title: "Week 4: Pain & Toxicology"
Week 4: Pain & Toxicology
1. Paracetamol Poisoning
Pharmacology & Toxicology
Normal Metabolism: Paracetamol → Phase II conjugation (sulphate/glucuronide) → Renally excreted
In Overdose: Phase II saturable → Phase I hydroxylation (cytochrome P450) → N-acetyl-p-benzoquinone imine (toxic metabolite)
- N-acetyl-p-benzoquinone imine = N-acetyl-p-benzoquinone imine
- Normally conjugated with glutathione → harmless excretion
- Overdose depletes glutathione → NAPQI accumulates → hepatotoxicity
- Massive overdose (>50g): paracetamol itself → mitochondrial toxicity
Types of Overdose
| Type | Definition | Hepatotoxic Dose |
|---|---|---|
| Single Immediate Release | One-time ingestion of regular paracetamol | >10g OR >200 mg/kg |
| Modified Release (modified release) | Panadol Osteo or sustained-release | >10g OR >200 mg/kg |
| Repeated Supratherapeutic | Excessive dosing over >24 hours | Variable (see below) |
Repeated Supratherapeutic Ingestion Thresholds
| Duration | Hepatotoxic Dose |
|---|---|
| Over 24 hours | >10g OR >200 mg/kg |
| Over 48 hours | >12g OR >300 mg/kg |
| >48 hours | >4g/day with symptoms |
Single Immediate Release: Management Algorithm
Time-Based Approach:
- Less than 2 hours: Activated charcoal (50g) + Paracetamol/alanine aminotransferase at 4 hours
- 2-8 hours: Paracetamol/ALT now → wait for result → use nomogram
- More than 8 hours: START N-acetylcysteine (N-Acetylcysteine) immediately + Paracetamol/ALT
- More than 24 hours: START NAC immediately
Paracetamol Overdose: Immediate Actions
Single immediate-release ingestion (time since ingestion)
Start N-acetylcysteine (N-Acetylcysteine) early — best within 8 hours of ingestion. If in doubt, START NAC while awaiting levels.
The Paracetamol Nomogram
- Plot serum paracetamol level (Y-axis) against time since ingestion (X-axis)
- ABOVE the line: Start NAC
- BELOW the line: No NAC required
- Double the line: Consider doubling Bag 2 dose
Check Units!
Nomogram uses mg/L (left axis) or μmol/L (right axis). Common error: putting μmol/L value on mg/L scale → appears normal when actually toxic!
N-Acetylcysteine (NAC)
Mechanism
- Provides cysteine for glutathione replenishment
- Directly binds NAPQI
- Can reduce NAPQI back to paracetamol
- Antioxidant → helps liver repair
2-Bag Regime
| Bag | Dose | Duration |
|---|---|---|
| Bag 1 | 200 mg/kg | Over 4 hours |
| Bag 2 | 100 mg/kg | Over 16 hours |
NAC protocol for paracetamol overdose: Double Bag 2 (200 mg/kg) if level is double the nomogram line (i.e., >50g ingestion or >1g/kg)
Cessation Criteria (2 hours before end of Bag 2)
- Paracetamol level under 10 mg/L
- alanine aminotransferase under 50 U/L (or peaked and decreasing)
- international normalised ratio (International Normalised Ratio) under 2
- No clinical symptoms (right upper quadrant pain, nausea, vomiting)
If criteria not met: Add Bag 3 (same as Bag 2) → repeat process
NAC Side Effects
| Common | Serious |
|---|---|
| Nausea, vomiting | Anaphylactoid reaction (rate-related) |
| Rash, bronchospasm, urticaria, angioedema, hypotension |
Anaphylactoid reaction management:
Stop NAC → Antihistamine + Adrenaline if severe → Once resolved, restart at slower rate
When to Call Liver Transplant Team
Modified King's College Criteria:
- international normalised ratio (International Normalised Ratio) >3 with liver derangement
- Creatinine >200
- pH under 7.3 despite resuscitation
- Hypotension despite resuscitation
- Any encephalopathy
Call early — they prefer to say "no worries" than be called too late.
