Aims and objectives Cover the following: Pathophysiology, clinical - - PowerPoint PPT Presentation

• Cover the following:
• Pathophysiology,

clinical presentation, investigations, management, complications

• High yield facts for SBAs
• Duration: 60 minutes
• Slides and recordings: app.bitemedicine.com

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Aims and objectives

History

A 52-year-old male is admitted to the surgical assessment unit with severe, constant epigastric pain and vomiting. The pain came

• n 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

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Case-based discussion: 1

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Question: 1

Neural tube Developing gut Developing liver Falciform ligament Developing pancreas Developing spleen Rotating gut 1 2 3 4 Pancreas Spleen Gastrosplenic ligament Gastrohepatic ligament

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Case-based discussion: 1

C…U…llen's sign U = umbilicus

History

A 52-year-old male is admitted to the surgical assessment unit with severe, constant epigastric pain and vomiting. The pain came

• n 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

! ! ! ! !

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

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Introduction

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Pathophysiology

Pancreas function

• Endocrine function
• Exocrine function

Gallbladder function

• Bile storage and release

Physiology

• Food stimulus
• Duodenum à CCK

1) Pancreas 2) Gallbladder

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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

Investigations:

• WCC 16
• Urea 22
• Creatinine 200
• AST 200
• ALT 180

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Case-based discussion: 1 cont…

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Question: 2

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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.

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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)

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Clinical features

Symptoms Signs Severe upper abdominal pain Tachycardic Band-like radiation to the back (~50% of cases) Fever 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

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Question: 3

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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: Ca2+ levels are required for severity scoring

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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.

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Investigations

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Question: 4

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Modified Glasgow score

A guide for high-dependency care referrals. Parameters 1 point for each of the following: P PO2 <8kPa A Age >55 years N Neutrophils WCC >15x109/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

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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

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Question: 5

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Complications

Systemic

• Hypocalcaemia
• Disseminated intravascular coagulation
• Functional ileus
• Renal failure

Think about the Modified Glasgow Score

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Complications

Systemic

• ARDS
• Pleural effusions
• Aspiration pneumonia
• Hypovolaemic shock

Think about the Modified Glasgow Score

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Question: 6

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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

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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
• f 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

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Top-decile question 1

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Top-decile question 2

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Recap

• Acute pancreatitis arises due to inflammation of the pancreas
• It is diagnosed by 2 of 3 criteria: 1) clinical features; 2) raised serum pancreatic enzymes; 3)

radiological features

• The majority of cases are caused by gallstone obstruction or ethanol abuse. A myriad of

rarer causes also exist – recalled by the mnemonic “IGETSMASHED”

• Severity of acute pancreatitis can be calculated using the Modified Glasgow score –

recalled by the mnemonic “PANCREAS”

• The focus of management is supportive and ensuring early recognition of complications
• Complications include ARDS, hypocalcaemia, DIC, renal failure, pancreatic pseudocyst and

necrotising pancreatitis

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References

• Glasbrenner and Adler (1993). Pathophysiology of acute pancreatitis.

https://pubmed.ncbi.nlm.nih.gov/8119636/

• Elfar et al (2007). The inflammatory cascade in acute pancreatitis: relevance to clinical disease.

https://pubmed.ncbi.nlm.nih.gov/18053834/

• Teach Me Surgery. Acute pancreatitis. https://teachmesurgery.com/hpb/pancreas/acute-pancreatitis/
• Oxford Medical Education. Acute pancreatitis.

http://www.oxfordmedicaleducation.com/gastroenterology/acute-pancreatitis/

• BMJ. Acute scorpion pancreatitis in Trinidad. https://www.bmj.com/content/1/5697/666
• Intechopen. Etiology of pancreatitis and risk factors. https://www.intechopen.com/books/acute-and-

chronic-pancreatitis/etiology-of-pancreatitis-and-risk-factors

• Genetic Home Reference. Hereditary pancreatitis. https://ghr.nlm.nih.gov/condition/hereditary-

pancreatitis#genes

• Life in the Fast Lane. Acute pancreatitis. https://litfl.com/pancreatitis-ccc/
• Radiopaedia. Necrotising pancreatitis. https://radiopaedia.org/articles/necrotising-pancreatitis
• NICE. Pancreatitis. https://www.nice.org.uk/guidance/ng104/resources/pancreatitis-pdf-66141537952453

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Presenter’s contact details

• LinkedIn: Richard Phillips
• Twitter: @RichyP56
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