PANCREATITIS

6th year MKU

Dr Alex Mogere
Consultant Physician
 Pancreas anatomy
• Is an elongated and tapered organ
• Pale grey
• Weighs about 60gms
• Situated in epigastric and left hypochondriac regions of
the abdominal cavity
• Has head ,body and tail
 Pancreatic fxns
• Endocrine and exocrine
• Endocrine: islet of Langerhans, alpha celss,beta
cells ,delta cells
• Exocrine : pancreatic juice; amylase,
lipase,trypsin,chymotrypsin,carboxypeptidase
 Exocrine cells
• Consists of a large no. of lobules made up of small acini ,
which consist of secretory cells
• Each lobuleis drained by a tiny duct and these unite
eventually to form the pancreatic duct
• Pancreatic duct joins the common bile duct to form
hepatopanreatic ampulla
• The duodenal opening of the ampulla is controlled by the
hepatopancreatic sphincter of the duodenal papilla
• The fxn of the exocrine pancreas is to produce juice cont.
enzymes that diges CHOs, proteins and fats
 Pancreatitis
Defn:
an inflammatory disease of the pancreas(commonly
described as autodigestion of the pancreas) & can be
classified into:-

Acute

Chronic
 Acute Pancreatitis
Two broad classifications as per Atlanta classification
Mild disease:
Interstitial pancreatitis

Severe disease:
Necrotizing pancreatitis
Mild self limiting disease
Interstitial Oedematous pancreatitis:

There is inflammation of pancreatic parenchyma &

peripancreatic tissue
Necrotizing
There is pancreatic & peripancreatic necrosis.

Degree of pancreatic necrosis correlates with severity of

attack & its systemic manifestation.
 pathogenesis
There is ↑ in intraacinar activation of proteolytic enzymes
→↑↑trypsin & other enzymes, → autodigestive injury to
the gland

Activated pancreatic enzyme, + microcirculatory

impairment
& the release of inflammatory mediators leads to worsening
of pancreatic damage + necrosis
 pathogenesis
 Some patients with severe pancreatic damage develop
systemic inflammatory response syndrome (SIRS)
probably mediated by:
 Activated pancreatic enzymes & cytokines released
into the circulation from inflamed pancreas
A compensated anti-inflammatory response
Syndrome (CARS) balances SIRS & lead to recovery;
 Pathogenesis
• Aetiological factors
• Activation of pancreatic enzymes
• Trypsinogen to trypsin
• Acivation of proteases which causes autodigestion of
pancreas and activation of other proteolytic enzymes
• Elastase---hemorrhage
• Phospholipase…fat necrosis
 Pathogenesis

An imbalance between SIRS & CARS →severe organ

failure with high morbidity & mortality.
 Acute pancreatitis
Common causes
 Gallstone ( including microlithiasis)
 Alcohol
 Hypertriglyceridemia
 Post ERCP
 Post trauma
 Drugs eg Azathioprine,anti-HIV drugs,HCTZ,6MP
Sulfonamides,estrogens,tetracycline
 Sphincter of Oddi Dysfunction
 Hypercalcaemia
 Idiopathic
 Genetic mutations
 Acute Pancreatitis
Causes to consider in patients with recurrent bouts of AP
without an obvious aetiology

 Microlithiasis
 Drugs
 Hypertriglyceridemia
 Pancreas divisum
 Pancreatic cancer
 SOD
 Cystic fibrosis
 Idiopathic
 Acute pancreatitis: Clinical features

1) Abdominal Pain

Mild to severe
Steady & boring in character

Localized in the Epigastrium & periumbilical region

Often radiates to:-
The back
As well as to the chest, flanks, & lower abdomen.

