancreatogastrostomy22. Nasopancreatic drainage alone has been used instead of placement of pancreatic duct stenting in treatment of pancreatic ascites22. The authors have reported nearly 90% of success in placement of nasopancreatic drain and disappearance of pseudocyst and ascites were observed on 4-6 weeks. Nasopancreatic drains allow repeated pancreatography to assess the progress of therapy and healing of the duct. This method provides the option of flushing of the drain to clear the blocks and allows removal of the drain once the duct disruption is healed. The disadvantages of this method are the discomfort to the patients due to the nasal tube and risk of accidental dislodgement.

The success of endotherapy ranges from 50-90% depending upon the duct changes8, 19-21. Success of endoscopic treatment was based on three factors in this study a) ability to pass the stent across the site of disruption of the duct, b) absence of strictures and stones and c) ability to traverse the stricture. Those patients who had only partial relief of symptoms and those with failed endotherapy would require surgery.

poor tolerance to feeds due to exocrine insufficiency. Enteral nutritional support should be attempted whenever possible as it maintains mucosal integrity and prevents bacterial translocation. Nasojejunal feeds have a theoretic benefit as it prevents stimulation of pancreas and minimises fistula output. In patients who do not tolerate enteral feeds well or those with catabolic response TPN should be used either alone or along with enteral feeds. Serous cavities should be emptied to promote approximation of serosal surfaces by drainage of ascitic/pleural fluid. Repeated aspiration of ascites or drainage of the ascites with the tube near the pseudocyst helps to drain the fluid by a controlled fistula. Similarly, aspiration or tube drainage should be done according to be patient's symptoms. Along with above measures, use of drugs with the aim to decrease the pancreatic exocrine secretion like somatostatin or octreotide also have a role in improving the pancreatic leak15-17. These drugs have been noted to decrease the fistula output (often within 24 hours of treatment) and accelerate the fistula closure. Depending upon the clinical situation a conservative therapy with above measures for 3-4 weeks helps in resolution of pancreatic leak in 25 – 60% of cases17,18. Patients with low sodium levels, albumin levels and those with a high fluid to serum protein levels had high chance for treatment failure18. Other agents attempted in closure of pancreatic leak are fibrin glue and nafamostat mesilate with variable results. Patients those who fails to respond to conservative measures or those patients who are

Endoscopic Retrograde Pancreatography (ERP) is the key step in planning of endoscopic treatment. ERP helps to delineate the anatomy of the duct, presence of strictures and site pancreatic leak (Figure 1). The principles of endotherapy include pancreatic sphincterotomy and placement of a transduodenal pancreatic stent across the site of ductal leak. This helps to obliterate the high-pressure gradient at the pancreatic sphincter, allowing preferential flow of pancreatic secretions along a low resistance path to the duodenum, thereby allowing the site of leak to heal. This has been reported in many series6, 8,13,19,20. It has been observed that a sphincterotomy and placement of stent close to the fistula, even if the stent could not be advance beyond the site of leak helps to heal the fistula or stabilizes patients clinical condition8. Other endoscopic approaches which are practised are endoscopic placement of nasopancreatic drainage21 and endosonography guided pancreatogastrostomy22. Nasopancreatic drainage alone has been used instead of placement of pancreatic duct stenting in treatment of pancreatic ascites22. The authors have reported nearly 90% of success in placement of nasopancreatic drain and disappearance of pseudocyst and ascites were observed on 4-6 weeks. Nasopancreatic drains allow repeated pancreatography to assess the progress of therapy and healing of the duct. This method provides the option of flushing of the drain to clear the blocks and allows removal of the drain once the duct disruption is healed. The disadvantages of this method are the discomfort to the patients

The success of endotherapy ranges from 50-90% depending upon the duct changes8, 19-21. Success of endoscopic treatment was based on three factors in this study a) ability to pass the stent across the site of disruption of the duct, b) absence of strictures and stones and c) ability to traverse the stricture. Those patients who had only partial relief of symptoms and

symptomatic should undergo endotherapy or surgery.

due to the nasal tube and risk of accidental dislodgement.

those with failed endotherapy would require surgery.

**7. Endotherapy**

Fig. 1. Endoscopic retrograde pancreatography showing leak of dye from tail duct.

#### **8. Surgery**

The surgical intervention is planned according to the ductal anatomy and site of leak (figure 2). Aims of the surgery in patients with chronic pancreatitis with pancreatic ascites are to a) wide drainage of pancreatic duct, often with a Lateral Pancreatojejunostomy (LPJ) b) removal of pancreatic stones and ductal strictures and c) drainage of the cysts and external drainage of abscess.

