Patient has gastritis vomited 2 times given raberprazol has pain throughout abdomen also stool was normal and clear what medicine can be given further to stop pain has extreme pain

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gastritis severe abdominal pain treatment antispasmodic analgesic medications clinical management

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I have enough information to give a thorough, clinically useful answer. Let me also note an important red flag - "pain throughout abdomen" in a gastritis patient warrants a caution about ruling out more serious causes.

Gastritis with Severe Abdominal Pain - Medication Management

Important clinical note: "Pain throughout the abdomen" (diffuse abdominal pain) is not typical of simple gastritis alone, which usually causes epigastric/upper abdominal pain. Before adding more medications, it is important to rule out complications like peptic ulcer perforation, pancreatitis, or appendicitis - especially if the pain is severe and diffuse.

Current Medication (Rabeprazole - Already Given)

Rabeprazole 20 mg is a proton pump inhibitor (PPI) - correct first-line choice for gastritis. It reduces acid production and promotes mucosal healing. However, it does not directly address pain acutely - it takes 2-5 days for full effect.

Medications to Add for Pain Relief

1. Antacids (Immediate Symptom Relief)
  • Syrup Antacid (Aluminium hydroxide + Magnesium hydroxide, e.g., Gelusil, Digene) - 10-20 mL after meals and at bedtime
  • Works within minutes by neutralising gastric acid
  • Can be given alongside rabeprazole
2. Antispasmodic (For Cramping / Spasmodic Abdominal Pain)
  • Dicyclomine (Dicyclomine HCl) 20 mg orally 3 times a day - reduces smooth muscle spasm
  • Hyoscine butylbromide (Buscopan) 10-20 mg orally or IM - fast-acting antispasmodic, very useful for acute cramp-type pain
  • Drotaverine (No-Spa) 40-80 mg orally TDS - smooth muscle relaxant, commonly used in India/Asia for gastric pain
3. Antiemetic (For Vomiting - Already Vomited x2)
  • Ondansetron 4-8 mg orally or IV - serotonin antagonist, very effective antiemetic
  • Domperidone 10 mg TDS before meals - also a prokinetic, helps gastric emptying and reduces nausea
  • Metoclopramide 10 mg - alternative antiemetic/prokinetic (avoid in young patients due to extrapyramidal risk)
4. Mucosal Protective Agent
  • Sucralfate 1 g before meals - coats and protects the gastric mucosa, useful in erosive gastritis
  • Pantoprazole + Sodium Alginate combination syrups (e.g., Gaviscon) - adds a protective barrier on top of the mucosa
5. If H. pylori is Suspected
  • Consider testing (urea breath test, stool antigen test)
  • If positive: add Amoxicillin 1g + Clarithromycin 500 mg twice daily for 14 days (triple therapy with rabeprazole)

Practical Add-On Regimen Summary

DrugDoseRoutePurpose
Rabeprazole 20 mgTwice daily (before meals)OralAcid suppression (already given)
Antacid syrup10-20 mL after meals + bedtimeOralImmediate acid neutralization
Hyoscine butylbromide (Buscopan)10-20 mg TDS or IMOral/IMAcute spasmodic pain relief
Domperidone 10 mgTDS before mealsOralAntiemetic + prokinetic
Sucralfate 1 gBefore meals (TDS)OralMucosal protection

Red Flags - When to Escalate / Investigate Further

If any of the following are present, do not rely on outpatient gastritis medications alone - refer/investigate urgently:
  • Diffuse/board-like rigidity of the abdomen (suggests perforation)
  • Fever with severe pain (suggests infection, peritonitis)
  • Sudden onset severe pain (suggests perforation or vascular cause)
  • Rebound tenderness (peritoneal irritation)
  • Pain radiating to back (pancreatitis - check serum amylase/lipase)
  • Haematemesis or black tarry stools (upper GI bleed)
  • Shock features (hypotension, tachycardia, cold extremities)
The stool being normal/clear is reassuring against an active upper GI bleed at this point.

