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Introduction :
Carcinoma of the pancreas is a highly malignant tumor with poor
prognosis (The overall 5-year survival rate for this disease is
less than 5%). It represents 95% of all malignant pancreatic tumors.
60% are round in the head of the pancreas, 20 per cent in the
body or rail of the pancreas and 20 pet cent involve the whole
pancreas. About 80% of tumors in the pancreas are focal. It primarily
occurs in the sixth to eighth decades of life with a male preponderance.
The risk factors include alcohol abuse, diabetes, smoking , asbestos
exposure, hereditary pancreatitis and chronic calcific pancreatitis.
Histologically 95 pet cent of pancreatic carcinomes are adenocarcinoma,
which usually originale from ductal elements.
Pathophysiology:
Pancreatic cancers can arise from both the exocrine and endocrine
portions of the pancreas. Of pancreatic tumors, 95% develop from
the exocrine portion of the pancreas, including the ductal epithelium,
acinar cells, connective tissue, and lymphatic tissue.
Typically, pancreatic cancer first metastasizes to regional lymph
nodes, then to the liver, and less commonly, to the lungs. It
can also directly invade surrounding visceral organs such as the
duodenum, stomach, and colon.
Clinical :
weight loss, abdominal pain, back pain, anorexia, nausea and vomiting,
generalized malaise and weakness.
Ultrasound :
The detection rate by any imaging procedure depends on an adequately
visualized gland. The tumors in the head present earlier than
the others, usually because they cause obstruction to the biliary
tract. Common bile duct dilatation occurs in 80 to 90 pet cent
of pancreatic head carcinomes, with small carcinomes common bile
duct dilatation may be the only ultrasound abnormality.
The ultrasonic findings include a focal mass which is generally
less echogenic than the normal gland. Pancreatic carcinoma is
often well defined with irregular margins. Its echogenicity varies
depending on the size and presence of necrosis and/or local bleeding.
The most important is a localized change in the echogenicity of
the pancreas, usually focal and hypoechoic. 95% were hyperechoic
(similar to this case). In addition, the borders of the mass are
irregular, and the mass is usually quite distinct from the rest
of the gland. Early small tumors are homogeneous and hypoechoic.
Larger tumors (>5cm in size) with hemorrhagic or necrotic changes
are nonhomogeneous and vary in echogenicity. The rest of the pancreas
may be normal or abnormal depending on the associated pancreatitis
due to ductal obstruction. Thickening of tissues around the coeliac
axis or mesenteric vessels may be due to invasion of the lymphatics.
The pancreatic duct may also be dilated. Obstruction of the common
bile duct can be produced by the direct effect of the mass in
the pancreatic head or adenopathy. In some cases, ductal dilatation
is the only sign of carcinoma.
Other associated findings in carcinoma include dilated pancreatic
duct (18%), dilated central and peripheral bile ducts, nodal metastasis,
liver metastasis, compression or tumor invasion involving portal
vein or its major tributaries, mesenteric vessel, inferior vena
cava, and splenic vein displacement; and ascites. Abrupt obstruction
with acute dilation of pancreatic duct proximal to obstruction
is strongly suggestive of carcinoma. Vascular displacement is
more common with tumors in the body and tail of pancreas.
Lymphatic spread is to the celiac, superior mesenteric, paracaval,
retrocaval and porta hepatis nodes. Vascular invasion is to the
liver, lungs and peritoneal cavity. Venons thromboses may occur
especially with the body or rail tumours. Less frcquently direct
invasion of duodenum, stomach, colon, gallbladder, adrenal gland
and kidney may occur.
Endoscopic ultrasonography (EUS):
EUS obviates the physical limitations of TUS by placing a high-frequency
ultrasonographic transducer on an endoscope, which is then positioned
in the stomach or duodenum endoscopically to help visualize the
head, body, and tail of the pancreas. In numerous series, EUS
has detection rates of 99-100% for all pancreatic carcinomas,
including those smaller than 3 cm. EUS is as accurate as other
methods for assessing the etiology of obstructive jaundice. An
additional significant diagnostic advantage is EUS-guided fine-needle
aspiration, which allows for the simultaneous cytologic confirmation
of pancreatic carcinoma at the time of EUS diagnosis. EUS appears
to be equivalent to dual-phase spiral CT scanning for assessing
tumor resectability potential.
Fine-needle percutaneous biopsy of abdominal mass lesions is a
safe and effective other method to obtain tissue samples for cytologic
and histologic analysis.
Differential :
The differential diagnosis of pancreatic masses is difficult because
chronic pancreatitis (particularly if the pathological changes
are focal) and pancreatic cancer show similar clinical and imaging
patterns, and the possibility of metastases, lymphoma, leukemia,
and myeloma, should be considered.
The presence of calcification or intraductal calculi makes chronic
partcreatitis more likely but does not exclude a carcinome.
Masses adjacent to the pancreas may be mistaken for pancreatic
masses: retroperitoneal varices, retroperitoneal masses, lymphatic
masses or nodes, renal tumours, arterial aneur-ysms. Marked dilatation
of the pancreatic duct alone does not necessarily indicate malignant
disease. Severe dilatation can result from malignant obstruction
of the pancreatic duct or chronic pancreatitis. Idiopathic fibrosis
within the pancreatic head can also cause marked biliary and pancreatic
ductal dilatation. Dilatation can also be seen with carcinoma
of the ampulla, cholangiocarcinoma near the ampulla, Crohn's disease
of the duodenum, and stenosis of the ampulla.
Treatment :
The only therapy that has definitively been shown to increase
the survival of patients with pancreatic cancer is surgical resection
: pancreaticoduodenectomy (Whipple operation). Some institutions
use neoadjuvant chemotherapy and radiation therapy to try to improve
the resectability potential of locally advanced cancers.
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