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Pancreatitis
22
FrancescoBasile, AntonioBiondi, GuidoBasile,
andMarcelloDonati
22.1 Introduction
The pancreatic parenchyma as well known is prone to a progressive atrophy during
the time, being reduced to less than its original weight overcoming 80years of age
[1]. Also a progressive increase of Wirsung’s duct over 8°years is to be observed [2].
So that in aged pancreas, a Wirsung’s width till 1cm can be occasionally observed
without any evidence of obstruction; also calcication of splenic and mesenteric
vessels can be registered without pathologic signicance; even a progressive perilobular brosis is very often present in the elderly [3]. Not only the exocrine function
but even the endocrine one was found to be progressively deteriorated with age;
clinical signicance of both remains not clear [4].
Anyway pancreatitis in the elderly represents a well-dened spectrum of diseases that we could rst divide, relating to clinical evolution in acute pancreatitis
and chronic pancreatitis. Those diseases represent completely different clinical conditions with different implications, early and long-term complications, and therefore must be separately considered.
If acute pancreatitis in the elderly can present a dramatic clinical evolution, with
complications, requiring sometimes a multidisciplinary approach and sometimes
also intensive care support, chronic pancreatitis shows usually an indolent clinical
evolution starting often when patients are young and showing “effects” in the
elderly.
F. Basile (*) • A. Biondi • M. Donati
Department of Surgery and Medical-Surgical Specialties, Surgical Clinic, Vittorio-Emanuele
University Hospital of Catania, Catania, Italy
e-mail: fbasile@unict.it
G. Basile
Department of Surgery and Medical-Surgical Specialties, Emergency Abdominal Surgery
Unit, University Hospital of Catania, University of Catania, Catania, Italy
© Springer International Publishing AG, part of Springer Nature 2018
A. Crucitti (ed.), Surgical Management of Elderly Patients,
https://doi.org/10.1007/978-3-319-60861-7_22
327
328
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F. Basile et al.
22.2 Acute Pancreatitis
22.2.1 Etiology
The main cause of acute pancreatitis also in the elderly is the cholelithiasis amounting for round 60% of cases. In 20–25% of cases, a history of alcoholic abuses can
be found in the anamnestic data of those patients [5] even in combination white
smoke [6]. While other causes like medicament adverse reaction, neoplastic disease, trauma, and infections account for 5–10% of acute pancreatitis, it remains
unclear the cause of about 10–15% that are dened idiopathic [7]. It’s nowadays
generally accepted that a big percentage of patients (round 70%) with an idiopathic
acute pancreatitis is affected by microlithiasis in duodenal juice, and this aspect
shows obviously also therapeutic implications [8]. The most important traumatic
cause of traumatic pancreatitis seems to be surgical or endoscopic procedures in the
elderly, instead of accident or violent trauma. Of course endoscopic procedures
amount for the most important cause of pancreatitis even if most of them are not
gaining clinical signicance [9]. Diuretics, steroids, and tetracycline are those
medicaments able to induce an acute pancreatitis generally; in the elderly the use of
many different drugs for coexisting disease seems to be a rising problem for causing
acute pancreatitis [10]. Etodolac, simvastatin, and isoniazid are medicaments more
recently associated with acute pancreatitis induction; diffusion of this side effect in
the elderly population is unknown.
A double binding exists between acute pancreatitis and pancreatic cancer, while
round 10% of patients affected by pancreatic cancer are showing an acute pancreatitis, and on the other hand, in patients affected by pseudocyst as a consequence of
acute pancreatitis rarely, a coexisting pancreatic cancer is to be observed (over
60years round 8%).
There are some other minor causes of pancreatitis that should be mentioned;
infectious disease like tuberculosis and fungal infections can be rarely responsible
in the elderly of pancreatitis so like hypecalcemia, hypertriglyceridemia, and peptic
ulcer.
22.3 Clinical Aspects, Diagnosis, andComplications
In the elderly like for young patients, the main symptom related to an acute pancreatitis is the epigastric pain, with typical belt-like irradiation. In a cholelithiasisinduced pancreatitis, also a right upper quadrant pain can be referred. A discrepancy
between the referred high grade of spontaneous abdominal pain and the clinical
objectivity of the abdomen are typical clinical aspects of pancreatitis. A rare clinical
sign of severe pancreatitis is the Cullen’s sign (periumbilical ecchymosis Fig.22.1).
