DAY 1 - Self-Introduction & "Why Emergency Medicine?"

Complete Interview Preparation Guide

PART 1: THE 2-MINUTE ELEVATOR PITCH

What It Is

The Structure (Use This Formula)

WHO YOU ARE → TRAINING → KEY EXPERIENCE → WHY EM → FUTURE GOAL

MODEL ANSWER - "Tell me about yourself"

"I'm Dr. [Name], a medical graduate from [College], Tamil Nadu. I completed my MBBS in [Year] and have since worked in [casualty/emergency/rural posting] for [X months/years].

During my internship, I was drawn to the Emergency Department more than any other posting - not just because of the acuity, but because of the way you had to think fast, act decisively, and care for every kind of patient regardless of their background.

One case that shaped my direction was a young man who came in with a seemingly simple headache - I assessed him, raised the concern for subarachnoid haemorrhage early, and the senior resident confirmed it. That moment of recognizing a life-threatening diagnosis early - that's what I want to do every day.

My strengths are clinical reasoning under pressure, communication, and teamwork. I'm comfortable in uncertainty, which I believe is the foundation of emergency medicine.

My long-term goal is to be an emergency physician who not only delivers excellent acute care but also contributes to building stronger emergency systems in India - particularly in tier-2 cities where EM is still developing.

I'm applying here because [Hospital/Program name] is known for [mention something specific - volume, teaching, diversity of cases], and I believe this is where I can grow into that physician."

PART 2: "WHY EMERGENCY MEDICINE?"

What the Interviewer Is Really Asking

• Are you committed, or is this a backup plan?
• Do you understand what EM actually involves (not just the TV version)?
• Do your values align with EM - uncertainty, diversity, shift work, high acuity?

MODEL ANSWER - "Why Emergency Medicine?"

"Emergency Medicine chose me as much as I chose it.

During my postings, I noticed that I came alive in the ED in a way I didn't elsewhere. The undifferentiated patient - someone who comes in saying 'I don't feel right' - that challenge of building a diagnosis from nothing excites me intellectually.

I also love that EM has no boundaries. In one shift, I manage a child with febrile seizures, a young adult with a psychiatric crisis, and an elderly patient with chest pain. That breadth keeps me engaged and always learning.

Beyond that, I genuinely believe Emergency Medicine is the safety net of a healthcare system. When everything else fails - no access, no referral, no money - the ED is open. I want to be part of that system.

I also don't mind the shift work, the uncertainty, or the emotional weight - I've experienced all three and I've found ways to manage them. I think that self-awareness is important for longevity in EM."

PART 3: STRENGTHS & WEAKNESSES

MODEL ANSWER - "What are your strengths?"

"My first strength is clinical decision-making under pressure. During a night shift in casualty, we had two critical patients arrive simultaneously - I was the only junior doctor present. I triaged both correctly, stabilised one, and escalated the other appropriately. The senior praised the priority call I made.

My second strength is communication - both with patients and the team. I've found that a calm, clear explanation to a frightened patient changes their cooperation entirely. I also know how to give a clean SBAR handover, which senior doctors appreciate.

My third strength is that I ask for help at the right time. I know my limits. I will not push beyond my competence when a patient's life is at stake - and I think that's actually a strength in EM."

MODEL ANSWER - "What is your weakness?"

"Honestly, I tend to be a perfectionist with documentation. In a fast-paced ED, I've sometimes spent too long writing detailed notes when I should have moved to the next patient. I've been working on this - using structured templates and bullet-point formats so I can document accurately but quickly. It's improving."

• "I work too hard" (cliche, dishonest)
• "I have no weaknesses" (arrogant)
• A weakness that is actually dangerous in EM (e.g., "I panic under pressure")

PART 4: LONG-TERM GOALS

MODEL ANSWER - "Where do you see yourself in 5-10 years?"

"In 5 years, I want to be a practising Emergency Medicine specialist - competent, confident, and contributing to teaching junior doctors. I'm particularly interested in [POCUS / Paediatric EM / Toxicology / Disaster Medicine - pick one that genuinely interests you].

In 10 years, I see myself in a senior or consultant role, possibly helping design better triage and emergency response systems for hospitals in semi-urban India - where EM infrastructure is still underdeveloped.

I'm also open to academic EM - research in areas like sepsis outcomes or trauma care in low-resource settings is something I find compelling."

PART 5: OTHER COMMON DAY 1 QUESTIONS

Q: "Why our program specifically?"

"I researched your program carefully. [Hospital name] sees a high volume of trauma and medical emergencies, and the teaching structure here - with bedside supervision and simulation labs - is what I need at this stage of training. I've also spoken to [a senior/residents here] and the feedback on the team culture was very positive. I want to train somewhere that challenges me and supports growth - this program does both."

Q: "What do you know about Emergency Medicine as a specialty in India?"

"EM in India is relatively young - it was recognized as a specialty by the MCI/NMC only in the 2000s. The MD Emergency Medicine program has been growing steadily, but there is still a significant gap - most Emergency Departments, especially in tier-2 and tier-3 cities, are staffed by GPs or residents from other specialties rather than trained EM physicians. Organizations like SEMI (Society for Emergency Medicine India) are working to change this. I think EM is at an inflection point in India, and those who train now will shape how the specialty develops over the next decade."

Q: "Tell me about a challenging case you handled."

• Situation - set the scene briefly
• Task - what was your role
• Action - what you did and why
• Result - what happened
• Reflection - what you learned

"During a night call in my internship, a 45-year-old man came in with sudden-onset severe headache. The initial assessment by triage labeled it as tension headache. I examined him and found neck rigidity and photophobia. I escalated immediately to the senior, who ordered a CT and LP - it confirmed subarachnoid haemorrhage. He was taken to the ICU and survived. What I learned was to never anchor on the first impression and to always trust your clinical examination over a triage label."

PART 6: COACHING NOTES

PART 7: QUESTIONS TO ASK THE PANEL

1. "What does a typical first month of the residency look like for a new trainee?"
2. "What qualities do you find distinguish the residents who thrive here from those who struggle?"
3. "Is there scope for involvement in simulation teaching or research during the program?"

PRACTICE CHECKLIST - Day 1

• Record yourself giving the 2-minute intro. Time it.
• Write down your real "why EM" story - don't borrow someone else's.
• Prepare 2 real clinical stories (one strength, one learning experience).
• Research the specific hospital/program you're applying to.
• Prepare 2 questions to ask the panel.
• Practice in front of a mirror or with a friend.

DAY 2 - Triage Systems

Complete Interview Preparation Guide

WHAT IS TRIAGE?

TRIAGE SYSTEM 1: ESI (Emergency Severity Index)

What It Is

The 5 ESI Levels

The ESI Decision Algorithm (3 Questions in Order)

• Needs immediate intervention (airway, breathing, circulation)?
• YES → ESI 1

• Should not wait, confused/lethargic, severe pain/distress?
• YES → ESI 2

• 0 resources → ESI 5
• 1 resource → ESI 4
• 2 or more resources → ESI 3

What Counts as a "Resource" in ESI?

• Blood tests / IV access
• IV fluids / medications
• ECG
• X-ray, CT scan, ultrasound
• IV/IM procedures
• Specialist consult

• History and physical examination
• Oral medications
• Prescription only
• Phone call to GP

ESI Vital Sign Thresholds (used at ESI 3 to upgrade to ESI 2)

ESI Interview Questions & Model Answers

"This is ESI 2 at minimum - possibly ESI 1. The presentation of chest pain with diaphoresis and pallor is a high-risk situation strongly suggesting ACS or aortic dissection. He appears hemodynamically compromised. He should not wait. I would place him in a resuscitation bay immediately, get IV access, ECG within 10 minutes, and notify the senior. If he is hypotensive or altered, he becomes ESI 1."

