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COMPLICATIONS IN PANCREATIC SURGERY

Despite recent technical advancements, post-operative complications  after pancreatic surgery (especially after pancreatic resections) remain  a major issue. The principal determinant of post-operative morbidity is  – paradoxically – the pancreas, a very soft and friable organ that  produces digestive enzymes. An early diagnosis and the correct  management of post-operative complications require a broad experience in  the field, and account for a favorable postoperative outcome. Here are  listed the principal complications after pancreatic surgeries. Click on  the links to learn more.

PANCREATIC FISTULA

Pancreatic fistula is the leading complication after pancreatic resections.  It is defined as the output via a drain, a drain track, or a surgical  wound (on or after postoperative day 3) of any measurable volume of  fluid containing pancreatic juice (amylase content greater than 3 times  the upper normal serum value). Drain fluid could have a ‘‘sinister  appearance’’ that may vary from a dark brown to greenish fluid to milky  water to clear ‘‘spring water’’ that looks like pancreatic juice.  Associated clinical findings may include abdominal pain  and distention with impaired bowel function, delayed gastric emptying,  fever, elevated serum leukocyte count, and increased C-reactive protein.
  
The origin of pancreatic fistula differs according to the type of pancreatic resection:

  • In pancreaticoduodenectomy,  pancreatic fistula represents the failure of healing/sealing of  pancreaticojejunostomy or pancreatico-gastrostomy. Incidence is between  10% and 20%.
  • In left pancreatectomy,  pancreatic fistula represents a parenchymal leak not directly related  to an anastomosis. The leak originates from the raw pancreatic surface  (closed with sutures or with a stapler). Incidence is 20-25%.
  • In middle segment pancreatectomy pancreatic  fistula derives from a failure of healing/sealing of the  pancreatic-enteric anastomosis performed on the distal stump, and/or it  may represent a parenchymal leak originating from the raw pancreatic  surface of the proximal stump. Incidence is 40-50%.
  • In enucleation pancreatic  fistula represents a parenchymal leak form the resection bed, often  because of inadvertent damage of a secondary duct or, less commonly,  because of damage to the main pancreatic duct. Its incidence is 35-40%.

The most widely recognized risk factors for pancreatic fistula are  directly linked to state and disease of the pancreas and  or/periampullary region. Principal among them is a soft pancreatic parenchyma.  The normal pancreas texture is soft and friable, and remains unaltered  when small and benign/borderline neoplasms develop. On the other hand,  ductal adenocarcinoma and – especially – chronic pancreatitis cause duct  obstruction and fibrotic replacement of the normal pancreatic  tissue. It has been widely accepted that a fibrotic pancreatic remnant  facilitates the pancreatico-enteric anastomosis, whereas a soft and  friable pancreatic parenchyma makes the anastomosis difficult to perform  and prone to inflammatory injury (due to the unaltered acinar  component), and leak.

The size of the main pancreatic duct has been also  implicated as a major predictor of fistula. Small non-dilated pancreatic  ducts, typically defined as less than or equal to 3 mm in diameter,  predispose patients to pancreatic fistulae. Small pancreatic duct and  soft parenchyma often coexist, making the risk of postoperative fistula  greater.

Despite refinements in surgical technique and postoperative care,  pancreatic fistula remains a major issue. Variations in surgical  technique (modification of pancreatic anastomosis technique in  pancreaticoduodenectomy or management of the pancreatic stump in distal  pancreatectomy) or in postoperative management did not modify the  incidence of fistula appreciably.
Clinically, pancreatic fistula can be associated with abdominal  collections, abscesses, infection, fever, abdominal distension and bowel  impairment, bleeding. A clinical grading system for  postoperative pancreatic fistula (A,B,C) has been proposed, by the  International Study Group of Pancreatic Fistula (ISGPF) and is  summarized below:

  • Pancreatic fistula grade A has no clinical impact and requires little change in management or deviation from the normal clinical pathway.
  • Pancreatic fistula grade B requires a change in  management or adjustment in the clinical pathway. Often the patient is  supported with artificial nutrition. The peripancreatic drains are  usually maintained in place or repositioned. Antibiotics are usually  required, somatostatin analogues may also be used. Grade B fistula  usually leads to a delay in discharge, or readmission after a previous  discharge may be required.
  • Pancreatic fistula grade C requires a major change  in clinical management. An invasive procedure is required, including  percutaneous drain placement of surgical re-exploration. The patient  typically requires an extended hospital stay with a major delay in  hospital discharge. There are often associated complications and the  possibility of post- operative mortality.