2. Acute Pain Management
Why Treat Acute Pain?
Untreated pain = sympathetic activation → harm:
- Respiratory: ↓functional residual capacity, ↓ventilation, atelectasis, pneumonia
- Cardiovascular: ↑heart rate (Heart Rate), ↑blood pressure (Blood Pressure), coronary vasoconstriction, ischaemia
- gastrointestinal (Gastrointestinal): Ileus, constipation
- Urinary: Retention
- Metabolic: Hypercoagulable, impaired wound healing
- Psychological: Anxiety, depression, sleep deprivation
Goals of Pain Management
Drinking, Eating, And Mobilising
The goal is NOT zero pain — it's return to function.
Set expectations:
"Our aim is to make you comfortable most of the time and treat pain when it occurs." Complete pain relief at all times is unrealistic.
Multimodal Analgesia
Principle: Multiple drugs with different mechanisms → better analgesia, reduced opioid requirements
| Drug Class | Example | Role |
|---|---|---|
| Simple analgesic | Paracetamol 1g four times daily (Quater In Die (four times daily)) | Cornerstone — reduces opioid need by 20-40% |
| non-steroidal anti-inflammatory drug | Ibuprofen 400mg three times daily (Ter Die Sumendum (three times daily)) | Especially good for movement pain |
| Opioid | Oxycodone, Morphine | Moderate-severe pain |
| Adjuvant | Pregabalin, Gabapentin | Neuropathic pain |
WHO Analgesic Ladder (Quick Guide)
Mild pain: regular paracetamol 1 g four times daily (Quater In Die (four times daily)) ± as needed (Pro Re Nata (as needed)) NSAID (if not contraindicated).
Moderate pain: regular paracetamol + NSAID + PRN (Pro Re Nata (as needed)) weak opioid (e.g., codeine 30-60 mg QID (Quater In Die (four times daily)) or tramadol 50-100 mg QID (Quater In Die (four times daily))).
Severe pain: regular paracetamol + NSAID + PRN (Pro Re Nata (as needed)) morphine sulfate solution 20-30 mg oral (Per Os (by mouth)) every 2 hours (adjust for age/renal impairment).
Inhalational Analgesia
Entonox is 50% nitrous oxide + 50% oxygen with rapid onset and short duration. Avoid in trapped gas conditions (e.g., pneumothorax, bowel obstruction) and head injury.
3. Opioids
Classification
| Category | Examples |
|---|---|
| Naturally occurring | Morphine, Codeine |
| Semi-synthetic | Oxycodone, Hydrocodone |
| Synthetic | Fentanyl, Methadone, Tapentadol |
Routes of Administration
| Route | Notes |
|---|---|
| intravenous (Intravenous) patient-controlled analgesia | Gold standard for post-op; patient controls boluses |
| Oral | When drinking/eating; immediate vs sustained release |
| intramuscular (Intramuscular)/subcutaneous (Subcutaneous) | Poor pharmacokinetic profile; needle stick risk |
| Transdermal (patch) | 12-24h onset — NOT for acute pain |
| Intranasal | Fentanyl in emergency department (Emergency Department); good for children |
IV (Intravenous) Opioids in Severe Pain
| Drug | Dose | Onset | Peak | Duration |
|---|---|---|---|---|
| Oxycodone | 1-2 mg | 5 min | 5-10 min | 2-3 hours |
| Fentanyl | 10-20 mcg | 3-5 min | 10-15 min | ~2 hours |
| Morphine | 1-2 mg | 5-10 min | 30-45 min | 3-4 hours |
PCA start: morphine 1 mg bolus with 5-minute lockout. In severe renal impairment, fentanyl is preferred.
Oral Opioids
| Drug | Onset | Duration | Notes |
|---|---|---|---|
| Oxycodone immediate release (Endone) | 30 min | 3-5 hours | Good bioavailability |
| Oxycodone sustained release (OxyContin) | 1-2 hours | 12 hours | twice daily (Bis Die (twice daily)) dosing |
| Tapentadol (Palexia) | 1 hour | 4-6 hours | Dual mechanism: μ + noradrenaline |
Tapentadol advantages:
- Less constipation, nausea than pure opioids
- Negligible serotonin effects (safer than tramadol with selective serotonin reuptake inhibitors)
- Equianalgesic conversion varies — consult eTG/local opioid conversion chart.
