This leads to acetylcholine- Anatomic: Pancreas divisum mediated pancreatic enzyme secretion. Proteases continue to be secreted Pancreatic cancer from the pancreas until the protein within the duodenum is digested. Intraductal papillary mucinous neoplasm IPMN At this point, pancreatic protease secretion is reduced to basic levels, Hereditary pancreatitis thus completing this step in the feedback process. The incidence of pancreatitis in alcoholics is trointestinal diagnosis. The annual incidence ranges pancreatic injury such as cigarette smoking.
Acute pancreatitis occurs from 13 to 45 cases per , persons. The median length of hospital stay creatography ERCP. Hospitalization has been shown to reduce pancreatitis after ERCP. Thus, acute trainee involvement.
Such patients are prone to recur- anisms by which these conditions trigger pancreatic inflammation have rent episodes of pancreatitis. Any factor e. Gallstones continue to bout of acute pancreatitis. Drugs cause pancreatitis either by a hypersensitivity reaction or by the Abdominal Pain generation of a toxic metabolite, although in some cases, it is not clear which of these mechanisms is operative Table Abdominal pain is the major symptom of acute pancreatitis.
Pain may Pathologically, acute pancreatitis varies from interstitial pancreatitis vary from a mild discomfort to severe, constant, and incapacitating pancreas blood supply maintained , which is generally self-limited to distress.
Characteristically, the pain, which is steady and boring in necrotizing pancreatitis pancreas blood supply interrupted , in which character, is located in the epigastrium and periumbilical region, and the extent of necrosis may correlate with the severity of the attack may radiate to the back, chest, flanks, and lower abdomen.
Nausea, and its systemic complications. Autodigestion is a currently accepted vomiting, and abdominal distention due to gastric and intestinal pathogenic theory; according to this theory, pancreatitis results when hypomotility and chemical peritonitis are also frequent complaints. Low-grade fever, tachycardia, and hypotension are fairly pancreas acinar cell rather than in the intestinal lumen.
A number of common. Shock is not unusual and may result from 1 hypovolemia factors e. Activated proteolytic enzymes, espe- tides, which cause vasodilation and increased vascular permeability; cially trypsin, not only digest pancreatic and peripancreatic tissues but and 3 systemic effects of proteolytic and lipolytic enzymes released also can activate other enzymes, such as elastase and phospholipase A2.
Jaundice occurs infrequently; when present, Spontaneous activation of trypsin also can occur. Abdomi- that evolves in three phases.
The initial phase is characterized by intra- nal tenderness and muscle rigidity are present to a variable degree, pancreatic digestive enzyme activation and acinar cell injury. Trypsin but compared with the intense pain, these signs may be less impres- activation appears to be mediated by lysosomal hydrolases such as cathepsin B that become colocalized with digestive enzymes in intra- sive.
Bowel sounds are usually diminished or absent. An enlarged pancreas from acute fluid collection, walled off necrosis, or a pseu-. The second phase of pancreatitis docyst may be palpable in the upper abdomen later in the course involves the activation, chemoattraction, and sequestration of leu- of the disease i.
There severe necrotizing pancreatitis with hemorrhage. The third phase of pancreatitis tually clinch the diagnosis if gut perforation, ischemia, and infarction is due to the effects of activated proteolytic enzymes and cytokines, are excluded. Serum lipase is the preferred test. However, it should be released by the inflamed pancreas, on distant organs. Activated noted that there is no correlation between the severity of pancreatitis proteolytic enzymes, especially trypsin, not only digest pancreatic and the degree of serum lipase and amylase elevations.
After 3—7 days, and peripancreatic tissues but also activate other enzymes such as even with continuing evidence of pancreatitis, total serum amylase elastase and phospholipase A2.
The active enzymes and cytokines then values tend to return toward normal. However, pancreatic lipase lev- digest cellular membranes and cause proteolysis, edema, interstitial els may remain elevated for 7—14 days. It should be recognized that hemorrhage, vascular damage, coagulation necrosis, fat necrosis, and amylase elevations in serum and urine occur in many conditions other parenchymal cell necrosis. Cellular injury and death result in the lib- than pancreatitis see Chap.
This finding explains why patients with diabetic ketoacidosis edema with profound effects on many organs. The systemic inflam- may have marked elevations in serum amylase without any other evi- matory response syndrome SIRS and acute respiratory distress syn- dence of acute pancreatitis. Serum lipase activity increases in parallel drome ARDS , as well as multiorgan failure, may occur as a result of with amylase activity and is more specific than amylase.
