Acute pancreatitis 2015

ACUTE PANCREATITIS

SAMIR EL ANSARY

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Acute pancreatitis

AP is an inflammatory condition of the pancreas

that has a broad spectrum of severity ranging

from mild and self-limited to severe and

associated with multiorgan failure.

Clinically it is associated with the acute onset of

abdominal pain and elevation of serum

biochemical markers.

The underlying pathophysiology is early and

inappropriate activation of digestive enzymes

within acinar cells.

•Different degrees of AP, and how are they

defined?

Mild AP

Pancreatic inflammation (of any cause) without

persistent organ failure or local complications.

Severe acute pancreatitis (SAP)

Associated with systemic complications,

including multiple-organ failure, and local

complications, such as necrosis, abscess,

and/or pseudocyst. This degree of pancreatitis requires aggressive therapy in an

intensive care setting to prevent significant morbidity or mortality.

Causes of AP?

Gallstone-related disease and excessive

alcohol intake comprising 70% of all cases.

hypertriglyceridemia (serum triglyceride level

above 1500 mg/dL), trauma, and

hypercalcemia.

Smoking is a risk factor for AP in a time- and

dose-dependent manner.

Causes of AP?

A large number of medications have been

implicated in causing AP, including angiotensin-

converting enzyme inhibitors, furosemide,

tetracycline, aminosalicylic acid, corticosteroids,

procainamide, thiazides, metronidazole, and

ranitidine.

Because of the varied duration between exposure and

development of symptoms, and the usual lack of a clear

mechanism, it is often difficult to identify a drug as the

sole cause of AP.

Causes of AP?

True idiopathic cases of AP are diminishing as

more genetic causes of the disease are

discovered.

Endoscopic retrograde

cholangiopancreatography (ERCP) causes

pancreatitis in approximately 5% of individuals

who undergo this procedure.

The presenting signs and symptoms of

AP?

AP is characterized by the sudden onset of

abdominal pain, classically located in the

epigastrium and usually associated with nausea

and/or vomiting.

Radiation of pain from the epigastrium

through to the back that is alleviated with the

patient leaning forward is a typical but not a

necessary feature.

Tachycardia related to pain or volume depletion

and low-grade fever may be present.

The presenting signs and symptoms of

AP?Two additional findings associated with severe

pancreatitis may be present

the Grey Turner and Cullen signs.•The Grey Turner sign is an ecchymosis of the

flank due to retroperitoneal hemorrhage. When present, it usually occurs 3 to 7 days after the onset of pain

and is indicative of severe pancreatitis.

•The Cullen sign is periumbilical ecchymosis

associated with both severe necrotizing

pancreatitis and retroperitoneal hemorrhage of

various causes.

•Are amylase and/or lipase measurements

helpful in the diagnosis?

The most commonly used diagnostic markers are

serum amylase and lipase.

Although serum amylase levels have a high

sensitivity in the first 24 hours the specificity is

very low.

In addition to pancreatitis, elevated amylase

levels are seen with many other conditions

including bowel infarction, renal failure,

perforated peptic ulcer, trauma to the salivary

glands, and macroamylasemia.

•Are amylase and/or lipase measurements

helpful in the diagnosis?

In contrast, serum lipase levels are both more

specific and more sensitive than amylase

measurements.

Of note, no correlation exists between

the absolute levels of amylase and

lipase and the severity of pancreatitis.

Role of imaging in the diagnosis

of AP

Abdominal plain radiographs may be

nonspecific or reveal an ileus if the pancreatitis

is severe.

Ultrasound evaluation of the pancreas itself is

often limited by overlying bowel gas and/or

patient discomfort. This test may, however,

detect signs of biliary abnormalities in cases

where this cause is suspected.

Role of imaging in the diagnosis

of AP

Computed tomography (CT) with oral and

intravenous (IV) contrast

Can offer information regarding severity of

disease and development of complications.

