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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_734_Библиотеки_им_академика_М_И_Перельмана.pdf
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J. A. Baril et al.
showing arterial complications of AP most often occur in the setting of acute on
chronic pancreatitis (92%) and less commonly during the index episode of pancreatitis (8%) [6].
The pathophysiology of pseudoaneurysm and hemorrhage from AP is thought to
be from the compartmentalization of pancreatic uid within the disrupted pancreatic capsule in the retroperitoneum. The proteolytic enzyme release in proximity of
the visceral arteries combined with the systemic inammatory environment of AP
effectively serves as the perfect storm for arterial disruption. Disruptions in walled
off necrosis or pseudocysts may also result in arterial bleeding [4]. Pseudoaneurysms
are most common in the splenic artery (35–50%), followed by the gastroduodenal
(20–30%) and pancreaticoduodenal (20–25%) arteries [4, 7]. Less common are the
mesenteric, colic, and hepatic arteries, yet all are recognized sources [4, 8].
The most common presenting symptom of arterial pseudoaneurysm in AP is
abdominal pain (62%) followed by gastrointestinal hemorrhage (26–29%) consistent with “hemosuccus pancreaticus.” [6, 9] Abdominal or back pain and hypovolemia are presenting symptoms of AP, which make vascular complications of AP
difcult to diagnose on history and physical alone. A high index of suspicion should
be had with any patient presenting with acute on chronic pancreatitis and evidence
of hypovolemia, anemia, or sudden onset pain. In patients with drains previously
placed for the management of pancreatic uid collections, a heraldic bleed via the
drain in many cases is the initial sign of a pseudoaneurysm. In one series of 28
patients, bloody drain output was a common presenting symptom (32%) followed
by asymptomatic patients whose pseudoaneurysm was incidentally found on CT
scan (21%) [5].
Computed tomography (CT) is the initial diagnostic method of choice for detecting visceral artery pseudoaneurysm or acute hemorrhage given its availability, cost,
and speed [10]. Compared with conventional angiography, cross-sectional CT angiography (CTA) detected bleeding in the setting of pancreatitis with a sensitivity and
specicity of 94.7% and 90%, respectively [11] (Fig.5.1). The practitioner’s experi-
ence, knowledge of the patient, and index of suspicion should not be discounted
when a CTA does not show an overt pseudoaneurysm; a visceral arteriogram should
be performed if the patient’s clinical picture matches that of hemorrhagic shock
with an unremarkable CTA.
Treatment for visceral artery pseudoaneurysm or hemorrhage in the hemodynamically stable patient with AP is angiography with embolization. There is a
breadth of literature supporting angiographic intervention with high rate of success
to stop hemorrhage. Initial interventional radiology (IR) embolization is successful
in 93–100% of published cases [5–7, 13]. However, rebleeding can occur in
3.5–12.5% of patients after successful embolization [1, 5–7, 14]. These data suggest
that embolization is particularly successful with low associated morbidity. An alternative IR approach is percutaneous stenting of the celiac or common hepatic artery
to preserve hepatic arterial blood supply while achieving proximal control of
hemorrhage.
Percutaneous thrombin injection is an important adjunct treatment for pseudoaneurysm. There are case reports of thrombin injection to successfully embolize
5 Acute Pancreatitis: Complications
Fig. 5.1 CTA showing a
pancreatic pseudocyst
eroding the splenic
artery [12]
89
pseudoaneurysms. However, this subset likely has a selection bias for successful
cases. Of the 23 patients published with percutaneous thrombin injection, four
patients had repeat bleeding as the thrombin is thought to be precise and without
collateral effects, yet is an absorbable, biodegradable embolization agent. Of those
four, two underwent repeat thrombin injection and one underwent coil angioembolization [4].
Surgical intervention for arterial pseudoaneurysm or hemorrhage is rare due to
poor outcomes when operating on patients in the setting of a massive systemic
inammatory condition. Surgery is indicated in the unstable patient after failed
angioembolization. The most common surgery reported for refractory hemorrhage
is distal pancreatectomy with or without splenectomy [15]. Prior to the advancement of IR techniques, surgery was more common for management of arterial complications with one-third to one-half of patients with bleeding pseudoaneurysm
undergoing surgery. Appropriately, the rate of surgical intervention has fallen to
11% in more recent studies with improved overall survival [1, 5, 15].
