Acute Pancreatitis – management in low-income countries
1.0 Introduction
Acute pancreatitis is a not uncommon condition causing acute abdominal pain
that has a wide spectrum of clinical consequences – from spontaneous resolution
through pancreatic necrosis causing intra-abdominal sepsis or bleeding to death
from multi-organ failure. Severe acute pancreatitis (SAP) challenges the most
advanced capacities of the intensive care unit. It may or may not require surgical
intervention. Numerous etiologic factors are implicated in acute pancreatitis
and the incidence of the condition is dependent on the prevalence of these.
Notwithstanding the variability of the above factors, the recognition, classification
and management of acute pancreatitis are important clinical skills for all physicians
treating patients with abdominal pain.(1) Guidelines have been
published for the diagnosis and management of acute pancreatitis. (2-4)
This Review will concentrate on how a modern understanding of this problem can
inform management in low-income countries.
2.0 Etiology/Epidemiology
Although a wide variety of conditions may give rise to acute pancreatitis (see
table
1) the two most common factors, causing 80-90% of cases generally, are gallstones
and excessive alcohol intake. (5) Gallstones, passing through
the bile duct into the duodenum, are believed to result in transient pancreatic
duct hypertension; alcohol has direct toxic action on pancreatic acinar cells
as well as causing spasm of the sphincter of Oddi. (6) Sowetan
South Africans suffer a particularly aggressive form of alcoholic pancreatitis.
(7;8) The relative importance of these etiologies
is related to their prevalence in the population. (9) What
is clear is that the first attack of pancreatitis carries the highest mortality
rate and that the elderly are at highest risk of morbidity and death. Other
associated causal factors are: anatomic abnormalities (pancreatic divisum),
drugs (azathioprine, estrogens, thiazide diuretics, etc.), infections (mumps,
coxsackie virus), hyperlipidemia(10), hypercalcemia from hyperparathyroidism(11),
tumours, auto-immune disorders (SLE) (12) and trauma. Iatrogenic
sources such as endoscopic retrograde choledochopancreatography (ERCP) and endoscopic
sphincterotomy (ES) are growing causes in the West.(13) Ascariasis,
obstructing bile or pancreatic ducts, has been implicated (14);
as has typhoid fever. (15) Finally a certain percentage of
cases, depending on the diligence of investigation, will remain idiopathic (16).
2.1. Pancreatitis and HIV
In the USA patients infected with HIV are said to experience a 35 to 800 times
increased risk of developing acute pancreatitis. (17) However
in a study of 44 patients from South Africa with abdominal pain, pancreatitis
was not seen. (18) Patients in more advanced stages with CD4
counts < 200 are said to be at increased risk. Drugs used in the treatment
of HIV, including anti-retrovirals such as didanosine (DDI) and pentamidine
or sulphonamides used to prevent or treat pneumocystis infection, are the most
common cause of pancreatitis. Opportunistic infection with CMV or toxoplasmosis
has also been implicated.
3.0 Surgical Anatomy/Physiology
The pancreas is a retroperitoneal secretory organ which extends obliquely from
the C loop of the duodenum to the splenic hilum and is typically divided into
head, body and tail. (5) Lesions of the head of the pancreas
cause jaundice by obstructing the common bile duct as it passes through the
pancreatic parenchyma. The deeply situated position of the body and tail explains
the poorly defined character and the often delayed recognition of pancreatic
pathology. Specifically it explains the fact that pancreatitis is characterized
by central abdominal pain radiating to the back.
The pancreas synthesizes more protein than any other exocrine gland and its
exocrine functions involve the secretion of enzymes essential for the digestion
of fats, carbohydrates and proteins. The main endocrine function of the pancreas
is the secretion of insulin – the hormone responsible for glucose homoeostasis.
To prevent autodigestion, pancreatic enzymes exist in the pancreas in the form
of proenzymes or zymogens. Trypsinogen requires activation into trypsin by enterokinase
found in the brush border of the duodenum. Trypsin then proceeds to activate
the other proenzymes. The sequestration of zymogens in organelle bound granules
and the presence of enzyme inhibitors further serve to protect the pancreas.