In the elderly the clinical presentation can be attenuated, also because pancreatitis
can often appear in patients in postoperatory recovery, under sedation or being intubated. Therefore the clinical course can be not so evident in a consistent proportion
of patients (till 40%). Even laboratory tests considering serum amylase and serum
22 Pancreatitis
Fig. 22.1 Cullen sign:
periumbilical ecchymosis
due to retroperitoneal
hemorrhagic lateral
abdominal extension till
subcutaneous area of a
necrotich hemorrhagic
acute pancreatitis
329
Fig. 22.2 Giant pancreatic pseudocyst as a complication of massive acute pancreatitis; 3D recon-
struction (a). On MRI it shows as a transverse diameter of 17cm (b)
lipase, and a threshold of 50ng/mL for urinary trypsinogen-2, can fail to demonstrate an acute pancreatitis in one every ten patients, delaying correct diagnosis and
treatment [11]. Interestingly the mortality of pancreatitis is similar in young as in
the elderly patients but in the young patients is more due to local complication like
necrosis (Fig.22.3) or pseudocysts (Fig.22.2), while in the elderly, septic and systemic complications are mainly responsible of death. In fact while in young patients,
abscess, necrotizing pancreatitis, and pseudocyst are more frequent complications;
in the elderly pulmonary or renal failure and gastrointestinal bleeding and septic
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Fig. 22.3 Pancreatic
head necrosis:
intraoperative nding
during a necrosectomy
F. Basile et al.
shock are the most important and frequent complications. The mortality rate in the
elderly can gain 20%, while in the young remains round 5–6%. This correlates well
with the fact that age is intended to be a worse prognosis factor already in Ranson’s
criteria.
Diagnostic and evolution of acute pancreatitis out of labor tests is based on
US and CT scan, even MRI is very useful to dene retroperitoneal extension of
disease, better identify choledocolitiasis or other coexistent diseases, and monitor complications’ evolution. Ultrasound is usually intended to be the rst-line
imaging modality in the most part of rst aid centers in order to conrm the
diagnosis and/or to rule out other kind of acute abdomen. Unfortunately US
examination considering the acute clinical settings shows a lot of limitations
(Turkvatan 2015); therefore CT scan is very often the very rst-line imaging
technique to assess severity of involvement of peripancreatic structures and to
check evolution of acute presentations. Rising interests in order to stage the
severity of the disease were gained by magnetic resonance imaging. (It is especially useful for imaging of patients with iodine allergies, characterizing collections, and assessment of an abnormal or disconnected pancreatic duct.)
Not only age showed an inuence on clinical evolution, but even the etiology is
related to hospital stay. Idiopathic pancreatitis has shown a worse clinical evolution
in front of biliary and alcohol-based pancreatitis; those patients are showing a longer hospital stay and a more severe clinical evolution [
12].
One of most diffused complications of surgical interest is represented by pancreatic pseudocyst (Fig.22.3). The risk of developing a pancreatic pseudocyst is
in recent studies (estimated around 7%), most of them are symptomatic, and no
specic studies are published for the elderly. Fluid collection becomes an emergency when infected leading in the elderly to a high mortality risk (Tables 22.1
and 22.2).
22 Pancreatitis
Table 22.1 Severity score of acute pancreatitis (an overview)
Score (year)
SOFA (1996/98)
(sequential multiorgan
failure assessment)
JSS (2009) (Japanese
severity criteria for
acute pancreatitis)
BISAP score (2009) Blood urea nitrogen >25mg/dl, impaired
APACHE-II (1985)
(Acute Physiology and
Chronic Health
Evaluation)
Balthazar-CTSI (1990)
(CT severity index)
Ranson (1974) Age, leucocitosis, glucose blood levels,
Factors Sensitivity
Arterial oxygen saturation, fraction of
inspired oxygen, serum creatinine, total
bilirubin, platelet count, itemized Glasgow
Coma Scale score, mean arterial pressure,
and use of vasopressors such as dopamine,
dobutamine, adrenaline and noradrenaline
5 clinical items
10 blood test items
CT ndings
SIRS signs
Age
mental status, systemic inammatory
response syndrome (SIRS), age >60 years,
and pleural effusions
Age, Glasgow Coma score. Vital
parameters, oxygenation, chemistry,
hematology
Based on CT scan ndings 66.7 67.1
LDH, SGOT, azotemy, Ca++ blood levels,
hematocrite reduction, PO
seizure of liquids
, basis lost,
2
331
Specicity
80% 79%
90% 79.8%
56% 91%
90% 86.8%
70–80% 44.3
Table 22.2 Complications after acute pancreatitis
Type of complications
Young Necrotizing pancreatitis, uid collection, abscess, pseudocyst 3–4%
Elderly Pneumonitis (respiratory failure), renal failure, septic shock 5–10%
Mortality
22.4 Therapy
The treatment of an acute pancreatitis doesn’t differ signicantly from the same
pathologic condition in the younger patients. Severe forms can require an intensive
care setting. Out of clinical symptoms and evolution, CT scan and US scan are necessary to check evolution of diseases even when paucisymptomatic. Acute pancreatitis
shows a variability of clinical presentation grades, ranging from light symptomatic to
acute violent painful variants in which severe and extended necrosis of the parenchyma induces even a peritoneal involvement and can cause severe complications.