"ESI 4 or ESI 5. She is stable, low-acuity, and will likely need only a throat examination - possibly a rapid strep test at most. If she needs only an examination and a prescription, she is ESI 5. If she needs a throat swab or test, she is ESI 4. I would confirm by asking about difficulty swallowing or voice changes to rule out peritonsillar abscess, which would change the category."

TRIAGE SYSTEM 2: Manchester Triage System (MTS)

What It Is

The 5 MTS Categories

How MTS Works

1. Patient presents with a complaint (e.g., "chest pain")
2. Nurse selects the matching flowchart (52 presenting complaint charts exist)
3. Works through discriminators - specific clinical features - from most urgent to least
4. First discriminator that matches = the triage category

Key MTS Discriminators (Know These)

MTS vs ESI - Key Differences

MTS Interview Questions & Model Answers

"Both are 5-level systems but their approach is fundamentally different. ESI asks two questions - how sick is this patient right now, and how many resources will they need? It is resource-prediction based. MTS, on the other hand, starts from the presenting complaint and uses specific clinical discriminators - structured yes/no criteria - to assign a category. MTS is more structured and less dependent on the individual nurse's resource estimation. ESI is quicker to apply once trained. For a busy Indian ED with mixed skill levels among triage nurses, ESI may actually be easier to implement, while MTS requires more specific training but produces more consistent outcomes."

TRIAGE SYSTEM 3: START Triage (Disaster/MCI)

What It Is

The 4 START Categories (Colour-Coded Tags)

The START Algorithm (30-60 seconds per patient)

• YES → Tag GREEN (minor), send to casualty collection point
• NO → Stay and assess

• NO → Reposition airway. Still no? → Tag BLACK (dead)
• YES → Check respiratory rate

• 30 breaths/min → Tag RED (immediate)

• < 30 breaths/min → Go to Step 4

• No radial pulse OR capillary refill > 2 seconds → Tag RED
• Pulse present AND cap refill < 2 seconds → Go to Step 5

• Cannot obey → Tag RED
• Can obey → Tag YELLOW

START Memory Aid

30 - 2 - Can Do

30 = RR threshold
2 = Cap refill threshold (2 seconds)
Can Do = Can they obey commands?

SALT Triage (Updated MCI System)

START/Disaster Interview Questions & Model Answers

"I would activate the hospital's Mass Casualty Incident plan immediately and call for additional help. On scene, I would apply START triage - first separating those who can walk (Green), then rapidly assessing the remaining patients using the 30-2-Can Do rule to assign Red, Yellow, or Black tags. Red patients are moved to immediate treatment areas first. I would not stop to treat any individual patient during triage - the goal is to sort everyone within minutes so we can allocate resources strategically. I would also ensure someone is managing scene safety, and communication to the hospital so resuscitation bays and theatres are prepared."

"RED - Immediate. Respiratory rate above 30 per minute places this patient in the Immediate category under START, regardless of the fact that they needed an airway manoeuvre. They are salvageable but require immediate intervention."

"BLACK - Expectant/Dead. Under START triage in a mass casualty scenario, a patient who does not breathe after airway repositioning is tagged Black. This is ethically difficult, but in MCI settings, spending resources on unsurvivable patients costs survivable patients their lives. This is one of the hardest aspects of disaster medicine - but it is the correct protocol."

PAEDIATRIC TRIAGE

Paediatric ESI Modifications

• Vital sign thresholds are age-dependent (children have higher normal HR and RR)
• A fever in a neonate (< 28 days) = automatic ESI 2 regardless of appearance
• Unimmunized febrile children are escalated more aggressively
• Pain assessment uses FACES scale or FLACC (for non-verbal children) rather than numeric scale

JumpSTART (Paediatric MCI Triage - < 8 years)

COMMON TRIAGE PITFALLS - KNOW THESE

QUICK COMPARISON TABLE

DAY 2 PRACTICE CHECKLIST

• Draw the START algorithm from memory (30-2-Can Do)
• Practise assigning ESI levels to 5 random patient scenarios
• Memorise the MTS colour-time targets (0-10-60-120-240 minutes)
• Know the difference between START and JumpSTART
• Be ready to discuss how triage works in your own hospital/internship posting

DAY 3 - BLS & ACLS Algorithms

Complete Interview Preparation Guide

PART 1: BASIC LIFE SUPPORT (BLS)

What Is BLS?

The Adult BLS Sequence (AHA 2020)

SAFETY → RESPONSE → SHOUT FOR HELP → CIRCULATION CHECK → CPR → AED

1. Scene Safety - ensure the environment is safe for you and the patient
2. Check Response - tap shoulders firmly, shout "Are you okay?"
3. No response - call for help / activate emergency response / send someone for AED
4. Check pulse + breathing simultaneously - carotid pulse, no more than 10 seconds
5. No pulse / no normal breathing - start CPR immediately
6. CPR ratio: 30 compressions : 2 breaths (1 rescuer or 2 rescuers without advanced airway)
7. With advanced airway: continuous compressions at 100-120/min + 1 breath every 6 seconds
8. AED arrives - power on, attach pads, follow prompts

High-Quality CPR - The Non-Negotiables

BLS Changes in AHA 2020 (Know These for Interviews)

• CAB not ABC - Compressions before Airway (since 2010, reaffirmed 2020)
• Dispatcher-assisted CPR - emphasized strongly
• Compression-only CPR is acceptable for untrained bystanders
• Mobile phone dispatch - simultaneous notification of emergency services
• No shock-first vs CPR-first debate - now unified: start CPR, use AED as soon as available

PART 2: ACLS - THE CORE ALGORITHMS

The Master Framework: H's and T's

H's and T's - Reversible Causes

ALGORITHM 1: SHOCKABLE RHYTHMS - VF / Pulseless VT (pVT)

Why They Are "Shockable"

VF/pVT Algorithm

Cardiac Arrest Confirmed
↓
Start CPR - High Quality (while charging defibrillator)
↓
SHOCK - Biphasic 200J (or manufacturer recommended)
↓
Immediately resume CPR x 2 minutes (do NOT check pulse right after shock)
↓
Rhythm check - still VF/pVT?
↓
SHOCK again
↓
CPR x 2 minutes
↓
IV/IO access - Epinephrine 1mg every 3-5 minutes
↓
Rhythm check - still VF/pVT?
↓
SHOCK again
↓
CPR x 2 minutes
↓
Amiodarone 300mg IV bolus (or Lidocaine 1-1.5 mg/kg if amiodarone unavailable)
↓
Continue: CPR → Rhythm check → Shock → Epinephrine → Amiodarone 150mg (2nd dose)

Drug Timing in VF/pVT

ECG Recognition

• Chaotic, irregular, no identifiable P waves or QRS
• Amplitude varies (coarse VF = better prognosis, fine VF = worse)

• Wide complex regular tachycardia > 150/min
• No pulse palpable

ALGORITHM 2: NON-SHOCKABLE RHYTHMS - PEA & Asystole

Why They Are "Non-Shockable"

• PEA (Pulseless Electrical Activity): Organised electrical activity on ECG but NO pulse. The heart is "seeing" signals but not contracting effectively.
• Asystole: No electrical activity at all ("flatline"). The worst prognosis of all arrest rhythms.

