1. CASE SCENARIO
History A 50-year-old civil services officer presents to the A&E with 2- days h/o vomiting and epigastric pain which radiates through to the back. He is not on any regular medication, but admits to drinking alcohol everyday for the last five years.

2. CASE SCENARIO
Examination
The patient is unable to lie flat for the examination.
His blood pressure is 150/80 mmHg and he has a pulse rate of 120/min. Palpation of his abdomen reveals tenderness in the epigastrium. The abdomen is not distended and he has normal bowel sounds. Rectal examination is unremarkable.

3. CASE SCENARIO Investigations Serum amylase 4672 IU/dL 0-100 IU/dL WBC
13.3 x 109 /L
x 109/L

4. QUESTIONS
What is the most likely diagnosis?
Which important differential diagnosis should be excluded?
How will you grade the severity of the condition?
What are its causes?
What are the other causes of the elevated serum marker of this condition?
How will you manage the condition?

5. ACUTE PANCREATITIS Faisal Ghani Siddiqui
MBBS; FCPS (General Surgery); PGDIP-BIOETHICS; MCPS-HPE; FICLS; (MHPE)

6. Pancreas is situated in the retroperitoneum.
It is divided into a head (30 per cent of the gland by mass) and a body and tail (together constitute 70 per cent).
The head lies within the curve of the duodenum, overlying the body of the second lumbar vertebra and the vena cava.

7. The aorta and the superior mesenteric vessels lie behind the neck of the gland.
Behind the neck of the pancreas, the superior mesenteric vein joins the splenic vein to form the portal vein.

8. Parenchymal Cells of Pancreas
Exocrine
(90%)
Endocrine
(10%)
Islets of Langerhans
(B, A, D cells)
80–90 per cent of pancreas is composed of exocrine acinar tissue organized into lobules. Acinar cells are clumped around a central lumen, which communicates with the duct system.
Clusters of endocrine cells, known as islets of Langerhans, are distributed throughout the pancreas. Islets consist of different cell types: 75 per cent are B cells (producing insulin); 20 per cent are A cells (producing glucagon); and the remainder are D cells (producing somatostatin) and a small number of pancreatic polypeptide cells. Within an islet, the B cells form an inner core surrounded by the other cells. Capillaries draining the islet cells drain into the portal vein, forming a pancreatic portal system.

9. Endocrine Cells of PancreasB
insulin A
glucagon
D somatostatin
Islets consist of different cell types:
75 per cent are B cells (producing insulin)
20 per cent are A cells (producing glucagon)
Remainder are D cells (producing somatostatin)

10. -inflammation of the gland parenchyma
PANCREATITIS
-inflammation of the gland parenchyma
of the pancreas
Pancreatitis is inflammation of the gland parenchyma of the pancreas.

11. Acute Pancreatitis Chronic For clinical purposes pancreatitis can be
acute, which presents as an emergency, and
chronic, which is a prolonged and frequently lifelong disorder resulting from the development of fibrosis within the pancreas.
Acute pancreatitis is defined as an acute condition presenting with abdominal pain and is usually associated with raised pancreatic enzyme levels in the blood or urine as a result of pancreatic inflammation. Acute pancreatitis may recur.
The underlying mechanism of injury in pancreatitis is thought to be premature activation of pancreatic enzymes within the pancreas, leading to a process of autodigestion. Anything that injures the acinar cell and impairs the secretion of zymogen granules, or damages the duct epithelium and thus delays enzymatic secretion, can trigger acute pancreatitis. Once cellular injury has been initiated, the inflammatory process can lead to pancreatic edema, hemorrhage and, eventually, necrosis. As inflammatory mediators are released into the circulation, systemic complications can arise, such as hemodynamic instability, bacteraemia (due to translocation of gut flora), acute respiratory distress syndrome and pleural effusions, gastrointestinal haemorrhage, renal failure and disseminated intravascular coagulation (DIC).
Acute pancreatitis may be categorised as mild or severe. Mild acute pancreatitis is characterised by interstitial oedema of the gland and minimal organ dysfunction. Eighty per cent of patients will have a mild attack of pancreatitis, the mortality from which is around 1 per cent. Severe acute pancreatitis is characterised by pancreatic necrosis, a severe systemic inflammatory response and often multi-organ failure. In those who have a severe attack of pancreatitis, the mortality varies from 20 to 50 per cent. About one-third of deaths occur in the early phase of the attack, from multiple organ failure, while deaths occurring after the first week of onset are due to septic complications.
Chronic pancreatitis is defined as a continuing inflammatory disease of the pancreas characterised by irreversible morpho- logical change typically causing pain and/or permanent loss of function. Many patients with chronic pancreatitis have painful exacerbations, but the condition may be completely painless.