Opioid equivalence (approx): 10 mg oral morphine ≈ 3 mg morphine SC (Subcutaneous)/IV (Intravenous) ≈ 5 mg oral oxycodone IR ≈ 40 mg oral tramadol ≈ 100 mg oral dihydrocodeine ≈ 120 mg oral codeine.
Fentanyl patch: 25 mcg/hour ≈ 90 mg oral morphine/day; use only for ongoing chronic pain (not acute).
Opioid Side Effects
| Side Effect | Notes |
|---|---|
| Sedation | FIRST sign of overdose — precedes respiratory depression |
| Respiratory depression | Late sign; monitor sedation scores |
| Nausea/vomiting | Common; antiemetics |
| Constipation | Universal; laxatives |
| Pruritus | Chest/neck/face distribution = opioid-induced |
| Urinary retention | Monitor output |
Signs of Opioid Toxicity:
- Sedation (earliest sign!)
- Pinpoint pupils
- Respiratory depression
Treatment: Stop opioid → O₂ → Naloxone 40-80 mcg intravenous (Intravenous) aliquots (titrate gently)
For opioid toxicity, titrate naloxone 40-80 mcg IV to respiratory rate rather than full alertness.
Opioid Pharmacology Pearls
Opioid receptors:
- μ: analgesia, respiratory depression, miosis, nausea/vomiting, pruritus
- κ: analgesia, sedation, dysphoria
- δ: analgesia
Q: Which morphine metabolite is more potent and accumulates in renal impairment? A: Morphine-6-glucuronide
Codeine is a prodrug requiring CYP2D6 conversion to morphine. Poor metabolisers have little analgesia; ultra-rapid metabolisers risk toxicity.
Fentanyl is highly lipid-soluble → short duration from redistribution; metabolites are inactive.
Pethidine (meperidine) forms norpethidine (long half-life, neurotoxic) and should be avoided in renal impairment. It can be used for post-op shivering.
Naloxone is effective for ~60 minutes; monitor for re-sedation in long-acting opioid toxicity.
What is the key concern?
Tolerance & Withdrawal
- Tolerance: Need increasing doses for same effect; can develop in 7 days
- Withdrawal: Hypertension, tachycardia, sweating, agitation
- Prevention: Taper slowly; warn patient about unusual feelings
4. Non-Opioid Analgesics
non-steroidal anti-inflammatory drugs
Q: Moderate pain: ibuprofen [___] mg can be effective and reduce opioid requirements. A: 400
Examples of COX-2 selective NSAIDs (with typical doses): celecoxib 200 mg, parecoxib 20 mg, valdecoxib 20 mg.
| Non-selective NSAID | Typical dose |
|---|---|
| Diclofenac | 50 mg |
| Ibuprofen | 400 mg |
| Ketorolac | 10 mg |
Contraindications
- Renal impairment / dehydration
- Active peptic ulcer disease / gastrointestinal (Gastrointestinal) bleeding
- Aspirin-sensitive asthma
- Concurrent nephrotoxics (aminoglycosides)
Avoid NSAIDs in renal impairment, active GI (Gastrointestinal) bleeding/PUD, aspirin-sensitive asthma, or with nephrotoxics.
Safe non-steroidal anti-inflammatory drug prescribing:
- Choose short half-life (ibuprofen, diclofenac)
- Check renal function and hydration
- Put a stop date on the chart (3-5 days)
Ceiling effect: Increasing dose beyond recommended doesn't improve analgesia — just increases side effects.
Tramadol
- Weak μ-receptor agonist + serotonin/noradrenaline reuptake inhibition
- Requires cytochrome P450 2D6 metabolism to M1 (active metabolite) — variable between patients
- Less constipating than pure opioids
- Less respiratory depression and lower abuse potential than pure opioids
Tramadol is a weak μ-opioid agonist and serotonin/noradrenaline reuptake inhibitor.