The premature activation of enzyme precursors or zymogens such as trypsinogen
within the substance of the pancreatic acinar cell is considered to be one of
the fundamental mediators of the pathophysiology of acute pancreatitis.
The major pancreatic duct of Wirsung usually (but not always) joins with the
terminal portion of the common bile duct at the ampulla of Vater, discharging
their contents of bile and pancreatic secretions in the medial aspect of the
second part of the duodenum. The sphincter of Oddi controls the pressure inside
the biliary and 2-3 mm pancreatic duct; the latter being maintained at a higher
level than biliary pressure. Spasm of the sphincter of Oddi and reflux of bile
into the pancreas is associated with acute pancreatitis. (19)
4.0 Pathophysiology
Pancreatic duct hypertension is felt to be a major initiator of the pathologic
processes leading to acute pancreatitis. This may come about through bile reflux,
ampullary obstruction, sphincter of Oddi spasm or hypersecretion (20)
and is the presumed mechanism of gallstone pancreatitis. The mechanism whereby
alcohol induces acute pancreatitis is less clear. Chronic excessive alcohol
intake is necessary. (21) Males and cigarette smokers are
at higher risks. Toxic metabolites of alcohol metabolism may play a role. (22)
Whatever the initiating event, the final common pathway of acute pancreatitis
appears to be inappropriate intracellular activation of trypsin causing acinar
cell damage and autodigestion. (23) This damage results in
recruitment of neutrophils and pancreatic inflammation. (24)
The local and systemic modulation of this inflammatory response will determine
the severity of the attack and the extent of complications. Cytokines, such
as tumour necrosis factor TNF, interleukins such as IL-1ß, -6 and -8,
as well as platelet activation factor, have all been associated with severity
of attack and pancreatic necrosis.
Two discrete forms of cell death have been identified. (25)
Apoptosis is a highly coordinated process mediated by caspases which result
in cytoplasmic and nuclear shrinkage and the breakdown of the cell into multiple
spherical bodies which retain membrane integrity. It is found more frequently
in less severe forms of pancreatitis. Necrosis is characterized by rapid loss
of membrane integrity, by cytoplasmic swelling and the release of lysosomal
and granular contents into the extracellular space. It is associated with more
severe forms of pancreatitis. Disturbances in the microcirculation occur. (26)
The balance between pro-inflammatory and anti-inflammatory mediators determines
the ultimate local and systemic effects. (27) If pro-inflammatory
mediators predominate the picture is one of systemic inflammatory response syndrome
(SIRS) which may lead to multi-organ dysfunction syndrome (MODS). (28)
The systemic complications of acute pancreatitis include pulmonary dysfunction
which occurs in 75% of cases and extends from hypoxemia through atelectasis
and pleural effusion to adult respiratory distress syndrome (ARDS). (29)
Shock and disseminated intravascular coagulation (DIC) are two other well recognized
systemic complications associated with cytokine release. Pancreatic encephalopathy
is another systemic complication of severe pancreatitis and is not well understood.
(30) Pathophysiologic changes in the gut have important consequences
in pancreatitis. (31) Reduced GI motility occurs and damage
to the gut barrier results in increased intestinal permeability and an increased
risk of bacterial translocation and sepsis. (32) These facts
have important therapeutic implications. (see 6.1.2. Nutritional
support)
5.0 Diagnosis
5.1. Clinical presentation
Acute pancreatitis presents with acute onset of usually epigastric abdominal
pain, often knife-like and radiating into the back and associated with nausea
and vomiting. As such it features in the differential diagnosis of the acute
abdomen. Patients are restless and lean forward; the supine positions may exacerbate
the pain. Examination may reveal hypotension, tachycardia and tachypnea. Fever
is not severe. There is usually guarding in the epigastrium with decreased bowel
sounds and there may be abdominal distension. Jaundice may be due to associated
cholangitis or alcoholic hepatitis. Cullen’s sign (peri-umbilical ecchymoses)
and Grey Turner’s sign (flank ecchymoses) may be seen late with necrotizing
pancreatitis.
