Mr. T, a 56-year-old man, presented with acute pancreatitis symptoms including epigastric pain and nausea. Investigations confirmed elevated pancreatic enzymes. He was initially treated conservatively but his condition deteriorated, requiring ICU admission and intubation. Imaging showed acute pancreatitis with peripancreatic fluid collection. Antibiotics were started after he developed a fever. Complications of acute pancreatitis like pancreatic necrosis and pseudocyst formation were discussed. The role of antibiotics, ERCP, and surgical or radiologic drainage of infected collections was also outlined.
2. Case study:
◦ Mr T, 56 y.o, Indian Male, taxi driver
◦ Presented to ED with 8 hours history of epigastric pain that radiates to the back
◦ Also complaint of nausea and vomiting
◦ Moderate drinker in the past, free of alcohol for the past 3 years
◦ No history of gall stone previously
◦ No hematemesis, no melena, normal bowel habit
◦ PMHx: nil
◦ PSHx: nil
◦ Meds: nil
3. ◦ O/E:
◦ BP:110/80, HR:85, RR:18, afebrile
◦ Looks distressed, sitting up
◦ Resp: normal
◦ CVS: normal
◦ Abdomen: decreased bowel sound, mildly distended, severe LUQ tenderness, no
peritoneal signs, Murphy sign: negative
6. Pancreas ◦ The pancreas lies behind the peritoneum of
the posterior abdominal wall and is oblique
in its orientation.
◦ The head of the pancreas is on the right side
and lies within the “C” curve of the
duodenum at the second vertebral level (L2).
◦ The tip of the pancreas extends across the
abdominal cavity almost to the spleen.
◦ Collecting ducts empty digestive juices into
the pancreatic duct, which runs from the
head to the tail of the organ.
7. ◦ The Duct of Wirsung is the main pancreatic duct
extending from the tail of the organ to the major
duodenal papilla or Ampulla of Vater .
◦ The duct of Wirsung is close, and almost parallel,
to the distal common bile duct before combining
to form a common duct channel prior to
approaching the duodenum.
◦ In approximately 70% of people, an accessory
pancreatic duct of Santorini (dorsal pancreatic
duct) is present.
◦ This duct may communicate with the main
pancreatic duct.
8. ◦ Definition
◦ A group of reversible lesions characterised by inflammation of the pancreas
Incidence
◦ Male:female ratio is 1:3- in those with gallstones and 6:1 in those with alcoholism
10. Pathogenesis of acute pancreatitis
Interstitial oedema
Impaired blood flow
Ischaemia
Acinar cell injury
Interstitial inflammation
oedema
Gallstone
Chronic alcoholism
Release of intracellular
proenzymes and
lysosomal hydrolases
Activation of enzymes
ACTIVATED ENZYMES
Delivery of proenzymes to
lysosomal compartment
Intracellular activation of
enzymes
Proteolysis
(proteases)
Fat necrosis
(lipase, phospholipase)
Haemorrhage
(elastase)
Alcohol, drugs
trauma, ischaemia,
viruses
Metabolic injury
(experimental)
Alcohol, duct obstruction
DUCT OBSTRUCTION ACINAR CELL INJURY DEFECTIVE INTRACELLULAR
TRANSPORT
11.
12. Clinical manifestation
The most common symptoms and signs include:
Severe epigastric pain radiating to the back, relieved by leaning forward
Nausea, vomiting, diarrhea and loss of appetite
Fever/chills
Hemodynamic instability, including shock
In severe case may present with tenderness, guarding, rebound.