Tramadol risks:
- Serotonin syndrome (especially with selective serotonin reuptake inhibitors)
- Lowered seizure threshold
- Variable efficacy (genetic polymorphism)
Neuropathic Pain
Features suggesting neuropathic pain:
- Burning, stabbing, electric shock descriptors
- Paroxysmal (comes and goes)
- Hyperalgesia or allodynia on exam
- Poor response to opioids
Treatment: Pregabalin or Gabapentin; refer to pain specialist
5. Abdominal Pain
Types of Abdominal Pain
| Type | Mechanism | Character |
|---|---|---|
| Visceral | Organ inflammation (before peritoneal irritation) | Vague, poorly localised, central |
| Somatic | Peritoneal irritation | Well-localised, sharp, worse with movement |
| Referred | Shared nerve pathways | Pain felt distant from source (e.g., shoulder tip) |
Classic example: Appendicitis
Starts as vague central/periumbilical pain (visceral) → migrates to right iliac fossa (somatic as peritoneum irritated)
Key Diagnoses Overview
| Diagnosis | Pain Location | Key Features |
|---|---|---|
| Appendicitis | Central → right iliac fossa | Migratory pain, McBurney's point, peritonism |
| Cholecystitis | right upper quadrant / epigastric | Murphy's sign, referred shoulder tip, 4 F's |
| Diverticulitis | left iliac fossa (usually) | Fever, ↑white cell count (White Cell Count), computed tomography (Computed Tomography) confirms |
| Pancreatitis | Epigastric → back | Severe, boring; ↑lipase; GET SMASHED causes |
| abdominal aortic aneurysm | Central / back | Pulsatile mass, shock, bedside ultrasound scan (Ultrasound Scan) |
| Renal colic | Loin → groin | Colicky, restless patient, haematuria |
| Mesenteric ischaemia | Central (vague) | Pain out of proportion, atrial fibrillation (Atrial Fibrillation), HIGH lactate |
| small bowel obstruction | Central, colicky | Vomiting, distension, no flatus, surgical scars |
| Ectopic pregnancy | Unilateral lower | Female, beta human chorionic gonadotropin+, free fluid on USS |
Appendicitis
- Risk factors: Any age (peak 10-30), slight male preponderance
- Pain: Migratory (central → right iliac fossa) in ~50-60%
- Exam: RIF tenderness, guarding, rebound; positive Rovsing's, obturator, psoas signs
- Labs: ↑white cell count (White Cell Count), ↑C-reactive protein (C-Reactive Protein) (may be normal early)
- Imaging: computed tomography (Computed Tomography) if uncertain; ultrasound difficult in adults
- Management: Analgesia, intravenous (Intravenous) fluids, antibiotics, surgical referral
Pancreatitis
- G - Gallstones (most common)
- E - Ethanol (most common)
- T - Trauma
- S - Steroids
- M - Mumps
- A - Autoimmune
- S - Scorpion venom
- H - Hyperlipidaemia / Hypercalcaemia
- E - endoscopic retrograde cholangiopancreatography
- D - Drugs
- Diagnosis: Lipase (NOT amylase — less specific)
- Imaging: computed tomography (Computed Tomography) lags behind clinical picture; used for complications
- Management: Analgesia, aggressive intravenous (Intravenous) fluids, nil by mouth (Nil By Mouth), nasogastric if vomiting
Severity Assessment
Lipase elevation does NOT predict severity — use prognostic scoring systems to identify severe pancreatitis early.