The clinical course is determined by the severity of the illness. While 80-90%
of patients recover with supportive care only, the remainder develop severe
pancreatitis (SAP) with a mortality rate ranging from 9-40% (27)
Of those who die, 60% do so in the first 6 days from MODS such as shock or ARDS.
After the 1st week the majority of deaths are a result of infectious causes
related to pancreatic necrosis or generalized sepsis. This two phase mortality
graph requires a two phase management strategy. In the first week of the illness
attention is directed at resuscitation and treating MODS. After the second week
treatment will have to be directed at local pancreatic complications.
5.2. Laboratory diagnosis
The hallmark in the biochemical diagnosis of acute pancreatitis is an elevated
serum amylase. However the sensitivity of this marker is reduced with late presentation,
hypertriglyceridemia and chronic alcoholism. (33) Lipase is
a more sensitive test, if available, and may suggest an alcoholic etiology.
(34) In cases of late presentation, measurement of urinary
amylase may be valuable as amylase excretion is increased relative to creatinine
clearance for 1-2 weeks. Elevated early serum transaminases suggest a biliary
origin. Multiple other markers have been used to predict the severity of the
episode, but these are unlikely to be available in low-income countries.(35)
The level of C reactive protein after 48 hours is an indicator of severity and
poor prognosis.
The following laboratory studies are recommended in the initial assessment of
a patient with acute pancreatitis: amylase, lipase, bilirubin, liver function
tests, CBC, electrolytes, creatinine, urea, arterial blood gas, Ca, PO4, chest
and abdominal xray.
5.3. Severity scoring/prognosis
There has been ongoing interest in attempting to predict those patients at highest
risk of severe disease and mortality. The earliest system was that of Ranson.
http://www.mdcalc.com/ransonscore
(see Table
2) It remains unsurpassed for predicting severity of disease and mortality.
(36) Note elevated amylase is not a sign of poor prognosis.
If the number of positive Ranson signs <2, the mortality is generally zero;
with three to five positive signs, mortality is increased to 10 to 20%. The
mortality rate increases to more than 50% when there are more than seven positive
Ranson signs. It is the least accurate in predicting intermediate grades (3-5
signs) of pancreatitis. However, this scoring system has been criticized, because
calculation of a number of values is delayed until 48 hours after presentation.
The Apache II scale is a general indicator of severity of illness and is calculated
at the time of presentation. If the score is >8 the pancreatitis will be
severe. (37) http://www.sfar.org/scores2/apache22.html#calcul
CT scoring systems have been used to identify local pancreatic complications
and predict adverse effects and mortality. (38) (see 5.4.
Imaging)
Based on these systems, attacks of acute pancreatitis should be classified as
mild or severe. (4) The latter is based on evidence of organ
failure persisting for more than 48 hours, (Ranson=3 or Apache II=8), or evidence
of a local complication (necrosis, pseudocyst or abscess). The accuracy of this
classification can be enhanced by clinical assessment and ancillary laboratory
tests such as CRP measurement.
5.4. Imaging
Merkle et al. have published a good review of the various imaging modalities
useful in pancreatitis. (39) Plain films of the abdomen may
show typical findings, but have low sensitivity and specificity. An abdominal
ultrasound is advisable early in the course of the disease to identify gallstones
and the possibility of ongoing choledocholithiasis. However U/S alone is a poor
indicator of pancreatitis itself. Computerized axial tomography CT is the modality
of choice for imaging pancreatitis. It should be performed in cases where the
diagnosis is unclear and for all cases of SAP. Balthazar has developed a scoring
system for grading severity of the local disease which accurately determines
the presence of pancreatic necrosis. (38) Contrast enhanced
CT may be detrimental in the acute setting, especially in under-resuscitated
patients. (40) CT plays an important role in interventional
efforts for local pancreatic complications. (41) In biliary
pancreatitis urgent ERCP is indicated to rule out choledocholithiasis if the
disease severe, if the common duct is dilated or if there is clinical jaundice
or cholangitis. (42) (see 6.2. biliary pancreatitis)
Endoultrasonography (EUS), if available, may play a role in detecting which
patients would benefit from ERCP.
6.0 Management
6.1. General management - prevention
Investigation into the management of acute pancreatitis has taken various directions.