Patients with chronic pancreatitis with large duct (>7mm) should undergo wide drainage of pancreatic duct often with a lateral panctreatojejunostomy and removal of pancreatic stones and ductal strictures5, 7, 8. Specific repair of the site or disruption is often unnecessary; however the area of disruption should be included in the anastomosis. Similarly, a mature pseudocyst also can be incorporated in the anastomosis. In patients with normal sized duct, identification of the site of leak is very important. In those with distal leak, a distal pancreatectomy with or without splenectomy is a good option. Spleen preservation is often difficult in these patients due to dense adhesions and inflammatory process. If the inflammation and fibrosis is significant a medial to lateral approach in distal pancreatectomy may be used to avoid excessive bleeding.

Pancreatic Ascites and Pleural Effusion 201

algorithmic approach may be adopted in managing this patients using conservative, endotherapy or surgical treatment according to the clinical scenario. A multidisciplinary approach of these modalities is essential for successful management of these patients.

Barish MA, Soto JA. MR cholangiopancreatography: techniques and clinical applications.

Bhasin DK. Endoscopic transpapillary nasopancreatic drainage alone to treat pancreatic ascites and pleural effusion. - - J Gastroenterol Hepatol 2006; 21: 1059-64 Bracher GA, Manocha AP, DeBanto JR, Gates LK, Slivka A, Whitcomb DC, et al. Endoscopic

Brooks JR. Pancreatic ascites. In: Brooks JR, editor. Surgery of the pancreas. Philadelphia:

Cameron JL. Chronic pancreatic ascites and pancreatic pleural effusions. Gastroenterology

da Cunha JE, Machado M, Bacchella T, Penteado S, Mott CB, Jukemura J, et al. Surgical

Dhar P, Tomey S, Jain P, Azfar M, Sachdev A, Chaudhary A. Internal pancreatic fistulae with serous effusions in chronic pancreatitis. Aus N Z J Surg 1996; 66: 608-11. Eckhauser F, Raper SE, Knol JA, Mulholland MW. Surgical management of pancreatic

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MacLauren IF. Pancreatic ascites. In: Howard JM, Jordan GL, Reber HA, editors. Surgical diseases of the pancreas. Philadelphia: Lea and Febigor; 1987. p. 591-602. Martineau P, Shwed JA, Denis R. Is octreotide a new hope for enterocutaneous and external

Materne R, Vranckx P, Pauls C, Coche EE, Deprez P, Van Beers BE.*.* Pancreaticopleural

Moosa AR. Surgical treatment of chronic pancreatitis: an overview. Br J Surg 1987; 74: 661-7.

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pancreaticogastrostomy. Gastrointest Endosc 2002; 56: 128-33.

Lipsett PA, Cameron JL. Internal pancreatic fistula. Am J Surg 163:216, 1992.

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findings. J Comput Assist Tomogr 1999; 23: 181-7.

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treatment of pancreatic ascites and pancreatic pleural effusions.

pseudocysts, pancreatic ascites, and pancreatopleural fistulae. Pancreas 1991; 6:

transpapillary therapy for disrupted pancreatic duct and peripancreatic fluid

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AJR Am J Roentgenol 1997; 169:1295–1303.

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WB Saunders; 1983, p. 230-2.

**10. References**

710-5.

74:134, 1978.

566-75.

102-6.

914.

Fig. 2. Operative picture showing disruption of pancreatic duct in the body region with pancreatic stent in situ coming out through the site of disruption.

In those with leak from the neck region Roux –en-Y anastomosis to the fistula site or pancreatogastrostomy has been described. In those patients with disconnected duct syndrome, often secondary to acute pancreatic necrosis, there is often a loss of tissue near the genu with fistula from either distal or proximal duct. A Roux-en-Y anastomosis to the distal duct and closure of the proximal duct or distal pancreatectomy with closure of proximal duct may be performed according to the clinical situation. In patients with long fistulous tract to skin, dissection of fistula and fistula-enterostomy has been reported with varying results23. Surgery for pancreatic ascites is often difficult due to the dense inflammatory process in the peripancreatic tissue, mesentery and due to the presence of pseudocysts and often identification of site of leak is difficult and cystojejunostomy to the leaking cyst is also an effective option24, 25.