Modified Glasgow (IMRIE) Score — assess within 48 hours:
| Factor | Threshold |
|---|---|
| P - partial pressure of oxygen | <8 kPa (60 mmHg) |
| A - Age | >55 years |
| N - Neutrophils (white cell count (White Cell Count)) | >15 × 10⁹/L |
| C - Calcium | <2 mmol/L |
| R - Renal (urea) | >16 mmol/L |
| E - Enzymes (lactate dehydrogenase) | >600 U/L |
| A - Albumin | <32 g/L |
| S - Sugar (glucose) | >10 mmol/L |
- P - partial pressure of oxygen <8 kPa
- A - Age >55
- N - Neutrophils (white cell count (White Cell Count)) >15
- C - Calcium <2
- R - Renal (urea) >16
- E - Enzymes (lactate dehydrogenase) >600
- A - Albumin <32
- S - Sugar >10
Interpretation:
- Score ≥3 = Severe pancreatitis → high dependency unit (High Dependency Unit)/intensive care unit (Intensive Care Unit) admission
- Score <3 = Mild pancreatitis → ward-based management
C-reactive protein (C-Reactive Protein) >150 mg/L at 48 hours is a reliable marker of severe pancreatitis and local complications. CRP rises with inflammation and necrosis.
Mesenteric Ischaemia
Classic triad:
- Severe abdominal pain
- Soft abdomen (pain out of proportion to exam)
- atrial fibrillation (Atrial Fibrillation) or vascular risk factors
Investigation: HIGH lactate, computed tomography (Computed Tomography) mesenteric angiogram
Treatment: Emergency surgery
AAA (Ruptured/Leaking)
- Risk factors: Male, >60, smoker, hypertension
- Pain: Central abdominal → back; can mimic renal colic
- Exam: Pulsatile expansile mass; hypotension if ruptured
- Investigation: Bedside ultrasound scan (Ultrasound Scan) (quick diagnosis)
- Management: 2 wide-bore cannulae, crossmatch 6 units, permissive hypotension, emergency vascular surgery
Permissive hypotension:
If patient is awake and talking with blood pressure (Blood Pressure) ~90 systolic — don't push fluids to raise BP to 120. Higher BP may dislodge clot → worse bleeding.
6. Practice Questions
What is the most appropriate next step?
What is the management?
What is the most appropriate next step?
7. Toxidromes
Toxidrome: A constellation of signs and symptoms suggesting a specific class of poisoning.
Major Toxidromes
| Toxidrome | Mechanism | Causes | Key Features |
|---|---|---|---|
| Opioid | μ-receptor agonism | Heroin, morphine, fentanyl, oxycodone | Miosis (pinpoint pupils), respiratory depression, sedation |
| Sedative-Hypnotic | gamma-aminobutyric acid enhancement | Benzodiazepines, barbiturates, gamma-hydroxybutyrate | Sedation, ataxia, respiratory depression |
| Sympathomimetic | Adrenergic crisis | Amphetamines, cocaine, methylenedioxymethamphetamine | Mydriasis, tachycardia, hypertension (Hypertension), hyperthermia, agitation |
| Serotonin | ↑ central 5-hydroxytryptamine (serotonin) | selective serotonin reuptake inhibitors, serotonin-noradrenaline reuptake inhibitors, tramadol, monoamine oxidase inhibitors | Clonus, hyperreflexia, hyperthermia, agitation |
| Anticholinergic | Muscarinic blockade | tricyclic antidepressants, antihistamines, atropine | "Mad, hot, dry, blind" - confusion, hyperthermia, dry skin, mydriasis |
| Cholinergic | ↑ acetylcholine at receptors | Organophosphates, carbamates | DUMBELLS: Diarrhoea, Urination, Miosis, Bradycardia, Emesis, Lacrimation, Lethargy, Salivation |
"Hot as a hare, blind as a bat, dry as a bone, red as a beet, mad as a hatter"
- Hot = hyperthermia
- Blind = mydriasis (dilated pupils)
- Dry = anhidrosis, urinary retention
- Red = flushing
- Mad = delirium, confusion
- D - Diarrhoea, Diaphoresis
- U - Urination
- M - Miosis
- B - Bradycardia, Bronchospasm
- E - Emesis
- L - Lacrimation
- L - Lethargy
- S - Salivation
Serotonin Syndrome
Clinical Triad:
- Autonomic: hyperthermia, diaphoresis, tachycardia, hypertension
- Neuromuscular: hyperreflexia, clonus (especially lower limbs), rigidity
- Mental status: agitation, confusion
Key differentiator: Lower limb clonus > upper limb. Hyperreflexia present (vs NMS which has rigidity and bradyreflexia).