One focus is on preventing post-ERCP pancreatitis. (43) Pancreatitis
complicates ERCP in 2-8% of procedures. Somatostatin, a natural peptide which
inhibits gastrointestinal hormones and thus pancreatic secretion, may play a
role in preventing post-ERCP pancreatitis. However octreotide, a synthetic analogue
of somatostatin, and proteinase inhibitors like gabexalate have not been effective
in this circumstance. (44) Similarly lexipafant, an antagonist
of the powerful cytokine, platelet activating factor, has not reduced mortality
in pancreatitis. (45) Specific pharmacologic manipulation
to reduce complications in acute pancreatitis has been similarly unrewarding
to date. Clinicians are therefore reduced to supportive measures in treating
acute pancreatitis.
6.1.1. Supportive measures
Resuscitation of the patient with acute pancreatitis is the foundation of supportive
management. Pancreatic inflammation leads to sequestration of large amounts
of retroperitoneal fluid and the hematocrit may rise considerably. Large amounts
of crystalloid (Ringers lactate or NS) solution should be infused to keep urinary
output > 0.5ml/kg/hr and blood pressure should be monitored along with CVP,
if necessary. Supplemental oxygen should be given to maintain O²sat>90%.
There is some evidence that early reversal of organ dysfunction may prevent
complications. (46) Patients are kept NPO for the first 48
hours at least. Nasogastric suction may be necessary if vomiting is persistent,
but has no other specific value. Narcotic analgesia is prescribed for pain.
While morphine has been traditionally withheld, because it is known to increase
sphincter of Oddi spasm, and meperidine usually given in its place, there is
no proof that morphine is deleterious. (47) Although antacid
therapy, in the form of PPIs or H² antagonists, is usually given, there
is little proof that this is efficacious.
While mild acute pancreatitis generally settles over the course of 3-7 days
with these supportive measures, severe acute pancreatitis (SAP) is a fulminant
disorder. A number of excellent reviews on the management of SAP have been published.
(48-50) Patients with SAP should be treated in an intensive
care unit and closely monitored. Resuscitation should be aggressive and shock
treated appropriately with fluid and inotropes and monitored with pulmonary
artery pressures if available. Transfer to a specialized center should be considered.
The management of specific problems is discussed below.
6.1.2. Nutritional support
In mild pancreatitis feeding may begin when pain and ileus have resolved. In
SAP with a high catabolic state and a prolonged ileus, nutritional support is
appropriate. The thinking around nutritional support for pancreatitis has shown
a considerable evolution. (51) Initially total parenteral
nutrition TPN was felt to be the preferred route and enteral feeding felt to
be relatively contraindicated. Today enteral feeding has been shown to be the
preferential route and should actually be instituted early to reduce the stress
response and disease severity. (52) Patients treated with
enteral feedings show a decreased risk of infectious complications, lower risk
of surgery and shorter hospital stay, not to mention decreased costs. (53)
Use of the gut seems to maintain normal flora, preventing bacterial translocation.
This is of considerable importance in low-income countries where facilities
for TPN may not exist. Enteral feedings may be instituted with specialized naso-jejunal
tubes, but naso-gastric feedings may also be used. The value of enteral feedings
provides an argument for feeding jejunostomy if surgery is undertaken during
the course of acute pancreatitis. There are technical issues of tube displacement.
Nasobiliary tubes used in ERCP procedures and placed in the jejunum endoscopically
are useful. (54) Low fat semi-elemental diets are usually
used which may be difficult to acquire in low-income countries. Development
of an affordable semi-elemental diet made from local ingredients would be extremely
valuable.