PEA / Asystole Algorithm

Cardiac Arrest Confirmed
↓
Start CPR - High Quality
↓
IV/IO access
↓
Epinephrine 1mg IV/IO ASAP - then every 3-5 minutes
↓
CPR x 2 minutes
↓
Rhythm check
↓
Still PEA/Asystole? → CPR x 2 min + Epinephrine + search for H's & T's
↓
Repeat cycle

Treating the H's and T's in PEA

PEA vs Asystole - The Critical Difference

ALGORITHM 3: POST-RESUSCITATION CARE (ROSC)

What Is ROSC?

Post-ROSC Goals (The "10 Commandments" of Post-Arrest Care)

• If not awake and following commands → intubate
• Target SpO2: 94-98% (avoid hyperoxia - free radical damage)
• Target PaCO2: 35-45 mmHg (avoid hypo/hyperventilation)
• Waveform capnography to confirm ET tube placement

• Target systolic BP: ≥ 90 mmHg (or MAP ≥ 65 mmHg)
• IV fluids if hypotensive, then vasopressors (norepinephrine first-line)
• 12-lead ECG immediately - look for STEMI
• If STEMI present → emergent coronary angiography (cath lab activation)

• For unconscious survivors → TTM at 32-36°C for 24 hours
• Updated AHA 2020/2023: TTM still recommended but temperature target debated (32-36°C acceptable; preventing fever > 37.5°C is mandatory)
• Avoid hyperthermia at all costs post-arrest

• Glucose: target 140-180 mg/dL (avoid hypoglycemia AND hyperglycemia)
• Correct electrolytes - K+, Mg2+, Ca2+

Post-ROSC BUNDLE (ABCDE approach)

A - Airway: intubate if unconscious
B - Breathing: SpO2 94-98%, normocarbia, avoid hyperventilation
C - Circulation: BP ≥90 systolic, ECG, activate cath lab if STEMI
D - Disability: avoid hyperthermia, TTM, glucose control
E - Exposure: identify reversible cause, treat complications

PART 3: SPECIAL SITUATIONS IN ACLS

Epinephrine - The Debate (Know for Advanced Interviews)

• Large RCT (8,000 patients) - Epi increased ROSC and survival to discharge (3.2% vs 2.4%)
• BUT: survivors in Epi group had worse neurological outcomes
• Conclusion: Epi saves hearts but may harm brains. Still recommended but with awareness of this trade-off.

Cardiac Arrest in Pregnancy

• Displace uterus manually to left (lateral tilt or manual displacement) - relieves aortocaval compression
• Standard CPR compressions higher on sternum (modified position)
• Perimortem Caesarean delivery within 5 minutes of arrest if > 20 weeks gestation - improves maternal and fetal survival
• Do NOT delay defibrillation - remove fetal monitors, shock is safe

Cardiac Arrest - Termination of Resuscitation

• No ROSC despite > 30-45 minutes of well-performed CPR
• No reversible cause identified
• Confirmed asystole for > 20 minutes without cause
• Senior physician decision, communicated clearly to team

PART 4: KEY INTERVIEW QUESTIONS & MODEL ANSWERS

"As soon as cardiac arrest is confirmed - no pulse, unresponsive, no normal breathing - I call a code blue, start a clock, and assign roles: one person for compressions, one for airway, one for IV access and drugs, one for documentation, and I take the team leader role.

I confirm the rhythm on the monitor. If it's VF or pVT, I charge the defibrillator immediately and deliver a shock at 200J biphasic while CPR is running, resume CPR immediately after, and recheck every 2 minutes. I add epinephrine after the second shock and amiodarone after the third.

If it's PEA or asystole, I start epinephrine immediately and focus the team on finding and fixing reversible causes - running through the H's and T's systematically.

Throughout, I'm monitoring CPR quality - rate 100-120, depth 5-6 cm, full recoil, minimal pauses. If we get ROSC, I shift to post-resuscitation care: intubate, target SpO2 94-98%, get a 12-lead ECG, and activate the cath lab if there's a STEMI."

"VF shows chaotic, irregular electrical activity with no identifiable QRS complexes - it is a shockable rhythm. PEA shows organised electrical activity - there may be a visible P wave and QRS - but there is no palpable pulse despite this. The treatment is completely different: VF gets immediate defibrillation; PEA gets no shock. Both get high-quality CPR and epinephrine, but with PEA the priority is identifying and reversing the underlying cause through the H's and T's."

"TTM is the deliberate cooling of post-cardiac arrest patients who remain unconscious after ROSC, targeting a core temperature between 32-36°C for 24 hours. The rationale is that hypothermia reduces cerebral metabolic demand, limits reperfusion injury, and reduces excitotoxicity after global cerebral ischaemia. Based on AHA 2020 guidelines, we recommend TTM for unconscious adult survivors of cardiac arrest regardless of whether the initial rhythm was shockable or not. Critically, we must prevent fever - hyperthermia post-arrest is independently associated with worse neurological outcomes and must be actively prevented."

"High-quality CPR means: rate of 100-120 compressions per minute, depth of at least 5 cm but no more than 6 cm in adults, full chest recoil between compressions without leaning, minimal interruptions with any pause kept under 10 seconds, and avoiding excessive ventilation. The compression fraction - the proportion of arrest time actually spent doing compressions - should be over 60%. Fatigue degrades quality, so I rotate compressors every 2 minutes during rhythm checks."

PART 5: ACLS DRUG QUICK REFERENCE

DAY 3 PRACTICE CHECKLIST

• Draw the VF/pVT algorithm from memory - including drug timing
• Draw the PEA/Asystole algorithm from memory
• Recite all 5 H's and 5 T's without notes
• State post-ROSC targets for SpO2, BP, glucose, and temperature
• Practise the full "walk me through a cardiac arrest" answer aloud (aim for 90 seconds)
• Know what PARAMEDIC-2 showed and what it means for practice

ACLS / BLS Quick Reference Cheat Sheet - PDF

What's in the PDF (6 colour-coded sections):

DAY 4 - Paediatric Emergencies

Complete Interview Preparation Guide (PALS-Based)

THE GOLDEN RULE OF PAEDIATRIC EM

"Children are not small adults."

PART 1: THE PALS SYSTEMATIC APPROACH

The PALS Framework - Always Use This Order

ASSESS → IDENTIFY → INTERVENE → REASSESS

Paediatric Assessment Triangle (PAT) - First 30 Seconds

TICLS - Assessing Appearance

PART 2: PAEDIATRIC RESPIRATORY EMERGENCIES

Step 1 - Identify the Type of Respiratory Problem

CROUP (Laryngotracheobronchitis)

• Age: 6 months - 3 years
• Cause: Parainfluenza virus most common
• Signs: Barking cough (seal-like), inspiratory stridor, hoarse voice, low-grade fever
• Scoring: Westley Croup Score (stridor, retractions, air entry, cyanosis, consciousness)

EPIGLOTTITIS

• Age: Any (classically 2-7 years, now rarer due to Hib vaccine)
• Cause: Haemophilus influenzae type b (Hib)
• Signs: The 4 D's - Dysphagia, Drooling, Dysphonia, Distress; tripod position; high fever
• Do NOT: examine the throat, lay flat, or do anything that might precipitate complete obstruction

1. Keep child calm, upright, with parent
2. Call senior + anaesthetics + ENT immediately
3. Controlled intubation in theatre under gas anaesthesia
4. IV Ceftriaxone after airway is secured
5. Dexamethasone IV

BRONCHIOLITIS

• Age: < 2 years (peak < 6 months)
• Cause: RSV (Respiratory Syncytial Virus) most common
• Signs: Coryzal prodrome → wheeze + crackles + tachypnoea + poor feeding + hyperinflated chest

• Nasal suctioning (clear secretions)
• High-flow nasal oxygen if SpO2 < 92%
• NG/IV feeds if poor oral intake
• NOT recommended: bronchodilators, steroids, antibiotics (unless secondary infection)
• Admit if: SpO2 < 92%, respiratory rate too fast to feed, apnoea, age < 3 months

ASTHMA ACUTE SEVERE (Paediatric)

1. Oxygen - high flow, target SpO2 ≥ 94%
2. Salbutamol (albuterol) - 2.5-5mg nebulised every 20 min x3, then hourly (OR MDI 4-8 puffs via spacer)
3. Ipratropium bromide - 250mcg nebulised with salbutamol (first 3 doses in severe)
4. Prednisolone - 1-2 mg/kg oral (max 40mg) or IV hydrocortisone 4 mg/kg if cannot swallow
5. Magnesium sulphate - 40 mg/kg IV over 20 min (max 2g) - for severe/life-threatening
6. IV Aminophylline - if no response (senior decision)
7. Intubation - last resort (very high risk in severe asthma)

PART 3: PAEDIATRIC SHOCK

What Is Shock in Children?

