Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1310_Библиотеки_им_академика_М_И_Перельмана.pdf
420 W.P. Lancaster and K.A. Morgan
pancreatic neck is developed. The gastroduodenal artery is ligated, confirming
continued perfusion of the hepatic artery. If the gallbladder is present, it is removed.
The common bile duct is dissected circumferentially and is divided. The stomach
is divided proximal to the pylorus with a surgical stapler. Just distal to the ligament
of Treitz, the proximal jejunum is divided and the jejunal mesentery as well as the
ligament of Treitz are taken down with an energy device. The proximal jejunum
and the fourth portion of the duodenum are then rotated under the superior
mesenteric vessels.
The pancreatic neck is divided over the portal vein, and the pancreatic head is
rotated laterally and dissected from the portal vein. The periarterial vascular and
lymphatic tissue between the uncinate process and the superior mesenteric artery is
divided, and the head of pancreas and duodenum are removed from the abdomen
and immediately placed in cold balanced-electrolyte preservative solution.
On the back table, the pancreatic head specimen is immediately prepared by
flushing the gastroduodenal artery stump with cold preservative solution. The
duodenum is removed and the pancreatic duct is cannulated with a 5 French
pediatric feeding tube (Fig. 32.2a).
Next, attention is turned to removing the body and tail of the pancreas. The
splenic artery is dissected and tagged but not yet ligated near its origin, the superior
margin of the pancreatic body. Similarly, the splenic vein is tagged, taking care to
preserve the coronary vein. Once the pancreas is dissected free from the surrounding structures, the splenic vessels are ligated and the distal pancreas and
spleen are removed from the abdomen and placed in cold preservative solution.
On the back table, the spleen is removed sharply. The splenic vein is opened
along its length to exsanguinate the specimen, and the splenic artery is flushed with
cold preservation solution. The pancreatic duct is cannulated with a 5 French
pediatric feeding tube, which is sutured in place (Fig. 32.2b, c). The pancreatic
body and tail are packaged with the head, and the pancreas is then taken on ice to
the islet cell laboratory for processing.
A 5 French KMP catheter to be used for islet infusion is threaded into the portal
vein to the bifurcation via a tributary of the middle colic vein. The catheter is
sutured to the transverse mesocolon. Reconstruction is undertaken with a retrocolic
end-to-side choledochojejunostomy. Gastrointestinal continuity is restored with an
antecolic Roux-en-Y gastrojejunostomy. The abdomen is closed with interrupted
fascial sutures, allowing an opening for the KMP catheter to exit at the inferior
aspect of the incision. The fascial sutures where the catheter emerges are placed, but
not tied.
Islet Cell Preparation
The prepared pancreas is transferred to the cGMP cell processing facility. A modified Ricordi method is utilized for islet harvest [9]. Isle ts are released from the
exocrine and connective tissues of the gland via enzymatic and mechanical digestion. Collagenase (Liberase MTF, Roche, Indianapolis, IN USA) is infused
32 Total Pancreatectomy with Islet Autotransplantation 421
Fig. 32.2 a The head of the
pancreas is prepared on the
back table in cold
preservation solution
immediately upon extraction.
The gastroduodenal artery is
flushed to exsanguinate the
organ. b Similarly, the body
and tail of the pancreas are
prepared. The splenic vein is
opened and the splenic artery
is flushed. c The main
pancreatic duct of the
prepared left pancreas is
cannulated with a 5 French
pediatric feeding tube, to be
used in the cell processing lab
for infusion of digestive
protease
422 W.P. Lancaster and K.A. Morgan
intraductally and/or injected directly into the pancreas for distension. The solution is
perfused through a closed heated circuit to optimize enzymatic effect, and aliquots
are examined periodically to determine timing of optimal islet separation. The islets
are then separated by centrifugation. Islet yield, viability, function, and sterility are
assessed. The isolated islets are then resuspended in 5% albumin solution with
prophylactic antibiotic (cephazolin) and with heparin (70 U/kg body weight).
Islet Transplantation
The patient is admitted to the intensive care unit intubated and sedated following
surgery. Once islet preparation is complete, the patient is transported to the interventional radiology suite, where catheter placement at the portal venous bifurcation
is confirmed under fluoroscopy and the islets are infused by gravity through the
catheter. Portal venous pressures are measured before, during, and after transplantation, as the portal system is a noncompliant system, and volume infusion can
significantly raise portal venous pressure. Large increases in pressure and pressures
greater than 30 mmHg have been shown to correlate with an increased incidence of
portal vein thrombosis. Therefore, pressures greater than 25 mmHg prompts a delay
in the infusion for 5 to 15 min. If the pressure does not come down in that time, the
remaining islets can be infused into the peritoneal cavity. A completion portal
venogram is performed (Fig. 32.3). The catheter is removed after transplant, and the
venous branch clipped in the wound. The previously placed fascial sutures are tied
and the skin closed.