Therapeutic options are surgical and endoscopic, or interventional radiologic methods
are reserved to severe and complicated forms. Of course a biliary stone-based pancreatitis can be approached with ERCP, instead of early treating those patients; MRI and
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F. Basile et al.
perendoscopic US of the biliary tract can avoid unnecessary early endoscopic exploration of biliary tract, due to the fact that most of the stones are passing spontaneously
in the duodenum [13, 14]. Laparoscopic cholecystectomy is also in the elderly the
necessary approach after reliefs of pancreatitis symptoms and laboratory signs in
order to avoid recurrences; the mandatory delay of 4–5weeks is able to reduce conversions to open cholecystectomy due to periportal inammation making hard sometimes the identication of CBD (common bile duct) [15].
Fluids collection can be nowadays safely routinely drained by interventional
radiology techniques [16] so that the high success rates of those methods are reducing surgical indications. Surgical exploration remains necessary in case of multilocular septic involvement and extended necrosis making surgical necrosectomy,
abdominal cavity lavage and drainage, and sometimes laparotomy mandatory.
Also a conservative approach especially in the elderly can be in selected patients
considered. The surgical exploration should be selectively considered also in the
treatment of complications like pseudocyst. Although the transgastric drainage of
pseudocyst becomes a standard of care, following some morphological features of
pseudocyst is driving the surgeon in the choice of the kind of treatment. In fact the
pseudocyst should be contiguous to gastric wall, not in an inferior position in order
to avoid complications. MRI and transendoscopic US can clarify which kind of
treatment should be adopted, underlying the importance of a multidisciplinary setting in the management of pancreatic pseudocysts.
22.5 Chronic Pancreatitis
22.5.1 Etiology andEpidemiology
Chronic pancreatitis in the elderly can be caused by many different factors such as:
– Alcohol abuses
– Autoimmune disease
– Pancreatic anatomical anomalies (pancreas divisum, etc.) [17]
There is also the idiopathic form that collects all other chronic pancreatitis in
which an etiology cannot be identied.
Recent studies [18] have shown the role of autoimmune mechanism in the
chronic pancreatitis classifying also this disease in two histological subgroups
(types 1 and 2).
The autoimmune pancreatitis should also be mentioned correlated to high levels
of IgG4-positive plasma cells inltration of the pancreas and sensible to steroids
treatment; this kind of acute pancreatitis was also associated to other clinical conditions like sclerosing cholangitis (50%), hilar lymphadenopathy (30%), and salivary
gland involvement (20%) [19]. The idiopathic form seems to show to peaks of incidence: till 20years and in the elderly after 65.
22 Pancreatitis
333
22.6 Symptoms andTherapy
Chronic pain especially postprandial pain and slow evidence of jaundice coming in
an indolent way are the rst clinical signs and symptoms of a chronic pancreatitis.
During the years it appears also some progressive symptoms of pancreatic insufciency. Instead of pancreatitis in the young patients, in the elderly the clinical course
is oligosymptomatic and pain is rarely present. Also signs of exocrine insufciency
are slowly clinically evident and in most cases don’t require a surgical approach.
The clinical problem can be sometimes the differential diagnosis with pancreatic
cancer due to gland atrophy and parenchymal changes to be differentiated from
pancreatic cancer. Exocrine pancreas substitution and compensation of diabetes are
therapeutical approach with medicaments. The surgical treatment of pain through
Frey’s procedure [20] (resection of pancreatic head for decompression of the
Wirsung’s duct) or Partington-Rochelle operation (longitudinal jejunum derivation
of Wirsung’s duct) [21] that are together with the alcoholization of celiac plexus for
the pain control, the most adopted surgical options in the young patients, for this
disease is rarely indicated in the elderly. Nowadays endotherapy [22] is the main
therapeutical approach for symptoms relief of chronic pancreatitis under US control
endoscopic sphincterotomy, and Wirsung’s incannulation is able to obtain clinical
resolution of pain. Even plastic ore metallic stent positioning is nowadays more
adopted and diffused. Surgery in the elderly was quite completely replaced by endoscopic procedures [23].