Disclaimer: This information is for clinical guidance only. Prescribing decisions must be made by a licensed physician after physical examination and full clinical assessment of the patient. Always individualise treatment based on patient age, comorbidities, allergies, and severity of presentation.

Pancreatitis

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acute pancreatitis CT scan imaging diagnosis

This diagnostic axial contrast-enhanced CT scan of the abdomen demonstrates findings consistent with severe acute pancreatitis. The pancreas exhibits heterogeneous enhancement with significant peripancreatic inflammatory stranding and fat plane blurring, characteristic of acute interstitial edematous pancreatitis progressing toward Balthazar Grade E. Free fluid is noted in the left paracolic gutter. The gallbladder is visible and contains a hyperdense focus, indicating a gallstone (cholelithiasis), suggesting a possible biliary etiology for the pancreatitis. Surrounding anatomical structures including the liver, spleen, and kidneys appear largely unremarkable in size and parenchymal density. This imaging is highly relevant for medical education regarding the radiological diagnosis and grading of acute pancreatitis, illustrating the loss of distinct organ borders due to extensive peripancreatic inflammation and fluid collection.

This diagnostic axial contrast-enhanced CT scan of the abdomen demonstrates findings consistent with severe acute pancreatitis. The pancreas exhibits heterogeneous enhancement with significant peripancreatic inflammatory stranding and fat plane blurring, characteristic of acute interstitial edematous pancreatitis progressing toward Balthazar Grade E. Free fluid is noted in the left paracolic gutter. The gallbladder is visible and contains a hyperdense focus, indicating a gallstone (cholelithiasis), suggesting a possible biliary etiology for the pancreatitis. Surrounding anatomical structures including the liver, spleen, and kidneys appear largely unremarkable in size and parenchymal density. This imaging is highly relevant for medical education regarding the radiological diagnosis and grading of acute pancreatitis, illustrating the loss of distinct organ borders due to extensive peripancreatic inflammation and fluid collection.

This diagnostic image is an axial computed tomography (CT) scan of the abdomen at the level of the pancreas and kidneys. The vertebral body is visible posteriorly, with the abdominal wall musculature and subcutaneous fat forming the external borders. Internally, the most prominent pathological finding is the presence of multiple hyperdense collections located within the peripancreatic space, indicated by a yellow arrow. These hyperdense areas are consistent with acute hemorrhage within or adjacent to the pancreatic parenchyma, suggesting a diagnosis of hemorrhagic pancreatitis. The pancreas itself appears poorly defined and edematous, accompanied by significant inflammatory fat stranding and haziness in the surrounding retroperitoneal tissue planes. Loops of small bowel with varying amounts of oral contrast and air are visible anteriorly and laterally. The kidneys are visible bilaterally, and the aorta is noted anterior to the vertebral body. This scan demonstrates the imaging features of severe acute pancreatitis, specifically showcasing how high-density blood (hematoma) appears on a non-contrast or portal venous phase CT relative to surrounding inflamed soft tissue.

This diagnostic image is an axial computed tomography (CT) scan of the abdomen at the level of the pancreas and kidneys. The vertebral body is visible posteriorly, with the abdominal wall musculature and subcutaneous fat forming the external borders. Internally, the most prominent pathological finding is the presence of multiple hyperdense collections located within the peripancreatic space, indicated by a yellow arrow. These hyperdense areas are consistent with acute hemorrhage within or adjacent to the pancreatic parenchyma, suggesting a diagnosis of hemorrhagic pancreatitis. The pancreas itself appears poorly defined and edematous, accompanied by significant inflammatory fat stranding and haziness in the surrounding retroperitoneal tissue planes. Loops of small bowel with varying amounts of oral contrast and air are visible anteriorly and laterally. The kidneys are visible bilaterally, and the aorta is noted anterior to the vertebral body. This scan demonstrates the imaging features of severe acute pancreatitis, specifically showcasing how high-density blood (hematoma) appears on a non-contrast or portal venous phase CT relative to surrounding inflamed soft tissue.

