Aims and objectives • Cover the following: • Pathophysiology, clinical presentation, investigations, management, complications • High yield facts for SBAs • Duration: 60 minutes • Slides and recordings: app.bitemedicine.com 2
Case-based discussion: 1 History A 52-year-old male is admitted to the surgical assessment unit with severe, constant epigastric pain and vomiting. The pain came on within 30 minutes of eating and radiates to his back. He speaks English poorly as he has recently immigrated from Trinidad and thus eliciting a past medical history is unsuccessful. On examination, he is tender in the epigastrium with guarding. There is a scent of alcohol on his breath. Observations HR 115, BP 98/76, RR 19, SpO2 95%, Temp 38.2 6
Question: 1 7
1 2 Neural tube Developing pancreas Developing spleen Developing gut Rotating gut Developing liver Falciform ligament 4 3 Pancreas Spleen Gastrosplenic ligament Gastrohepatic ligament
Case-based discussion: 1 History A 52-year-old male is admitted to the surgical assessment unit with severe, constant epigastric pain and vomiting. The pain came on within 30 minutes of eating and radiates to his back. ! ! ! ! ! He speaks English poorly as he has recently immigrated from Trinidad and thus eliciting a past medical history is unsuccessful. On examination, he is tender in the epigastrium with guarding. There is a scent of alcohol on his breath. C…U…llen's sign Observations HR 115, BP 98/76, RR 19, SpO2 95%, Temp U = umbilicus 38.2 9
Introduction Definition • Acute pancreatitis arises due to inflammation of the pancreas • Characterised clinically by acute abdominal pain + rise in pancreatic enzymes in blood/urine Epidemiology • In the UK there is an estimated 30 per 100,000 cases each year • 25% of cases are severe • Of the severe cases, 25% will die • Overall mortality rate of 5% Risk factors • Advancing age • Afro-Caribbean ethnicity • Family history 10
Pathophysiology Pancreas function • Endocrine function • Exocrine function Gallbladder function Bile storage and release • Physiology Food stimulus • Duodenum à CCK • 1) Pancreas 2) Gallbladder 11
Pathophysiology Mechanisms Irrespective of the cause, the pathophysiological pathways converge with: • Obstruction of the pancreatic secretory transport • Premature activation of pancreatic pro-enzymes (zymogens), such as trypsinogen to • trypsin There are a number of host defence mechanisms that counter and remove premature • zymogen activation. These include: Pancreatic secretory trypsin inhibitors (PSTI) • Alpha-1 anti-trypsin • Alpha-2 macroglobulin • However, these systems can become overwhelmed if there is excess activation of zymogens, • leading to pancreatic autodigestion and further enzyme activation This causes a positive cycle of inflammation and enzyme release • 12
Case-based discussion: 1 cont… Investigations: • WCC 16 • Urea 22 • Creatinine 200 • AST 200 • ALT 180 13
Question: 2 14
Explanation Why gallstones? This patient has an ALT of 180U/L. • 1. An ALT of >150U/L has an 85% positive predictive value for gallstone-related pancreatitis. 2. His raised AST and ALT suggest a cholestatic picture, likely due to gallstones. 3. Finally, the onset of the pain came on shortly after eating, which is in keeping with gallstones. Why not alcohol? 1. Despite the patient smelling of alcohol, this should not automatically make alcohol the most likely cause. There is no past medical history to back this up. 2. It is estimated that ~50% of cases of acute pancreatitis are due to gallstones compared to 20% being caused by alcohol abuse. 15
Aetiology Causes I – iatrogenic • G – gallstones • E – ethanol abuse • T – trauma (usually sharp trauma, e.g. knife stabbing or gunshot wound) • S – scorpion and spider bites (e.g. Tityus trinatis scorpion in Trinidad) • M – mumps virus (+ measles, HIV, EBV, hepatitis-A) • A – autoimmune (e.g. IgG4-related disease, Sjogren’s disease) • S – steroids • H – hypercalcaemia, hyperlipidaemia • E – endoscopic retrograde cholangiopancreatography (ERCP) • D – drugs (e.g. valproate, azathioprine, thiazide diuretics) • 16
Clinical features Symptoms Signs Severe upper abdominal pain Tachycardic Band-like radiation to the back (~50% of Fever cases) Nausea Hypotensive (if displaying signs of SIRS) Vomiting Jaundice Anorexia Abdominal distension and tenderness Dyspnoea Cullen’s sign Steatorrhoea Grey Turner’s sign Poor urinary output Fox’s sign 18