A serum lipase this cascade of local and distant effects. Patients with more severe disease may pancreatitis, and chronic pancreatitis. Five genetic variants have Hemoconcentration may be the harbinger of more severe disease been identified as being associated with susceptibility to pancreatitis.
Hyperglycemia is common and is due to multiple factors, gene PRSS1 , 2 pancreatic secretory trypsin inhibitor SPINK1 , including decreased insulin release, increased glucagon release, and an 3 the cystic fibrosis transmembrane conductance regulator gene CFTR , increased output of adrenal glucocorticoids and catecholamines. Investigations of other genetic variants are currently under way, understood.
Although earlier studies suggested that the response of and new genes will be added to this list in the future. Multiple medical, the parathyroid gland to a decrease in serum calcium is impaired, sub- ethical, and psychological issues arise when these genes are discovered, sequent observations have failed to confirm this phenomenon. Intrap- and referral to genetic counselors is recommended.
Homogeneous collection with fluid density This term applies only to areas of peripancreatic fluid Confined by normal peripancreatic fascial planes seen within the first 4 weeks after onset of interstitial edematous pancreatitis and without the features of a No definable wall encapsulating the collection pseudocyst. Adjacent to pancreas no intrapancreatic extension Pancreatic pseudocyst An encapsulated collection of fluid with a well-defined Well circumscribed, usually round or oval inflammatory wall usually outside the pancreas with Homogeneous fluid density minimal or no necrosis.
PART Disorders of the Gastrointestinal System. Laboratory studies may reveal leukocytosis, hypocalcemia, and patients with pancreatitis, mild hypocalcemia, and little or no obvious hyperglycemia. Although not required for diagnosis, markers of severity ascites.
Serum alkaline phosphatase and aspartate The differential diagnosis should include the following disorders: aminotransferase levels are also transiently elevated, and they parallel 1 perforated viscus, especially peptic ulcer; 2 acute cholecystitis and bil- serum bilirubin values and may point to gallbladder-related disease iary colic; 3 acute intestinal obstruction; 4 mesenteric vascular occlusion; or inflammation in the pancreatic head.
Finally, the electrocardiogram is occasionally abnormal in acute may be found in both disorders. Pain of biliary tract origin is more right pancreatitis with ST-segment and T-wave abnormalities simulating sided or epigastric than periumbilical or left upper quadrant and can be myocardial ischemia.
Ultrasound is helpful in establishing An abdominal ultrasound is recommended in the emergency ward the diagnosis of cholelithiasis and cholecystitis. Intestinal obstruction due as the initial diagnostic imaging modality and is most useful to evalu- to mechanical factors can be differentiated from pancreatitis by the his- ate for gallstone disease and the pancreatic head.
Acute mesenteric vascular occlusion is usually suspected in as follows: 1 interstitial pancreatitis, 2 necrotizing pancreatitis, elderly debilitated patients with brisk leukocytosis, abdominal distention, 3 acute pancreatic fluid collection, 4 pancreatic pseudocyst, 5 and bloody diarrhea, confirmed by CT or magnetic resonance angiogra- acute necrotic collection ANC , and 6 walled-off necrosis WON phy.
Vasculitides secondary to systemic lupus erythematosus and pol- Table and Fig. Radiologic studies useful in the diag- yarteritis nodosa may be confused with pancreatitis, especially because nosis of acute pancreatitis are discussed in Chap.
Diabetic Table Any severe acute pain in the abdomen or back should suggest the possi- bility of acute pancreatitis. Patients also have associated nausea, initions as outlined below. Contrast-enhanced CT scan of the abdomen performed on admission for a patient with clinical and biochemical parameters suggestive of acute pancreatitis. Note the abnormal enhancement of the pancreatic parenchyma arrow suggestive of interstitial pancreatitis.
Contrast-enhanced CT scan of the abdomen performed on the same patient 6 days later for persistent fever and systemic inflammatory response syndrome. The pancreas now demonstrates significant areas of nonenhancement consistent with development of necrosis, particularly in the body and neck region arrow. Note that an early CT scan obtained within the first 48 h of hospitalization may underestimate or miss necrosis.
Contrast-enhanced CT scan of the abdomen performed on the same patient 2 months after the initial episode of acute pancreatitis. CT now demonstrates evidence of a fluid collection consistent with walled-off pancreatic necrosis arrow. Courtesy of Dr. In the early phase of The late phase is characterized by a protracted course of illness and acute pancreatitis, which lasts 1—2 weeks, severity is defined by clinical may require imaging to evaluate for local complications.
The impor- parameters rather than morphologic findings. Most patients exhibit tant clinical parameter of severity, as in the early phase, is persistent SIRS, and if this persists, patients are predisposed to organ failure.
