MockCC13 Pancreatitis

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Stem: A 45-year-old, diagnosed & managed for acute pancreatitis 2 weeks ago.
Now presents with vomiting, SOB & epigastric pain which is not improved with PPIs.
Examination revealed tachycardia & tachypnoea.

Which enzymes to be checked apart from amylase & lipase?

Lactate dehydrogenase

Is amylase and lipase valuable? and why?

Lipase levels are more specific to the pancreas.
While amylase is not specific and can be normal if measured too early or too late because of its short half-life.

What are Causes of post-cholecystectomy pancreatitis ?

Iatrogenic injury
infectious
retained stones
stricture.

Patient comes with jaundice and ascending cholangitis 6 months after surgery, reason?

Retained stone causing obstruction
Stricture

5 weeks after the initial attack patient presented with epigastric fullness, vomiting and dyspepsia, diagnosis?

Pancreatic pseudocyst

Define pseudocyst and what are its contents?
Collection of amylase-rich fluid enclosed in a wall of fibrous or granulation tissue.

Difference between cancer & pseudocyst?
Tumour- Pseudocyst
Fluid viscosity: Elevated -Low
Tumour marker CA19-9: High -Low
Amylase: Low- High

What is the difference between true cyst and pseudocyst?

Pseudocyst is not closed and doesn't have a lining of epithelial cells separating it from the nearby tissue, instead its wall made up of fibrous and granulation tissue.

In case of pancreatic necrosis, what investigation of choice?

CT abdomen with IV contrast pancreatic protocol (thin CT slices).

What are the findings to look for in CT?

Fat stranding
Oedema
Collection
Pseudocyst
Abscess
Necrosis

What are the biochemical findings?

Hyperglycaemia
Hypocalcaemia
Hypomagnesemia
Hypoalbuminemia.

Why is the calcium level low?

In early stages
Auto-digestion of mesenteric fat by pancreatic enzymes and release of free fatty acids (chelate calcium), which form calcium salts (saponification of fat).
Later stages, due to complication like:
-Sepsis
-Hypoalbuminemia
-Transient hypoparathyroidism

Why is there hyperglycaemia?

Destruction of B cells of islets of Langerhans that normally secret insulin.
Could be due to stress response (cortisol and catecholamines).

How could you classify obstructive jaundice according to cause?

Intra-luminal: stone
Trans-luminal: cholangiocarcinoma
Extra-luminal: cancer of head of pancreas

What could the cause for silent obstructive jaundice?

Carcinoma of head of pancreas

How would you manage a patient with acute pancreatitis?

CCrISP protocol using the ABCDE approach
Admission to HDU/ICU.
Analgesia
Aggressive fluid rehydration
Supplemental oxygen
Monitoring
-Central venous pressure
-Urine output
-Blood gases
-Liver function, U&E
-Clotting profile
-Serum calcium
-Blood glucose
-Nasogastric drainage (only initially)
Antibiotics if
-If suspected cholangitis
-Sepsis
-Necrosis
-Pre-invasive intervention (ERCP).
Octreotide → decrease pancreatic secretions
PPI → prevent stress ulcers
CT scan if
-Organ failure
-Clinical deterioration
-Signs of sepsis
ERCP within 72 hours for
-Severe gallstone pancreatitis
-Or signs of cholangitis
Supportive therapy for organ failure if it develops → (inotropes, ventilatory support, hemofiltration, etc.)
If nutritional support is required → nasojejunal tube.

What scoring for pancreatitis do you know? Talk about each of them
Glasgow criteria: PANCREAS

PaO₂ < 8 kPa (normal: 10–13 kPa)
Age > 55
Neutrophils > 15,000
Calcium < 2 mmol/L (after 48h)
Renal (urea) > 16 mmol/L (normal: 2.5–6.7)
Enzymes (LDH) > 600 (after 48h)
Albumin < 32 g/L (after 48h)
Sugar (glucose) > 10 mmol/L
(at least 3 of the above = severe episode = ITU admission)

Ranson's criteria

Estimates mortality of patients with pancreatitis, based on initial and 48-hour lab values.
Criteria at time of patient admission to hospital
Age > 55
WBC > 16,000
Glucose > 11 mmol/L (> 200 mg/dL)
AST > 250 IU/L
LDH > 350 IU/L
Within 48 hours
Hct drops 10% or greater
Fluid sequestration > 6 L
Calcium < 2.0 mmol/L (< 8 mg/dL)
PO₂ < 60 mmHg (< 8 kPa)
BUN rises more than 1.98 mmol/L (> 5 mg/dL) after IV fluid hydration
Base deficit > 4 mmol/L
Mortality prediction
0–2 points: Mortality is 1%
3–4 points: Mortality is 16%
5–6 points: Mortality is 40%
7–11 points: Mortality almost 100%

What are the early and delayed complications of acute pancreatitis?
Early

Necrosis
ARDS
Pleural effusion
Electrolyte disturbance:
Hyperglycaemia
Hypocalcaemia
Hypomagnesemia
Hypoalbuminemia
Late
!Pseudocyst
Splenic vein thrombosis

How to treat splenic vein thrombosis in a patient with haemorrhagic pseudocyst?

Multidisciplinary approach including:
-Gastroenterologist/hepatologist
-Haematologist
-Interventional radiologist
→ For radiological intervention (coiling)

Complications of coiling?
Injury to surrounding structures
Haemorrhage
Failure
Infection

Abx in pt with acute pancreatitis?

Quinolones or according to Trust guidelines

Management of pain?

According to WHO analgesic ladder but I will try to avoid morphine and NSAID.
Starting with non-opioid like paracetamol, then weak opioid like (codeine), then strong opioid (pethidine), then PCA (patient-controlled analgesia), and epidural analgesia.

Why not morphine?

Causes constriction of sphincter of Oddi.

Is it true or theoretical?

Theoretical

What is CRP?

Nonspecific acute phase reactant protein made by the liver released into the blood in response to inflammation.

Causes of tachypnoea in this patient?

ARDS as complication
Sympathetic overactivation
Compression of diaphragm by pseudocyst

Exocrine enzymes of the pancreas?

Amylase: breaks down carbohydrates into simple sugars like glucose.
Proteases: break down proteins into amino acids. The main proteases are trypsin, chymotrypsin, and carboxypeptidase.
Lipase: breaks down fats into fatty acids and glycerol.

Other than the enzymes what is present in pancreatic juice?

Bicarbonate: neutralizes the acidic chyme from stomach, creating an alkaline environment that is optimal for the activity of pancreatic enzymes.
Water: helps to dilute the chyme and facilitate transport of nutrients.
Electrolytes: such as sodium, potassium. The secretion of pancreatic juice is stimulated by factors including:
-Acetylcholine: released by the vagus nerve, stimulates the secretion of pancreatic enzymes.
-Cholecystokinin (CCK): a hormone released by the duodenum in response to the presence of fatty acids and amino acids, stimulates the secretion of pancreatic enzymes and contraction of the gallbladder.
-Secretin: a hormone released by the duodenum in response to the presence of acid, stimulates the secretion of bicarbonate-rich fluid by the pancreas.

How is the pancreatic secretion stimulated?

Acid load in the duodenum plays a crucial role in stimulating pancreatic secretion. When acidic chyme enters the duodenum from the stomach, it triggers the release of secretin, which stimulates the pancreas to secrete bicarbonate-rich fluid. This fluid neutralizes the acid, creating an alkaline environment that is necessary for the activity of pancreatic enzymes.

isurg

MockCC13 Pancreatitis