Management:
- Stop offending agent
- Benzodiazepines for agitation
- Cyproheptadine (5-HT antagonist)
- Cooling for hyperthermia
Neuroleptic Malignant Syndrome (neuroleptic malignant syndrome (Neuroleptic Malignant Syndrome))
| Feature | neuroleptic malignant syndrome (Neuroleptic Malignant Syndrome) | Serotonin Syndrome |
|---|---|---|
| Onset | Days | Hours |
| Causes | Antipsychotics, dopamine withdrawal | selective serotonin reuptake inhibitors, monoamine oxidase inhibitors, opioids |
| Muscle tone | "Lead pipe" rigidity | Hyperreflexia, clonus |
| Reflexes | Decreased | Increased |
| creatine kinase | Very high | Mildly elevated |
Management: Stop antipsychotic, cooling, intravenous (Intravenous) fluids, bromocriptine or dantrolene
Sodium Channel Blocker Toxicity
electrocardiogram (Electrocardiogram) signs of sodium channel blockade (e.g. tricyclic antidepressant overdose):
- QRS complex (QRS Complex) >100 ms
- Terminal R wave in aVR >3 mm
- R/S ratio >0.7 in aVR
Treatment: sodium bicarbonate to achieve pH 7.5-7.55
Clinical Approach: RRSI DEAD
- R - Resuscitation
- R - Risk assessment
- S - Supportive care
- I - Investigations/monitoring
- D - Decontamination (charcoal if <2 hrs)
- E - Enhanced elimination (dialysis, urinary alkalinisation)
- A - Antidotes
- D - Disposition
Key Antidotes
| Toxin | Antidote |
|---|---|
| Paracetamol | N-acetylcysteine (N-Acetylcysteine) |
| Opioids | Naloxone |
| Benzodiazepines | Flumazenil (use with caution) |
| Beta-blockers | Glucagon, High-dose insulin-euglycaemic therapy |
| Calcium channel blockers | Calcium, High-dose insulin-euglycaemic therapy |
| Digoxin | Digibind (Fab fragments) |
| Tricyclics | sodium bicarbonate |
| Warfarin | Vitamin K, Prothrombinex, fresh frozen plasma |
| Methanol/Ethylene glycol | Fomepizole or Ethanol |
| Organophosphates | Atropine, Pralidoxime |
| Cyanide (smoke inhalation) | Hydroxocobalamin ± sodium thiosulfate |
Antidote Dosing Pearls (adult, local protocol)
| Scenario | Typical regimen | Notes |
|---|---|---|
| Beta-blocker overdose | Glucagon 5-10 mg IV bolus, then 1-5 mg/hr infusion | Nausea/vomiting common; consider HIET |
| Calcium channel blocker overdose | Calcium chloride 10% 10-20 mL IV (or calcium gluconate 10% 30-60 mL), repeat as needed | Calcium chloride via central line if possible |
| HIET for BB/CCB | Insulin 1 unit/kg IV bolus + dextrose, then 0.5-1 unit/kg/hr infusion | Monitor glucose and potassium closely |
| Digoxin toxicity | Digoxin-specific Fab if life-threatening arrhythmia or potassium over 5.5 mmol/L | Avoid calcium ("stone heart") |
| Organophosphate poisoning | Atropine 1-2 mg IV, double every few minutes to dry secretions + pralidoxime | Endpoint is airway dryness, not pupils |
High-dose insulin euglycaemic therapy (HIET) improves inotropy in beta-blocker/CCB toxicity but requires close glucose and potassium monitoring.
HIET improves cardiac output by providing myocardial carbohydrate substrate and enhancing inotropy, not by lowering the drug level.
Beta-blocker overdose: use glucagon or high-dose insulin euglycaemic therapy (HIET).
Organophosphate toxicity is treated with atropine + pralidoxime.
Atropine treats muscarinic effects (secretions, bronchospasm, bradycardia); pralidoxime reactivates acetylcholinesterase to reverse nicotinic weakness. Give pralidoxime early before enzyme "aging".