These patients may require supportive measures such as. CHAPTER Acute and Chronic Pancreatitis Three organ systems should be assessed to define organ failure: respi- renal dialysis, ventilator support, or need for supplemental nutrition ratory, cardiovascular, and renal.
Organ failure is defined as a score via the nasojejunal or parenteral route. The radiographic feature of of 2 or more for one of these three organ systems using the modified greatest importance to recognize in this phase is the development of Marshall scoring system. Necrosis generally prolongs important clinical finding in regard to severity of the acute pancreatitis hospitalization and, if infected, may require operative, endoscopic, or episode.
Organ failure that affects more than one organ is considered percutaneous intervention. Mild acute Risk Factors for Severity pancreatitis is without local complications or organ failure. Most patients with interstitial acute pancreatitis have mild pancreatitis. Organ failure can be single or multiple. CT identification of local complications, particularly necrosis, is critical in patients who are not responding to therapy because patients with infected and sterile necrosis are at greatest risk of mortality Figs.
The prevalence of organ failure is perhaps slightly higher in infected versus sterile necrosis. The management of acute pancreatitis begins in C D the emergency ward. Acute necrotizing pancreatitis: computed tomography CT scan. Contrast-enhanced confirmed, aggressive fluid resuscitation is initiated, CT scan showing acute pancreatitis with necrosis.
Acute assessed, and a search for etiologies that may impact fluid collection: CT scan. Contrast-enhanced CT scan showing fluid collection in the retroperitoneum arrow compressing the air-filled stomach arising from the pancreas in a patient with asparaginase- acute care is begun.
Patients who do not respond to induced acute necrotizing pancreatitis. Walled-off pancreatic necrosis: CT scan. CT scan showing aggressive fluid resuscitation in the emergency ward marked walled-off necrosis of the pancreas and peripancreatic area arrow in a patient with necrotizing should be considered for admission to a step-down Disorders of the Gastrointestinal System.
Addendum: In past years, both of these CT findings Figs. Spiral CT showing a pseudocyst small arrow with a tion, hemodynamic monitoring, and management of pseudoaneurysm light area in pseudocyst. Note the demonstration of the main pancreatic duct big necrosis or organ failure. A, B, C, courtesy of Dr. The patient is made NPO to tory changes or peripancreatic stranding.
Symptoms generally resolve rest the pancreas and is given intravenous narcotic analgesics to control with a week of hospitalization. According to the Revised Atlanta Serial bedside evaluations are required every 6—8 h to assess vital signs, criteria, the natural history of pancreatic and peripancreatic necrosis oxygen saturation, and change in physical examination to optimize. Pancreaticopleural fistula: pancreatic duct leak on endoscopic retrograde cholangiopancreatography.
Pancreatic duct leak arrow demonstrated at the time of retrograde pancreatogram in a patient with acute exacerbation of alcohol-induced acute or chronic pancreatitis. Pancreaticopleural fistula: computed tomography CT scan. Contrast-enhanced CT scan coronal view with arrows showing fistula tract from pancreatic duct disruption in the pancreatic pleural fistula.
Pancreaticopleural fistula: chest x-ray. Large pleural effusion in the left hemithorax from a disrupted pancreatic duct. Analysis of pleural fluid revealed elevated amylase concentration.
A targeted resus- atitis, and drug-induced pancreatitis. Treatment of hyperparathyroidism citation strategy with measurement of hematocrit and BUN every or malignancy is effective at reducing serum calcium. AIP is responsive 8—12 h is recommended to ensure adequacy of fluid resuscitation and to glucocorticoid administration. Pancreatic duct stenting and rectal monitor response to therapy, noting less aggressive resuscitation strat- indomethacin administration are effective at decreasing pancreatitis egy may be needed in milder forms of pancreatitis.
Drugs that cause pancreatitis should be discontinued. A decrease in hematocrit and BUN during the first 12—24 h is strong evidence that sufficient fluids are being administered. Enteral nutrition should be considered 2—3 days after admis- fluid rates are maintained at the current rate. Adjustments in fluid sion in subjects with more severe pancreatitis instead of total parenteral resuscitation may be required in patients with cardiac, pulmonary, or nutrition TPN.
Enteral feeding maintains gut barrier integrity, limits renal disease. A rise in hematocrit or BUN during serial measurement bacterial translocation, is less expensive, and has fewer complications should be treated with a repeat volume challenge with a 2-L crystalloid than TPN. The choice of gastric versus nasojejunal enteral feeding is bolus followed by increasing the fluid rate by 1.