13. Diagnosis
AP established by the presence of 2 of the 3 following criteria:
◦ (i) Abdominal pain consistent with the disease
◦ (ii) Serum amylase and / or lipase greater than three times the upper limit of
normal
◦ (iii) Characteristic findings from abdominal imaging
Contrast-enhanced computed tomography (CECT) and / or magnetic resonance
imaging (MRI) of the pancreas should be reserved for patients in whom
◦ The diagnosis is unclear
◦ Who fail to improve clinically within the first 48– 72 h after hospital admission
◦ Evaluate complications
14. INITIAL ASSESSMENT AND RISK STRATIFICATION
◦ Hemodynamic status should be assessed immediately upon presentation
and resuscitative measures begun as
◦ Risk assessment should be performed to stratify patients into higher- and
lower-risk categories to assist triage, such as admission to an intensive care
◦ Patients with organ failure should be admitted to an intensive care unit
ICU or intermediary care setting whenever possible
16. Clinical findings associated with a SEVERE course for
initial risk assessment
◦ Age >55
◦ Obesity( BMI>30)
◦ Altered mental status
◦ Comorbid diseases
◦ SIRS (presence of >2)
-RR >20
-Pulse> 90
-Temp >38 /<36
-TWC >12000 /<4000
◦ Urea>20 or rising urea
◦ HCT> 44 or rising hematocrit
◦ Elevated creatinine
◦ Radiology findings:
-Pleural effusion
-Pulmonary infiltrates
-Multiple or extensive extrapancreatic
collection
17. INITIAL MANAGEMENT
◦ Aggressive hydration, defined as 250-500ml per hour of isotonic crystalloid
solution should be provided to all patients, unless cardiovascular, renal, or other
related comorbid factors exist
◦ Early aggressive intravenous hydration is most beneficial during the first 12 – 24 hr,
and may have little benefit beyond this time period
◦ Adequate prompt fluid resuscitation
- Fluids are given intravenously
- Aim to maintain urine output >0.5 ml/kg body weight
18. Nutrition in acute pancreatitis
◦ In mild AP, oral feedings can be started immediately if there is no nausea and
vomiting, and the abdominal pain has resolved
◦ In mild AP, initiation of feeding with a low-fat solid diet appears as safe as a clear
liquid diet
19. Management in a nutshell.
◦ Fluid resuscitation and correction of electrolyte imbalance
◦ Analgesia
◦ Bowel rest
◦ Strict urine output measuring
◦ DXT monitoring
◦ Stress ulcer prophylaxis
◦ **Ryles tube
◦ **Antibiotic
20. Case study: Mr T (Day 2)
◦ Overnight patient was oliguric ++, tachypneic, hypotensive
◦ IV infusing around 300 cc/H –over 7L of fluid given
◦ Transferred to ICU for intensive monitoring, fluid resuscitation & was
subsequently intubated
◦ Blood works were repeated
22. ◦ CT abdomen: Acute pancreatitis
with peripancreatic fluid with no
necrotic pancreatic tissue.
◦ Patient was started on IV Carbenem
after having repeated temperature.
25. 39-year and 43-year-old men with acute pancreatitis and pseudocysts formation. a) Axial contrast-enhanced CT scan shows
ovoid shape peripheral rim enhancing lesion (arrowhead), indicative of pseudocyst, in lesser sac and detectable peripancreatic
fluid collection and fat infiltration (arrows). b) Axial contrast-enhanced (b) CT scan shows two pseudocysts (arrowhead) in
head of pancreas and pancreaticoduodenal groove, respectively.
26. THE ROLE OF ANTIBIOTICS IN AP
◦ Infected necrosis should be considered in patients with pancreatic or extrapancreatic necrosis
who deteriorate or fail to improve after 7– 1 0 days of hospitalization
◦ Once blood and other cultures are found to be negative and no source of infection is identified,
antibiotics should be discontinued.
◦ In stable patients with infected necrosis, surgical, radiologic, and/ or endoscopic drainage should
be delayed by preferably 4 weeks to allow the development of a wall around the necrosis (walled-
off pancreatic necrosis).
28. TREATMENT OF STERILE NECROSIS
◦ Sterile necrosis is best managed medically during the first 2–3 wk
◦ After this interval, if abdominal pain persists and prevents oral intake,
debridement should be considered.
◦ This is usually accomplished surgically, but percutaneous or endoscopic
debridement is a reasonable choice in selected circumstances with the appropriate
expertise.
29. TREATMENT OF STERILE NECROSIS
◦ When sterile necrosis is debrided surgically, a common sequela is the development
of infected necrosis and the need for additional surgery
◦ Patients with sterile necrosis, there was a trend to greater mortality among those
operated on within 4 days
◦ If surgery is delayed for at least 2-3 wk ,the diffuse inflammatory process in the
retroperitoneum resolves considerably, and gives rise to an encapsulated structure
that envelops the necrotic pancreas and peripancreatic area
◦ This structure has frequently been called organized necrosis.