This diagnostic image is a coronal reformatted computerized tomography (CT) scan of the abdomen demonstrating findings consistent with acute pancreatitis. The primary pathological feature is the enlargement and edema of the pancreatic parenchyma, which exhibits heterogeneous density. There is notable blurring of the pancreatic margins with associated peripancreatic fat stranding and minor fluid collections, indicating active inflammatory changes. Anatomical context shows the liver with relatively normal morphology and density. Bowel loops are visible with normal gas distribution patterns. Consistent with the patient's surgical history of cholecystectomy, the gallbladder is absent from its fossa. The image serves as a clinical illustration of the radiologic manifestations of pancreatitis, focusing on organ morphology, parenchymal inflammation, and secondary changes in the surrounding retroperitoneal fat. It is intended for medical education regarding abdominal imaging and the diagnosis of acute gastrointestinal inflammatory conditions.

This diagnostic image is a coronal reformatted computerized tomography (CT) scan of the abdomen demonstrating findings consistent with acute pancreatitis. The primary pathological feature is the enlargement and edema of the pancreatic parenchyma, which exhibits heterogeneous density. There is notable blurring of the pancreatic margins with associated peripancreatic fat stranding and minor fluid collections, indicating active inflammatory changes. Anatomical context shows the liver with relatively normal morphology and density. Bowel loops are visible with normal gas distribution patterns. Consistent with the patient's surgical history of cholecystectomy, the gallbladder is absent from its fossa. The image serves as a clinical illustration of the radiologic manifestations of pancreatitis, focusing on organ morphology, parenchymal inflammation, and secondary changes in the surrounding retroperitoneal fat. It is intended for medical education regarding abdominal imaging and the diagnosis of acute gastrointestinal inflammatory conditions.

I now have comprehensive textbook content on pancreatitis diagnosis. Here is the full breakdown:

Acute Pancreatitis - Diagnosis & Investigations

Diagnostic Criteria (Atlanta Revised Criteria 2012)

Diagnosis requires at least 2 of the following 3 criteria:
  1. Abdominal pain characteristic of acute pancreatitis - acute onset, severe, constant epigastric pain, often radiating to the mid-back
  2. Serum lipase or amylase >3× upper limit of normal
  3. Characteristic findings on abdominal imaging (CT/MRI/USG)
If two of the three criteria are met clinically, imaging is not mandatory for diagnosis. - Schwartz's Principles of Surgery, p. 1472

Clinical Features

FeatureDetail
PainSevere epigastric/upper abdominal, radiates to back ("band-like"), worse lying down, relieved slightly on leaning forward
Nausea/VomitingVery common
FeverLow-grade, may be high in infected necrosis
Abdominal tendernessEpigastric tenderness, guarding in upper abdomen
Cullen's signPeriumbilical bruising (retroperitoneal haemorrhage - rare, severe)
Grey Turner's signFlank bruising (retroperitoneal bleed - rare, severe)
TetanyFrom hypocalcaemia in severe cases

Investigations

1. Primary Blood Tests (Most Important)

TestFindingsNotes
Serum Lipase>3× ULN (diagnostic)Preferred over amylase - greater sensitivity & specificity. Preferred first-line test.
Serum Amylase>3× ULNRises within hours, peaks in 24-72h, returns to normal in 3-5 days. Can be falsely normal in hypertriglyceridaemia.
Urine AmylaseElevatedStays elevated longer than serum amylase - useful in delayed presentations
CBC (FBC)WBC elevated (leukocytosis)WBC >16,000 = Ranson criterion
Blood GlucoseElevated (hyperglycaemia)Due to decreased insulin production
Serum CalciumLow (<8 mg/dL) = bad signSaponification of peripancreatic fat
Serum LDHElevatedRanson criterion
Serum AST/ALTElevatedALT >3× = gallstone aetiology likely
BUN/CreatinineElevatedIndicates hemoconcentration, third-space fluid loss
HaematocritElevated (hemoconcentration)Fall >10 points in 48h = Ranson criterion
Serum CRP>150 mg/L at 24h = severeGood severity marker
TriglyceridesCheck if no gallstone/alcohol causeHypertriglyceridaemia is a cause
ABG (Blood Gas)PO₂ <60 mmHg = severeWatch for ARDS/respiratory failure
LFTs + GGTBilirubin, ALP raised if biliary cause
AlbuminLow in severe disease