If currently under investigation. A multidisciplinary team approach is recom- admission to an intensive care unit. The Bedside Index of Severity in Acute mended including gastroenterology, surgery, interventional radiology, Pancreatitis BISAP incorporates five clinical and laboratory parameters and intensive care specialists, and consideration should also be made obtained within the first 24 h of hospitalization Table —BUN for transfer to a pancreas center.
The benefits of percutaneous aspiration of necrosis in assessing severity. Presence of three or more of these factors was asso- with Gram stain and culture should be considered or discussed if there ciated with substantially increased risk for in-hospital mortality among are ongoing signs of possible pancreatic infection such as sustained patients with acute pancreatitis.
It is reasonable to acute pancreatitis. Incorporating these indices with the overall patient start broad-spectrum antibiotics in a patient who appears septic while response to initial fluid resuscitation in the emergency ward can be useful awaiting the results of Gram stain and cultures.
If cultures are negative, at triaging patients to the appropriate hospital acute care setting. Repeated fine-needle aspi- admission BUNs tend to respond to initial management and are triaged ration and Gram stain with culture of pancreatic necrosis may be done to a regular hospital ward for ongoing care.
If SIRS is not present every 5—7 days in the presence of persistent fever. In general, sterile necrosis is most often managed conservatively Patients with higher BISAP scores and elevations in hematocrit and unless complications arise. Once a diagnosis of infected necrosis is estab- admission BUN that do not respond to initial fluid resuscitation and lished and an organism identified, targeted antibiotics should be insti- exhibit evidence of respiratory failure, hypotension, or organ failure tuted.
Pancreatic debridement necrosectomy should be considered should be considered for direct admission to an intensive care unit. Symptomatic local complications as outlined in the review of medications, selected laboratory studies liver profile, serum Revised Atlanta criteria may require definitive therapy. An abdominal ultrasound is the initial imaging fully reported by some pancreatic centers. One-third of the patients modality of choice and will evaluate the gallbladder and common duct successfully treated with the step-up approach did not require major and assess the pancreatic head.
Patients with gallstone WON. Taken together, a more conservative approach to the man- pancreatitis are at increased risk of recurrence, and consideration agement of infected pancreatic necrosis has evolved under the close should be given to performing a cholecystectomy during the same supervision of a multidisciplinary team. If conservative therapy can be admission or within 4—6 weeks of discharge. Initial therapy may include insulin, hepa- lections resolve over time. Outpatient therapies include control of diabetes fluid collections after 6 weeks that would meet the definition of a pseu- if present, administration of lipid-lowering agents, weight loss, and docyst.
Only symptomatic collections should be drained with surgery avoidance of drugs that elevate lipid levels. Patients should be Pancreatic fluid collections continually monitored for the development pneumonia, urinary tract Pancreatic pseudocyst infection, and line infection.
Continued culturing of urine, monitoring Disruption of main pancreatic duct or secondary branches of chest x-rays, and routine changing of intravenous lines are important Pancreatic ascites during hospitalization. Follow-up evaluation Obstructive jaundice should assess for development of diabetes, exocrine insufficiency, Systemic recurrent cholangitis, or development of infected fluid collections.
In one series of 31 patients diagnosed initially as having idiopathic or recurrent PART Thus, with symptoms of increasing abdominal pain or shortness of breath in the condition is defined by the presence of histologic abnormalities, the setting of an enlarging fluid collection. Diagnosis can be confirmed including chronic inflammation, fibrosis, and progressive destruction on magnetic resonance cholangiopancreatography MRCP or ERCP.
Hyperlipidemia Whitcomb and associates studied several large families with heredi- Chronic renal failure tary chronic pancreatitis and were able to identify a genetic defect that Medications—phenacetin abuse affects the gene encoding for trypsinogen. Several additional defects of Toxins—organotin compounds e.
The defect prevents the destruction Idiopathic of prematurely activated trypsin and allows it to be resistant to the Early onset intracellular protective effect of trypsin inhibitor.
It is hypothesized that this continual activation of digestive enzymes within the gland Late onset leads to acute injury and, finally, chronic pancreatitis. This gene functions as a cyclic AMP—regulated chloride channel. Attempts to elucidate the relationship between the Type 1 autoimmune chronic pancreatitis genotype and pancreatic manifestations have been hampered by the IgG4 systemic number of mutations.
The ability to detect CFTR mutations has led to Type 2 autoimmune chronic pancreatitis the recognition that the clinical spectrum of the disease is broader than Recurrent and severe acute pancreatitis previously thought. Two studies have clarified the association between.
In these studies, the patients Obstructive were adults when the diagnosis of pancreatitis was made; none had Pancreas divisum any clinical evidence of pulmonary disease, and sweat test results were Duct obstruction e. The prevalence of such mutations is Preampullary duodenal wall cysts unclear, and further studies are certainly needed.