Many patients with grade B and C postoperative pancreatic fistula can  be discharged with drains in situ and observed in the outpatient  setting.

POST-PANCREATECTOMY HEMORRHAGE

Postoperative hemorrhage is one of the most severe complications  after pancreatic resections, with an incidence between 2% to 8%. The  International Study Group of Pancreatic Surgery (ISGPS) developed an  objective, generally applicable definition of PPH based on 3 parameters:

  • Onset (early/late)
  • Location (intraluminal/extraluminal)
  • Severity (mild/severe)

Postoperative hemorrhage manifests with blood loss from drains or  nasogastric tube, and/or clinical signs of hypovolemia (loss of blood  volume). Unless the bleeding requires emergency treatment, all patients  should be initially monitored (hemoglobin, red blood cell count,  hematocrit, blood pressure, pulse, urine output). A CT-scan may be able  to demonstrate the bleeding site and the associated abdominal  collections.

Early post-pancreatectomy hemorrhage occurs in the  first 24 hours postoperatively. It is caused most likely by technical  failure of appropriate hemostasis during the index operation or an  underlying perioperative coagulopathy. If feasible, it can be treated by  blood transfusions; otherwise, re-exploraton and hemostasis are  required. Re-exploration within 24 hours from the index operation does  not modify substantially the post-operative course.

Late post-pancreatectomy hemorrhage occurs typically  from complications of the operation, with a usual delay of several days  or even weeks (eg, after intraabdominal abscesses, erosion of a  peripancreatic vessel secondary to pancreatic fistula or intraabdominal  drains, ulceration at the site of an anastomosis, or in association with  an arterial pseudoaneurysm that has developed). A so-called  “sentinel bleeding”, a small amount of blood loss via abdominal drains  or nasogastric tube several hours before massive hemorrhage, may be  present (30% to 100%). Diagnostic angiography may localize the bleeding  site, and embolization can be performed. Otherwise, surgical  re-exploration may be needed, especially to treat a massive bleeding or  to treat a concomitant complication (e.g. pancreatic fistula). Endoscopy  may play a role in intraluminal bleeding.  Late hemorrhage is a serious  event associated with mortality rates of 15-20%.

Intraluminal bleeding occurs into the bowel lumen. In pancreaticoduodenectomy and middle segment pancreatectomy bleeding  may originate suture lines of the pancreato-enteric anastomosis because  of enzymatic digestion of the blood vessel wall on the pancreatic stump  surface by pancreatic exocrine enzymes secondary to a pancreatic leak.  Other sites of intraluminal bleeding include the gastro-enteric or the  duodeno-enteric anastomosis. Such bleedings usually depend  on gastric/duodenal ulcer or diffuse gastritis. Intraluminal bleeding  presents with dark blood in the nasogastric tube (if present), or with  hematemesis and/or melena (black stools), and/or signs of hypovolemic  shock. The treatment of bleeding from the enteric anastomosis is  endoscopic, while bleeding from the pancreatic anastomosis may require  surgical re-exploration.

Extraluminal bleeding occurs in the abdomimal  cavity, and may originate from arterial or venous vessels in the areas  of resection (especially retroportal lamina), or eroded and ruptured  pseudoaneurysms, that are secondary to intra-abdominal infection with  involvement of peripancreatic vessels, or vascular injury during  resection. Intraluminal bleeding presents withblood loss from  intra-abdominal drains and/or signs of hypovolemic shock. The treatment  may be either surgical or angiographic.

The severity of bleeding can be differentiated into 2 categories based on the amount of blood loss or transfusion requirements: mild bleeding  involves no clinical impairment, drop of hemoglobin level by <3  g/dl, and transfusion <3 units of packed red blood cells within 24  hours. Severe bleeding involves a large volume blood  loss (drop of hemoglobin level by >3 g/dl), clinically significant  impairment (eg, tachycardia, hypotension, oliguria, hypovolemic  shock), need for blood transfusion >3 units of packed red blood cells  within 24 hours, and need for invasive treatment (interventional  angiographic embolization, or relaparotomy).

Post-pancreatectomy hemorrhage remains a major complication that at  least requires a careful clinical monitoring, Recognizing this event in a  timely fashion may prevent severe and fatal outcomes. A  multidisciplinary expert team is mandatory to ensure the best treatment  24 hours/day.