Other centers perform intraoperative islet infusion, keeping the patient under
anesthesia in the operating room during the islet harvest and autotransplanting the
islets into the portal vein under direct visualization.
Technical Pearls for Total Pancreatectomy with Islet Autotransplantation
• Perfusion of the pancreas should be maintained during surgery to minimize warm ischemic time by ligating the vascular supply only when the
organ is ready to be removed.
• Careful attention should be taken to preserve the left gastric (coronary)
vein to maintain gastric vascular outflow and to minimize the incidence of
postoperative delayed gastric emptying.
• A pylorus ablating procedure can be utilized to reduce the incidence of
postoperative delayed gastric emptying.
• A Roux-en-Y alimentary reconstruction may improve posto perative gastric emptying and reduce risk of marginal ulceration when utilizing the
pylorus ablating procedure with antrum intact.
32 Total Pancreatectomy with Islet Autotransplantation 423
Fig. 32.3 Portal venogram after completion of islet infusion. Catheter enters through a portal
venous tributary and the catheter tip is below the bifurcation
Postoperative Care
The patient is then transported back to the intensive care unit and extubated. Blood
glucose levels are checked every 30 min for 2 h and then hourly thereafter. An
insulin infusion is used to maintain blood glucose levels between 70–110 mg/dL.
This is discontinued on postoperative day 3 and transitioned to low-dose
long-acting insulin and sliding scale short-acting insulin, as needed. All patients
are maintained on some dose of long-acting insulin except those with significant
concerns for hypoglycemia, in order to rest the islets during engraftment.
A low-dose heparin infusion (250 U/h) is begun on the morning of postoperative
day 1 if the hemoglobin has been stable. This is continued for 3 days, and the
patient is transitioned to oral aspirin 81 mg.
A duplex ultrasound of the portal venous system is performed on the first
postoperative day and again prior to discharge, to evaluate for portal vein thrombosis, which can be other wise unrecognized and is well treated with therapeutic
anticoagulation.
424 W.P. Lancaster and K.A. Morgan
The islet preparation is sent for culture, and if gram stain or the final culture is
positive, the patient is given prophylactic antibiotics to cover the offending
organism for 3 days. The positive islet cultures do not seem to translate into
meaningful clinical infections [10].
Postoperative pain control is achieved with a combination of epidural anesthesia,
ketamine infusion, and intravenous narcotics. Non-narcotic adjuncts are maximally
utilized. The ketamine infusion is tapered in 24 h, and the epidural is removed on
the third day after surgery. Intravenous narcotics are slowly tapered with the
addition of oral narcotics, as the patient is able to tolerate PO intake.
The nasogastric tube is removed on the first postoperative day and full liquids
are begun, including oral nutritional supplements. Patients are advanced to full
diabetic diet on the second day after surgery, as tolerated. Oral pancreatic enzymes
are administered with diet. Early ambulation is supported [11].
Potential Complications
Complications associated with TPIAT are those seen with other major pancreatic
surgeries, with the notable exception of postoperative pancreatic fistula.
Complications specific to islet autotransplantation include hemorrhage (from the
anticoagulation given at infusion), portal vein thrombosis, and systemic inflammatory response. Acinar mantle cells surround the islets to keep them stable and
intact. These cells, however, are a source of tissue thromboplastin, which is
thrombogenic. Anticoagulation is administered with the islets during infusion to
prevent portal vein thrombosis. Tissue thromboplastin as well as other factors
associated with exocrine pancreatic tissue can incite systemic inflammatory
response.
Long-Term Outcomes
After TPIAT, patients can expect pain relief and improvements in quality of life. On
the Short Form Quality of Life questionnaire, significant improvements in all
domains as early as 6 months postoperatively have been demonstrated by multiple
centers. Narcotic weaning may be challenging, depending on patient history, support system, coping skills, and physician management. Thirty percent of patients
will be insulin-free long-term (25% of adults, 55% of children) and 90% will have
some demonstrable function of autotransplanted islets (serum c-peptide levels >
0.6 ng/ml) long-term [13] 1214]. Exocrine pancreatic insufficiency requires lifelong
oral pancreatic enzyme supplementation and monitoring of nutritional health [ 15 ].
32 Total Pancreatectomy with Islet Autotransplantation 425
References
1. Bellin MD, Gelrud A, Arreaza-Rubin G, Dunn TB, Humar A, Morgan KA, et al. Total
pancreatectomy with islet autotransplantation: summary of an NIDDK workshop. Ann Surg.
2015;261(1):21–9.
2. Chinnakotla S, Radosevich DM, Dunn TB, Bellin MD, Freeman ML, Schwarzenberg SJ,
et al. Long-term outcomes of total pancreatectomy and islet autotransplantation for
hereditary/genetic pancreatitis. J Am Coll Surg. 2014;218(4):530–43.