In addition, the ther- Posttraumatic pancreatic duct scars apeutic and prognostic implication of these findings with respect to managing pancreatitis remains to be determined. CFTR mutations are common in the general population. It is unclear whether the CFTR mutation alone can lead to pancreatitis as an autosomal recessive disease. A study evalu- Although alcohol has been believed to be the primary cause of ated 39 patients with idiopathic chronic pancreatitis to assess the risk chronic pancreatitis, other factors contribute to the disease because associated with these mutations.
Patients with two CFTR mutations not all heavy consumers of alcohol develop pancreatic disease. There compound heterozygotes demonstrated CFTR function at a level is also a strong association between smoking and chronic pancreatitis. The presence of an digestion and predisposes to dysregulation of duct cell CFTR function.
Both continued alcohol of pancreatitis fold. Knowledge of the genetic defects and down- and smoking exposure are associated with pancreatic fibrosis, calcifica- stream alterations in protein expression has led to the development tions, and progression of disease.
Table lists recognized causes of chronic chronic pancreatitis. Specifically, PSCs are believed to play a role in main- pancreatitis and pancreatic exocrine insufficiency. It is believed that alcohol or additional stimuli lead with characteristic laboratory, histologic, and morphologic findings.
The characteristic pancreatic histopathologic induce PSC activity with subsequent new collagen synthesis. In addition findings include lymphoplasmacytic infiltrate, storiform fibrosis, and to being stimulated by cytokines, oxidants, or growth factors, PSCs also abundant IgG4 cells. It is a disorder limited to the pancreatitis even after removal of noxious stimuli. AIP and IDCP are highly responsive in the head of the pancreas mimicking carcinoma to initial glucocorticoid treatment.
Eating may exacerbate the pain, leading to a fear magnetic resonance cholangiopancreatography. The spectrum of abdominal pain ranges from mild to quite severe, with narcotic dependence Although AIP was initially described as a primary pancreatic as a frequent consequence.
Maldigestion is manifested as chronic disorder, it is now recognized that it is associated with other diarrhea, steatorrhea, weight loss, and fatigue. Patients with chronic pancreatitis have ulcerative colitis, mediastinal fibrosis and adenopathy, autoimmune significant morbidity and mortality and use appreciable amounts of thyroiditis, tubulointerstitial nephritis, retroperitoneal fibrosis, chronic societal resources.
Despite steatorrhea, clinically apparent deficiencies PART Mild of fat-soluble vitamins are surprisingly uncommon. Physical findings symptoms, usually abdominal pain, and recurrent acute pancreatitis in these patients are usually unimpressive, so that there is a disparity are unusual. Furthermore, AIP is not a common cause of idiopathic between the severity of abdominal pain and the physical signs that recurrent pancreatitis. Weight loss from pancreatic atrophy and new onset of diabetes The diagnosis of early or mild chronic pancreatitis can be challeng- Disorders of the Gastrointestinal System.
An ing because there is no biomarker for the disease. In contrast to acute obstructive pattern on liver tests is common i. Elevation of serum bilirubin and aminotransferases. Elevated serum levels of IgG4 provide a marker alkaline phosphatase may indicate cholestasis secondary to common for the disease, particularly in Western populations.
Serum IgG4 is bile duct stricture caused by chronic inflammation. CT scans reveal abnormalities in the impaired glucose tolerance with elevated fasting blood glucose levels. ERCP of patients with suspected pancreatic steatorrhea. The fecal elastase or MRCP reveals strictures in the bile duct in more than one-third level will be abnormal and small-bowel histology will be normal in of patients with AIP; these may include common bile duct strictures, such patients.
The radiographic evaluation of a patient with suspected chronic This has been termed autoimmune IgG4 cholangitis. Characteristic his- pancreatitis usually proceeds from a noninvasive to more invasive tologic findings include extensive lymphoplasmacytic infiltrates with approach. Abdominal CT imaging Fig. In addition to excluding a pseudocyst The Mayo Clinic HISORt criteria indicate that AIP can be diagnosed and pancreatic cancer, CT may show calcification, dilated ducts, or by the presence of at least one or more of the following: 1 histology; an atrophic pancreas.
Although abdominal CT scanning and MRCP 2 imaging; 3 serology elevated serum IgG4 levels ; 4 other organ greatly aid in the diagnosis of pancreatic disease, the diagnostic test involvement; and 5 response to glucocorticoid therapy, with improve- with the best sensitivity and specificity is the hormone stimulation ment in pancreatic and extrapancreatic manifestations. This usually correlates decreasing the size of the pancreas, and reversing histopathologic well with the onset of chronic abdominal pain.