#### **9. Conclusion**

Pancreatic ascites or pleural effusion are rare complications of acute or chronic pancreatitis wherein there is leakage of pancreatic juice to a serous cavity from a disrupted pancreatic duct or leaking pseudocyst. Preoperative workup should be aimed at the nutritional assessment of the patient and the pancreatic ductal imaging using CT scan or MRI. An algorithmic approach may be adopted in managing this patients using conservative, endotherapy or surgical treatment according to the clinical scenario. A multidisciplinary approach of these modalities is essential for successful management of these patients.

#### **10. References**

200 Pancreatitis – Treatment and Complications

Fig. 2. Operative picture showing disruption of pancreatic duct in the body region with

In those with leak from the neck region Roux –en-Y anastomosis to the fistula site or pancreatogastrostomy has been described. In those patients with disconnected duct syndrome, often secondary to acute pancreatic necrosis, there is often a loss of tissue near the genu with fistula from either distal or proximal duct. A Roux-en-Y anastomosis to the distal duct and closure of the proximal duct or distal pancreatectomy with closure of proximal duct may be performed according to the clinical situation. In patients with long fistulous tract to skin, dissection of fistula and fistula-enterostomy has been reported with varying results23. Surgery for pancreatic ascites is often difficult due to the dense inflammatory process in the peripancreatic tissue, mesentery and due to the presence of pseudocysts and often identification of site of leak is difficult and cystojejunostomy to the

Pancreatic ascites or pleural effusion are rare complications of acute or chronic pancreatitis wherein there is leakage of pancreatic juice to a serous cavity from a disrupted pancreatic duct or leaking pseudocyst. Preoperative workup should be aimed at the nutritional assessment of the patient and the pancreatic ductal imaging using CT scan or MRI. An

pancreatic stent in situ coming out through the site of disruption.

leaking cyst is also an effective option24, 25.

**9. Conclusion**

**14**

Audrius Šileikis *Vilnius University,*

*Lithuania*

**Emphysematous Pancreatitis**

**1. Introduction**

**Emphysematous (gas-forming) infections of the abdomen and pelvis**

Emphysematous (gas-forming) infections of the abdomen and pelvis represent potentially life-threatening conditions that require aggressive medical and often surgical management. The initial clinical manifestation of these entities may be insidious, but rapid progression to sepsis will occur in the absence of early therapeutic intervention. Conventional radiography and ultrasonography are often the initial imaging modalities used to evaluate patients with abdominopelvic complaints. However, when a differential diagnosis remains, or if further localization or confirmation of tentative findings is needed, computed tomography (CT) should be considered the imaging modality of choice. CT is both highly sensitive and specific in the detection of abnormal gas and well suited to reliable depiction of the anatomic location and extent of the gas. Of equal importance may be the capability of CT to help reliably identify benign sources of gas, because treatment (if any) varies dramatically depending on the source. Knowledge of the pathophysiologic characteristics, common predisposing conditions, and typical imaging features associated with gas-forming infections of the gall-bladder, stomach, pancreas, and genitourinary system will help make early diagnosis and successful treatment possible. In addition, such knowledge will aid in further diagnostic work-up, surveillance of potential complications, and evaluation of therapeutic response. The presence of gas within the parenchyma of solid organs or the walls of hollow viscera may be due to a variety of pathologic or benign entities. Besides infection with gas-forming bacteria, other possible sources include bland tissue infarction with necrosis, enteric fistula formation, and reflux from an adjacent hollow viscus. Gas should be differentiated from atmospheric air introduced at recent instrumentation or surgery. Gas associated with infection is generally thought to consist of carbon dioxide and nitrogen secondary to the fermentation of glucose by some species of bacteria. Poor glycolysis at the tissue level in diabetic patients results in increased glucose concentrations within the interstitial fluid. Other clinical factors that contribute to the increased production or slowed removal of gas include a depressed cell-mediated immune response, local tissue necrosis, and the presence of arteriosclerosis. The increased pH of bile associated with gallbladder inflammation and the focal tissue ischemia seen in gynecologic neoplasms are examples of specific underlying processes that help optimize bacterial culture media. In addition to broad-spectrum antimicrobial therapy and possible surgery, correction of associated underlying conditions such as urinary outflow obstruction, acid-base and electrolyte

### **Emphysematous Pancreatitis**

Audrius Šileikis *Vilnius University, Lithuania*

#### **1. Introduction**

202 Pancreatitis – Treatment and Complications

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Smith EB. Hemorrhagic ascites and hemothorax associated with benign pancreatic disease.

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World J Gastroenterol 2004; 10: 2419-2422.