Pain is worse in the supine position

Less in the sitting position, with the trunk flexed & knees drawn up
 Acute Pancreatitis:Clinical features.
2). Nausea vomiting
&
abdominal distention
Due to gastric & Intestinal hypomotility;
 AP: Physical signs
In severer disease, the following may also be noted:
 Distressed anxious pt.
 Low grade fever
 Tachycardia
 Hypotension
 A/P: Physical signs
 Shock
Could result from:
- Hypovolaemia

- Î Formation & release of kinin peptides which cause

vasodilatation & Î vascular permeability

-Systemic effect of proteolytic & lipolytic enzymes released

into the circulation
 A/P: Physical signs
 Jaundice

 Erythematous skin nodules due to subcutaneous fat

necrosis

 Pulmonary findings

 Abdominal tenderness & muscle rigidity:

Present out of proportion to the degree of pain
 A.P: Physical signs cont.
 Absent OR reduced bowel sound

 Cullen's sign:
A faint blue discoloration may occur around the umbilicus.
This is secondary to the haemoperitoneum

 Turners sign:
A blue- red- purple or green-brown, discoloration of the flanks
secondary to tissue catabolism of Hb may occur.
 A/P: Physical signs
NOTE:
Cullen‘s & Turners sign

Are features of severe necrotizing Pancreatitis

However they rarely occur

 INVESTIGATIONS: Diagnostic
LABORATORY

1. Serum amylase
Do within - 72hrs
As tends to level off even on a background of continuing
pancreatitis

2. Serum lipase
Remain elevated up to 14 days
 INVESTIGATIONS: Diagnostic
Laboratory tests cont:
Other Enzymes which can be tested include:
1) Trypsinogen activation peptide↑
2).Urinary & Serum trypsinogen levels are high in AP
Other lab tests
3)LFTS,U/E+creatinine,TBC,CRP,Ca,Mg lipid profile, blood
sugar
 Investigations: Diagnostic
IMAGING
C-T scan: with contrast: Do after 72hrs
Could be of value in:-
a) indicating severity of the disease
e.g. Infected necrotizing pancreatitis
b) Aetiology of the disease
 Diagnosis
Other imaging modalities

1. MRI / MRCP

2. EUS: Most useful for detecting stone in CBD

 DIAGNOSIS OF AP
Requires presence of any 2 of the following three diagnostic
parameters.
1). Acute onset of persistent , severe epigastric pain often
radiating to the back
2). Elevation of serum lipase or amylase ≥3ULN
3). Characteristic findings of acute pancreatitis on
imaging(CT,MRI, US)
*You don’t need to do imaging to make a diagnosis if
1&2 are +ve.
 Scoring systems in AP
Ransons score:
• Clinical predilection rule
• Predicts prognosis and mortality risk
• GALAW&CHOBBS(on admission and 48hrs)
BISAP,
APACHE II score,
MCTSI score,
 AP: TREATMENT
Depends on disease severity

1) Pain relief:
Acetaminophen, NSAID, Opiods:

What to use will depend on severity of pain

Could give: codein,tramadol,morphine

 AP: TREATMENT
2) Fluid:

Aggressive hydration 5-10mls /kg/hr≈ 250-500mls/hr for

48hrs then adjust downwards.

Preferred lactated ringers solution unless there is

hypercalcaemia then give N/S

Correct electrolytes if deranged

 AP TREATMENT
3) Asses patient & decide on where to admit: ward or ICU
 Haematocrit >44%
 BUN >20mg/dl (>7.14mmol/l)
 CRP >150mg/L
 Systolic BP↓↓
 Elderly >60yrs
 Organ damage
?renal,?pulmonary,cadiovascular
 AP TREATMENT
Is there evidence of SIRS: Presence of ≥2 of the
following (monitor from day 1):-
 Fever of >380C or <360C
 Heart rate >90beats/min
 Respiratory Rate >20 beats/min or arterial carbon
dioxide tension (PaCO2) <32mmHg
 Abnormal WBC >12,000/µL or <4,000/µL
or >10% immature(bands) forms.
 AP TREATMENT

Asses & monitor:

Acute Physiology and Chronic Health Examination
( APACHE)

APACHE II >8 in 1st 24hrs of admission: Indicates severe

disease.
Indicators of severe disease include:
 CRP >150mg/l, at 48hrs of disease onset
 APACHE score >8 in 1st.24hrs of admission
 Presence of SIRS
 Presence of Organ Failure in initial 72hrs
 CECT done at 72hrs with evidence of +/-infected necrosis
 Treatment
4). Nutrition:
Early enteral /gastric feeding