Types of Shock - Know All Four

Compensated vs Decompensated Shock

Shock Management - The PALS Approach

• High-flow oxygen
• IV/IO access (intraosseous if IV fails after 2 attempts in < 90 seconds)
• Monitor: HR, SpO2, BP, CRT, urine output

• Septic/hypovolemic shock: 10-20 mL/kg isotonic saline (0.9% NaCl or Lactated Ringer's) IV/IO over 5-20 min
• Reassess after each bolus
• Maximum total: up to 60 mL/kg in first hour (evidence supports 20 mL/kg boluses with reassessment - FEAST trial caution in resource-limited settings)
• Cardiogenic shock: 5-10 mL/kg cautiously - avoid fluid overload

Septic Shock - PALS/SSC Paediatric Bundle (1 hour)

• Blood cultures (before antibiotics if possible)
• IV antibiotics within 1 hour (broad-spectrum: Ceftriaxone ± Vancomycin)
• 20 mL/kg fluid bolus - reassess
• Lactate measurement
• Consider vasopressors early (norepinephrine first-line)
• Target: CRT < 2 sec, HR normalise, MAP age-appropriate, urine output > 1 mL/kg/hr

Anaphylaxis in Children

• Epinephrine (adrenaline) 1:1000 solution - 0.01 mg/kg IM into outer thigh (max 0.5 mg)
• Repeat every 5-15 min if no improvement
• High-flow oxygen
• IV fluid bolus 10-20 mL/kg
• Antihistamine (chlorphenamine) + hydrocortisone IV (second-line, not first-line)
• Observe minimum 4-6 hours (biphasic reaction risk)

PART 4: FEBRILE SEIZURES

Definitions

Management of Active Febrile Seizure

Seizure occurring →
│
├── Airway: position, suction, oxygen
├── Timing: start the clock
├── IV/IO access
│
├── Seizure > 5 minutes?
│     ↓ YES
│     Benzodiazepine (1st line):
│     • Midazolam buccal/intranasal: 0.2 mg/kg (max 10 mg) — preferred if no IV
│     • Lorazepam IV/IO: 0.05-0.1 mg/kg
│     • Diazepam IV/IO: 0.1-0.3 mg/kg (rectal: 0.5 mg/kg)
│
├── Seizure continues after 5-10 min (2nd benzodiazepine dose)?
│     ↓ YES
│     Repeat benzodiazepine x1
│
├── Seizure continues after 20 min? → STATUS EPILEPTICUS
│     ↓
│     2nd line: Phenobarbitone 20 mg/kg IV over 15-20 min
│     OR Phenytoin/Fosphenytoin 20 mg/kg IV
│     OR Levetiracetam 30-60 mg/kg IV
│
└── Seizure continues > 45 min → Refractory status
      ↓
      RSI + intubation + ICU (thiopental/midazolam infusion)

Post-Seizure Assessment

• Meningitis (always consider - LP if any doubt, especially < 18 months)
• Encephalitis
• Electrolyte disturbance (hyponatraemia can trigger seizures)

• Age < 12 months (cannot assess meningism reliably)
• Age 12-18 months (consider)
• Complex febrile seizure
• Meningeal signs present
• Not fully recovered

Parental Counselling After Febrile Seizure

1. Risk of recurrence: ~30% will have another febrile seizure
2. Risk of epilepsy: only slightly above general population (~2-3%) for simple febrile seizure
3. Does NOT cause brain damage (simple febrile seizure)
4. Antipyretics reduce discomfort but do NOT prevent recurrence
5. What to do if seizure recurs: position safely, time it, call emergency if > 5 minutes

PART 5: DEHYDRATION

Assessment of Dehydration Severity

Dehydration Management (ORS vs IV)

• Oral Rehydration Solution (ORS) - 50-100 mL/kg over 4 hours
• Small, frequent amounts (5-10 mL every 2-3 min)
• If vomiting - NG tube for ORS is preferred over IV fluids

• IV/IO 20 mL/kg 0.9% NaCl bolus - repeat as needed
• Then calculate deficit + maintenance + ongoing losses
• For DKA-associated dehydration - special protocol (slower rehydration to prevent cerebral oedema)

First 10 kg:   100 mL/kg/day
Next 10 kg:    50 mL/kg/day
Each kg above 20: 20 mL/kg/day

OR in hourly rates (4-2-1 rule):
First 10 kg:   4 mL/kg/hr
Next 10 kg:    2 mL/kg/hr
Each kg above 20: 1 mL/kg/hr

PART 6: KEY PAEDIATRIC VITAL SIGN NORMALS

Minimum SBP = 70 + (2 × age in years)

PART 7: PAEDIATRIC DRUG DOSES (MUST KNOW)

PART 8: INTERVIEW QUESTIONS & MODEL ANSWERS

"First, I ensure the airway is clear and the child is in a safe position. I check vital signs, oxygen saturation, and do a rapid glucose. I look for the source of fever - ears, throat, chest, urine. I assess for meningism - neck stiffness, Kernig's, Brudzinski's - and check the level of consciousness. This child is 2 years old with a single, generalised, brief seizure - this fits a simple febrile seizure profile. However, I cannot be complacent. If there is any concern for meningitis, altered consciousness beyond post-ictal, or if the child is under 12-18 months, I have a low threshold for LP. I treat the fever symptomatically, reassure the parents, explain the recurrence risk of 30%, and observe until the child is fully back to baseline."

"This child is in shock. My priority is: oxygen immediately, IV access - if I can't get IV within 90 seconds, I go intraosseous without hesitation. I give a 20 mL/kg bolus of 0.9% saline over 5-20 minutes and reassess. I take blood cultures, glucose, lactate, FBC, CRP, electrolytes. I start broad-spectrum antibiotics - this presentation is septic shock until proven otherwise, and the 1-hour bundle applies. If the child does not respond to 2-3 fluid boluses, I start vasopressors and escalate to paediatric ICU. Throughout, I'm reassessing CRT, HR, and consciousness after each intervention."

"In compensated shock, the child's physiological mechanisms - tachycardia and increased systemic vascular resistance - are successfully maintaining blood pressure. The BP appears normal but there are early signs: tachycardia, prolonged CRT of 2-3 seconds, cool peripheries, and decreased urine output. In decompensated shock, these mechanisms fail - BP drops, the child becomes increasingly obtunded, CRT exceeds 3 seconds, and the skin becomes mottled and grey. Critically, bradycardia in a shocked child is a sign of imminent arrest - the heart is exhausted. This is why we intervene aggressively at the compensated stage - by the time BP drops, the child is in danger."