DELAYED GASTRIC EMPTYING

Delayed gastric emptying consists in a functional gastroparesis, and  it is one of the most common complications after pancreatic resection  (especially after pancreaticoduodenectomy).  Its incidence varies widely across surgical institutions (5-25%).The  definition of delayed gastric emptying encompasses different clinical  items, including:

  • Prolonged naso-gastric tube or necrssity of naso-gastric tube reinsertion
  • Inability to tolerate a solid diet
  • Vomit and gastric distension
  • Use of prokinetic drugs

The causes for delayed gastric emptying are still unclear and are  probably multifactorial, involving disruption of pylorus innervation,  motilin deficiency due to duodenum resection, and technical aspects.  Several studies have suggested a greater incidence of delayed gastric  emptying after pylorus-preserving than after Whipple  pancreaticoduodenectomy, whereas others found the opposite effect.  Another operative factors that may impact the rate delayed gastric  emptying is method of reconstruction of gastric drainage (antecolic versus  retrocolic). Finally, delayed gastric emptying is often secondary to  pancreatic fistula, biliary fistula and abdominal collections.

When a delayed gastric emptying is suspected, it may be necessary to  exclude a gastric outlet obstruction. This can be done by a gastrografin  swallow X-ray (that allows the radiologist to see the movement of the  dye through the digestive anastomosis), or an upper endoscopy (that  allows visualization of the digestive anastomosis and of associated  problems, such as anastomotic ulcers).

Three different grades (A, B, and C) were defined based on the impact on the clinical course and on postoperative management:

  • Delayed gastric emptying grade A usually does not  lead to a marked change in management other than by minor disturbances  in the return to intake of solid food or reinsertion of nasogastric tube  for a brief period.
  • Delayed gastric emptying grade B requires treatment  with prokinetic drugs and parenteral or enteral nutritional support,  and usually a prolonged reinsertion of the nasogastric tube.
  • Delayed gastric emptying grade C necessitates a  major change in clinical management, and possibly treatment of  associated postoperative complications, such as pancreatic fistula or  intra-abdominal abscesses. Consequently, further diagnostic workup and  radiologic or operative interventions are often needed.

Delayed gastric emptying may lead to significant patient discomfort,  and its treatment may be difficult. A multidisciplinary team including  experienced gastroenterologists and dietitians is necessary to provide  the best care.

POSTOPERATIVE PANCREATITIS

Post-operative pancreatitis depends on local inflammation triggered  by enzymatic digestion at the level of pancreatic remnant. Patients with  a soft, acinar pancreas are more prone do develop postoperative  pancreatitis, despite other patient-related factors may contribute to  the pathogenesis. Early postoperative pancreatitis (day 1-3) usually  contributes to the formation of a pancreatic leak. The diagnosis relies  on elevated serum amylase levels, a dark-brown drain fluid, and poorly  controlled postoperative pain. Postoperative pancreatitis necessitates  changes in clinical managemement, including artifical nutrition.
Biliary fistula
Biliary fistula is defined as the output via a drain of any  measurable volume of fluid containing bile. Drain fluid is typically  greenish and thick. Most of the times biliary fistula does not cause  serious clinical manifestations, although in few cases  associated clinical findings may include abdominal pain and distention  with impaired bowel function, delayed gastric emptying, fever, elevated  serum leukocyte count, and increased C-reactive protein. Bile leakage  may occur after pancreaticoduodenectomy or total pancreatectomy,  and represents the failure of healing/sealing of hepatico-jejunostomy.  Occasionally, biliary fistula may depend on a leakage from the cystic  duct remnant. The incidence of biliary fistula is 3-5%. Treatment  options include fasting and artificial nutrition to allow healing of the  anastomosis. It may be necessary to place a percutaneous transhepatic  biliary drainage if high-output fistulas do not resolve spontaneously.
Pulmonary complications
Patients undergoing pancreatic surgery are at increased risk for  pulmonary complications postoperatively. Major upper abdominal  surgery alters postoperative pulmonary function, and reduces the  efficiency of efforts to cough for as long as one week. These  mechanisms lead to a decrease in functional residual and vital capacity  for many days, and subsequently to atelectasis or pneumonia. Frail,  elderly patients or patients with comorbidities are at increased risk of  developing pneumonia. Postoperative pulmonary complications  increase hospital morbidity, and prolong hospital stay. Therefore,  postoperative chest physiotherapy was implemented. Respiratory exercises  during hospitalization has been shown to improve respiratory  performance as well as preventing postoperative pulmonary complications.