2. Imaging

Ultrasound Abdomen (First-Line Imaging)

  • Should be done in ALL patients with acute pancreatitis
  • Primary purpose: identify gallstones (biliary aetiology - commonest cause)
  • Can show: oedematous pancreas, peripancreatic fluid, dilated CBD
  • Limitation: bowel gas often obscures pancreas in acute setting

CT Abdomen with Contrast (CECT) - Not Routine

  • Not required routinely for diagnosis
  • Indications for CT:
    • Diagnostic uncertainty (criteria not met)
    • Assessing complications (necrosis, abscess, pseudocyst)
    • No improvement after 48-72 hours of treatment
    • Suspected infected necrosis
  • Ideally done 48-72 hours after onset (necrosis may not be apparent earlier)
CT Severity Index (CTSI - Balthazar Grade):
GradeCT FindingsScore
ANormal pancreas0
BPancreatic enlargement1
CPancreatic inflammation + peripancreatic fat changes2
DSingle peripancreatic fluid collection3
ETwo or more fluid collections OR pancreatic gas4
  • Add necrosis score (0-4) to Balthazar grade for total CTSI
  • CTSI 0-3 = mild; 4-6 = moderate; 7-10 = severe
Here is what acute pancreatitis looks like on CT:
Acute pancreatitis CT - peripancreatic inflammation and gallstone
Contrast-enhanced CT showing pancreatic oedema, peripancreatic fat stranding, and gallstone - classic biliary pancreatitis
Hemorrhagic pancreatitis CT
CT showing haemorrhagic pancreatitis - hyperdense peripancreatic collections indicating haemorrhage

MRCP (MR Cholangiopancreatography)

  • Best for evaluating bile duct and pancreatic duct anatomy
  • Preferred when CBD stones or duct disruption is suspected without wanting to risk ERCP
  • No radiation, no contrast nephrotoxicity

ERCP

  • Diagnostic ERCP is not indicated for pancreatitis alone
  • Therapeutic ERCP indicated only for: cholangitis or biliary obstruction (CBD stones not clearing)

3. Severity Scoring Systems

Ranson's Criteria

(Scored at admission + 48 hours - sourced from Schwartz's Principles of Surgery)
For non-gallstone pancreatitis:
At AdmissionAt 48 Hours
Age >55 yearsHaematocrit fall >10 points
WBC >16,000/mm³BUN rise >5 mg/dL
Blood glucose >200 mg/dLSerum calcium <8 mg/dL
Serum LDH >350 IU/LArterial PO₂ <60 mmHg
Serum AST >250 U/dLBase deficit >4 mEq/L
Fluid sequestration >6 L
Interpretation:
  • <3 criteria: Mild disease, low mortality (<5%)
  • 3-6 criteria: Moderate-severe disease
  • 6 criteria: Severe, 50% mortality risk

BISAP Score (Bedside Index for Severity in Acute Pancreatitis)

Can be calculated within first 24 hours. Score 1 point for each:
  • B - BUN >25 mg/dL
  • I - Impaired mental status (GCS <15)
  • S - SIRS (systemic inflammatory response syndrome) present
  • A - Age >60 years
  • P - Pleural effusion on imaging
Score ≥3 = significant risk of severe disease and mortality.