The role of endoscopic features in patients with AIP. Here, the step-up approach has become established, with prior drainage either endoscopic or percutaneous followed by delay for maturing of the wall and then debridement by endoscopic or minimally invasive surgical methods.
Open surgery is only indicated when this approach fails. Other indications for surgery in acute pancreatitis are for the treatment of acute compartment syndrome, non-occlusive intestinal ischaemia and necrosis, enterocutaneous fistulae, vascular complications and pseudocyst.
Surgery also has a role in the prevention of recurrent acute pancreatitis by cholecystectomy. Despite the more restricted role, surgeons have an important contribution to make in the multidisciplinary care of patients with complicated acute pancreatitis.
There have been dramatic changes in the role of surgery for acute pancreatitis AP over the last 20 years, and some have predicted its demise. The most common indication for intervention is for infected local complications of AP, and these have recently been re-defined Fig.
Other indications for intervention include complications of acute pancreatitis, and these may require surgery alone or combined with other treatment modalities, including interventional radiologic and endoscopic techniques. The purpose of this chapter is to provide a current overview of the role of surgery in AP, in the context of these wider changes in intervention.
The local complications of acute pancreatitis defined by chronicity, infection and content adapted from Windsor JA, Petrov MS. Acute pancreatitis re-classified. Gut ; 4—5. Acute pancreatitis is now rarely diagnosed by surgery in advanced healthcare systems. The situation where this might still be the case is when patients with AP present late, and there is a non-diagnostic elevation of serum pancreatic enzyme concentration.
The other indication is when a patients presents with signs of severe peritonitis, warranting an urgent laparotomy. If these patients can be stabilised, cross-sectional imaging will usually allow the radiological diagnosis of acute pancreatitis, avoiding the need for surgical diagnosis. The incidence of intra-abdominal hypertension IAH and abdominal compartment syndrome ACS in AP appears to be related to a more aggressive resuscitation strategy [ 2 ].
Pressures are usually measured by a catheter in the bladder, but this is far from routine practice. In patients with AP, ACS is associated with extensive pancreatic necrosis, multi-organ failure, a longer stay in ICU and hospital and higher mortality [ 3 ]. Early recognition and prompt treatment of ACS help to decrease morbidity and improve patient survival.
It has been found that the duration of IAH is of greater importance than the absolute increase in intra-abdominal pressure. The mechanism by which IAH affects end-organs such as the heart, lungs and kidneys has not been established.
The gut-lymph hypothesis [ 6 ] is a plausible explanation, with impairment of gut microcirculation leading to a breakdown of the gut barrier and the generation of toxic gut lymph which bypasses the liver entering the circulation immediately upstream of the organs affected [ 7 ].
Non-operative strategies [ 8 ] to prevent and reverse IAH in the setting of AP should be initially considered, with surgical intervention usually reserved for the setting of persistent organ dysfunction. Medical interventions to lower IAP target three important contributors: 1 distension and volume of hollow organs such as with paralytic ileus , 2 space occupying lesions such as ascites, blood and fluid collections and 3 conditions that limit abdominal wall expansion such as agitation or incomplete relaxation in ventilated patients.
The levels of sedation and analgesia should be optimised to avoid agitation and increased abdominal wall tone. A brief trial with neuromuscular blocking agents helps to decrease abdominal muscular tone and increases abdominal wall compliance thus reducing IAP. Enteral decompression with nasogastric or rectal tubes can be helpful in managing ileus and gastric dilation.
Prokinetic agents such as erythromycin and metoclopramide may help mitigate paralytic ileus. Another drug, neostigmine, a parasympathomimetic agent, has been used for treatment of ACS related to acute colonic pseudo-obstruction ACPO after conservative measures have failed. It exerts its effect by two mechanisms: increasing the amount of available acetylcholine and indirectly stimulating nicotinic and muscarinic receptors in the smooth muscles of intestine.
Valle et al. The use of neostigmine in AP is not included in any current guidelines [ 10 ]. Currently, there is no consensus regarding the optimal timing for surgical decompression of ACS or the best technique in patients with AP. The most commonly used method for surgical decompression is a midline laparostomy extending from the xiphisternum to the pubis.
This approach allows an inspection of bowel viability and the diagnosis of ischaemia. Although early complications, such as intestinal fistulas, have been greatly reduced with careful management and improved understanding of the open abdomen, there is still the medium-term requirement of skin grafting and longer-term requirement for elective repair of the ensuing incisional ventral hernia.