◦ By this time, organ failure has usually subsided, and many patients are now
asymptomatic and do not require additional therapy.
30. Indication of ERCP
ERCP is indicated for clearance of bile duct stones in patients with :
- Severe worsening biliary pancreatitis
- Cholangitis
- Poor candidates for cholecystectomy
- Post cholecystectomy
- Strong evidence of persistent biliary obstruction
31. ERCP ◦ ERCP is an endoscopic technique for visualization of the
bile and pancreatic ducts.
◦ Physician inserts a side-viewing endoscope in the
duodenum facing the major papilla.
◦ The side-viewing endoscope (duodenoscope) is specially
designed to facilitate placement of endoscopic accessories
into the bile and pancreatic duct.
◦ The endoscopic accessories may be passed through the
biopsy channel into the bile and pancreatic ducts.
◦ A catheter is used to inject dye into both pancreatic and
biliary ducts to obtain x-ray images using fluoroscopy
◦ During this procedure, the physician is able to see two sets
of images: the endoscopic image of the duodenum and
major papilla, and the fluoroscopic image of the bile and
pancreatic ducts.
The gland has both exocrine and endocrine functions.
In its exocrine capacity, the acinar cells produce digestive juices, which are secreted into the intestine and are essential in the breakdown and metabolism of proteins, fats, and carbohydrates
. In its endocrine function capacity, the pancreas also produces insulin and glucagon, which are secreted into the blood to regulate glucose levels.
The pancreas receives blood from branches of both the coeliac artery and superior mesenteric artery. The splenic artery runs along the top margin of the pancreas, and supplies the neck, body and tail of the pancreas through its pancreatic branches, the largest of which is called the greater pancreatic artery. The superior pancreaticoduodenal artery and inferior pancreaticoduodenal artery runs along the anterior and posterior surfaces of the head of the pancreas at its border with the duodenum. These supply the head of the pancreas.[4]
The body and neck of the pancreas drain into the splenic vein; the head drains into the superior mesenteric and portal veins.
Serum amylase alone cannot be used reliably for the diagnosis of AP and serum lipase is preferred.
Serum lipase appears to be more specific and remains elevated longer than amylase after disease presentation.
Upper limit of normal greater than 3– 5 times may be needed in diabetics who appear to have higher median lipase compared with nondiabetic patients for unclear reasons
Transfer to ICU) (or possibly a step-down care unit should be considered If there are :
Signs that suggest that the pancreatitis is severe or is likely to be severe
Need for very aggressive fluid resuscitation to overcome hemoconcentration, especially in an older person who may have underlying cardiovascular disease
If a patient does not have hypoxemia but is showing signs of labored respiration, transfer should be considered to monitor pulmonary status carefully in anticipation
An early elevated :
Hematocrit
Blood urea nitrogen
Creatinine
Should prompt clinicians to institute more intensive early resuscitation measures.
Antibiotics should be given for an extrapancreatic infection, such as cholangitis, catheter-acquired infections, bacteremia, urinary tract infections, pneumonia
Routine use of prophylactic antibiotics in patients with severe AP is not recommended
The use of antibiotics in patients with sterile necrosis to prevent the development of infected necrosis is not recommended
IMRIE: age, twc, calcium,urea,glucose
Kidney shutting down
After 1: Initial CT-guided (FNA) for Gram stain and culture to guide use of appropriate antibiotics or
Empiric use of antibiotics after obtaining necessary cultures for infectious agents, without CT FNA, should be given
In patients with infected necrosis, antibiotics known to penetrate pancreatic necrosis, such as carbapenems, quinolones, and metronidazole
Guidewire cannulation
Pancreatic duct stents in pt doin ampullectomy, endoscopic sphincter of oddi manometry
/ or post-procedure rectal (NSAID) suppositories should be utilized to lower the risk of severe post-ERCP pancreatitis in high-risk patients :diclofenac/indomethacin
Sphincter of Oddi dysfunction is diagnosed when the basal sphincter pressure is greater than 40 mm Hg.