"Stridor is an inspiratory sound indicating upper airway obstruction - the narrowing is above the carina. My first thought is: is this croup or epiglottitis? Croup presents with a barking cough, gradual onset, and I can examine the child carefully. Epiglottitis is a surgical emergency - the child is toxic, drooling, in the tripod position, and I must NOT examine the throat or agitate them in any way. I call anaesthetics and ENT immediately and plan for controlled intubation in a controlled environment.

Wheeze is an expiratory sound indicating lower airway obstruction. In a child under 2 with wheeze and a coryzal illness, I think bronchiolitis first - treatment is largely supportive. In a child over 2 with wheeze and no recent URTI or atopic history, I think asthma and start bronchodilators. The examination, investigations, and treatment pathways are completely different."

DAY 4 PRACTICE CHECKLIST

• Recite the PAT components (Appearance, Work of Breathing, Circulation to skin) and what TICLS stands for
• Draw the febrile seizure management flowchart from memory
• State the minimum acceptable systolic BP formula (70 + 2×age)
• List the 4 types of shock and one clinical clue for each
• Recall the intraosseous rule: IV failure after 2 attempts in 90 seconds → IO
• State paediatric defibrillation dose: 2 J/kg → 4 J/kg → 4 J/kg
• Practise the "6-month-old in shock" answer aloud (aim for 60-90 seconds)

DAY 5 - Trauma & Primary Survey (ATLS 10th Edition)

Complete Interview Preparation Guide

THE ATLS PHILOSOPHY - UNDERSTAND THIS FIRST

"Treat the greatest threat to life first."

1. Treat the greatest threat to life first - regardless of the "most obvious" injury
2. Do not move to the next step until the current step is managed - or at least addressed

THE ATLS SEQUENCE

PREPARATION → TRIAGE → PRIMARY SURVEY (ABCDE) → RESUSCITATION
→ ADJUNCTS → SECONDARY SURVEY → DEFINITIVE CARE

PART 1: THE PRIMARY SURVEY - ABCDE (with C-ABCDE update)

The Traditional ABCDE

The C-ABCDE Update (ATLS 10th Edition)

C → Catastrophic Haemorrhage Control (tourniquet, wound packing)
A → Airway
B → Breathing
C → Circulation
D → Disability
E → Exposure

STEP A: AIRWAY + C-SPINE

Airway Assessment - Talk to the Patient First

• Can they speak a full sentence clearly? → Airway is patent (for now)
• Stridor / gurgling / hoarse voice → immediate intervention needed
• Unconscious patient → assume airway is at risk

Manoeuvres (in order of invasiveness)

1. Jaw thrust (preferred in trauma - maintains C-spine alignment)
2. Chin lift (acceptable if no C-spine concern)
3. Suction - clear blood, vomit, secretions
4. Oropharyngeal airway (OPA) - unconscious patients without gag reflex
5. Nasopharyngeal airway (NPA) - semi-conscious patients with intact gag; avoid in base of skull fracture
6. Definitive airway - RSI + endotracheal intubation

When Do You Need a Definitive Airway?

C-Spine Immobilisation

• Apply hard cervical collar + head blocks + tape + long board
• Assume C-spine injury in any blunt trauma until cleared
• Cannot clear C-spine in: unconscious patient, intoxicated patient, distracting injury, midline neck tenderness
• Use NEXUS criteria or Canadian C-Spine Rule to decide imaging

1. No posterior midline cervical tenderness
2. No focal neurological deficit
3. Normal level of alertness
4. No evidence of intoxication
5. No painful distracting injury

STEP B: BREATHING + VENTILATION

The 4 Immediately Life-Threatening Chest Injuries (ATOM FC)

Tension Pneumothorax - The Classic Scenario

• Absent breath sounds on affected side
• Trachea deviated AWAY from the affected side
• Distended neck veins (JVD)
• Hypotension
• Tachycardia

1. Needle decompression - 2nd intercostal space, midclavicular line, large-bore needle (14G)
2. Listen for rush of air (confirms diagnosis)
3. Follow immediately with chest tube - 4th/5th ICS, anterior axillary line

STEP C: CIRCULATION + HAEMORRHAGE CONTROL

Haemorrhage Classes (Know All Four)

Haemorrhage Control - The Priority

• Direct pressure (first always)
• Tourniquet (limb haemorrhage - apply proximal to wound, note time)
• Wound packing with haemostatic gauze (junctional bleeding - groin, axilla, neck)

Chest → Haemothorax (chest tube / thoracotomy)
Abdomen → Intra-abdominal bleeding (FAST → surgery)
Pelvis → Pelvic fracture (pelvic binder → angioembolisation)
Retroperitoneum → Aortic injury (CT → surgery)
Long bones → Femur fracture (~1-1.5L per femur)

IV Access in Trauma

• Two large-bore peripheral IVs (14-16G antecubital) - first choice
• If unsuccessful → intraosseous (IO) access: tibial plateau or humeral head
• Central line - only if no peripheral/IO access; do not delay resuscitation

Massive Transfusion Protocol (MTP)

When to Activate MTP

• Ongoing haemorrhage with haemodynamic instability
• Estimated blood loss > 10 units pRBC in 24h anticipated
• Shock index (HR/SBP) > 1 (e.g., HR 120, SBP 100 = index 1.2)
• ABC Score ≥ 2 (penetrating, SBP ≤ 90, HR ≥ 120, positive FAST)

The 1:1:1 Ratio (Damage Control Resuscitation)

Packed Red Blood Cells (pRBC) : Fresh Frozen Plasma (FFP) : Platelets
              1          :          1         :        1

The Lethal Triad of Trauma Death

        ACIDOSIS
           ↑
HYPOTHERMIA ←→ COAGULOPATHY

• Acidosis: Restore perfusion with blood products (not saline)
• Hypothermia: Warm IV fluids, warm blankets, warm OR
• Coagulopathy: FFP + platelets + TXA early

Tranexamic Acid (TXA)

• Dose: 1g IV over 10 min, then 1g IV over 8 hours
• Time window: Must be given within 3 hours of injury (CRASH-2 trial)
• After 3 hours: May be harmful (increases mortality) - do NOT give
• Mechanism: Anti-fibrinolytic - prevents clot breakdown

Permissive Hypotension (Damage Control Resuscitation)

• Target SBP 80-90 mmHg (not normal BP)
• Rationale: aggressive fluid resuscitation dilutes clotting factors, dislodges clots, and worsens coagulopathy
• Exception: TBI - maintain SBP > 90 mmHg (brain needs perfusion pressure)

STEP D: DISABILITY (NEUROLOGICAL STATUS)

Rapid Neuro Assessment

• A - Alert
• V - Responds to Voice
• P - Responds to Pain
• U - Unresponsive

Check Pupils

• Unequal pupils (anisocoria) → raised ICP / tentorial herniation on ipsilateral side
• Fixed dilated bilateral → brainstem compression, herniation, or drugs
• Pinpoint pupils → opiates, pontine lesion

Check Glucose

• Hypoglycaemia mimics brain injury - always rule out with bedside BGL

STEP E: EXPOSURE + ENVIRONMENT

Full Exposure

• Remove ALL clothing (cut off if necessary)
• Log roll to examine the back (4-person log roll to maintain C-spine)
• Check: spine, perineum, posterior wounds

Prevent Hypothermia

• Trauma patients lose heat rapidly (wet, cut clothing, cold OR)
• Hypothermia < 35°C worsens coagulopathy
• Warm blankets, warm IV fluids, raise ambient temperature