430-4.

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Gastrointest Surg 2003;7:542–6

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therapy and role of octreotide. Arch Surg 1992; 127: 707-12.

#### **Emphysematous (gas-forming) infections of the abdomen and pelvis**

Emphysematous (gas-forming) infections of the abdomen and pelvis represent potentially life-threatening conditions that require aggressive medical and often surgical management. The initial clinical manifestation of these entities may be insidious, but rapid progression to sepsis will occur in the absence of early therapeutic intervention. Conventional radiography and ultrasonography are often the initial imaging modalities used to evaluate patients with abdominopelvic complaints. However, when a differential diagnosis remains, or if further localization or confirmation of tentative findings is needed, computed tomography (CT) should be considered the imaging modality of choice. CT is both highly sensitive and specific in the detection of abnormal gas and well suited to reliable depiction of the anatomic location and extent of the gas. Of equal importance may be the capability of CT to help reliably identify benign sources of gas, because treatment (if any) varies dramatically depending on the source. Knowledge of the pathophysiologic characteristics, common predisposing conditions, and typical imaging features associated with gas-forming infections of the gall-bladder, stomach, pancreas, and genitourinary system will help make early diagnosis and successful treatment possible. In addition, such knowledge will aid in further diagnostic work-up, surveillance of potential complications, and evaluation of therapeutic response. The presence of gas within the parenchyma of solid organs or the walls of hollow viscera may be due to a variety of pathologic or benign entities. Besides infection with gas-forming bacteria, other possible sources include bland tissue infarction with necrosis, enteric fistula formation, and reflux from an adjacent hollow viscus. Gas should be differentiated from atmospheric air introduced at recent instrumentation or surgery. Gas associated with infection is generally thought to consist of carbon dioxide and nitrogen secondary to the fermentation of glucose by some species of bacteria. Poor glycolysis at the tissue level in diabetic patients results in increased glucose concentrations within the interstitial fluid. Other clinical factors that contribute to the increased production or slowed removal of gas include a depressed cell-mediated immune response, local tissue necrosis, and the presence of arteriosclerosis. The increased pH of bile associated with gallbladder inflammation and the focal tissue ischemia seen in gynecologic neoplasms are examples of specific underlying processes that help optimize bacterial culture media. In addition to broad-spectrum antimicrobial therapy and possible surgery, correction of associated underlying conditions such as urinary outflow obstruction, acid-base and electrolyte

Emphysematous Pancreatitis 205

Fig. 1. Emphysematous pancreatitis in a 66-year-old woman. Digital scout image from a CT scan demonstrates a mottled collection of gas bubbles in the midportion of the upper

Fig. 2. Emphysematous pancreatitis in a 66-year-old woman. Contrast-enhanced CT scans obtained at the same level as a show gas surrounding the body and tail of the pancreas (white arrows) and extending more cephalic within the anterior pararenal space.

abdomen and extending into the left upper quadrant.

imbalances, hypovolemia, and hyperglycemia is imperative. In the setting of gas-forming infections, clinical outcome will, in large part, depend on whether early diagnosis and treatment are achieved. The presence of comorbid conditions and equivocal physical examination findings may prevent rapid diagnosis or delay appropriate initial therapy. Consequently, appropriate radiologic imaging with prompt, accurate interpretation plays an important role in the diagnosis and management of these diseases.

#### **2. Main heading, emphysematous pancreatitis**

The most common causes of acute pancreatitis are the passage of gallstones and alcohol abuse. An overall mortality rate of 4% rapidly escalates to more than 50% when complications (eg, abscess formation, superinfection with gas-forming bacteria) occur. The infecting organisms are usually coliform bacteria and may reach the pancreatic bed by way of the bloodstream or lymphatic channels, a fistula from adjacent bowel, transmural passage from the transverse colon, or reflux of enteric organisms into the pancreatic duct or biliary tree via a patulous ampulla of Vater. Gas may be detected in up to 22% of pancreatic abscesses; however, its presence alone is not specific for the diagnosis of infection. Other sources of intraductal or parenchymal pancreatic gas include reflux from the duodenum following sphincterotomy, endoscopic instrumentation, enteric fistula (commonly involving the transverse colon), and end-organ infarction. Patients with emphysematous pancreatitis are usually debilitated and often have underlying immunocompromised conditions such as poorly controlled diabetes or chronic renal failure, atherosclerosis, tuberculosis, HIV infected individuals.