Digoxin toxicity: give Digibind (Fab fragments).
Digoxin-specific Fab is indicated for life-threatening arrhythmias or hyperkalaemia (potassium over 5.5 mmol/L).
Each digoxin Fab vial binds about 0.5 mg digoxin; if ingestion is unknown and unstable, an empiric 10 vials is commonly used per toxicology advice.
After digoxin Fab, serum digoxin levels rise (bound + unbound) and are not reliable; monitor clinically and follow potassium.
Organophosphate poisoning: atropine is titrated to dry secretions, not pupil size; doses are much higher than cardiac bradycardia dosing.
TCA overdose with wide QRS: treat with sodium bicarbonate.
Q: Antidote for suspected cyanide toxicity (smoke inhalation with severe lactic acidosis)? A: Hydroxocobalamin ± sodium thiosulfate
Toxic alcohol ingestion (methanol or ethylene glycol): give fomepizole (or ethanol if unavailable) and involve toxicology early.
8. Abdominal Emergencies in ED
Cannot-Miss Diagnoses
Surgical emergencies — must diagnose urgently:
- Ruptured abdominal aortic aneurysm → pulsatile mass, shock, >60yo male
- Mesenteric ischaemia → pain out of proportion, AF, high lactate
- Testicular/ovarian torsion → sudden onset, young patient
- Small bowel obstruction with strangulation → vomiting, distension, peritonism, ↑lactate
- Perforated viscus → peritonism, free air on erect CXR
- Ectopic pregnancy → female of reproductive age, positive βHCG, free fluid
Surgical vs Medical Abdomen
| Feature | Surgical Abdomen | Medical Abdomen |
|---|---|---|
| Peritonism | Present (guarding, rebound, rigidity) | Absent |
| Bowel sounds | Absent or high-pitched (obstruction) | Present |
| Localisation | Often well-localised initially | May be diffuse |
| Progression | Worsening, new signs | Stable or improving |
| Examples | Appendicitis, perforation, torsion | Pancreatitis, gastroenteritis, IBS |
9. Abdominal Imaging
Abdominal X-ray (AXR)
3/6/9 Rule for bowel diameter:
- Small bowel: >3 cm = dilated
- Large bowel: >6 cm = dilated
- Caecum: >9 cm = dilated (perforation risk)
AXR findings to look for:
| Finding | Suggests |
|---|---|
| Dilated small bowel + air-fluid levels | Small bowel obstruction |
| Dilated large bowel | Large bowel obstruction or pseudo-obstruction |
| Free air under diaphragm | Perforated viscus (erect CXR more sensitive) |
| Sentinel loop | Localised ileus (pancreatitis, appendicitis) |
| Calcifications | Gallstones (10% radio-opaque), renal stones (90% radio-opaque), AAA |
Erect CXR for Free Air
Free air under diaphragm = perforation until proven otherwise.
Best seen on erect CXR (more sensitive than AXR). Patient must be upright ≥10 minutes.
CT Abdomen Indications
- Haemodynamically stable trauma (unstable → theatre or IR)
- Suspected perforation with equivocal plain films
- Appendicitis (if clinical diagnosis uncertain)
- Diverticulitis (severity assessment)
- Pancreatitis complications (necrosis, abscess — not for initial diagnosis)
- Mesenteric ischaemia (CT mesenteric angiogram)
- Renal colic (CT KUB — non-contrast for stones)
10. Chronic Pain Overview
Chronic pain = pain persisting >3 months (or beyond expected healing time).
Key concept: Central sensitisation — the nervous system amplifies pain signals, making normal stimuli painful (allodynia) and painful stimuli more painful (hyperalgesia).