EXOCRINE PANCREATIC INSUFFICIENCY

Exocrine pancreatic insufficiency with maldigestion  is caused by a deficiency of pancreatic enzymes production due to  fibrotic replacement of normal pancreatic tissue or loss of pancreatic  parenchyma. This condition is major consequence of chronic pancreatitis,  but may also follow pancreatic resections. In pancreatic resections,  the development of exocrine insufficiency depends on the type and the  extension of resection, on the associated bowel resection, and on  individual factors.

Digestion is often impaired after pancreaticoduodenectomy,  and patients may experience steatorrhea and weight loss. This condition  is often transient, and depends more on bowel resection than on the  loss of pancreatic parenchyma. The duodenum, in fact, functions as an  intestinal pacemaker and activates pancreatic enzymes. Most patients  return to a normal bowel and pancreatic function within few months.  Long-term exocrine insufficiency may depend on anastomosis failure with  subsequent pancreatic duct obstruction and secondary chronic  pancreatitis. signs of exocrine insufficiency are not present until 85  to 90% of the pancreas is unable to secrete enzymes. After left pancreatectomy, exocrine isufficiency is uncommon.

Total pancreatectomy is  invariably associated with exocrine insufficiency and impairment of  gastrointestinal motility. However, these conditions tend to ameliorate  over time (with an appropriate replacement therapy) such that the  reported 1-year quality of life seems to be comparable to patients who  underwent pancreaticoduodenectomy.

Symptoms of exocrine pancreatic insufficiency  are mainly related to lipids and protein maldigestion, and include (in a  variable degree) malabsorption, diarrhea, steatorrhea, and weight loss.  Recurring abdominal pain  may be present. Breakdown of carbohydrates  can be partially taken over by amylase in the saliva and enzymes in the  small intestine; while breakdown of proteins may be partially taken over  by gastric peptidase and enteropeptidase. Deficiency of liposoluble  vitamins is usually present.
Quantification of exocrine pancreatic insufficiency requires  functional tests. Among them, determination of fecal elastase-1, fecal  chymotripsin, and stool fat content are the most widely available.

The mainstays of exocrine pancreatic  insufficiency treatment are a balanced low-fat diet, supplementation  with trace elements and vitamins, and enzyme replacement therapy.  A pancreatic enzyme preparation (pancreatine) contains lipases,  alpha-amylase, and proteases. The strenght of the preparation is defined  as the content of lipase per capsule (microspheres or  minimicrospheres), where 10.000 = 10.000 lipase units. Up to 40.000  lipase units per capsule are commercially available.
The capsules must be taken with meals or immediately thereafter.  Enzyme preparations are acid-resistant and become activated under basic  pH, in the small intestine. Nevertheless, proton-pump inhibitors may be  associated to maximize their activation, especially in the case of  gastric hyperacidity. Therapeutic success is primarily determined on a  clinical basis.

ENDOCRINE PANCREATIC INSUFFICIENCY

Some patients develop endocrine pancreatic insufficiency after  pancreatic resection, consisting in impaired carbohydrate metabolism up  to diabetes mellitus. Diabetes after  pancreatic resection depends on  loss of Langerhans islets and deficiency in the production of insulin.

After partial pancreatic resection, it is common to experience a  temporary impairment of carbohydrate metabolism, especially in those  patients who receive parenteral nutrition. This condition can be  resolved with an adequate diet and a mild antidiabetic therapy. If  diabetes develops, insulin is needed to control hyperglycemia and  prevent long-term complications. Insulin is given subcutaneously using  pre-filled pens. In some patients, diabetes may develop several years  after the resection, and depends on chronic obstructive pancreatitis of  the remnant.
 
The relationship between partial pancreatic resections and diabetes  mellitus is still unclear. Patients undergoing left pancreatectomy seem  to be at greater risk of developing some form of diabetes in the long  term, because the bulk of Langerhans islets is naturally located in the  pancreatic tail.

Total pancreatectomy results  in a complete loss of pancreatic endocrine function, with  full-manifestations of pancreoprival diabetes. The absence of both  insulin and glucagon (that oppose one another) increases the risk for  hyperglycemia and hypoglycemia. Significan glycemic fluctuations may  occur, with marked post-prandial hyperglycemia and sudden hypoglycemia  after insulin administration or during prolonged fasting. Therefore, it  is important to provide a diabetes treatment plan that includes frequent  blood sugar monitoring and flexible insulin therapy to help decrease  the risk of high and low blood sugar.
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