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Acute Pancreatitis

40

 

Ajay Kumar and Akshat Kumar

 

A 45-year-old nonalcoholic male patient presented with severe continuous upper abdominal pain for 1 day, associated with vomiting and mild abdominal distension. He had history of right hypochondrium pain 6 months back. His vital signs were stable. Abdomen examination showed mild tenderness and distension. Bowel sounds were sluggish. Investigations showed leukocytosis (13,000), serum bilirubin of 2.5 mg/dl, and fourfold increase in transaminases. Serum amylase was 1,420 IU and serum lipase was 1,200 IU. Ultrasonography of the abdomen showed 7-mm gallstones, normal common bile duct (CBD), and bulky pancreas with peripancreatic fluid collection. He was diagnosed to have biliary pancreatitis.

Acute pancreatitis (AP) can have significant morbidity and mortality. Outcome of AP is determined by its severity, which is, to a large extent, determined by the amount of pancreatic necrosis. Organ failure or infected necrosis is associated with adverse outcome.

Step 1: Initiate resuscitation and take focused history

Initiate resuscitation, as mentioned in Chap. 78.

Take detailed history.

Most of the patients (95%) present with acute epigastric abdominal pain. About 50% of these patients will have this pain referred to the back. This can be accompanied by nausea, vomiting, and abdominal distension or fever. Give attention to

A. Kumar, M.D., D.M. (*)

Department of Gastroenterology & Hepatology, Indraprastha Apollo Hospitals, New Delhi, India

e-mail: ajaykge@hotmail.com

A. Kumar, M.B.B.S.

Mayo Clinic, Rochester, NY, USA

R. Chawla and S. Todi (eds.), ICU Protocols: A stepwise approach,

319

DOI 10.1007/978-81-322-0535-7_40, © Springer India 2012

 

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A. Kumar and A. Kumar

 

 

Table 40.1 Etiology of AP

 

Biliary tract stone disease

Traumatic

Viral infections (mumps)

Idiopathic pancreatitis

Postoperative—duct exploration

Drugs

Iatrogenic—post-endoscopic retrograde

Parasites—ascaris and clonorchis

cholangiopancreatography (ERCP)

 

Pancreatic neoplasm

Hypertriglyceridemia

Ethanol abuse

 

history of alcohol intake, previous gallstone disease, drug intake, and hypertriglyceridemia or known malignancy.

History should be directed toward the known causes of pancreatitis (Table 40.1) in a suspected case.

Step 2: Perform focused detailed examination

The patient may have signs of shock or may be hemodynamically stable depending on the severity of disease.

The patient may have low-grade fever, mild jaundice, abdominal distension, tenderness, ileus, ascites, and pleural effusion.

Step 3: Send investigations

Complete hemogram.

Serum amylase—initially elevated but may decrease after 2–3 days if the necrosis is widespread. False positive occurs in gastrointestinal perforation, renal failure, severe burns, and diabetic ketoacidosis.

Serum lipase—it persists longer than amylase. If the necrosis is widespread, it may be normal.

Serum calcium is usually low.

Arterial blood gas (ABG) and electrolytes, blood glucose, and serum triglyceride test.

Renal functions test.

Altered liver function tests suggest biliary etiology.

C-reactive protein.

Blood culture.

Chest and abdominal skiagram helps to rule out perforation and ileus.

Ultrasound of the whole abdomen.

Step 4: Assessment of severity

The outcome depends on severity.

According to the Atlanta classification, severity is defined by the presence of organ failure and/or local complications. The Mayo group defines an additional group of moderate severity, which is characterized by local complications without organ failure.

Various scoring systems (Table 40.2), such as Ranson’s and Acute Physiology and Chronic Health Examination (APACHE) II, have been used in evaluating the severity of AP for many years. They have their own limitations.