 Particularly in moderate to severe pancreatitis to

avoid gut bacterial translocation → sepsis

 High protein ,low fat diet

 Within 24-72hrs
 :MONITOR
BP, Pulse rate ,temperature,RR
Urine output: Aim at >0.5-1.0cc/kg /hr
P02: maintain >95%
If <90% do blood gases
Glucose level
UE/creatinine
CRP
WBC
 AP: RX
In severe disease: Necrotizing

1. NO Prophylactic antibiotics & antifungal unless

infection suspected.
Give imipenem

2. Role for surgery ?

 AP: Rx
Other measures in Rx.

Find cause & correct e.g.

1.Biliary stone DO ERCP
2. Alcohol STOP
3. Drugs stop
4. SOD, Pancreas divisum DO ERCP
5. Dyslipidimia: Correct
 CHRONIC PANCREATITIS
Is a continuous ,prolonged ,inflammatory and fibrosing
process of the pancreas.
Strictures and calcification may also occur in pancreas.
may present as :-
Episodes of acute inflammation in a previously injured
pancreas
OR

AS chronic damage, with persistent pain or malarbsorption

 CP: CAUSES
1. Alcohol/chronic

2. Idiopathic

3. Auto Immune pancreatitis

Î serum IgG4
Periampullary Bx. show Lymphocytic infiltrate
 CP: CAUSES
4) Tropical Pancreatitis ( Africa & Asia )
Associated with severe protein- calorie malnutrition with
hypoalbuminemia

There is interaction between genetic susceptibility(with

↑ prevalence of mutations of trypsin inhibitor gene
SPINK) & environmental triggers.
Commonly found in children & young adults
 CP: CAUSES
5) Trauma

6) Hypercalcaemia

7) Hereditary
 Trypsinogen & Inhibitory protein
defects
 Cystic fibrosis
 CP: CAUSES
8) Congenital abnormalities of the pancreatic duct e.g.
Pancreas divisum
9) Gall stones
10) Biliary tract disease
 Pathophysiology CP
• The 2 mjr types are:
• Chronic obstructive pancreatitis and chronic calcifying
pancreatitis
• Toxicity of alcohol causes obstruction of duct with protein
precipitates. The precipitates block the pancreatic duct
and eventually calcify,the fibrosis ensues
• Pseudocysts and abscesses commonly follow
 CP: CLINICAL FEATURES

 Upper abdominal Pain

 Obstructive jaundice
 Oily,smelly stools/steatorrhoea
 Features of Malabsorption/wt loss

 Features of insulin deficiency

 Complications of CP
• Infections
• Pseudocyst
• DM
• Abscess
• Resp complics
• SIRS
• PE,DIC
 CP: DIAGNOSIS
 Serum amylase / lipase
Usually not significantly elevated in CP

 Classic triad of :-
Pancreatic calcification
Steatorrhea
Diabetes mellitus
Usually establishes the diagnosis of CP & exocrine pancreatic
insufficiency
 CP: DIAGNOSIS
IMAGING
1. Plain radiograph
May show calcification
2. Abdominal C-T scan
3. MRI / MRCP
4. Endoscopic Ultrasound ( EUS )
5. ? ERCP
 CP: Rx.
 Relieve pain: NSAID,OPIOD,antispasmodic
 Prevention/alleviation of shock..n/saline/colloids
 Support on maldigestion
Pancreatic enzyme supplement: eg pancreozymine
 Diabetes: control with insulin
 Prevent/tx infections
 Control fluid &electrolyte imbalances
 Treat complications: Endoscopic, Surgical
 Cont. CP TX
• NG suction to reduce vomiting and gastric distension
• Avoid alcohol
• Oxygen for hypoxic pts with acute respiratory distress
syndrome
• Antacids
• Calcium-if there is hypocalcemia tetany
• Diet low in fat and high protein and CHOs
• Small frequent feeds
• Surgery—abscess,acute pseudocyst,severe peritonitis
 Cont. CP TX
• ERCP-to remove duct obstruction