#### **2.1 Secondary heading**

Retrospective review of literature, and our one experience of treatment 8 patients with emphysematous pancreatitis in our department from 2003 to 2011.

#### **2.1.1 Tertiary heading, left justified**

Early radiographic detection of retroperitoneal gas is critical in the evaluation of superimposed emphysematous infection of the pancreas. Conventional abdominal radiography may demonstrate mottled gas overlying the midabdomen (Fig 1).

This finding is not specific for pancreatitis because abscesses involving the lesser sac or perinephric space may also have this appearance. Diagnostic US is often of limited value in the evaluation of acute pancreatitis or its complications secondary to an adjacent air-filled small bowel loop from ileus. When identified, pancreatic gas will manifest as multiple irregular echogenic foci, often with posterior dirty acoustic shadowing. A significant volume of gas may limit the detection of adjacent fluid collections. CT is the modality of choice for detecting parenchymal gas as well as evaluating its extent and location (Fig 2, 3).

Fluid collections or portal venous air are readily identified, and, although intravenously administered contrast material is not necessary for the visualization of air, it is useful for evaluating potential complications including parenchymal necrosis and abscess formation. The prognosis for emphysematous pancreatitis is grave, and successful treatment requires

imbalances, hypovolemia, and hyperglycemia is imperative. In the setting of gas-forming infections, clinical outcome will, in large part, depend on whether early diagnosis and treatment are achieved. The presence of comorbid conditions and equivocal physical examination findings may prevent rapid diagnosis or delay appropriate initial therapy. Consequently, appropriate radiologic imaging with prompt, accurate interpretation plays

The most common causes of acute pancreatitis are the passage of gallstones and alcohol abuse. An overall mortality rate of 4% rapidly escalates to more than 50% when complications (eg, abscess formation, superinfection with gas-forming bacteria) occur. The infecting organisms are usually coliform bacteria and may reach the pancreatic bed by way of the bloodstream or lymphatic channels, a fistula from adjacent bowel, transmural passage from the transverse colon, or reflux of enteric organisms into the pancreatic duct or biliary tree via a patulous ampulla of Vater. Gas may be detected in up to 22% of pancreatic abscesses; however, its presence alone is not specific for the diagnosis of infection. Other sources of intraductal or parenchymal pancreatic gas include reflux from the duodenum following sphincterotomy, endoscopic instrumentation, enteric fistula (commonly involving the transverse colon), and end-organ infarction. Patients with emphysematous pancreatitis are usually debilitated and often have underlying immunocompromised conditions such as poorly controlled diabetes or chronic renal failure, atherosclerosis, tuberculosis, HIV

Retrospective review of literature, and our one experience of treatment 8 patients with

Early radiographic detection of retroperitoneal gas is critical in the evaluation of superimposed emphysematous infection of the pancreas. Conventional abdominal

This finding is not specific for pancreatitis because abscesses involving the lesser sac or perinephric space may also have this appearance. Diagnostic US is often of limited value in the evaluation of acute pancreatitis or its complications secondary to an adjacent air-filled small bowel loop from ileus. When identified, pancreatic gas will manifest as multiple irregular echogenic foci, often with posterior dirty acoustic shadowing. A significant volume of gas may limit the detection of adjacent fluid collections. CT is the modality of choice for

Fluid collections or portal venous air are readily identified, and, although intravenously administered contrast material is not necessary for the visualization of air, it is useful for evaluating potential complications including parenchymal necrosis and abscess formation. The prognosis for emphysematous pancreatitis is grave, and successful treatment requires

radiography may demonstrate mottled gas overlying the midabdomen (Fig 1).

detecting parenchymal gas as well as evaluating its extent and location (Fig 2, 3).

emphysematous pancreatitis in our department from 2003 to 2011.

an important role in the diagnosis and management of these diseases.

**2. Main heading, emphysematous pancreatitis**

infected individuals.

**2.1 Secondary heading**

**2.1.1 Tertiary heading, left justified**

Fig. 1. Emphysematous pancreatitis in a 66-year-old woman. Digital scout image from a CT scan demonstrates a mottled collection of gas bubbles in the midportion of the upper abdomen and extending into the left upper quadrant.

Fig. 2. Emphysematous pancreatitis in a 66-year-old woman. Contrast-enhanced CT scans obtained at the same level as a show gas surrounding the body and tail of the pancreas (white arrows) and extending more cephalic within the anterior pararenal space.