3. Morgan KA, Theruvath T, Owczarski S, Adams DB. Total pancreatectomy with islet
autotransplantation for chronic pancreatitis: do patients with prior surgery have different
outcomes? Am Surg. 2012;78(8):893–6.
4. Dunderdale J, McAuliffe JC, McNeal SF, Bryant SM, Yancey BD, Flowers G, Christein JD.
Should pancreatectomy with islet cell autotransplantation in chronic alcoholic pancreatitis be
abandoned? J Am Coll Surg. 2013;216(4):591– 6.
5. Cote GA, Yadav D, Slivka A, Hawes RH, Anderson MA, Burton FR, et al. Alcohol and
smoking as risk factors in an epidemiology study of patients with chronic pancreatitis. Clin
Gastroenterol Hepatol. 2001;9(3):266–73.
6. Whitcomb DC, Gorry MC, Preston RA, Furey W, Sossenheimer MJ, Ulrich CD, et al.
Hereditary pancreatitis is caused by a mutation in the cationic trypsinogen gene. Nat Genet.
1996;14(2):141–5.
7. Dorlon M, Owczarski SM, Wang H, Adams D, Morgan K. Increase in postoperative insulin
requirements does not lead to decreased quality of life after total pancreatectomy with islet
cell autotransplantation for chronic pancreatitis. Am Surg. 2013;79(7):676–80.
8. Morgan KA, Borckardt J, Balliet W, Owczarski SM, Adams DB. How are chronic pancreatitis
patient selected for total pancreatectomy with islet autotransplantation? Are there psychometric predictors? J Am Coll Surg. 2015;220(4):693–8.
9. Ricordi C, Lacy PE, Finke EH, Olack BJ, Scharp DW. Automated method for isolation of
human pancreatic islets. Diabetes. 1988;37(4):413–20.
10. Johnson CN, Morgan KA, Owczarski SM, Wang H, Fried J, Adams DB. Autotransplantation
of culture positive islet product: is dirty always bad? HPB (Oxford). 2014;16(7):665–9.
11. Morgan KA, Lancaster WP, Walters ML, Owczarski SM, Clark CA, McSwain JR, et al.
Enhanced recovery after surgery protocols are valuable in pancreas surgery patients. J Am
Coll Surg. 2016;222(4):658–64.
12. Morgan K, Owczarski SM, Borckardt J, Madan A, Nishimura M, Adams DB. Pain control
and quality of life after pancreatectomy with islet autotransplantation for chronic pancreatitis.
J Gastrointest Surg. 2012;16(1):129–33.
13. Sutherland DE, Radosevich DM, Bellin MD, Hering BJ, Beilman GJ, Dunn TB, et al. Total
pancreatectomy and islet autotransplantation for chronic pancreatitis. J Am Coll Surg.
2012;214(4):409–24.
14. Chinnakotla S, Beilman GJ, Dunn TB, Bellin MD, Freeman ML, Radosevich DM, et al.
Factors predicting outcomes after a total pancreatectomy and islet autotransplantation lessons
learned from over 500 cases. Ann Surg. 2015;262(4):610–22.
15. Crosby J, Bellin MD, Radosevich DM, Chinnakotla S, Dunn TB, Pruett TL, et al.
Gastrointestinal symptoms before and after total pancreatectomy with islet autotransplantation: the role of pancreatic enzyme dosing and adherence. Pancreas. 2015;44(3):453 – 8.
Necrotizing Pancreatitis: Best Approaches
Attila Nakeeb and Nicholas J. Zyromski
Introduction
In the United States approximately 290,000 patients develop acute pancreatitis
annually. More than 80% of cases of acute pancreatitis are due to either alcohol
consumption or gallstone disease. More uncommon causes include metabolic disorders, trauma, tumors, and iatrogenic injuries (ERCP, surgery). The severity of
acute pancreatitis ranges from edema to necrosis of the gland. The edematous form
of the disease (mild acute pancreatitis) occurs in about 80–85% of patients and is
self-limited, with recovery in a few days. In the 15–20% of patients wi th the most
severe form of pancreatitis, hospitalization is prolonged, and commonly associated
with the systemic in flammatory response syndrome (SIRS), multi-organ failure, and
infection of the pancreatic necrosis. In these patients, mortality can be as high as
20% [1, 2].