40 Acute Pancreatitis

321

 

 

Table 40.2 Method to predict the severity of AP

 

(1) Ranson’s criteria

 

 

0 h

Age

>55 years

White blood cell count

>16,000/mm3

Blood glucose

>200 mg/dL (11.1 mmol/L)

Lactate dehydrogenase

>350 U/L

Aspartate aminotransferase

>250 U/L

 

48 h

Hematocrit

Fall by ³10%

Blood urea nitrogen

Increased by >5 mg/dL

 

(1.8 mmol/L) despite fluids

Serum calcium

<8 mg/dL (2 mmol/L)

PO2

<60 mmHg

Base deficit

>4 mEq/L

Fluid sequestration

>6,000 mL

The presence of one to three Ranson’s criteria represents mild pancreatitis; the mortality rate rises significantly with four or more criteria

The presence of three or more Ranson’s criteria within the first 48 h is indicative of severe pancreatitis

(2) The BISAP score for early mortality prediction (within the first 24 h)

Five parameters

Blood urea nitrogen (BUN) >25 mg/dL

Impaired mental status

SIRS 2 or more

Age >60 years

Pleural effusion

Predictive accuracy of BISAP is similar to APACHE II

The BISAP score of more than 3 predicts persistent organ failure (p < 0.0001) and necrosis (p < 0.0004)

Mortality increases from BISAP score of 1–5

Patients with predicted severe disease should be shifted to the specialist center or ICU, and aggressive management should be rapidly instituted

A new prognostic scoring system, the bedside index for severity in acute pancreatitis (BISAP), has been found to be an accurate means for risk stratification in patients with AP (Table 40.2). Its components are clinically relevant and easy to obtain. This score is simple, easy, and inexpensive. The prognostic accuracy of BISAP is similar to those of the other scoring systems.

The simple score like SIRS alone has also been used for predicting mortality. SIRS is defined by the presence of two or more of the following criteria: pulse of

more than 90 beats/min, respirations of more than 20/min, or PaCO2 of less than 32 mmHg, temperature of more than 100.4°F or less than 96.8°F, and white blood cell count of more than 12,000 or less than 4,000 cells/mm3, or more than 10% immature neutrophils. It is very simple and inexpensive and can be done multiple times. SIRS of two or more for over 48 h predicts mortality of 25%.

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A. Kumar and A. Kumar

 

 

Table 40.3 CT grading of AP

(A) Balthazar–Ranson’s grading system (can be done without contrast)

ANormal appearing pancreas

BFocal or diffuse enlargement of pancreas

CPancreatic gland abnormalities associated with mild peripancreatic inflammatory changes (stranding)

DFluid collection in a single location, usually within anterior pararenal space

ETwo or more fluid collections near the pancreas and/or presence of gas in or adjacent to the pancreas

(B) Severity of AP

CT grade

Score

A

0

B

1

C

2

D

3

E

4

Necrosis (needs IV contrast)

Score

None

0

<33%

2

33%–50%

4

³50%

6

 

CT severity index (0–10)

 

CT grade (0–4) + necrosis (0–6) = total score

• MRI of the abdomen should be done if CECT is contraindicated

Step 5: Do imaging

Ultrasound is noninvasive and the best tool available for the initial evaluation of pancreatitis. This may reveal gallstones or edema of the pancreas.

CT scan should be postponed till 72 h or more.

A contrast-enhanced CT (CECT) of the abdomen is one of the finest modalities available to morphologically diagnose and quantify the necrosis, which predicts prognosis (Table 40.3). These changes may not appear in the first few days.

The only indication for early CT scan is when one is not certain about the diagnosis.

The follow-up CT scan is required if one suspects the development of a complication.

CT should be done with a proper pancreatic protocol. Dynamic CECT is must for this (100–150 mL of contrast at 3 mL/s). Necrosis is diagnosed by less than 50 HU enhancement (normal pancreas 100–150 HU).

Step 6: Start treatment

All patients with AP who have severe pain, vomiting, dehydration, and raised amylase should be hospitalized.

40 Acute Pancreatitis

323

 

 

The patient who is hemodynamically unstable and has tachypnea, hypoxia, and decreased urine output indicates severe course and should be admitted to the ICU.

There are a number of drugs which have been specifically used to inhibit the process of pancreatitis but have not been shown to have any therapeutic benefit in controlled trials.

General supportive care is the mainstay of the treatment in AP.

(A)Fluids

Patients with severe pancreatitis should be resuscitated with aggressive fluid resuscitation.

These patients have a huge fluid loss in the third space, which leads on to hemoconcentration, and relative pancreatic bed ischemia, which can further increase the pancreatic necrosis. So rapid restoration of intravascular fluid volume is the priority.