PART 2: FAST EXAM (Focused Assessment Sonography in Trauma)

What FAST Looks For

1. Perihepatic (Morrison's pouch - right upper quadrant)
2. Perisplenic (splenorenal - left upper quadrant)
3. Pelvis (pouch of Douglas / rectovesical pouch)
4. Pericardium (subxiphoid view - cardiac tamponade)

eFAST (Extended FAST)

• Absent lung sliding + no B-lines → Pneumothorax
• B-lines + absent sliding → Haemothorax

FAST Interpretation

PART 3: PELVIC FRACTURES

Why Pelvic Fractures Are Deadly

• Pelvic ring disruption tears the presacral venous plexus and iliac vessels
• Can lose 3-5 litres of blood into the retroperitoneum
• External haemorrhage not visible - patients die from "hidden" pelvic bleeding

Signs of Pelvic Fracture

• Pelvic instability on spring test (do ONCE only - not repeatedly)
• Leg length discrepancy
• Perineal bruising, scrotal/labial haematoma
• Blood at urethral meatus (do NOT catheterise - do retrograde urethrogram first)
• High-riding prostate on PR exam

Pelvic Binder - Application

1. Position binder at the level of the greater trochanters (NOT the iliac crests)
2. Apply firm circumferential compression
3. Commercial binders (T-POD, SAM Sling) preferred; bedsheet as improvised option
4. Binder closes the pelvic ring, reduces volume, tamponades venous bleeding

• Angioembolisation (arterial bleeding)
• Pre-peritoneal pelvic packing (in some centres)
• External fixator (temporary bony stability)

PART 4: SECONDARY SURVEY

AMPLE History

Head-to-Toe Examination

Mechanism of Injury - Always Document

PART 5: INTERVIEW QUESTIONS & MODEL ANSWERS

"This patient is in haemorrhagic shock - tachycardic, hypotensive, and has a reduced GCS. I activate the trauma team immediately and start with the primary survey.

A - Airway: GCS 10 is borderline, but I assess whether he can protect his airway. With ongoing haemodynamic instability and a falling GCS, I have a low threshold for early intubation. C-spine is immobilised throughout.

B - Breathing: I look, listen, feel for breath sounds bilaterally. If there are absent breath sounds with tracheal deviation - I needle decompress immediately without waiting for imaging. I get eFAST running simultaneously.

C - Circulation: Two large-bore IVs, activate massive transfusion protocol now - 1:1:1 pRBC:FFP:platelets. I give TXA 1g IV immediately - we are within the 3-hour window. I do NOT give crystalloid as primary resuscitation fluid. FAST exam to look for free fluid. Permissive hypotension target: SBP 80-90 mmHg - but with GCS of 10 I keep it closer to 90.

D - Disability: GCS 10, pupils checked, glucose checked.

E - Exposure: Full exposure, log roll, keep warm.

If FAST is positive and he remains haemodynamically unstable despite MTP - he goes directly to the operating theatre for damage control laparotomy. CT is for stable patients - not this man."

"The lethal triad is the combination of hypothermia, acidosis, and coagulopathy - they form a vicious cycle where each one worsens the others. Hypothermia impairs clotting enzyme function. Coagulopathy leads to ongoing blood loss and worsening acidosis. Acidosis further impairs clotting and cardiac function.

Prevention is the cornerstone of damage control resuscitation: I avoid hypothermia with warm fluids and blankets; I correct acidosis by restoring perfusion with blood products rather than saline; and I prevent coagulopathy with early 1:1:1 transfusion and TXA. Damage control surgery - abbreviated laparotomy to control bleeding, followed by ICU resuscitation and return to theatre when the triad is corrected - is based entirely on this concept."

"TXA must be given within 3 hours of injury. The CRASH-2 trial showed that giving TXA after 3 hours is not only ineffective but may actually increase mortality - likely because late fibrinolysis is actually a protective response at that point. So I would not give TXA if the time of injury is unknown and likely over 3 hours ago, if the patient has active thromboembolic disease, or if there is a contraindication to antifibrinolytics. I would also be cautious in isolated head injury, as the CRASH-3 trial showed benefit only when given very early."

"The pelvic binder is placed at the level of the greater trochanters - not the iliac crests. This is critical because the goal is to compress the pelvic ring at its widest point and close the book in an open-book fracture. Placing it at the iliac crests is too high and ineffective. The binder reduces the pelvic volume by closing the ring, which tamponades the presacral venous plexus - the main source of bleeding in most pelvic fractures."

"The primary survey is a rapid, systematic assessment to find and immediately treat life-threatening injuries - it follows the ABCDE sequence and runs simultaneously with resuscitation. Every step has a specific life threat it targets, and we do not move on until that threat is addressed. The secondary survey is a thorough head-to-toe physical examination that happens only after the primary survey is complete and the patient is haemodynamically responding to resuscitation. It is where we look for injuries that are serious but not immediately life-threatening - fractures, abdominal tenderness, neurological deficits. The AMPLE history is taken during the secondary survey."

QUICK REFERENCE - TRAUMA MNEMONICS

DAY 5 PRACTICE CHECKLIST

• Recite ABCDE and what life threat each step addresses
• State the 4 immediately life-threatening chest injuries (ATOM FC) with treatment for each
• Draw the haemorrhage class table (I-IV) from memory
• State TXA dose, route, and time window
• Explain the lethal triad and damage control resuscitation
• Describe correct pelvic binder placement (greater trochanters - not iliac crests)
• Explain when FAST positive + unstable → OR vs FAST positive + stable → CT
• Practise the "high-speed RTA" answer aloud - aim for 90 seconds

DAY 6 - Head & Spinal Trauma

Complete Interview Preparation Guide

THE CORE CONCEPT IN HEAD TRAUMA

"The primary brain injury is done. Your job is to prevent the secondary brain injury."

• SBP < 90 mmHg - even one episode doubles mortality in TBI
• SpO2 < 90% - even one episode doubles mortality in TBI

PART 1: GLASGOW COMA SCALE (GCS)

The Full Scale

TBI Severity Classification

GCS Limitations (Know for Interview)

• Cannot assess verbal in intubated patients - document as "V1T" (T = tube)
• Affected by alcohol/drugs, metabolic disturbances, sedation
• Eye opening affected by periorbital swelling
• Not predictive of specific brain injury type
• Motor score is the most prognostically significant component

PART 2: RAISED INTRACRANIAL PRESSURE (ICP)

The Monro-Kellie Doctrine

Volume of Brain + Volume of CSF + Volume of Blood = CONSTANT

Signs of Raised ICP

• Headache (worse in the morning, with Valsalva)
• Nausea / vomiting (often sudden, projectile)
• Papilloedema (takes hours to develop - not reliable in acute setting)
• Subtle personality change

HYPERTENSION (rising BP)
BRADYCARDIA
IRREGULAR RESPIRATION

Cerebral Herniation Syndromes

Emergency Management of Raised ICP

1. Head of bed 30° (promotes venous drainage without compromising CPP)
2. Ensure SBP ≥ 90 mmHg - hypotension kills TBI patients
3. SpO2 ≥ 95% - intubate if needed
4. Avoid hyperthermia - target normothermia
5. Avoid hypoglycaemia and hyperglycaemia
6. Loosen cervical collar - tight collar impairs venous drainage

1. Mannitol 0.25-1 g/kg IV over 15-20 min (osmotic agent - draws water out of brain) OR Hypertonic saline (3% NaCl) 250 mL IV (preferred in hypotensive TBI - raises BP simultaneously)
2. Hyperventilation (temporary bridge only): PaCO2 target 35 mmHg (reduces cerebral blood flow by vasoconstriction) - use only for minutes as a bridge to surgery, NOT as sustained treatment
3. Call neurosurgery immediately