APACHE II Score

  • Score ≥8 at 24 hours = predicted severe pancreatitis
  • More complex but widely used in ICU settings

CRP

  • Single simple marker: CRP >150 mg/L at 24 hours = similar accuracy to Ranson's for predicting severity

Common Causes (to guide investigations)

CauseInvestigation
Gallstones (most common)USG abdomen, LFTs, MRCP
Alcohol (second most common)History, GGT
HypertriglyceridaemiaFasting lipid profile, serum triglycerides
Drugs (e.g., azathioprine, thiazides, steroids)Medication history
Trauma / ERCPHistory
HypercalcaemiaSerum calcium, PTH
AutoimmuneIgG4 levels
IdiopathicDiagnosis of exclusion

Summary: Minimum Investigation Panel for Suspected Pancreatitis

UrgencyTests
ImmediateSerum lipase (or amylase), FBC, RFT, LFTs, blood glucose, serum calcium, ABG (if severe), CRP
Same dayUSG abdomen (gallstones), serum triglycerides, fasting lipid profile
If no improvement at 48-72hCECT abdomen (assess necrosis/complications)
If biliary cause suspectedMRCP
Sources: Rosen's Emergency Medicine, p.3878-3912 | Schwartz's Principles of Surgery, p.1471-1475

Generate management protocol for acute pancreatitis treatment

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ACUTE PANCREATITIS - MANAGEMENT PROTOCOL

Based on: Rosen's Emergency Medicine, Schwartz's Principles of Surgery, Current Surgical Therapy 14e, Revised Atlanta Classification 2012

STEP 1 - SEVERITY CLASSIFICATION (First 24-48 Hours)

Revised Atlanta Classification 2012

GradeCriteria
MildNo organ failure, no local or systemic complications
Moderately SevereTransient organ failure (<48 h) OR local/systemic complications
SeverePersistent organ failure (>48 h) - respiratory, cardiovascular, or renal (Modified Marshall score ≥2)

Quick Bedside Severity: BISAP Score (within 24h)

Score 1 point each for:
  • B - BUN >25 mg/dL
  • I - Impaired mental status (GCS <15)
  • S - SIRS present
  • A - Age >60 years
  • P - Pleural effusion on imaging
Score ≥3 = high risk, consider ICU admission

STEP 2 - IMMEDIATE RESUSCITATION (First 6-24 Hours)

A. IV Fluid Resuscitation (Highest Priority)

ParameterRecommendation
Fluid of choiceLactated Ringer's (LR) - preferred over Normal Saline
Why LR?NS causes hyperchloraemic metabolic acidosis which activates trypsinogen and worsens pancreatic injury. LR also has anti-inflammatory effects.
Initial rate5-10 mL/kg/h for first 2 hours (IAP/APA guidelines)
Maintenance1.5-3 mL/kg/h for next 12-24 hours
Total target in 24h2-4 litres overall (goal-directed)
ACG recommendation250-500 mL/h
Fluid resuscitation goals (targets):
  • Heart rate < 120/min
  • Mean arterial pressure (MAP): 65-85 mmHg
  • Urine output: >0.5-1 mL/kg/h
  • BUN and haematocrit trending down
Caution: Overly aggressive fluids can cause abdominal compartment syndrome, respiratory failure, and worsen sepsis. Monitor closely.
If hypotensive despite fluids: Start norepinephrine to maintain MAP ≥65 mmHg.

B. Electrolyte Correction

ElectrolyteAction
HypocalcaemiaReplace only if ionised Ca²⁺ is low, QT prolonged, or Chvostek/Trousseau signs present. Correct hypomagnesaemia first.
HypomagnesaemiaReplace before calcium
HyperglycaemiaMonitor blood glucose; insulin if needed (hyperglycaemia worsens pancreatic injury and immune function)

STEP 3 - PAIN MANAGEMENT

Pain is the cardinal symptom and its relief is a clinical priority. No single analgesic has been proven superior. (Schwartz's Principles of Surgery)