6.1.3. Antibiotics
Since infectious complications account for up to 80% of deaths in SAP primarily
from necrotizing pancreatitis, it is not surprising that the role of antibiotics
has been extensively investigated. While pancreatic necrosis can be adequately
diagnosed by CT scan, distinguishing between sterile and infected necrosis requires
aspiration of contents. The bacteriologic spectrum of infected pancreatic necrosis
is generally polymicrobial with staph aureus, aerobic and anaerobic gram-negative
bacilli and fungal infection all common pathogens. Appropriate antibiotic regimes
need to be broad spectrum. The evidence for reduction in mortality from pancreatic
necrosis is conflicting. (55;56) Some meta-analyses
seem to suggest a lower mortality rate with the use of prophylactic antibiotics,
particularly with beta-lactams active against staph aureus, but no absolute
reduction in the rate of infected necroses or abscesses. Some guidelines recommend
prophylactic antibiotics in SAP, some do not. (2;48)
Prolonged use is discouraged and results in super-infection with resistant and
opportunistic organisms. (50) The roles of selective gut decontamination
or use of probiotic agents such as live lactic acid bacilli to maintain normal
gut flora are being investigated.
6.1.4. Surgery
It is recognized in high income countries that surgery for acute pancreatitis
should be reserved for specific problems and complications. (see 6.2.
biliary pancreatitis and 7.2.1. pancreatic necrosis)
However in situations with limited resources a laparotomy for undiagnosed acute
abdomen occasionally reveals acute pancreatitis. Fat necrosis may be seen in
the transverse mesocolon or in the mesentery. Blood stained fluid may be a sign
of hemorrhagic pancreatitis. The pancreas itself is best examined by entering
the lesser sac through dissecting the omentum off the transverse colon. A boggy
enlarged pancreas with peripancreatic fluid will be found.
In these cases cholecystectomy and cholangiogram may be appropriate, if gallstones
are palpated or strongly suspected, and exploration of the bile duct if common
duct stones are found. A feeding jejunostomy may also be added if prolonged
nutritional support is anticipated by evidence of severe pancreatitis. A recent
report from China suggests the utility of peritoneal lavage in acute pancreatitis.
(57) This procedure has been used in the past in the West
and has been discarded. (58)
6.2. Biliary pancreatitis
Gallstones are a frequent cause of pancreatitis, but pancreatitis is a poor
indicator of choledocholithiasis. (42) Biliary pancreatitis
is caused primarily by the passage of stones through the sphincter, not the
presence of choledocholithiasis itself. However 15% of patients (in regions
of high prevalence of gallstones) will have CBD stones. Microlithiasis and sludge
may also be the cause of what otherwise appears to be idiopathic pancreatitits.
Most importantly pancreatitis will be recurrent in up to 30% of cases of untreated
biliary pancreatitis. (59) The two main issues have been the
timing of cholecystectomy and the role of ERCP/ES in SAP.
6.2.1. Timing of cholecystectomy
Cholecystectomy is indicated to prevent recurrent attacks. The older practice
of waiting 6-8 weeks after an attack has been revised with newer data concerning
risk of recurrence and with the use of laparoscopic cholecystectomy (LC). Patients
with mild pancreatitis are now advised to have a LC prior to discharge. Intra-operative
cholangiogram should be carried out at this time and if bile duct stones are
found some method of removing them either intra- or post-operatively should
be undertaken. (59) In patients with SAP, without evidence
of choledocholithiasis, cholecystectomy should be delayed until the patient
has adequately recovered from the illness.
6.2.2. ERCP/ES
Patients with pancreatitis, of any degree, who have evidence of obstructive
jaundice, with dilated CBD or choledocholithiasis or cholangitis should have
urgent ERCP followed by sphincterotomy if stones are found. (59)
In the absence of this modality surgical cholecystectomyand CBD visualization
and exploration is probably indicated. Controversy exists over the indication
for urgent ERCP in the absence of these. In mild pancreatitis it is not indicated.
(60) In SAP, when improvement is not evident within 72 hours,
urgent ERCP is indicated to diagnose obstructing stones. This should probably
be undertaken in centers specializing in pancreatic care. (61)
7.0. Complications
The systemic and local complications in SAP are responsible for its high mortality
rate. Systemic complications are responsible for most early deaths, whereas
local complications account for deaths after the first week.
7.1. Systemic
7.1.1. Shock
While there is some evidence that shock can induce pancreatitis by changes in
the microcirculation, we are interested here in shock arising in the course
of pancreatitis. (62) It appears that the pathogenesis of
shock in pancreatitis is entirely related to hypovolemia, with no evidence of
a myocardial depressant effect. Shock is also a strong marker of SAP and mortality.