Features that may be identified on CT include

evidence of inflammation (pancreatic

parenchymal edema or peripancreatic fat

stranding), peripancreatic or intrapancreatic

fluid collections, pancreas perfusion, and

presence and extent of pancreatic necrosis.

•Should all patients have imaging studies

done at the time of presentation?

The timing of performing CT in the evaluation of

AP has been frequently debated and studied.

Obtaining CT early in the course of illness has

not been shown to establish alternative

diagnoses or change clinical management.

The need for cross-sectional imaging should be

evaluated on a case-by-case basis and reserved

for those who do not improve clinically after

several days of supportive therapy and/or in

whom worrisome symptoms such as fever or

leukocytosis develop.

•Should all patients have imaging studies

done at the time of presentation?

Advanced imaging should be considered early in

a patient's course of illness if the diagnosis itself

is uncertain or if suspicion exists of a

complication from AP that, if identified, would

significantly alter management, or if alternative

diagnoses requiring surgical management are

considered.

•What if the patient cannot receive

contrast for imaging?

Magnetic resonance imaging (MRI) has a

growing role in the diagnosis and management

of AP and is a reasonable option in patients

who cannot receive iodinated contrast for CT.

Enhanced MRl requires the administration of

gadolinium, which has been implicated in

severe toxic side effects (nephrogenic

systemic fibrosis) in patients with

compromised renal function.

•What if the patient cannot receive

contrast for imaging?

Good correlation has been noted, however,

when comparing magnetic resonance

cholangiopancreatography (MRCP), with or

without gadolinium contrast, with CT in the

evaluation AP.

MRCP also has the added benefit of being able to

better define the pancreatic and biliary ductal system

in cases where this cause is suspected but the pretest

probability is too low to proceed directly to ERCP.

Determination of the severity and

prognosis of AP

Recognizing and differentiating mild AP from

Severe AP is important so that patients can be

triaged to the appropriate setting and

treatment plan.

Over decades, several clinical predictors have

emerged.

Although all are imperfect, they are

considered superior to clinical judgment alone.

Ranson criteriaWere one of the earliest and widely used

scoring systems.

Their major disadvantage was that they

required 48 hours to complete.

The Acute Physiology and Chronic Health

Evaluation (APACHE) II system, developed

to evaluate critically ill patients, has also been

used to differentiate mild AP from SAP {

Severe AP }.

The major disadvantage of this system is that many find it

cumbersome as it requires 12 physiologic measures to calculate.

A CT severity index

(Balthazar score )Has been developed and often used to predict

severity of pancreatitis on the basis of

radiographic features.

The bedside index of severity in AP

(BISAP) score integrates the systemic

inflammatory response syndrome (SIRS)

criteria and can be calculated relatively

quickly on admission.

RANSON PROGNOSTIC SIGNSETIOLOGY OF PANCREATITIS

{ GALL STONES AND NON GALL STONES }

At initial presentation :

•70

•White blood cell count (k/mm3)

•Lactate dehydrogenase (U/L)

During first 48 hours

•Decrease in hematocrit

•Elevation in blood urea nitrogen (mg/dl )

•Base deficit (mmol/L)

•Fluid sequestration (L)

The treatment for AP

The mainstay of treatment in AP is aggressive

supportive and symptomatic therapy that

includes volume repletion, pain control,

nutritional support, correction of electrolyte

abnormalities, treatment of infection (if

present), and treatment of associated or

causative conditions.

Adequate volume repletion and restoration

of perfusion to pancreatic microcirculation is

imperative to stave off progression of disease

and development of local complications.

Inadequate volume repletion is associated

with higher rates of pancreatic necrosis.

No randomized trials exist to guide rate or

volume of fluid administration. Most experts

recommend isotonic crystalloid infusion rates

of 250 to 300 Ml/hr or greater for the first 48

hours or enough to maintain urine output at 0.5

ml/kg/hr.

Narcotics are usually necessary to establish

pain control.