PART 3: INTRACRANIAL HAEMATOMAS

EPIDURAL HAEMATOMA (EDH)

Head injury → Brief loss of consciousness → LUCID INTERVAL
(patient wakes up, appears normal) → Rapid deterioration
→ Ipsilateral fixed dilated pupil + contralateral hemiplegia
→ Cushing's triad → death if untreated

• Biconvex (lens-shaped / lenticular) hyperdense lesion
• Does NOT cross suture lines (dura is attached at sutures)
• Most commonly temporal/temporoparietal

SUBDURAL HAEMATOMA (SDH)

• Crescent-shaped hyperdense lesion (acute)
• DOES cross suture lines (because bridging veins span the whole subdural space)
• Midline shift indicates mass effect

• Elderly (cerebral atrophy stretches bridging veins)
• Alcoholics (cerebral atrophy + coagulopathy)
• Patients on warfarin / NOACs / aspirin
• Infants (non-accidental injury - "shaken baby")

• Small SDH with no midline shift → observation, correct coagulopathy, reverse anticoagulation
• Large SDH with midline shift > 5mm or GCS drop → craniotomy / burr hole drainage

SUBARACHNOID HAEMORRHAGE (SAH)

"Worst headache of my life" - thunderclap headache - sudden onset, maximal at onset, occipital

• Hyperdense blood in basal cisterns, sylvian fissure, sulci
• Sensitivity of CT within 6 hours: ~98% (very high if done early)
• After 6 hours: sensitivity drops → LP required if CT negative (xanthochromia in CSF = positive)

• Rebleeding - highest risk in first 24 hours
• Vasospasm - days 4-14 post-bleed → delayed ischaemic neurological deficit (DIND)
• Hydrocephalus - blood blocks CSF drainage
• Hyponatraemia - SIADH or cerebral salt wasting

• Nimodipine 60mg every 4 hours (calcium channel blocker - reduces vasospasm)
• Neurosurgical: coil embolisation (endovascular) or surgical clipping

INTRACEREBRAL HAEMATOMA (ICH)

COMPARISON TABLE - HAEMATOMAS

PART 4: CONCUSSION

Definition

Features

• Headache, dizziness, confusion, amnesia (retrograde and/or anterograde)
• No loss of consciousness required for diagnosis
• Symptoms typically resolve in days-weeks

Red Flags Requiring Immediate CT (not just concussion)

• GCS < 15 at 2 hours after injury
• Suspected open or depressed skull fracture
• Signs of basal skull fracture (see below)
• Post-traumatic seizure
• Age ≥ 65
• Vomiting ≥ 2 episodes
• Retrograde amnesia > 30 minutes
• Dangerous mechanism (pedestrian vs vehicle, ejection from vehicle, fall > 1 metre)

Signs of Basal Skull Fracture (Know All Five)

PART 5: SPINAL CORD INJURIES

Spinal Cord Anatomy Essentials

POSTERIOR COLUMNS → Ipsilateral fine touch, vibration, proprioception
LATERAL CORTICOSPINAL TRACTS → Ipsilateral voluntary motor
LATERAL SPINOTHALAMIC TRACTS → Contralateral pain and temperature

The Spinal Cord Syndromes - MUST KNOW ALL FIVE

1. COMPLETE CORD INJURY

• Loss of ALL motor + sensory + autonomic below the level
• No sacral sparing
• Poor prognosis for recovery

2. ANTERIOR CORD SYNDROME

• Bilateral loss of motor (corticospinal tracts) below level
• Bilateral loss of pain + temperature (spinothalamic tracts) below level
• PRESERVED vibration and proprioception (posterior columns intact)

3. POSTERIOR CORD SYNDROME

• Loss of vibration, proprioception, fine touch below level (posterior columns gone)
• PRESERVED motor, pain, temperature

4. CENTRAL CORD SYNDROME

• Arms weaker than legs (central cervical cord fibres run more medially)
• Variable sensory loss below level
• Bladder dysfunction (urinary retention)
• Sacral sparing often present

5. BROWN-SÉQUARD SYNDROME

• Ipsilateral: Loss of motor, vibration, proprioception, fine touch (SAME side as lesion)
• Contralateral: Loss of pain and temperature (OPPOSITE side - spinothalamic tracts cross within 1-2 levels of entry)

Summary Table - Spinal Cord Syndromes

Neurogenic Shock vs Spinal Shock

Spinal Cord Injury Management

1. C-spine immobilisation (hard collar + board)
2. Maintain SBP > 90 mmHg (target MAP 85-90 mmHg in first 7 days per some guidelines)
3. Avoid hypoxia (SpO2 > 95%)
4. High-dose methylprednisolone - controversial and no longer standard of care in most guidelines (NASCIS-3 showed modest benefit with significant complications - do not recommend routinely)
5. Catheterise (neurogenic bladder)
6. DVT prophylaxis
7. Spine surgery referral

PART 6: IMAGING IN HEAD & SPINAL TRAUMA

CT Head - Indications

• GCS < 13 at any point since injury
• GCS < 15 at 2 hours after injury
• Suspected open/depressed skull fracture
• Signs of basal skull fracture
• Post-traumatic seizure
• Focal neurological deficit
• Age ≥ 65 + any LOC or amnesia
• Coagulopathy + any LOC or amnesia

• LOC or amnesia + dangerous mechanism (< 65 yrs, no coagulopathy)

CT Spine - Indications

• Age ≥ 65
• Dangerous mechanism
• Paraesthesias in extremities

• Simple rear-end MVC, sitting position in ED, ambulatory at any time, delayed onset of neck pain, absence of midline tenderness
• If YES → assess rotation 45° each side

• YES → no imaging needed
• NO → CT C-spine

MRI Spine - When to Use

• Neurological deficit with normal CT
• Suspected cord injury without radiographic abnormality (SCIWORA)
• Ligamentous injury assessment
• Not first-line in acute trauma (takes time, motion artefact)

PART 7: INTERVIEW QUESTIONS & MODEL ANSWERS

"This is a classic presentation of an epidural haematoma with a lucid interval. The initial loss of consciousness was from the primary impact. The lucid interval occurred as he compensated temporarily. The subsequent deterioration with a fixed dilated right pupil indicates the expanding arterial bleed - almost certainly from the middle meningeal artery from a temporal bone fracture - is now causing uncal herniation compressing the right oculomotor nerve, giving the ipsilateral fixed dilated pupil and contralateral motor deficit pattern.

This is a neurosurgical emergency. I call neurosurgery immediately. I intubate now - GCS 9 and deteriorating is not a patient I wait on. I give mannitol 0.5 g/kg IV or hypertonic saline as a temporising measure to reduce ICP while preparing for emergency craniotomy. CT head will confirm the biconvex haematoma but should not delay the surgical call. Target SBP ≥ 90 and SpO2 ≥ 95%. Outcome is excellent if we get him to theatre quickly - the brain itself is often undamaged in EDH."

"There are five main spinal cord syndromes: complete cord injury, anterior cord syndrome, posterior cord syndrome, central cord syndrome, and Brown-Séquard syndrome. The differences depend on which tracts within the cord are damaged.

Brown-Séquard is caused by a cord hemisection - classically a penetrating injury like a stab wound to one side of the spine. Because the motor and posterior column fibres travel on the same side they originate, while the spinothalamic fibres cross within one to two levels of entry, you get a dissociated picture: ipsilateral loss of motor function and proprioception, with contralateral loss of pain and temperature sensation. It sounds counterintuitive but makes perfect anatomical sense. It carries the best prognosis of any incomplete cord injury."