Shock appearing early on in the course of SAP is usually characterized by low
cardiac output and high systemic vascular resistance - indicative of hypovolemia.
The treatment is vigorous fluid resuscitation with invasive monitoring. Shock
associated with pancreatic necrosis and sepsis may show signs of high output
and low systemic vascular resistance. In these cases inotropic support may be
necessary as well as the treatment of sepsis.
7.1.2. ARDS
Pulmonary complications of acute pancreatitis range from hypoxemia without radiologic
changes through pleural effusion and atelectasis to ARDS. (29)
15-20% of patients with pancreatitis will develop ARDS and these have > 50%
mortality. Pathophysiology is mediated through the cytokine storm described
above. ARDS is established by reduced lung compliance and impaired gas exchange.
(63) Treatment is primarily supportive and ventilation is
the hallmark. Ventilatory strategies include low tidal volumes (6ml/kg) and
the use of positive end expiratory pressure PEEP. Prone positioning and partial
liquid ventilation are being investigated.
7.1.3. Sepsis
It is important and difficult to distinguish the systemic inflammatory response
syndrome SIRS which is a manifestation of the systemic cytokine release induced
by acute pancreatitis from sepsis as a result of infecting organism. (64)
They are clinically identical although SIRS occurs in the first phase of SAP.
Vigorous search for a source of sepsis is appropriate. Repeated cultures may
be necessary. Line sepsis may occur especially in patients on TPN. Fungal infection
may supervene especially when prophylactic antibiotics have been used for a
prolonged period. Sepsis from the pancreas itself is discussed below. (see 7.2.1.)
7.2. Local
A number of local complications specific to SAP occur and will be discussed
below. One non-specific, but important, local complication which has systemic
consequences is the abdominal compartment syndrome. (65) The
clinical syndrome is one of a tense, distended abdomen, increased peak inspiratory
airway pressures with hypercapnia, and shock with hypotension and oliguria.
Measurement of the intra-abdominal pressure through an indwelling urinary catheter
is an easy and accurate method. Abdominal pressures > 20mmHg are clinically
significant and warrant intervention. The syndrome is seen in a number of clinical
conditions and SAP is one. The treatment is decompressive laparotomy and maintenance
of an open abdomen approach. This should be considered if the intra-abdominal
pressure > 25mmHg (35cmH²O).
7.2.1. Pancreatic necrosis/abscess
Pancreatic necrosis is the most feared and lethal local complication of SAP
with mortality rates for infected collections ranging from 20-50%. Its management
has been the subject of intensive study. (66-70) The first
step is the identification of the patient at risk for pancreatic necrosis. These
are patients with SAP as defined above with Ranson score=3 and ApacheII=8. There
is controversy whether these patients should have a baseline contrast enhanced
CT scan (CECT) at 72 hours or whether this study should be based on clinical
deterioration or failure to improve. The presence or absence or intra- or peri-pancreatic
necrosis is defined by nonenhancement of these tissues on dynamic CECT. Using
Balthazar’s classification the area of involvement must be >3cm or
30% of pancreatic tissue. (38) Mortality rises with extent
of necrosis. (Table
3) Various pitfalls to the detection of pancreatic necrosis exist and the
radiologist should be familiar with the technique. Whether all patients with
proven pancreatic necrosis should receive broad spectrum antibiotics is unclear,
but evidence suggests a role for decreasing or at least delaying infectious
complications with broad spectrum antibiotics – particularly imipenem
and 3rd generation cephalosporins. (56)
The next decision is whether the collection is sterile or infected. The presence
of gas in the necrotic tissues suggests infection, but is not universally present.
Since there is a marked difference in survival based on whether the necrosis
is sterile or infected, fine needle aspiration of all necrotic collections is
recommended. Sterile collections should be simply observed and followed. Drainage
of these actually increases infection rates. (48) Infected
necrotic collections or pancreatic abscesses require broad spectrum antibiotics
and drainage. (50) Delay of surgery into the 2nd or 3rd week
should be attempted as this leads to better results. Yousaf gives a good description
of various techniques including necrosectomy which may require repeated explorations
facilitated through laparostomy. Alternatively the abdomen may be closed over
drains and irrigated. The value of percutaneous radiologic interventions has
been revealed recently and lower mortality rates are associated with these techniques.