Risk Factors for Chronification
| Factor | Mechanism |
|---|---|
| Catastrophising | Cognitive amplification of pain experience |
| Fear-avoidance | Avoiding activity → deconditioning → more pain |
| Poor sleep | Impairs descending inhibition |
| Depression/anxiety | Shared neurobiological pathways with pain |
| Inadequately treated acute pain | Peripheral and central sensitisation |
| Opioid dependence | Opioid-induced hyperalgesia |
Non-Pharmacological Approaches
Biopsychosocial approach:
- Exercise — graded activity, physiotherapy (strongest evidence)
- Psychology — CBT, acceptance and commitment therapy
- Education — understanding pain neuroscience reduces catastrophising
- Sleep hygiene — improving sleep improves pain
- Social — return to work, social engagement
Opioids are NOT first-line for chronic non-cancer pain.
Long-term opioids → tolerance, dependence, opioid-induced hyperalgesia, endocrine dysfunction, falls. Focus on functional goals (DREAM), not pain scores.
11. Antiemetics
| Drug | Receptor Target | Dose | Best For |
|---|---|---|---|
| Ondansetron | 5-HT₃ antagonist | 4-8 mg IV/PO | Post-op, chemotherapy, gastroenteritis |
| Metoclopramide | D₂ antagonist + prokinetic | 10 mg IV/PO TDS | Gastroparesis, post-op (avoid in bowel obstruction) |
| Cyclizine | H₁ antagonist | 50 mg IV/PO TDS | Vestibular causes, opioid-induced |
| Dexamethasone | Anti-inflammatory (central) | 4-8 mg IV | Post-op (adjunct), raised ICP |
| Droperidol | D₂ antagonist (butyrophenone) | 0.625-1.25 mg IV | Post-op, opioid-induced (caution: QT prolongation) |
Do NOT give metoclopramide in bowel obstruction!
Prokinetic action against a mechanical obstruction → perforation risk.
12. Respiratory Failure Cases (Clinical Application)
Applying Type 1 vs Type 2 Respiratory Failure
| Feature | Type 1 (Hypoxaemic) | Type 2 (Hypercapnic) |
|---|---|---|
| PaO₂ | Low (<60 mmHg) | May be low |
| PaCO₂ | Normal or low | High (>45 mmHg) |
| Mechanism | V/Q mismatch, shunt, diffusion impairment | Alveolar hypoventilation |
| Common causes | Pneumonia, PE, ARDS, pulmonary oedema | COPD exacerbation, neuromuscular, overdose |
| O₂ therapy | High-flow safe | Controlled O₂ (risk of worsening hypercapnia) |
ABG Interpretation Framework
Systematic ABG approach:
- pH — acidotic (<7.35) or alkalotic (>7.45)?
- PaCO₂ — respiratory component (normal 35-45 mmHg)
- HCO₃⁻ — metabolic component (normal 22-26 mmol/L)
- Compensation — is the other system compensating?
- A-a gradient — normal <15 mmHg (increases with age: age/4 + 4)
Clinical Scenario: COPD Exacerbation
| Parameter | Value | Interpretation |
|---|---|---|
| pH | 7.28 | Acidotic |
| PaCO₂ | 68 mmHg | High → respiratory acidosis |
| HCO₃⁻ | 32 mmol/L | High → chronic compensation (metabolic alkalosis) |
| PaO₂ | 52 mmHg | Hypoxaemic |
| Diagnosis | Acute-on-chronic Type 2 respiratory failure | COPD with acute exacerbation |
| Treatment | Controlled O₂ (target SpO₂ 88-92%), NIV if pH <7.35 | Salbutamol + ipratropium + prednisolone + antibiotics |
Clinical Scenario: Pneumonia
| Parameter | Value | Interpretation |
|---|---|---|
| pH | 7.48 | Alkalotic |
| PaCO₂ | 28 mmHg | Low → respiratory alkalosis (hyperventilating) |
| HCO₃⁻ | 24 mmol/L | Normal (no compensation yet = acute) |
| PaO₂ | 55 mmHg | Hypoxaemic |
| A-a gradient | Elevated | Suggests parenchymal disease (not hypoventilation) |
| Diagnosis | Type 1 respiratory failure | Pneumonia causing V/Q mismatch |
| Treatment | High-flow O₂ safe, antibiotics, consider NIV if worsening |
What is the diagnosis?
Week 4 Study Checklist
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