Stepwise Analgesic Approach

StepDrugDoseNotes
Step 1 (Mild pain)Paracetamol (Acetaminophen)1 g IV/oral every 6 hoursFirst choice; 650 mg/8h if liver disease
Step 2 (Moderate pain)Ketorolac/NSAIDsKetorolac 30 mg IVAvoid in renal impairment, critically ill
Step 2 altMetamizole (Dipyrone)2 g IV every 8 hoursRecommended in Schwartz's for moderate pain
Step 3 (Severe pain)Buprenorphine0.3 mg IV every 4 hoursFirst-line opioid per Schwartz's
Opioid sparingLow-dose Ketamine0.1-0.3 mg/kg IVGood adjunct; reduces opioid requirement
AntiemeticOndansetron / Metoclopramide4-8 mg IVFor nausea/vomiting control
Morphine: Classically avoided due to theoretical sphincter of Oddi spasm. No clinical trials confirm it worsens pancreatitis, but most guidelines still recommend avoiding it when alternatives are available.
Pentazocine, meperidine, procaine HCl are also effective opioid options.

STEP 4 - NUTRITION

Old Practice vs Current Evidence

Old (Incorrect)Current Evidence-Based
Keep patient NPO until pancreatitis resolvesEarly oral feeding (<24h) if tolerated is recommended
Enteral feeding worsens pancreatitisEnteral feeding is safe and beneficial

Nutrition Guidelines

ScenarioApproach
Mild pancreatitis, tolerating orallyStart oral diet early (<24h) - low fat, soft diet as tolerated
Cannot tolerate oral (nausea/vomiting)Nasogastric or nasojejunal (NG/NJ) enteral feeding
NJ vs NG routeBoth are comparable in safety and efficacy
If enteral not possibleTotal Parenteral Nutrition (TPN) - last resort
Why avoid prolonged NPO?Causes gut mucosal atrophy, bacterial overgrowth, gut translocation, increases infectious complications
Early enteral nutrition reduces: infectious complications, organ failure severity, need for surgical intervention, and mortality compared to parenteral nutrition. (Current Surgical Therapy 14e)

STEP 5 - ANTIBIOTICS

Key Principle: Prophylactic antibiotics are NOT recommended

ScenarioAntibiotic Use
Mild/moderate sterile pancreatitisNO antibiotics
Severe pancreatitis (SIRS present but no proven infection)NO prophylactic antibiotics
Suspected sepsis / clinically deterioratingSTART empirical antibiotics
Infected pancreatic necrosis (confirmed by CT/culture)YES - start antibiotics
Extrapancreatic infection (cholangitis, pneumonia, bacteraemia)YES - treat infection

Antibiotic Choice for Infected Necrosis

DrugReason
Carbapenems (Meropenem, Imipenem)Best pancreatic penetration - superior to cephalosporins and fluoroquinolones
Ciprofloxacin + MetronidazoleAlternative combination
Piperacillin-TazobactamAlternative
Probiotics are contraindicated - a multicentre RCT showed more than doubled mortality with probiotics in severe pancreatitis (possible intestinal ischaemia). (Current Surgical Therapy 14e)

STEP 6 - ENDOSCOPIC INTERVENTION (ERCP)

Indications

IndicationAction
Cholangitis with biliary obstructionERCP within 24-72 hours (emergency)
CBD stone obstruction without cholangitisERCP within 72 hours
Biliary pancreatitis without obstructionERCP NOT routinely required
Diagnostic purposesERCP NOT indicated - use MRCP instead

STEP 7 - SURGICAL / INTERVENTIONAL MANAGEMENT

For Necrotising Pancreatitis

SituationAction
Asymptomatic sterile necrosis / pseudocystConservative management only - these may resorb spontaneously
Infected necrosis with clinical deteriorationUrgent percutaneous drainage + antibiotics
Infected/symptomatic necrosis, stable patientDelay intervention to ≥4 weeks to allow collection to "wall off"
Symptomatic sterile necrosis >8 weeksConsider drainage (endoscopic/percutaneous/surgical)

Drainage Options (in order of preference)