Emphysematous Pancreatitis 207

Parameter Case 1 Case 2 Case 3 Case 4 Case 5 Case 6 Case 7 Case 8 Age, years 72 66 74 67 79 80 80 73 Sex female male male female male male male female Appache II 18 23 16 8 17 22 10 18

localization head head head tail head tail head head

CT detection\* 7 3 3 4 2 2 11 6

operation\*\* 15 4 3 - 3 3 13 7

operation closed open open - open+G open open open

debridment 2 1 1 3 0 1 1

stay, days 114 60 78 22 14 3 41 43 Outcome recovery recovery recovery recovery dead dead recovery recovery

Pr E. coli - E. coli;

The trigger of the development of emphysematous pancreatitis in all cases was passage of gallstones. All of these patients had calculous cholecystitis and choledocholithiasis. Most of them CT scan showed pancreatic necrosis, retroperitoneal and intrapancreatic gas trapping in the first week of the disease. Necrosis with intrapancreatic gas trapping occurred more frequently in pancreatic head (six cases), less in pancreatic tail (two cases). Six patients, for whom vasopressor-noradrenaline doses were increased to 0,4 µg/kg/min to provide sustainable hemodynamics due to bacteremic shock, had been successfully treated by extensive pancreatic necrosectomy, open packing with debridement immediately after CT diagnosis of emphysematous pancreatitis. One female patient was treated with antibiotics (ciprofloxacin and metronidazole), oxygen therapy, fluid and electrolyte correction and

Table 1. Patients data treated in our department. IS - ischemic stroke; MI - myocardial infarction; ISH - ischemic heart disease; CaV - gastric cancer; CaP - prostate cancer; \*Time of intrapancreatic gas CT detection, days from the onset of the disease; \*\*Time of the operation,

days from the onset of the disease; closed - closed lavage; open - open packing; G gastrectomy; Pr - Providentia rettgeri; Bf-Bacteroides fragilis; Ef - Enterococcus faecalis;

illnesses IS IS MI ISH ISH;

E. coli E. coli;

30-50% 30-50% <30% <30% <30% >50% <30% 30-50%

12,5 10,2 7,0 11,3 6,9 11,7 6,0 5,8

CaV

MI;

CaP ISH IS;

Bf Ef E. coli E. coli

ISH

CT evidence of necrosis degree

Necrosis

Glucose during admission mmol/l

Comorbid

Time of gas

Time of the

Type of the

Number of

Cultures of necrotic pancreas tissue

Hospital

Fig. 3. Contrast-enhanced CT scans in a 66-year-old woman with emphysematous pancreatitis. There are extensive inflammatory changes involving the surrounding fat (white arrows).

aggressive management of the infection with systemic antimicrobial therapy and control of septic shock. Usually emphysematous pancreatitis occurs at the onset of the disease – first week of the illness, but some times it can manifest later on. There is at present a tendency to operate patients with infected necrosis as soon as the diagnosis is made, regardless of the clinical status. It is well known that pancreatic abscesses represent a distinct clinical entity and that they are treatable by nonoperative management, including percutaneous drainage. Similarly, selected patients with localized infected necrosis amenable to endoscopic, transgastric drainage can be managed with this interventional technique. There are some patients with retroperitoneal gas in the setting of severe acute pancreatitis who were treated with focused long-term (3–7 weeks) antibiotics; allegedly the infected necrosis resolved without any interventional drainage or necrosectomy. The emergence of a few cases treatable medically, though small in number, may be due in part to better intensive care and in part to improved antibiotic therapy. However, the lesson learnt from these cases is that some patients may improve without intervention. The above observations suggest the need to correlate clinical versus imaging and bacteriologic findings in acute pancreatitis with infected pancreatic necrosis. Not all patients with infected pancreatic necrosis may need intervention. 368 patients with severe acute necrotic pancreatitis were treated in our department from year 2003 to 2011, including 8 (2%) patients who had developed emphysematous pancreatitis. The data of these patients are presented in Table 1.

The patient's age averaged was 73,9 ± 4,8 years. All of them had manifestation of atherosclerosis (ischemic stroke, myocardial infarction, ischemic heart disease) four had metabolic syndromes such as hyperglycemia, one gastric and another one prostate cancer.

Fig. 3. Contrast-enhanced CT scans in a 66-year-old woman with emphysematous

emphysematous pancreatitis. The data of these patients are presented in Table 1.