33
Case Presentation
A 68-year-old-male with a history of coronary artery disease, atrial fibrillation, and
diabetes mellitus, is transferred to a tertiary referral center 2 weeks into a course of
severe necrotizing pancreatitis due to hypertriglyceridemia. On presentation, the
A. Nakeeb (&) N.J. Zyromski
Indiana University School of Medicine, 545 Barnhill Drive, Emerson Hall 539,
Indianapolis, IN 46202, USA
e-mail: anakeeb@iupui.edu
N.J. Zyromski
e-mail: nzyromsk@iupui.edu
© Springer International Publishing AG 2017
T.M. Pawlik et al. (eds.), Case-Based Lessons in the Management of Complex
Hepato-Pancreato-Biliary Surgery, DOI 10.1007/978-3-319-50868-9_33
427
428 A. Nakeeb and N.J. Zyromski
Fig. 33.1 IV contrast-enhanced CT scan showing pancreatic and peripancreatic necrosis and
small gas bubbles, suggesting infected necrosis
Fig. 33.2 CT scan showing percutaneous drain placed in a necrotic collection
patient was febrile to 39.5 °C and required norepinephrine to maintain a systolic
blood pressure > 90 mmHg. He required mechanical ventilation for hypoxemia and
required continuous veno-venous hemodialysis for an acute kidney injury.
Contrast-enhanced computed tomography (CT) scan (Fig. 33.1) revealed necrotizing pancreatitis with evidence of infected pancreatic and peripancreatic necrosis
33 Necrotizing Pancreatitis: Best Approaches 429
Fig. 33.3 Four-week post video-assisted retroperitoneal debridement CT scan demonstrating near
complete resolution of the peripancreatic necrosis
in the lesser sac and tracking into the left pericolic gutter. He was started on
broad-spectrum antibiotics and taken to interventional radiology for placement of a
percutaneous drain into the infected fluid collection (Fig. 33.2). After percutaneous
drainage his clinic course stabilized, and at four weeks he was taken to the operating room for a video-assisted retroperitoneal pancreatic debridemen t (VARD).
Postoperatively he was able to be extubated, and his renal function recovered.
Follow-up CT 1-month post debridement showed near complete resolution of his
peripancreatic and pancreatic necrosis (Fig. 33.3).
Pathophysiology and Determination of Severity
Acute pancreatitis is a consequence of the intra-acinar cell cleavage of trypsinogen
to trypsin, with subsequent activation of other enzym es. The local inflammatory
response in the pancreas is associated with the liberation of oxygen-derived free
radicals and cytokines, including interleukin (IL)-1, IL-6, IL-8, tumor necrosis
factor alpha (TNFa), and platelet-activating factor (PAF) [3]; these mediators play
an important role in the transformation of a local inflammatory response to systemic
illness. The revised Atlanta classification of acute pancreatitis [4] stratifies patients
with acute pancreatitis into mild, moderately severe, or severe categories based on
the presence of organ failure and the presence of local or systemic complications.
Organ failure is assessed by the modified Marshall scoring system (Table 33.1).
Organ failure is defined by a score of two or more for the respiratory, cardiovascular, or renal systems. Local complications include acute peripancreatic fluid
collections, pancreatic pseudocysts, acute necrotic collections (sterile or infected),
430 A. Nakeeb and N.J. Zyromski
Table 33.1 Modified Marshall scoring system for organ dysfunction
Organ system Score
Respiratory (Pa0
Renal (serum Cr, mg/dl) <1.4 1.4–1.8 1.9–3.6 3.6–4.9 >4.9
Cardiovascular (systolic BP,
mm Hg)
a
A score of 2 or greater defines organ failure
/FiO2) >400 301–400 201–300 101–200 <101
2
a
01 2 3 4
>90 <90
fluid
responsive
<90
not fluid
responsive
<90
pH < 7.3
<90
pH < 7.2
and walled of pancreatic necrosis (sterile or infected). Patients with mild pancreatitis have no evidence of organ failure or local or systemic complications.
Moderately severe acute pancreatitis is defined by transient organ failure (resolves
within 48 h) and/or local or systemic complications without persistent organ failure.
Severe acute pancreatitis is characterized by persistent organ failure of one or
multiple systems.
Medical Therapy
Initial therapy for patients with pancreatitis is mostly supportive. Severe acute
pancreatitis is divided into two clinical phases; an early vasoactive and a late septic
phase. The vasoactive phase typically occurs during the first 2 weeks and is
dominated by the consequences of SIRS. Severe pancreatitis is associated with a
marked increase in microvascular permeability, leading to large volume losses of
intravascular fluid into the tissues, thereby decreasing perfusion of the lungs, kidneys, and other organs. The single most important elem ent in preventing multiple
organ failure is vigorous fluid resuscita tion with electrolyte solutions in order to
optimize cardiac output and to maintain hemodynamic stability. The management
of the first phase of severe pancreatitis is summarized here:
Management of the First Phase of Severe Pancreatitis
• Fluid resuscitation
• Respiratory support
• Cardiovascular support
• Relief of pain
• Limitation of systemic complications
• Treatment of metabolic complications
• Nutritional support
• Prevention of infection