  1. Endoscopic drainage (EUS-guided, e.g., cyst-gastrostomy) - least invasive, requires walled-off collection
  2. Percutaneous image-guided drainage - for immature or inaccessible collections
  3. Video-assisted retroperitoneal debridement (VARD) or minimally invasive surgery
  4. Open necrosectomy - highest risk, last resort; mortality 75% if done in first 2 weeks
Surgical mortality: 75% if <2 weeks, 45% at 2-4 weeks, 8% if >30 days from onset. Always delay if clinically possible. (Current Surgical Therapy 14e)

Cholecystectomy (for Gallstone Pancreatitis)

  • Mild disease: Laparoscopic cholecystectomy before discharge or within 2-4 weeks (same admission preferred)
  • Severe disease: Delay cholecystectomy; perform after full recovery

STEP 8 - MONITORING

Parameters to Track

ParameterFrequencyTarget
Heart rateContinuous<120/min
Blood pressure / MAPContinuousMAP 65-85 mmHg
Urine outputHourly>0.5-1 mL/kg/h
Blood glucose4-6 hourly140-180 mg/dL (in ICU)
Serum BUN, creatinineDailyTrending down
HaematocritDailyTrending down (falling Hct = adequate fluids)
Serum calciumDaily>8 mg/dL
ABG / SpO₂As neededPO₂ >60 mmHg
CRPEvery 48hTrending down
Serum amylase/lipaseNot useful for monitoring severity - do not repeat routinely

STEP 9 - ICU ADMISSION CRITERIA

Admit to ICU if any of:
  • Persistent organ failure >48h (respiratory: PaO₂ <60 / renal: creatinine >170 / cardiovascular: BP <90 despite fluids)
  • BISAP score ≥3 or Ranson score ≥3
  • APACHE II score ≥8
  • Necrotising pancreatitis on CT
  • Ongoing haemodynamic instability despite resuscitation
  • Need for vasopressors

SUMMARY FLOWCHART

Suspected Acute Pancreatitis
         |
Confirm: ≥2 of 3 criteria (pain + lipase/amylase >3x ULN + imaging)
         |
     SEVERITY?
    /         \
  MILD        MODERATELY SEVERE / SEVERE
   |                    |
Oral diet        IV LR fluid resuscitation
Early oral        (5-10 mL/kg/h → 1.5-3 mL/kg/h)
feeding          Pain control (Paracetamol → Opioids)
Monitor          Antiemetics
Discharge        NPO only if vomiting severely → NG/NJ feed
when              |
tolerated    Monitor BUN/Hct/UO/HR/MAP
              |
         BILIARY CAUSE?        INFECTED NECROSIS?
              |                       |
         ERCP if                Carbapenems + delay
         cholangitis/           intervention to ≥4 weeks
         obstruction            (percutaneous drain if deteriorating)
              |
         Cholecystectomy
         before discharge

DRUGS SUMMARY TABLE

DrugDosePurpose
Lactated Ringer's IV5-10 mL/kg/h → 1.5-3 mL/kg/hFluid resuscitation (first choice)
Paracetamol1 g IV/PO q6hAnalgesia (first line)
Metamizole2 g IV q8hModerate pain
Buprenorphine0.3 mg IV q4hSevere pain (opioid of choice)
Ketamine (low dose)0.1-0.3 mg/kg IVOpioid-sparing analgesia
Ondansetron4-8 mg IV q8hAntiemetic
Meropenem/ImipenemStandard dosingInfected necrosis only
InsulinSliding scale/infusionIf hyperglycaemia persistent
NorepinephrineTitrate to MAP ≥65 mmHgVasopressor if hypotensive

Sources: Rosen's Emergency Medicine (9th Ed), pp. 3874-3900 | Schwartz's Principles of Surgery (11th Ed), pp. 1471-1475 | Current Surgical Therapy (14th Ed) | Revised Atlanta Classification 2012 (Banks et al., Gut)
Disclaimer: This protocol is a clinical reference guide. All treatment decisions must be individualised based on the patient's clinical state, comorbidities, local institutional guidelines, and physician judgement.
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