12. WHAT IS ACUTE PANCREATITIS?
Acute inflammation of pancreatic parenchyma
Presents as an emergency
With abdominal pain and vomiting
Associated raised pancreatic enzyme levels in blood or urine
Acute pancreatitis is defined as:
an acute condition, presenting with
abdominal pain, and
usually associated with raised pancreatic enzyme levels in the blood or urine as a result of pancreatic inflammation

13. Impairment of secretion of zymogen granules
Injury to
acinar cells
Impairment of secretion
of zymogen granules
Premature activation of the enzymes; Autodigestion
Local inflammation
Systemic complications
UNDERLYING MECHANISM OF INJURY IN PANCREATITIS
The underlying mechanism of injury in pancreatitis is thought to be premature activation of pancreatic enzymes within the pancreas, leading to a process of autodigestion. Anything that injures the acinar cell and impairs the secretion of zymogen granules, or damages the duct epithelium and thus delays enzymatic secretion, can trigger acute pancreatitis. Once cellular injury has been initiated, the inflammatory process can lead to pancreatic edema, hemorrhage and, eventually, necrosis. As inflammatory mediators are released into the circulation, systemic complications can arise, such as hemodynamic instability, bacteraemia (due to translocation of gut flora), acute respiratory distress syndrome and pleural effusions, gastrointestinal haemorrhage, renal failure and disseminated intravascular coagulation (DIC).

14. ACUTE PANCREATITIS -AETIOLOGY
80%
Gallstones
Alcohol
Viral infections: mumps
Abdominal trauma: bicycle handle injury
Iatrogenic: ERCP
Drugs: steroids; azathioprine
Hypocalcemia
Pancreas divisum
Idiopathic

15. Categories of Acute Pancreatitis
Mild
Interstitial edema
Minimal organ dysfunction
Low mortality rate (1%)
Severe
Pancreatic necrosis
Severe SIRS / MOF
High mortality rate (20-50%)
Acute pancreatitis may be categorized as mild or severe.
Mild acute pancreatitis is characterized by interstitial edema of the gland and minimal organ dysfunction. 80% of patients will have a mild attack of pancreatitis, the mortality from which is around 1%
Severe acute pancreatitis is characterized by pancreatic necrosis, a severe systemic inflammatory response and multi-organ failure. The mortality varies from 20 to 50 %. About one-third of deaths occur in the early phase of the attack, from multiple organ failure, while deaths occurring after the first week of onset are due to septic complications.