IV morphine or hydromorphone at 2- to 4-hour

intervals should be considered.

Occasionally, continuous infusion with

additional patient-administered boluses is

necessary.

Antisecretory agents have been considered

for use in pancreatitis.

The inhibitory effect of octreotide, a

pharmaceutical analog of somatostatin, on

pancreatic enzyme secretion has led to its

study in the treatment of AP.

The largest randomized trial comparing

placebo with octreotide in the treatment of

moderate or severe pancreatitis

found no significant difference

With regard to mortality, rate of new

complications, rate of surgical intervention,

duration of pain, or length of hospital stay.

BALTHAZAR CT GRADING OF AP

AND CT SEVERITY INDEX•A Normal pancreas

•B Enlarged pancreas

•C Inflammation of pancreas or

•D One peripancreatic fluid collection

•E More than one peripancreatic fluid

collection and /or air in retroperitoneum

NECROSIS FACTOR :

Percentage of necrosis .

*CT grade points + necrosis points.

•How should patients with

pancreatitis be fed?

Enteral feeding

Is the preferred method of nutritional support

for all patients who are seen with pancreatitis.

It is thought to help maintain the intestinal

mucosal barrier, thereby preventing

translocation, which is thought to be a major

source of infection.

Enteral feeding

No strong evidence exists that nasojejunal

feeding is advantageous over nasogastric

feeding.

Still, many experts recommend fluoroscopic or

endoscopic placement of a jejunal, or

postpyloric, feeding tube if possible.

Parenteral nutritionshould be initiated in patients unable to

tolerate oral feeding because of pain,

ileus, and/or nausea.

Opinion with regard to the timing of

initiation of parenteral nutrition

ranges from 2 to 5 days after

presentation.

•Should all patients with AP

receive antibiotics?

No. The use of prophylactic antibiotics to

prevent infection of pancreatic necrosis has

been controversial but is not currently

recommended.

No significant benefit has been found with

regard to mortality, rates of infected

necrosis,need for operative treatment, or overall

infections when administering prophylactic

antibiotics.

Broad-spectrum antibiotics should be

administered if objective evidence exists of

infected necrosis on the basis of clinical status

(i.e., fever) or cultured aspirate.

Some experts believe antibiotics are warranted

when evidence is seen on CT of necrosis in >

30% of the pancreas.

In such cases, the use of antibiotics should be

limited to 7 to 14 days because of the risk of

fungal superinfection.

If the patient's condition continues to

deteriorate, he or she should be

evaluated for minimally invasive

and/or surgical debridement or

necrosectomy .

The bedside index of severity in AP

BlSAP SCORE :1 point for each of the following if present. 0 ooints if absenl

•BUN >25 mg/dL (8.9 mmol/L)

•Impaired mental state status

•SIRS (two or more of the following) :

•Pulse > 90 beats/min

•Respiratory rate >20/min or

•PaC02 < 32 mm Hg

•Temperature >38" C or <36" C

•WBC >12,000 or <4000 cells/mm3

or > 10% immarure neutrophils

•Age > 60 yr

•Pleural effusion

The most common bacteria responsible

for infected pancreatic necrosis?

Culprit infective agents are usually gut derived,

including

Escherichia coli, Bacteroides, and

Enterococcus.

Staphylococcus and Pseudomonas

are also potential pathogens and should be

considered.

Fungal infectionof necrosis

Is rare but more common when prophylactic

antibiotics are given.

It is unclear whether fungal superinfection has

any impact on mortality.

Role of surgery for AP

Surgery may be necessary for delayed

complications of AP (i.e., pancreatic

pseudocysts, persistent sterile necrosis) or for

cholecystectomy to prevent future episodes of

biliary pancreatitis.

Surgical necrosectomy is the gold standard

treatment for infected pancreatic necrosis

resulting from severe AP.

Retrospective reviews addressing timing of

intervention found that postponing surgery

until 4 or 6 weeks after admission correlated

with decreased mortality compared with

earlier intervention.