The patient's age averaged was 73,9 ± 4,8 years. All of them had manifestation of atherosclerosis (ischemic stroke, myocardial infarction, ischemic heart disease) four had metabolic syndromes such as hyperglycemia, one gastric and another one prostate cancer.

arrows).

pancreatitis. There are extensive inflammatory changes involving the surrounding fat (white

aggressive management of the infection with systemic antimicrobial therapy and control of septic shock. Usually emphysematous pancreatitis occurs at the onset of the disease – first week of the illness, but some times it can manifest later on. There is at present a tendency to operate patients with infected necrosis as soon as the diagnosis is made, regardless of the clinical status. It is well known that pancreatic abscesses represent a distinct clinical entity and that they are treatable by nonoperative management, including percutaneous drainage. Similarly, selected patients with localized infected necrosis amenable to endoscopic, transgastric drainage can be managed with this interventional technique. There are some patients with retroperitoneal gas in the setting of severe acute pancreatitis who were treated with focused long-term (3–7 weeks) antibiotics; allegedly the infected necrosis resolved without any interventional drainage or necrosectomy. The emergence of a few cases treatable medically, though small in number, may be due in part to better intensive care and in part to improved antibiotic therapy. However, the lesson learnt from these cases is that some patients may improve without intervention. The above observations suggest the need to correlate clinical versus imaging and bacteriologic findings in acute pancreatitis with infected pancreatic necrosis. Not all patients with infected pancreatic necrosis may need intervention. 368 patients with severe acute necrotic pancreatitis were treated in our department from year 2003 to 2011, including 8 (2%) patients who had developed

Table 1. Patients data treated in our department. IS - ischemic stroke; MI - myocardial infarction; ISH - ischemic heart disease; CaV - gastric cancer; CaP - prostate cancer; \*Time of intrapancreatic gas CT detection, days from the onset of the disease; \*\*Time of the operation, days from the onset of the disease; closed - closed lavage; open - open packing; G gastrectomy; Pr - Providentia rettgeri; Bf-Bacteroides fragilis; Ef - Enterococcus faecalis;

The trigger of the development of emphysematous pancreatitis in all cases was passage of gallstones. All of these patients had calculous cholecystitis and choledocholithiasis. Most of them CT scan showed pancreatic necrosis, retroperitoneal and intrapancreatic gas trapping in the first week of the disease. Necrosis with intrapancreatic gas trapping occurred more frequently in pancreatic head (six cases), less in pancreatic tail (two cases). Six patients, for whom vasopressor-noradrenaline doses were increased to 0,4 µg/kg/min to provide sustainable hemodynamics due to bacteremic shock, had been successfully treated by extensive pancreatic necrosectomy, open packing with debridement immediately after CT diagnosis of emphysematous pancreatitis. One female patient was treated with antibiotics (ciprofloxacin and metronidazole), oxygen therapy, fluid and electrolyte correction and

Emphysematous Pancreatitis 209

This patient did not undergo a puncture for the bacteriological proof of infection based on the supposition of the possibility to confirm the radiological suspicion of infected pancreatic necrosis during the operation. Since no surgical interventions were performed on the nonoperated patient previously, there was no enteric fistula, and pancreatic necrosis was localized in the middle of parenchyma, we therefore considered clinical and CT data to be sufficient in this case for the proof of infection of pancreatic necrosis. Following successful conservative treatment, however, the patient avoided the operation, and, therefore, the causative agent of the infected pancreatic necrosis was not verified. CT follow-up for this female patient was performed in 8 weeks and in 3 months respectively showing complete

Fig. 5. CT scan showing resolution of intrapancreatic and retroperitoneal gas after 8 weeks

draw valid conclusions.

We suggest that the main factor determining such different outcomes of emphysematous pancreatitis in patients of similar age and with similar comorbidities and extend of the necrosis is the varying localization of necrosis in the pancreas. Necrosis in the pancreas head showing higher vascularization than the pancreatic tail is associated with a lower frequency of massive intoxication and organ failure necessitating surgical intervention. Other authors reported some cases of successful antibiotic treatment of infected pancreatic necrosis located in the pancreatic tail as well. In these cases, however, infected pancreatic necrosis was identified later on, not at the onset of the disease, and the number of the cases is too small to

intrapancreatic and retroperitoneal gas disappearing (fig. 5).