16. ACUTE PANCREATITIS –CLINICAL FEATURES
Pain
Vomiting
Tachypnea, tachycardia, shock
Fever
Jaundice
Abdominal distension
Grey Turner / Cullen’s sign

17. Cullen’s sign
Grey-Turner’s sign

18. ACUTE PANCREATITIS –INVESTIGATIONS
Laboratory investigations
Serum amylase / lipase levels
Radiological
Plain X ray abdomen (Ileus; calcifications)
X-ray chest (pneumoperitoneum; pleural effusion))
Ultrasound (gallstones; pancreatic edema)
Contrast enhanced CT (Pancreatic necrosis)

19. OTHER CAUSES OF HYPERAMYLASEMIA
Perforated peptic ulcer
Mesenteric infarction
Acute cholecystitis
Generalized peritonitis
Intestinal obstruction
Ruptured ectopic pregnancy
Diabetic ketoacidosis
Bowel perforation
Renal failure
Ruptured aortic aneurysm

20. The colon cutoff sign describes abrupt termination of gas shadow within the proximal colon at the level of the radiographic splenic flexure, usually with decompression of the distal colon.
Inflammatory exudate in acute pancreatitis that extends into the phrenicocolic ligament by directly spreading through the lateral attachment of the transverse mesocolon gives rise to this sign. Infiltration of the phrenicocolic ligament results in functional spasm and/or mechanical narrowing of the splenic flexure at the level where the colon returns to the retroperitoneum.
This transition point, or cutoff, is further accentuated by distention of the intraperitoneal transverse colon from the focal adynamic ileus, which is also a result of the underlying inflammatory process. This appearance can mimic a true colonic obstruction.
Colon cut-off
sign

21. A sentinel loop is a focal area of adynamic ileus close to the intra-abdominal inflammatory process.
The sentinel loop sign may aid in localizing the source of inflammation. For example, a sentinel loop in the upper abdomen may indicate pancreatitis, while one in the right lower quadrant may be due to appendicitis.
Sentinel loop

22. Pleural effusion

23. ASSESSMENT OF SEVERITY –SCORING SYSTEMS
Ranson’s criteriae
Used to grade severity
Helps decide whether patients should be managed
on ward, or
in HDU or intensive care

24. RANSON’S CRITERIAE On admission: Within 48h: Age: >55 years
WBC count: >16 x 109 L
LDH: >600 IU/L
AST: >120 IU/L
Glucose: >10 mmol/L
Fluid sequestration: >6 L
Estimates on mortality are based on the number of points scored: 0–2: =2 per cent; 3–4: =15 per cent; 5–6: =40 per cent; >7: =100 per cent
Within 48h:
Hematocrit fall: >10 per cent
Urea rise: >0.9 mmol/L
Calcium: >2mmol/L
pO2: >60 mmHg
Base deficit: >4

25. ASSESSMENT OF SEVERITY –OTHER SCORING SYSTEMS
Glasgow
APACHE-II

26. ACUTE PANCREATITIS -MANAGEMENT
NPO
Analgesics
Fluid resuscitation
Supplement oxygen
Antibiotics
Continuous monitoring for systemic / local complications
Treat the cause

27. ACUTE PANCREATITIS - COMPLICATIONS
Local
Sterile pancreatic necrosis
Infective pancreatic necrosis
Pancreatic abscess
Pancreatic pseudocyst
Abscess formation
Splenic / portal vein thrombosis
Systemic
Renal failure
Respiratory failure
Cardiac failure
Septic shock
Multi-organ failure and death

28. CASE SCENARIO
History A 50-year-old civil services officer presents to the A&E with 2- days h/o vomiting and epigastric pain which radiates through to the back. He is not on any regular medication, but admits to drinking alcohol everyday for the last five years.

29. CASE SCENARIO
Examination
The patient is unable to lie flat for the examination.
His blood pressure is 150/80 mmHg and he has a pulse rate of 120/min. Palpation of his abdomen reveals tenderness in the epigastrium. The abdomen is not distended and he has normal bowel sounds. Rectal examination is unremarkable.

30. CASE SCENARIO Investigations Serum amylase 4672 IU/dL 0-100 IU/dL WBC
13.3 x 109 /L
x 109 /L

31. QUESTIONS
What is the most likely diagnosis?
Which important differential diagnosis should be excluded?
How will you grade the severity of the condition?
What are its causes?
What are the other causes of the elevated serum marker of this condition?
How will you manage the condition?