Another approach is to use transverse bilateral extended incision below the costal margins to form a full-thickness laparostomy. This incision is more likely to achieve primary closure than the midline incision. A third option is subcutaneous vertical linea alba fasciotomy which is achieved through three short horizontal skin incisions. This allows the linea alba to be split, sometimes using a laparoscope for visual control although the least effective for decompression is associated with less complications, such as fistulae [ 11 ].
The judicious use of intravenous resuscitation fluids improved non-operative management, and the wider use of percutaneous drainage for collections has resulted in a decrease in the incidence of ACS in patients with AP.
Although surgical decompression results in prompt recovery from ACS, it is associated with a significant morbidity including intra-abdominal bleeding, persistent infection, development of post-operative fistulas, and hernias [ 12 ].
A number of factors contribute to the risk of non-occlusive mesenteric ischaemia NOMI and intestinal infarction in patients with AP. Risk factors may include under-resuscitation with significant persisting reflex splanchnic vasoconstriction, the metabolic demand of early enteral feeding, non-selective inotropes and the development of intra-abdominal hypertension [ 13 ].
When NOMI occurs, it is usually an early event and within the first week of the onset of symptoms. When suspected, due to the development of an acute abdomen and a rising serum lactate, an urgent CT scan should be arranged. There may be evidence of pneumatosis intestinalis with intramural gas in the intestinal wall, and sometimes in the portal vein and liver. Occasionally mild NOMI can be managed conservatively by addressing the risk factors, but usually, it requires surgery and bowel resection [ 14 ].
Probiotics have been shown to reduce infectious complications by limiting small-bowel bacterial overgrowth, restoring gastrointestinal barrier function and modulating the immune system. Probiotic prophylaxis should therefore not be administered in this category of patients. Historically, the most common reason for surgical intervention in patients with AP was to treat pancreatic necrosis, and it is this indication for surgery that has undergone the most change.
There have been phases in the evolving role of surgery in AP, going from resection to debridement to drainage. Another notable trend has been the move away from early to delayed intervention.
The early surgical mindset was to operate early to remove all necrotic tissue, both sterile and infected. Open surgical debridement has been the standard treatment not only for the removal of infected pancreatic and peri-pancreatic necrosis but also for symptomatic sterile necrosis especially through the —s.
The trend for early intervention was not persisted with. Different strategies were advocated following debridement, including closing the abdomen over packs, wide bore drains with postoperative irrigation or leaving the abdomen open to facilitate further debridements [ 21 ].
Less invasive techniques have been developed and implemented [ 23 ], and these have largely replaced the need for open procedures. The development of minimally invasive necrosectomy has been in the context of the trend towards less invasive treatments generally, and an increasing convergence of the technologies within the fields of laparoscopic surgery, interventional radiology and therapeutic endoscopy. Nine different minimally invasive intervention techniques, based on the method of visualisation laparoscopic, endoscopic, nephroscopic and the route of entry transperitoneal, retroperitoneal and transmural have been published [ 23 ].
A more comprehensive classification of interventions for AP, based on visualisation, route and purpose, includes the increasingly important contributions of interventional radiology [ 24 ]. Two other important trends have occurred, including the recognition that a delay in intervention allows a lesser procedure with better outcomes because it allows the development of a wall i.
The other realisation is that there is a role for non-operative management in selected patients, including all unfit patients, most patients with sterile necrosis and some with infected necrosis. The major end-point was a combination of major complications and mortality. The results from this study have changed the surgical approach to AP. Sixty per cent of patients who were drained went on to have a minimally invasive necrosectomy, and two patients required open necrosectomy out of 43 patients in the step-up arm.
The principle of delay is now embedded within the latest guidelines [ 27 ]. There are many approaches to minimally invasive necrosectomy [ 23 ]. The selection of the best approach depends on the availability of relevant expertise and the topography of the lesion to be treated.
When the WON is central, transgastric approaches are the best approach. When there are prominent extensions into paracolic gutters, then flank percutaneous drainage is preferred, and the drain is used to access these more lateral lesions.
This can be done by cutting down onto the drain to create a short transverse incision to facilitate extraction of the necrosum with blunt forceps and laparoscopic guidance, as in the videoscope-assisted retroperitoneal debridement VARD procedure [ 28 ].
This is an efficient method for debridement. An alternative approach is to use the approach used by urologists for percutaneous nephrolithotomy, with dilation of the drain track, insertion of an Amplatz sheath and high flow operating rigid nephoscope [ 29 ]. This less efficient method of debridement is often done as an adjunct to upsizing and placement of wide-bore drains e. The diminishing role of open surgical treatment of infected local complications of AP and the rise of minimally invasive necrosectomy has almost been eclipsed by the evolution in the role of percutaneous drainage PCD.
