(neo)-adjuvante prinzipien beim pankreas-karzinom · how do you diagnose acute pancreatitis (ap)?...

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Acute Pancreatitis University Hospital Berne, Clinic for Visceral Surgery and Medicine Jan Hendrik Niess

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Acute Pancreatitis

University Hospital Berne, Clinic for Visceral Surgery and Medicine

Jan Hendrik

Niess

How do you diagnose acute pancreatitis (AP)?

Presence of two of the following three criteria

- abdominal pain consistent with disease

- lipase or serum amylase greater than three times

upper the normal limit

- characteristic findings of abdominal imaging

- renal diseases

- appendicitis

- cholecystitis

- diabetics

When is the lipase false positive ?

What abdominal imaging modality needs to be

performed in early AP?

- Transabdominal ultrasound

- Search for biliary aetiology

- needs to be performed on admission (since sludge can develop

during AP evolution)

- sensitivity for GB lithiasis 95%

- sensitivity for CBD lithiasis 30-80%

- (pancreatic swelling only in 25 – 50%; bowel gases may mask the

pancreatic region)

What problems does CE-CT have at early AP?

- High sensitivity (90%) and specificity for AP

- In most cases AP can be diagnosed without imaging modality

- Has a low sensitivity and specificity for the detection of lithiasis

- Necrosis are not marked at early time points (prior to 48 to 72h)

When should CE-CT carried out?

In patients not improving with 72 hours (persistent pain, fever, nausea,

unable to begin oral feeding) to assess local complications

What is the aetiology of AP?

• Gallstones (40-70%)

• Alcohol (25-35%)

• Medications (http://www.mucosalimmunology.ch/images/content/PPT-presentations_free_access/bible_class/Drug-inducedpancreatitis.pdf)

• (i.e. azathioprine, furosemide, valproic acid)

• Primary and secondary hypertriglyceridemia ( > 1,000 mg/dl)

• Hypercalcemia and hyperparathyroidism

• Autoimmune

• Infectious (coxackie, mumps, CMV, HSV, HAC, HBV, HCV)

• Post -ERCP

• SPINK, PRSS1, CFTR mutations

• Congenital anomaly of the pancreas (Pancreas divisum)

• 5-14% pf patients with a benign or malign mass present with AP

Work-up of patients with AP?

- Ultrasound at admission

- Lab tests

- Ca2+

- ALT, AST, Bili g-GT

- Fasting TG (if > 1000 mg/dl, repeat 4 weeks after resolution of AP)

- Immunoglobulins

- Consider genetic testing in young patients (< 30 years) and with a

positive family history of pancreatic diseases.

- Consider anomalies of the pancreas

- Consider in patients > 40 years a benign or maligne mass as cause

for the pancreatitis

- Abdominal imaging after resolution of pancreatitis

How is the severity of AP defined?

Note:

dynamics

of OF

Am J Gastroenterol. 2013 Sep;108(9):1400-15

How can severe AP predicted?

- There is no lab parameter, which predicts severe AP

- AP-specific scoring systems (BISAP, APACHE etc.) are of importance for clinical

studies, but have limited value within the first 48 hours of AP

- Clinical assessment is most important in monitoring AP patients

Patient characteristics

Age > 55 years

Obesity (BMI > 30 kg/m2)

Altered mental status

Comorbidities

How can severe AP predicted?

The systemic inflammatory response syndrome (SIRS)

Pulls > 90 beats/min

Respiration > 20/min

Temperature <36; > 38

Laboratory findings

blood urea nitrogen (BNU) > 20 mg/dl

Haematocrit > 44

Radiology findings

pleural effusions

pulmonary infiltrates

Multiple or extrapancreatic collections

How is AP managed ?

Fluid management

• Aggressive hydration 250-500 ml per hour of isotonic crystalloid

solution. Most efficient in the first 12-24 hours, and may have little

benefit beyond

• Lactated Ringer’s solution may be the preferred isotonic crystalloid

replacement fluid.

• Fluid requirements should be reassessed at frequent intervals

within 6 h of admission and for the next 24 – 48 h. The goal of

aggressive hydration should be to decrease the blood urea nitrogen

Pain control

When should ERCP performed?

Am J Gastroenterol. 2013

Sep;108(9):1400-15

What are risk factors for stones ?

N Engl J Med. 2014 May 15;370(20):1955

How should antibiotics used ?

Consider

Mortality

Sterile necrosis 10%

Infected necrosis 30%

but it takes approximately 7 to 10 days before necrosis will become infected

This means

- Antibiotics should be given for the treatment of extrapancreatic infections

(cholangitis, pneumonia, urinary tract infections ……..).

- Routine use of prophylactic antibiotics in patients with severe

AP is not recommended (any longer)

- There are only few antibiotics that penetrate into necrotic regions

(carbapenems, quinolones, metronidazole and 4th generation cephalosporins)

- Consider the development of pancreatitis for the choice of the antibiotic used

for the treatment of extrapancreatic infections in early AP

How should nutrition be managed in AP patients?

N Engl J Med. 2014 Nov 20;371(21):1983-93

• Intravenous fluids in the first 72 hours

If patients actively asks for food an oral diet can be offered

• Start on demand oral diet after 72 hours

• If an oral diet is not tolerated within 96 hours after onset of pancreatitis,

then place a naso-enteral feeding tube for nutrition

What is the management of necrosis?

Sterile necrosis: conservative management; no drainage or necrosectomy to prevent

iatrogenic infection

(Exceptions: compartment syndrome, bowel ischemia, acute bleeding, gastrointestinal

or biliary obstruction)

Infected necrosis (confirmed or suspicious) - gas inclusion in CT

- fine needle aspiration and microbiology

conservative treatment with broad spectrum antibiotics for at least 3 to 4 weeks

if possible (wait for the encapsulation and demarcation of necrosis)

Invasive approaches for the treatment of

infected necrosis?

• Percutaneous catheter drainage

• Endoscopic transluminal drainage

• Minimally invasive retroperitoneal necrosectomy

• Minimally invasive laparoscopic necrosectomy

• Endoscopic (transluminal) necrosectomy

• Open necrosectomy

CLINICAL GASTROENTEROLOGY AND HEPATOLOGY 2012;10:1190–1201

Minimale invasive retroperitoneal necrosectomy

Endoscopic transluminal drainage and necrosectomy

CLINICAL GASTROENTEROLOGY

AND HEPATOLOGY 2012;10:1190–1201

Axios

Stent System

Gastrointestinal Endoscopy

2012; 75:870–876

CLINICAL GASTROENTEROLOGY

AND HEPATOLOGY 2012;10:1190–

1201

Summary – Management of acute pancreatitis