Expert panels recommend delaying

necrosectomy at least 3 to 4 weeks after

hospitalization if possible, while

administering antibiotics and allowing the

necrosis to organize.

Principles of surgical management of

infected pancreatic necrosis include

debridement of all infected necrotic

material and drainage of the remaining

pancreatic bed.

Debridement is done bluntly and

gently, with hydrosonic irrigation

frequently used, to avoid vascular

injury.

Adequate debridement may require

multiple trips to the operating room.

The current favored drainage option

includes closure of the abdomen over

multiple large closed sump drains

with or without irrigation.

These patients are usually critically ill

and require vigorous supportive care.

•When should minimally invasive or image-

guided therapy be considered?

Although surgical necrosectomy remains the

gold standard for definitive management of

pancreatic necrosis, percutaneous and

endoscopic therapies have a growing role in

at least adjunctive management.

Percutaneous drainage (followed by surgery

if necessary) has been associated with fewer

major complications than open necrosectomy

alone but did not offer any mortality benefit.

•One third to one half of patients who undergo

percutaneous drainage have no need for surgical

necrosectomy. CT-guided percutaneous drainage of

necrotizing pancreatic collections may be considered

as a bridge to necrosectomy in patients with sepsis

who are too ill

to proceed directly to surgery.

Drainage of a walled-off necrotic cavity by

endoscopic ultrasonography (EUS) via transgastric

or transduodenal approach has been shown to be

effective; however, this modality should be considered

only in a carefully selected patient population and is

dependent on local expertise.

Additional treatment options for acute

biliary pancreatitis

Early ERCP has previously been the standard of

care for patients with AP suspected to be due to

gallstones.

All patients who have signs or symptoms of

cholangitis should have early ERCP to relieve

biliary obstruction.

Other patients with AP in which cholangitis

is not present should be evaluated on a

case-by-case basis with the understanding

that investigations have shown that early

ERCP in patients with predicted mild or

severe pancreatitis does not significantly

reduce the risk for overall complications or

mortality.

Pancreatic pseudocysts

Pancreatic pseudocysts are localized fluid

collections rich in amylase and other

pancreatic enzymes surrounded by a wall of

fibrous tissue that are not lined by epithelium.

Pseudocysts can form as a result of

pancreatic necrosis during an episode of

pancreatitis or because of disruption in the

normal duct anatomy due to stenosis,

calculus, or trauma.

Pancreatic pseudocysts may be

asymptomatic, present with pain alone, or

present with a variety of other clinical

complications including

bleeding, infection, or rupture.

Rare complications include gastric outlet

and/or biliary obstruction and thrombosis of

splenic or portal veins with development

of gastric varices.

Diagnosis is usually made on the basis of

clinical and radiographic evidence.

The best approach to the

management of pseudocysts

Pancreatic pseudocysts require treatment if

they become symptomatic or develop a

complication .

Surgical, percutaneous, and endoscopic

approaches have all been used to manage

these collections.

No randomized trials have been performed to

compare these modalities.

Endoscopic drainage has advantages of

being less invasive, more cost-effective, and

associated with lower lengths of stay than

surgery, but its use may be limited on the

basis of anatomy.

Modality of treatment for pancreatic

pseudocysts should be based on a

combination of factors including patient

comorbidities and clinical status, site and

characteristics of the lesion, and available

local expertise.

COMMON CAUSES OF ACUTE

PANCREATITIS :•Biliary-Gallstones, parasites, or

malignancy

•Alcohol

•Drugs

•Trauma, toxins

•Idiopathic, ischemic, infectious, inherited

•Metabolic-hyperlipidemia, hypercalcemia

•ERCP

•Smoking

GOOD LUCK

SAMIR EL ANSARY

ICU PROFESSOR

AIN SHAMS

CAIRO

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Wellcome in our new group ..... Dr.SAMIR EL ANSARY