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Benign andMalignant Lesions
oftheLiver
FrancescaRomanaPonziani, GiuliaGibiino,
andAntonioGasbarrini
23.1 Introduction
Primary liver cancer represents approximately 4% of all new cancer diagnosed
worldwide and is the third most common cause of cancer-related deaths among men
and the sixth among women, respectively [1].
Hepatic tumors may derive from hepatocytes, bile duct epithelium, or mesenchymal tissue or spread to the liver from primary tumors in remote or adjacent organs.
In adults, hepatic metastases are more common than primary malignant tumors
of the liver, whereas in children, primary malignant tumors outnumber both metastases and benign lesions. Except for cavernous hemangiomas, benign hepatic tumors
are rare in all geographic regions and in all age groups. It is widely accepted that the
risk of developing hepatocellular carcinoma (HCC) is age dependent [2]; hence, in
Western countries, the diagnosis of HCC is more frequent in patients aged 70 or
more, and being faced with elderly cirrhotic patients with HCC has become frequent in clinical practice [2–4].
23
23.2 Primary Malignant Tumors
23.2.1 Hepatocellular Carcinoma
Hepatocellular carcinoma is the most common primary malignant tumor of the
liver, accounting for 85–90% of all primary liver cancers. It is the fth most common cancer in men and the eighth most common in women, ranking fourth in annual
cancer mortality rates [5]. The global age distribution of HCC varies by region,
F.R. Ponziani (*) • G. Gibiino • A. Gasbarrini
Internal Medicine, Gastroenterology and Hepatology, Agostino Gemelli Hospital, Rome, Italy
e-mail: Antonio.Gasbarrini@unicatt.it
© Springer International Publishing AG, part of Springer Nature 2018
A. Crucitti (ed.), Surgical Management of Elderly Patients,
https://doi.org/10.1007/978-3-319-60861-7_23
335
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incidence rate, gender, and etiology. In Western low-risk populations, men are generally more susceptible to HCC, and the highest rates occur among persons aged 75
and older [6, 7].
The mechanisms of HCC pathogenesis are complex and usually involve liver
injury followed by inammation, necrosis, and hepatocytes proliferation. The perpetuation of this destructive- regenerative process results in the development of liver
cirrhosis, which is characterized by regenerating nodules that progress to dysplastic
nodules and ultimately to HCC [8]. Indeed, cirrhosis is present in about 80–90% of
patients with HCC being, therefore, the most frequent risk factor. Other risk factors
are hepatitis B virus (HBV) and hepatitis C virus (HCV) infections, aatoxin, alcohol intake, obesity, and diabetes.
Worldwide, around 400 million people are estimated to be chronically infected
by HBV [9]. The HBV appears to be directly and indirectly carcinogenic, and HCC
develops in as many as 25% of them [10].
HBV continues to be the major HCC risk factor worldwide, being the main leading factor to date compared to HCV, although its importance is expected to decrease
during the coming decades due to the widespread diffusion of HBV vaccination in
the newborns [5]. Approximately 170 million people in the world are chronically
infected with HCV and are at increased risk of HCC development.
In Japan, Italy, and Spain, HCV is the cause of about 75% of HCCs, and, in other
industrialized countries, chronic HCV infection, often in combination with alcohol
abuse, is emerging as a major cause of this tumor. Patients with HCV-induced HCC
are generally older than those with HBV-related tumors, and HCV infection was
usually acquired in adult life [11].
Together, HBV and/or HCV chronic infections account for 80–90% of all HCC
worldwide [12]. The variable age-specic patterns in different countries are related
to differences in the dominant hepatitis virus in the population, the age at viral
infection ,and the existence of other risk factors. According to EASL recommendations, in patients with chronic hepatitis, antiviral therapies leading to maintained
HBV suppression in chronic hepatitis B and to sustained viral response in hepatitis
C are recommended, since they have been shown to prevent progression to cirrhosis
and hence HCC development [
10].
Heavy alcohol intake, dened as ingestion of >50–70g/day for prolonged periods, is a well-established risk factor for HCC, and there is also evidence of a synergistic effect of heavy alcohol intake with HCV or HBV chronic infection [13].
Nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis
(NASH), often associated with metabolic syndrome, are other well-known risk factors for HCC.
The relationship between cigarette smoking and HCC has been widely examined
in both low- and high-risk areas, and discordant ndings have been reported [5].
Although the typical clinical features of HCC (including abdominal pain and
weight loss in patients with cirrhosis) are not always present and difcult to be recognized in patients with liver cirrhosis, nowadays more patients are being diagnosed
at an early tumor stage, when they have no specic symptoms or signs. This is probably the result of the surveillance programs adopted among patients with cirrhosis,
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