Their fluid requirement in 24 h may vary from 5 to 7 L, generally in the form of crystalloids.

Use vasopressors after ensuring adequate intravascular volume.

Invasive hemodynamic monitoring should be done especially in cases of poor cardiac functions and in patients who are hemodynamically unstable with the aim of keeping the urine output above 0.5 mL/kg/h, hematocrit below 30%, and central venous pressure of 6–8 cmH2O.

(B)Relief of pain

Try conventional analgesics by the IV route.

Opioids are not contraindicated. Transdermal fentanyl patch of 25–50 mcg may be used to relieve pain.

Avoid nonsteroidal anti-inflammatory drugs (NSAIDs).

(C)Antibiotics

The use of antibiotics in AP has been quite controversial and still remains so. In the initial phase, clinical features are primarily of inflammation (SIRS) and do not require antibiotics.

Only definite indication of therapeutic antibiotics is cholangitis due to CBD stones. Gram-negative pathogens such as Escherichia coli and anaerobes are the typical pathogens. The third-generation cephalosporins, fluoroquinolone are good initial choices.

The other rationale of antibiotics has been for prophylactic use to prevent infection of the pancreatic necrosis. For this purpose, multiple studies have been performed over the past 15 years, on the basis of which guidelines have been changing every few years. Current guidelines do not recommend the use of prophylactic antibiotics.

In practice, lot of these patients of severe pancreatitis will be in the ICU with the central line and urinary catheters, and some of them may be on ventilator support or dialysis. Thus, they are prone to hospital-acquired sepsis. Antibiotic choice for these patients depends on the local epidemiology of infections in the ICU and the sensitivities of these organisms. To treat the hospital-acquired sepsis, antibiotics may be used as per the hospital guidelines.

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A. Kumar and A. Kumar

 

 

(D)Nutrition

AP is a hypercatabolic state and can lead to severe nutritional deficiencies.

While mild pancreatitis patients can start oral intake in 5–7 days, most of the severe AP patients cannot be fed orally for a significant period and thus require nutritional support.

Moreover, traditionally the only way of treating pancreatitis was to give rest to the pancreas by not feeding and by nasogastric tube aspiration. Now, nasogastric tube aspiration is advisable only in patients of gastric ileus who are repeatedly vomiting.

In such patients, enteral nutrition with the nasojejunal (NJ) tube should be started as early as within 48 h. The NJ tube is placed 30 cm distal to the ligament of Treitz under endoscopic/fluoroscopic guidance or at the bedside by gastric insufflations technique. It helps in nutrition as well as in prevention of sepsis.

Recently, there has been some evidence which shows that nasogastric feeding in patients who cannot tolerate oral feed is as good as NJ feed, but this remains controversial.

Administer enteral solutions as a continuous 24-h pump-driven infusion. Start with 500 mL/day and increase the diet gradually (250– 500 mL/day) until the patient’s targeted calorie needs are tolerated.

If the nutritional target cannot be met exclusively by the enteral route after a 5- to 7-day trial, consider combined enteral and parenteral nutritional support (TPN plus EN).

Earlier, total parenteral nutrition was used for nutritional support. It is expensive and increases the risk of line sepsis. Fasting promotes gut atrophy with decreased mucosal lymphocytes and immunoglobulin A (IgA), which predisposes to bacterial translocation and infection of the pancreatic necrosis. So TPN is recommended only when enteral nutrition is not possible or to supplement inadequate enteral nutrition.

Monitor serum glucose and give IV insulin infusion if indicated.

Avoid overfeeding and improve glucose tolerance by supplying some calories as lipids and maintain the triglyceride level below 400 mg.

When patients can resume orally, they should initially be fed lowcalorie and low-fat diet, which should be gradually increased. This can be continued till the patient starts taking adequately orally, which may be after 2–3 weeks.

Step 7: Early ERCP in acute biliary pancreatitis

Early ERCP (48–72 h) is indicated only in patients of acute biliary pancreatitis with evidence of cholangitis. If in doubt, endoscopic ultrasound/magnetic resonance cholangiopancreatography (EUS/MRCP) can be done to decide if the stone is still retained in CBD. It should be undertaken only by experts as it has high failure and complication rate.

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