Venous Thrombosis
Venous thrombosis is a more common complication of acute pancreatitis when
compared with arterial bleeding. Among a meta-analysis of over 10,000 patients
with acute and chronic pancreatitis, splanchnic venous thrombosis was found in
16.6% of patients with AP and 11.6% of patients with CP [16]. Another metaanalysis found rates of splenic vein thrombosis of 22.6% and 12.4% in AP and CP
[17]. Venous thrombosis in AP is related to both local and systemic inammation
generating a prothrombotic state, and venous ow disruptions as a result of external
compression during AP [18]. Often there is a clear association between the vessel
with venous thrombosis and areas of necrosis and collections resulting from AP
[19]. Thrombosis is most common in the splenic vein (11.2%), followed by the
portal vein (6%) and mesenteric veins (2.7%) [16].
90
J. A. Baril et al.
Portal venous thrombosis (PVT) is more easily diagnosed via transabdominal
ultrasonography (US) (Fig.5.2). Sensitivity and specicity for PVT is between 60
and 100% via US.Endoscopic ultrasound (EUS) has comparable sensitivity and
specicity, 81 and 93%, but is more invasive and does not visualize the intrahepatic
portal venous system with as much detail [20]. For venous thromboses outside the
portal venous system, CT or magnetic resonance angiography are the diagnostic
modalities of choice with sensitivities reaching 95%, improved from 71% in the
early 2000s [8, 20] (Fig.5.3).
Portal venous thrombosis is treated with either systemic anticoagulation or portal
venous stenting. Image-guided portal vein stenting is currently used to treat malignant stenosis [21, 22]. Stenting is sometimes performed before or after surgery for
pancreatic adenocarcinoma in cases of portal vein stenosis [23–25]. There is less
published data on the use of portal vein stenting for PV thrombosis or compression
Fig. 5.2 US imaging
showing thrombosed left
portal vein (black
arrow) [20]
Fig. 5.3 Coronal oblique
venous phase CT of a
patient with AP with
thrombosed splenic vein
(white arrows) and a
segmental branch of right
portal vein (single white
arrow) with hepatic artery
buffer response in the form
of differential
hyperenhancement of the
affected liver segment
(black arrows) [20]
5 Acute Pancreatitis: Complications
91
in AP; many cases focus on retroperitoneal decompression via percutaneous drains
to alleviate pressure on the portal venous circulation.
Splenic vein thrombosis can usually be safely watched and treated with systemic
anticoagulation. Complications of splenic vein thrombosis can include sinistral portal hypertension and esophageal varices. Gastroesophageal varices occur in up to
20% of patients with splenic vein thrombosis; however, bleeding from these is rare
(12.3%) when compared to varices from those with hepatic cirrhosis [17]. In patients
who have sinistral portal hypertension or asymptomatic gastric or esophageal varices secondary to splenic vein thrombosis as a result of acute on chronic pancreatitis,
splenectomy is not routinely performed [8]. However, in such patients who are
symptomatic or undergoing a planned pancreatic surgery, splenectomy can be performed during the same operation and does not lead to increased morbidity or mortality [26, 27]. Similarly, mesenteric vein thrombosis is usually treated with systemic
anticoagulation. Surgery is reserved for cases of mesenteric ischemia with overt
peritonitis which require emergent laparotomy and bowel resection [28].
Intra-Abdominal Hypertension
Intra-abdominal hypertension (IAH) is a unique complication of pancreatitis which
can range in severity from asymptomatic to life-threatening. IAH, dened as sustained intra-abdominal pressures greater than 12 mm hg, may occur in severe
AP.The incidence of IAH in severe AP ranges from 50% to 80% [29–33]. A combination of retroperitoneal inammation, aggressive uid resuscitation, visceral
edema, ileus, and peripancreatic uid collections result in IAH in AP [34].
Management of IAH includes correcting a positive uid balance as able, evacuate intra-luminal gastrointestinal contents, evacuate extraluminal abdominal uid,
and improving abdominal wall compliance. Each management pillar has a range of
interventions from nasogastric decompression and goal directed uid management,
to drainage of intra-abdominal collections and dialysis to achieve negative uid balance [35]. Early recognition is key in preventing progression to abdominal compartment syndrome (ACS) and reducing morbidity and mortality.
ACS is dened as sustained IAH >20mmHg with new organ dysfunction as a
result [36]. Acute kidney injury (AKI) is the most common organ dysfunction seen
in ACS and can rapidly progress to anuria requiring renal replacement therapy [35,
37]. Pulmonary complications include the inability to ventilate due to elevated IAH
resulting in prohibitively high airway pressures. Conversely, increased PEEP is
unlikely to contribute more than 1–2mmHg to the intra-abdominal pressure [38].