nasojejunal feeding for 9 days, followed by necrosectomy and continued lavage due to failure of organs. One patient at the same time had emphysematous pancreatitis and cholecystitis. All operated on patients had infected pancreatic necrosis which was confirmed bacteriologically. Escherichia coli infection was present in six patients, additionally Bacteroides fragilis, Providentia retgeri and Enterococcus faecalis were cultured respectively. Emphysematous pancreatitis requires urgent surgical management at the onset of disease due to multisystem organ failure and patient instability. Ordinarily early surgical interventions mortality rates are reported as at least 50%, and morbidity can approach 100%. Ideally, surgery should be delayed at the earliest of 3rd or 4'th week of illness until the necrosis has demarcated and organized. At that time, the necrosectomy is technically easier, and there is generally improved mortality and morbidity. However, we found that in cases of emphysematous pancreatitis, pancreatic necrosis is already demarcated and organized at the first week, which is enough to repeat one or two additional necrosectomies for the patient full recovery. The hospital stay was significantly shorter too. In comparison for the other our patients with open packing: an average of time of the operation from the onset of the disease was 29 days, overall hospital stay - 93 days and 4,2 additional necrosectomies for the patient full recovery. We also found that minimally invasive procedures in patients with emphysematous pancreatitis are not available, since fluid collections are absent. One patient (case 4) with overt inflammatory indices – C-reactive protein 177,7 mg/l, white blood cells 16x109, febrile temperature 38,7 Co – on first presenting presenting, underwent conservative treatment regimen after radiological detection of emphysematous pancreatitis (fig.4.).

Fig. 4. CT scan showing less than 30% pancreas tail necrosis with intrapancreatic and retroperitoneal gas.

nasojejunal feeding for 9 days, followed by necrosectomy and continued lavage due to failure of organs. One patient at the same time had emphysematous pancreatitis and cholecystitis. All operated on patients had infected pancreatic necrosis which was confirmed bacteriologically. Escherichia coli infection was present in six patients, additionally Bacteroides fragilis, Providentia retgeri and Enterococcus faecalis were cultured respectively. Emphysematous pancreatitis requires urgent surgical management at the onset of disease due to multisystem organ failure and patient instability. Ordinarily early surgical interventions mortality rates are reported as at least 50%, and morbidity can approach 100%. Ideally, surgery should be delayed at the earliest of 3rd or 4'th week of illness until the necrosis has demarcated and organized. At that time, the necrosectomy is technically easier, and there is generally improved mortality and morbidity. However, we found that in cases of emphysematous pancreatitis, pancreatic necrosis is already demarcated and organized at the first week, which is enough to repeat one or two additional necrosectomies for the patient full recovery. The hospital stay was significantly shorter too. In comparison for the other our patients with open packing: an average of time of the operation from the onset of the disease was 29 days, overall hospital stay - 93 days and 4,2 additional necrosectomies for the patient full recovery. We also found that minimally invasive procedures in patients with emphysematous pancreatitis are not available, since fluid collections are absent. One patient (case 4) with overt inflammatory indices – C-reactive protein 177,7 mg/l, white blood cells 16x109, febrile temperature 38,7 Co – on first presenting presenting, underwent conservative treatment regimen after radiological detection of emphysematous pancreatitis (fig.4.).

Fig. 4. CT scan showing less than 30% pancreas tail necrosis with intrapancreatic and

retroperitoneal gas.

This patient did not undergo a puncture for the bacteriological proof of infection based on the supposition of the possibility to confirm the radiological suspicion of infected pancreatic necrosis during the operation. Since no surgical interventions were performed on the nonoperated patient previously, there was no enteric fistula, and pancreatic necrosis was localized in the middle of parenchyma, we therefore considered clinical and CT data to be sufficient in this case for the proof of infection of pancreatic necrosis. Following successful conservative treatment, however, the patient avoided the operation, and, therefore, the causative agent of the infected pancreatic necrosis was not verified. CT follow-up for this female patient was performed in 8 weeks and in 3 months respectively showing complete intrapancreatic and retroperitoneal gas disappearing (fig. 5).

Fig. 5. CT scan showing resolution of intrapancreatic and retroperitoneal gas after 8 weeks

We suggest that the main factor determining such different outcomes of emphysematous pancreatitis in patients of similar age and with similar comorbidities and extend of the necrosis is the varying localization of necrosis in the pancreas. Necrosis in the pancreas head showing higher vascularization than the pancreatic tail is associated with a lower frequency of massive intoxication and organ failure necessitating surgical intervention. Other authors reported some cases of successful antibiotic treatment of infected pancreatic necrosis located in the pancreatic tail as well. In these cases, however, infected pancreatic necrosis was identified later on, not at the onset of the disease, and the number of the cases is too small to draw valid conclusions.

Emphysematous Pancreatitis 211

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