Wide bore catheters with multiple side holes will be particularly useful if
the liquefaction has developed sufficiently to allow for percutaneous drainage,
as in the case of pancreatic abscess. (71) Sufficient expertise
needs to be available. (66) The precarious nature of these
patients must be stressed and many of them may not be salvageable in resource
limited settings.
7.2.2. Fluid collections and pseudocysts
Peri- and intra-pancreatic fluid collections develop in the course of SAP. (72)These
may or may not develop as a result of ductal disruption and they may persist
or resolve spontaneously in the course of the illness. A combination of US and
CT is better at assessing these collections than CT alone. A policy of watchful
waiting is appropriate for pseudocysts. As long as no complication (infection,
bleeding, increased size) develops pseudocysts should be observed. Pseudocysts
> 6cm or which have persisted for > 6 weeks are unlikely to resolve spontaneously
and should be treated. A combination of percutaneous, endoscopic and surgical
techniques is available and their use should be guided by local expertise. (73;74)
7.2.3. Vascular complications
A wide variety of vascular complications from acute pancreatitis may occur.
(75) These range from disruption of a major blood vessel causing
pseudoaneurysm or bleeding through thrombosis of vessels causing intestinal
ischemia (often transverse colon) and perforation to splenic vein thrombosis
causing hypersplenism and varices.
8.0. Conclusions
While most cases of acute pancreatitis can be managed with a low level of supportive
care, severe acute pancreatitis SAP challenges the capacity of the most highly
developed intensive care units. These cases will be particularly challenging
in the context of resource limited environments. Clinical scoring can be used
to identify the high risk patient in whom complications and mortality can be
anticipated and for whom transfer to specialized centers would be appropriate.
An understanding of pathophysiology allows anticipation of various clinical
events.
9.0. Recommendations
1) Serum amylase determinations should be available in all hospitals dealing
with acute abdominal complaints.
2) History, physical examination, laboratory and imaging studies should allow
non-operative diagnosis of acute pancreatitis in the majority of cases.
3) All cases of pancreatitis should be classified using Ranson and Apache II
systems as either mild or severe.
4) The initial treatment of all cases of pancreatitis requires vigorous fluid
resuscitation to maintain BP and urinary output and supplemental O² to
maintain O² sat > 90%.
5) Prolonged fasting or nasogastric suction is not necessary in the majority
of cases.
6) Narcotic analgesia should be used for pain control. Morphine is not contraindicated.
7) Prophylactic antibiotics are not appropriate for mild pancreatitis.
8) Mild cases of biliary pancreatitis should have cholecystectomy prior to discharge.
9) Severe acute pancreatitis SAP is a discrete clinical entity requiring the
following:
a) All cases of SAP should be cared for in a centre with CT scan and advanced
intensive care capacity including invasive monitoring and ventilatory support.
b) Patients with severe suspected biliary pancreatitis who are not improving
or who have associated jaundice, dilated common bile duct or cholangitis should
have early ERCP with ES if choledocholithiasis is found. In the absence of ERCP
capacity an argument may be made for early open cholecystectomy and common duct
exploration in these patients.
c) Enteral feeding via nasogastric or nasojejunal tubes and semi-elemental formulations
should be instituted early on.
d) Patients with SAP should have contrast enhanced CT assessment to assess for
the presence of pancreatic necrosis.
e) Patients with CT severity index >3 might benefit from prophylactic broad
spectrum antibiotics.
f) Patients with pancreatic necrosis involving more than 1/3 of the pancreas
or signs of sepsis should have fine needle aspiration to determine the presence
of pancreatic infection.
g) Sterile pancreatic collections should be observed.
h) Infected pancreatic collections should be drained. The method of drainage,
percutaneously versus open, should be determined by local expertise.
10) Asymptomatic pancreatic pseudocysts < 6 cm. should be observed for 6
weeks prior to intervention.
Brian Ostrow MD, FRCSC
Office of International Surgery
University of Toronto
Canada
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