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Investigations Diagnosis - ANY 2 of: 1. Clinical features consistent with pancreatitis (e.g. classical-sounding pain) 2. Elevation of serum amylase or serum lipase (at 3x the upper limit of normal). 3. Radiological features consistent with pancreatitis (e.g. inflammation, necrosis on CT imaging) Bloods: Serum amylase : Most common. Rises faster than lipase but less specific • Serum lipase : More specific. Not routine • LFTs: Albumin and transaminases are required for severity scoring • FBC: WCC is required for severity scoring • U&E: Urea required for severity scoring • Clotting screen : It is important to monitor clotting for development of DIC • ABG: Arterial sampling is required for severity scoring • Serum glucose: Blood sugars are required for severity scoring • Serum LDH: Lactate dehydrogenase is required for severity scoring (if AST is not available) • Serum calcium: Ca 2+ levels are required for severity scoring • 20
Investigations Imaging CXR: Used to assess for development of ARDS, as well as pleural effusions and atelectasis. • AXR: Used to exclude bowel obstruction, as the clinical picture can overlap with acute pancreatitis. • To consider: Abdominal US: this may be used to identify any gallstones or evidence of duct dilatation. • CT imaging: • A dynamic contrast-enhanced CT is not ordered routinely for diagnosis. • It may be required if one of the other 2 diagnostic criteria are not met. • Features indicative of acute pancreatitis include local oedema and swelling, as well as non- • enhancing areas that suggest pancreatic necrosis. A CT scan to assess for complications or severity of disease is usually only performed after 6-10 • days of admission. 21
Investigations 22
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Modified Glasgow score A guide for high-dependency care referrals . Parameters 1 point for each of the following: P PO 2 <8kPa A Age >55 years N Neutrophils WCC >15x10 9 /L C Calcium <2mmol/L R Renal function Urea >16mmol/L E Enzymes AST >200U/L OR LDH >600U/L A Albumin <32g/L S Sugar Blood glucose >10mmol/L 24
Management First line IV fluid resuscitation : aggressive fluid management is required to compensate for the “third space • losses” Catheterisation : monitoring urine output will rapidly identify any renal dysfunction, as well as aid • with plotting a fluid balance chart Oxygen supplementation : if the oxygen saturations <94%, supplementary oxygen is required • Opiate analgesia : dosage of analgesia should be titrated with the severity of the pain • Feeding : “resting” the pancreas is not evidence based and thus early enteral nutrition is • encouraged to prevent intestinal atrophy and may reduce bacterial translocation from the GI tract to pancreas 25
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Complications Systemic • Hypocalcaemia Think about the • Disseminated intravascular coagulation Modified Glasgow Score • Functional ileus • Renal failure 27
Complications Systemic • ARDS Think about the • Pleural effusions Modified Glasgow Score • Aspiration pneumonia • Hypovolaemic shock 28
Question: 6 29
Complications Local Necrotising pancreatitis • A severe subtype of acute pancreatitis, whereby • necrosis presents within the first 24-48 hours It should be suspected in those who continue to have • pain, nausea and fever despite supportive management The key diagnostic factor is non-enhancing low • attenuating pancreatic tissue on CT imaging It carries a poor prognosis and has a high risk of • becoming infected Chronic pancreatitis • Recurrent episodes of acute pancreatitis can lead to • a chronic picture Defined as irreversible inflammation and/or • fibrosis of the pancreas with progressive decline in endocrine and exocrine function 30
Complications Local Peri-pancreatic fluid collection • Occurs <4 weeks after initial presentation • Oedema in the inflamed pancreas causes the • pancreatic capsule to swell Leakage of pancreatic lipases can lead to destruction • of peri-pancreatic fat and result in peripancreatic fluid collection This can resolve or develop into a pseudocyst or • abscess Pancreatic pseudocyst • Occurs >4 weeks after initial presentation • They present with abdominal pain and a palpable • mass , particularly if they rupture or become infected 31
Top-decile question 1 32
Top-decile question 2 33
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