Initially, PCD was an adjunctive treatment, being used to drain infected residual or recurrent collections after open surgery. To this has been the evolution of PCD as a primary treatment.
This effectively buys time and this allows the systemic response to settle and for the maturation encapsulation of target lesions for later and safer definitive treatment. And now, PCD is being increasingly used as definitive and sole treatment, although there remains significant room for improvement [ 30 ].
In summary, several key points can be made about the surgical treatment of infected acute fluid collections and walled off necrosis.
Treatment of infected acute fluid collections and walled off necrosis should be delayed as long as possible by providing optimum intensive care support and drainage to allow for encapsulation. The step-up approach is the standard of care, with initial drainage percutaneous or endoscopic followed by minimally invasive necrosectomy percutaneous or endoscopic , and open necrosectomy only if these approaches fail. The decrease in the use of laparostomy, open necrosectomy and packing for the treatment of AP has contributed to a decline in the incidence of enterocutaneous small and large bowel fistulae in these patients.
The majority of these fistulas can be managed conservatively, using established principles [ 31 ]. This includes defining the anatomy, controlling sepsis, optimising nutrition and undertaking surgical resection after failed conservative management. Although fistulae increase the morbidity, they do not appear to increase the mortality of patients with necrotising pancreatitis [ 32 ]. The reclassification of the local complications has led to a narrower definition of pseudocyst.
It is now defined as an encapsulated collection of fluid with a well-defined inflammatory wall usually outside the pancreas with minimal or no necrosis [ 33 ]. And, it is only defined when it has been present for a least 4 weeks after the onset of interstitial oedematous pancreatitis. If the patient has necrotising pancreatitis, the collection will almost always contain necrotic pancreatic and sometimes peripancreatic tissue.
This is a limitation of CT scanning in AP patients. The majority of fluid collections and pseudocysts resolve spontaneously without active treatment. Those that persist and are associated with symptoms or complications should be treated.
Persistence without symptoms or complications is not an indication for intervention, despite the widely held surgical opinion that a cysto-gastrostomy is required when a pseudocyst of greater than 6 cm and present for more than 6 weeks [ 34 ].
In the absence of symptoms or complications, it is reasonable to take an expectant approach. Symptoms may develop, including early satiety, epigastric discomfort, impaired gastric emptying and gastro-oesophageal reflux [ 35 ]. The fluid content of a pseudocyst is enzyme-rich including pancreatic elastase and this can lead to weakening of blood vessels in the wall of the pseudocyst, leading to pseudoaneurysm formation and bleeding.
Pseudocysts can also rupture leading to pancreatic ascites. Treating a pseudocyst by percutaneous drainage without first ensuring that there is no distal obstruction in the main pancreatic duct by MRCP is ill advised. The presence of a pancreatic duct stricture or stone increases the likelihood that percutaneous drainage will result in an external pancreatic fistula [ 36 ].
In this setting, it is best to perform internal drainage. Historically, this has meant performing a cysto-gastrostomy or Roux en Y cysto-jejunostomy, and more recently, these have been performed laparoscopically [ 35 ]. But today, it is preferable to consider treating a pseudocyst using an endoscopic transmural approach, either through the posterior stomach wall or medial duodenal wall. The insertion of a double pigtail stent, or multiple stents, is all that is required for a pseudocyst.
This is in contrast to walled off necrosis, where it is best to use a purpose designed, wall-opposing, self-expanding metal stent that also permits endoscopic debridement [ 37 ]. Rarely, it is possible to successfully treat a pseudocyst by the placement of a transampullary drain directly into the pseudocyst cavity after first defining a communication between the main pancreatic duct and the pseudocyst cavity by endoscopic retrograde pancreatography [ 38 ].
A pseudocyst is more likely to persist and become symptomatic when there has been disruption of the main pancreatic duct by the necrotising process. If an endoscopic approach is not feasible because of the location and topography of the pseudocyst, then a surgical approach is warranted [ 39 ]. Patients with gallstone acute pancreatitis can present with associated cholestasis and cholangitis, suggestive of choledocholithiasis.
Too often, ERCP has been undertaken for predicted severe acute pancreatitis and for cholestasis. A recent meta-analysis finds that the primary indication for endoscopic treatment is concomitant cholangitis [ 40 ]. If the presentation of a patient with AP and cholangitis has been delayed beyond 72 h, it may be safer to decompress the biliary tree by percutaneous transhepatic biliary drainage since duodenal oedema and patient instability can significantly increase the risks of an endoscopic approach.
Note that cholestasis per se does not require urgent endoscopic intervention; indeed, testing liver function tests over 48 h will often reveal improvement which suggests that the offending CBD stone has passed into the duodenum already.
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