Mr. MR, a 37-year-old male, presented with severe epigastric pain radiating to his left side after drinking a minimum of 9 beers the previous day. On examination, he had abdominal tenderness localized to his epigastrium. Laboratory tests found elevated lipase and amylase levels. He was given IV fluids and analgesics and diagnosed with mild acute pancreatitis likely caused by alcohol consumption. He was discharged two days later after his symptoms resolved with conservative management.
2. CASE REPORT
▪ Mr MR is a 37 year old male with no known known comorbidities, nil
allergies, no recent admissions, no history of trauma, no surgical
history, and no history of blood transfusions. He denies smoking but
refers to occasionally consume alcohol, with preference to beers and
ciders. He resides in Bedworth park with a work colleague, in a work
residence, where they work in construction. His baseline is
independent and functional.
▪ Presents with a history of vomiting multiple times after having had a
minimum of 9 beers the previous day, now presents with severe
epigastic pain radiating to the left hypochondrium, exacerbated by
movement, alleviated by sitting up and leaning forward.
3. Physical exam
▪ General exam:
Patient does not look chronic ill, no signs of wasting, appears to be in discomfort. No
jaundice, no pallor, no cianosis, no clubbing, no oedema, no lymphadenopathy, no
dehydration
▪ Systemic exam
▪ Resp: Good air entry bilaterally, no additional sounds
▪ CVS: good S1 and S2, no S3, no murmurs
▪ Abdomen: not distended, no surgical scars, no guarding, no rebound tenderness,
soft but tender to palpation on epigastrium, bowel sounds present.
▪ PR: normal anal mucosa, No haemorrhoids, good sphincter tone, no Palpable
masses, brown stool on glove, no tenderness.
6. Progress
▪ Patient was discharged two days later on analgesics after observed
recuperation, on discharge he no longer presented any abdominal
pain, and had resumed feeds, he consumed food without vomiting,
and he had no moreAbdominal tenderness to pPalpation.
8. CAUSES
▪ I – Idiopathic
▪ G – Gallstones
▪ E – Ethanol (alcohol consumption)
▪ T – Trauma
▪ S – Steroids
▪ M – Mumps
▪ A – Autoimmune
▪ S – Scorpion sting (the one
everyone remembers)
▪ H –
Hyperlipidaemia/Hypercalcemia
▪ E – ERCP
▪ D – Drugs (furosemide, thiazide
diuretics and azathioprine
9. PRESENTATION
▪ Site:epigastric pain
▪ Onset:sudden
▪ Character: Boring/sharp pain
▪ Radiation: Radiating to the back
▪ Alleviation: it is alleviated by sitting up and leaning forward (tripoding position)
▪ Timing: escalates in intensity abd peaks within 10-20 minutes of onset.
▪ Exacerbation: it gets worse when lying supine
▪ Severity: severe
▪ Associated vomiting, nausea
▪ Abdominal tenderness
14. INVESTIGATIONS
▪ Bloods-FBC:WBC (when its high it is asociated with worse prognosi).U&E(to rule out
hypercalcemia)
▪ Serum amylase: level> 3 X normal upper limit: sensitivity to 50% and specificity
99%. If elevated for > 10 days indicates complications(pseudocyst formation)
▪ Serum lipase: Level > 3 X normal upper limit:Severity 64% and Specificity 97% Its
more accurate because it remains elevated longer than serum amylase.
▪ LFTs- ALT level > 150U/L has a positive predictive value of 85% for gallstones as the
underlying Cause.
▪ ABG
▪ ECG
▪ Abdo U/S
15. MANAGEMENT
▪ Initial resuscitation (ABCDE approach)
▪ IV fluids
▪ Nil by mouth
▪ Analgesia
▪ Careful monitoring
▪ Treatment of gallstones in gallstone pancreatitis (ERCP / cholecystectomy)
▪ Antibiotics if there is evidence of a specific infection (e.g., abscess or
infected necrotic area)
▪ Treatment of complications (e.g., endoscopic or percutaneous drainage of
large collections)
16. COMPLICATIONS
▪ Necrosis of the pancreas
▪ Infection in a necrotic area
▪ Abscess formation
▪ Acute peripancreatic fluid collections
▪ Pseudocysts (collections of pancreatic juice) can develop 4 weeks
after acute pancreatitis
▪ Chronic pancreatitis
18. CONCEPT AND ETIOLOGY
▪ Concept: Progressive inflammation
that results in irreversible damage to
the structure and function of the
pancreas.
▪ Etiology-
-Alcohol abuse
-Smoking
-Autoimmune
-Idiopathic
-Metabolic(hyperglycemia,
hyperparathyroidism)
-Drugs(steroids, azathioprine)
-Trauma
-Genetics(cystic fibrosis)
-Congenital(sphincter of Oddi
dysfunction, pancreas divisum)
19. PATHOGENESIS
-progressive destruction of the pancreas by repeated flare-ups of mild
and sublingual types of acute pancreatitis
-Characterized by diffused scarring and strictures in the pancreatic
duct.
-The islets of Langerhans (endocrine function)have a greater resistance
to injury than do the exocrine tissues.
20. Clinical manifestation
▪ Epigastric abdominal pain, radiates to the back alleviated by bending
forward and is exacerbated after eating.
▪ Pain initially is episodic but becomes persistent as the disease
progresses.
▪ Features of Pancreatic insufficiency:
-Steatorrhoea: Exocrine enzyme deficiency
-Cramping abdominal pain, Bloating, diarrhea
-Malabsorption and weight loss.
21. RED FLAGS
▪ Polydipsia, polyuria, polyphagia, blurred vision
▪ Unexplained weight loss, Courvoisier's sign
▪ Jaundice(painless),pruritus, dark urine, acholic stools
▪ Sxs of addiction to narcotics: uncontrollable cravings, slurred speech,
sweating and physical substance dependance
22. INVESTIGATIONS
▪ Bedside: ABG, Hgt, Urine dipstick and inspection of the urine
,Temperature
▪ Routine :Full blood count, CRP, LFT, Amylase &Lipase
▪ Imaging (Diagnostic): Abdominal X-ray, CT scan/ultrasound,
ERCP(which can also be therapeutic)/MRCP
▪ CEA,CA 19-9 and Biopsy if necessary
▪ Fecal elestase level
▪ IgG4 blood test if in suspicions of autoimmune pancreatitis
▪ Check bone density routinely(Xray)
23. MANAGEMENT
▪ Supportive: Risk Factors control(Counseling about life style
changes)e.g. No alcohol, no greasy/fatty food, less meat, low fat,
blend small meals, high in protein diet, limit sugar intake and refined
carbohydrates, eat complex carbs, if obese, reduce obesity(exercise
or dietitians consult for further management)
▪ Other supportive: IV hydration, Monitor and control pain, Monitor
blood glucose, Monitor stools: greasy?,Monitor urinary output: dark
brown?
24. Cont. Of MANAGEMENT
▪ Medicine: Analgesics ,pancratic enzyme replacement (for
malabsorption in exocrine dysfunction )- Creon/pancreatin,Vitamin
supplements
▪ For endocrine dysfunction- Insulin, annual monitoring of HbA1c
▪ Steroids- incase of autoimmune etiology
▪ Non surgical: ERCP ,ESWL
▪ Surgical: Frey's procedure/Whipples procedure