Other signs of organ dysfunction include hemodynamic instability and metabolic
derangements which can occur in severe AP without ACS.Organ dysfunction in
severe AP is difcult to attribute to AP or ACS.Nonetheless, IAH and ACS should
be measured early and treated aggressively with medical management and, when
needed, surgical intervention.
92
J. A. Baril et al.
Surgical decompression is necessary in patients with continued ACS despite
maximal non-surgical management to decrease intra-abdominal pressures. Mortality
can reach 50% in patients with AP and ACS [39]. Among patients with severe AP,
the incidence of ACS is not well documented. However, among patients admitted to
the intensive care unit with severe AP, incidence of ACS has been reported between
27 and 38% of patients [32, 39]. In a single-center study of 2345 episodes of AP,
226 required ICU admission of which 26 (11.5%) required surgical decompression
for ACS [40]. Early laparotomy was associated with improved outcomes compared
to patients with laparotomy >72h after admission.
Thoracic Complications
Acute pancreatitis can have effects on the respiratory system ranging from asymptomatic pleural effusions to acute respiratory distress syndrome (ARDS). The presence of pleural effusion is a poor prognostic indicator in acute pancreatitis and is a
criterion on the Bedside Index for Severity in Acute Pancreatitis (BISAP) score
[41]. Pleural effusion is present in 4–17% of patients with AP with the majority
being sympathetic in nature and requires thoracentesis only when symptomatic
[42]. Rarely, in approximately 0.6% of AP, a pancreaticopleural stula forms. These
are most common in alcohol-induced pancreatitis and in pancreatic duct disruption.
Treatment of duct disruption with endoscopic stenting can resolve the stula, yet
there are no clear treatment guidelines due to the paucity of the event [43]. Like with
pleural effusion, addressing the pancreatitis is the primary treatment to mitigate
additional pulmonary injury.
As a more severe sequela, ARDS occurs in severe AP as a result of inammatory
cytokines, endothelial and epithelial damage to pneumocytes and pulmonary vasculature, as well as interstitial neutrophil inltration [44]. Dened as PaO2/FiO2 ratio
of <200, ARDS has a high mortality between 30 and 60% and is the cause of early
death in most elderly patients who die of severe AP [44]. Pancreatitis was the cause
of 3.4% of ARDS cases from over 900,000 ARDS cases analyzed in the US between
2006 and 2014 [45] but has also been reported in 12.8% of ARDS admissions to
ICUs in Beijing [46]. Like pleural effusions, treatment of ARDS should focus on
supportive care and addressing the underlying pancreatitis. Effective measures
include lung protective ventilation with lower tidal volumes, judicious use of uids,
reducing ventilator dyssynchrony, and prone positioning [47, 48]. High PEEP strategies (25–35cmH
patients [49]. The use of steroids has not proven effective in reducing mortality in
ARDS. [50]
Pancreatic pseudocyst can present in the mediastinum through the esophageal or
aortic hiatus. Most frequently, this is due to pancreatic duct disruption (PDD) and
presents with dysphagia or chest pain [43]. They are diagnosed by CT scan but can
also be seen on upper EUS.Stenting of the pancreatic duct can often resolve the
pseudocyst. However, drainage via EUS with transesophageal or transgastric
O) to increase lung recruitment increases mortality in ARDS
2
5 Acute Pancreatitis: Complications
93
methods are sometimes needed if duct stenting is not successful as mediastinal
pseudocyst rarely spontaneously resolve.
Gastrointestinal Complications
Gastric outlet obstruction (GOO) is an uncommon complication of AP with an incidence of approximately 5%. In early pancreatitis, within four weeks of disease
onset, GOO is most often caused by compression from pancreatic necrosis or pseudocyst and less commonly from edema of the stomach and/or duodenum [51].
Treatment previously was upfront surgery with gastrojejunostomy, but now minimally invasive techniques with gastric decompression, jejunal feeding, and drainage
of uid collections are successful in most cases [52, 53].
Colonic complications are rare and include stula, necrosis, and stricture [54].
Bowel perforation secondary to necrosis warrants a colectomy with wide drainage
and possible stoma creation. The colonic mesentery is at grave risk during any
urgent acute pancreatitis-associated surgery. Colonic stricture often presents as a
late complication following the episode of pancreatitis due to acute or chronic ischemia to segments of the colon. Among patients with colonic stricture, surgical
resection may be performed successfully with a primary anastomosis in an elective
setting after resolution of the acute pancreatitis episode [55–57].
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J. A. Baril et al.
Part III
Chronic Pancreatitis