"This patient is high risk despite a trivial mechanism. Elderly patients on anticoagulation can develop significant intracranial haemorrhage from minor trauma because anticoagulation prevents haemostasis and cerebral atrophy stretches bridging veins. I get an urgent CT head without contrast - this is a NICE guideline indication: anticoagulated patient with any LOC, amnesia, or neurological symptom. I check his INR, reverse his anticoagulation proactively - vitamin K + 4-factor PCC (prothrombin complex concentrate) if INR is supratherapeutic or if CT shows haemorrhage. If CT shows a subdural haematoma with any mass effect, neurosurgery is called. If CT is negative and he has a persistent headache or is not back to baseline, I admit for observation and reassessment."

"They can be distinguished by the combination of blood pressure and heart rate. In haemorrhagic shock, the reflex response is tachycardia - the body compensates for volume loss by increasing heart rate. In neurogenic shock, the injury is at the thoracic spinal cord level T1-L2, which cuts off the sympathetic outflow. The result is vasodilation and loss of the cardiac accelerator fibres - so you get hypotension with paradoxical bradycardia, and the skin below the level of injury is warm and dry rather than cool and clammy. This distinction matters because treating neurogenic shock with large volumes of crystalloid can cause fluid overload - the problem is vascular tone, not volume deficit. First-line treatment is vasopressors, particularly norepinephrine."

DAY 6 PRACTICE CHECKLIST

• Recite GCS components and scores from memory - including what decorticate vs decerebrate means
• Draw the EDH vs SDH table (shape, source, density, suture crossing, lucid interval)
• Name all 5 signs of basal skull fracture
• Describe the Brown-Séquard pattern precisely (ipsilateral motor, contralateral pain/temp)
• State the Monro-Kellie doctrine in one sentence
• Explain the difference between neurogenic shock and spinal shock
• State two immediate measures for raised ICP while awaiting CT
• Practise the "fixed dilated pupil after head injury" answer aloud

DAY 7 - Chest Pain & Acute Coronary Syndromes (ACS)

Complete Interview Preparation Guide

THE CORE CONCEPT

"Time is myocardium. Every minute of ischaemia kills 2 million cardiomyocytes."

1. Rule IN the life-threatening causes immediately (STEMI, aortic dissection, tension PTX, PE, tamponade)
2. Risk-stratify everyone else - not all chest pain is ACS, and not all ACS is obvious

PART 1: LIFE-THREATENING CAUSES OF CHEST PAIN

The "Killer Six" - Rule Out These First

PART 2: ACS SPECTRUM

Understanding the ACS Spectrum

PLAQUE RUPTURE → Thrombus Formation
        │
        ├── Complete occlusion → STEMI
        │   (transmural ischaemia, ST elevation)
        │
        ├── Partial occlusion → NSTEMI
        │   (subendocardial ischaemia, troponin rise, NO ST elevation)
        │
        └── No troponin rise, no ECG changes → UNSTABLE ANGINA
            (but same mechanism, high risk of progression)

PART 3: ECG INTERPRETATION IN ACS

ECG Territories - Know This Cold

STEMI Criteria

• ≥ 1 mm (0.1 mV) in ≥ 2 contiguous limb leads
• ≥ 2 mm (0.2 mV) in ≥ 2 contiguous precordial leads (V1-V3 in men)
• ≥ 1.5 mm in V2-V3 in women (lower threshold)

• Tall broad R wave in V1-V2
• ST depression in V1-V2 (the mirror of posterior ST elevation)
• Do posterior leads V7-V9 → ST elevation confirms it

• Get right-sided leads (V3R, V4R)
• ST elevation in V4R ≥ 1mm = RV MI
• Critical management difference: Avoid nitrates (cause catastrophic hypotension), avoid diuretics, give IV fluids for preload

STEMI Equivalents (No Classic ST Elevation - But Same Emergency)

Sgarbossa Criteria (LBBB + suspected STEMI)

NSTEMI / Unstable Angina ECG Changes

• ST depression (horizontal or downsloping) ≥ 0.5mm
• T-wave inversions (new or dynamic)
• Transient ST changes during pain
• Normal ECG (does NOT rule out ACS - up to 6% of MIs have normal ECG at presentation)

PART 4: HIGH-SENSITIVITY TROPONIN (hs-cTn)

What Troponin Is

Rise and Fall Kinetics

The 0h/1h Algorithm (ESC 2020 - Most Important)

hs-cTn at TIME 0 (presentation)
↓
Very LOW (below assay-specific threshold) + low clinical probability
→ Rule OUT (discharge with safety net)

OR

hs-cTn at 0h AND 1h
↓
0h level very high → Rule IN (NSTEMI confirmed)
0h to 1h delta (rise) significant → Rule In
0h low + 1h low + small delta → Rule Out
Inconclusive → repeat at 3h or serial ECGs

• Large absolute rise at 0h = likely NSTEMI
• Small absolute value but significant rise over 1h = likely NSTEMI (delta rule)
• Persistently low with negligible rise = very unlikely ACS

Causes of Troponin Rise Other Than ACS (Type 2 MI and Non-Ischaemic)

PART 5: RISK STRATIFICATION

HEART Score (Most Common in EM)

TIMI Score (Unstable Angina / NSTEMI)

1. Age ≥ 65
2. ≥ 3 CAD risk factors (family history, hypertension, hypercholesterolaemia, DM, active smoker)
3. Known CAD (stenosis ≥ 50%)
4. ASA use in last 7 days (implies aspirin-resistant plaque)
5. Severe angina (≥ 2 episodes in 24h)
6. ST deviation ≥ 0.5mm
7. Positive cardiac marker (troponin)

PART 6: MANAGEMENT

STEMI Management - The Timeline

Patient arrives with chest pain
↓
10-Minute ECG (door-to-ECG time) → STEMI identified
↓
Activate Cath Lab (door-to-balloon time target: < 90 min)
↓
Dual antiplatelet therapy (DAPT) - Loading doses:
  • Aspirin 300mg oral (if not on aspirin already)
  • P2Y12 inhibitor: Ticagrelor 180mg OR Prasugrel 60mg OR Clopidogrel 600mg
↓
Anticoagulation: Unfractionated Heparin IV bolus (70-100 units/kg)
↓
Primary PCI (balloon inflation) - this is reperfusion
↓
Post-PCI: DAPT continued, statin, beta-blocker, ACEi

Thrombolytics - When PCI Is Not Available

• Prior intracranial haemorrhage (ever)
• Ischaemic stroke within 3 months
• Structural cerebrovascular lesion (AVM)
• Intracranial neoplasm
• Active internal bleeding (not menses)
• Suspected aortic dissection
• Significant closed head trauma within 3 months

Signs of Successful Thrombolysis (within 90 min)

• Resolution of chest pain
• ST elevation reduces by ≥ 50%
• Reperfusion arrhythmia (accelerated idioventricular rhythm - AIVR - a good sign)
• Peak troponin earlier than expected (washout)

NSTEMI / Unstable Angina Management

• Aspirin 300mg loading dose
• Ticagrelor 180mg (preferred over clopidogrel per ESC/ACC guidelines)
• Anticoagulation: Fondaparinux 2.5mg SC (preferred) OR LMWH (enoxaparin)
• Oxygen only if SpO2 < 94% (routine oxygen is NOT beneficial and may be harmful)
• Nitrates for pain (IV GTN if ongoing ischaemia)
• Morphine (use cautiously - may reduce P2Y12 absorption)
• Beta-blocker (if no contraindication)

Aortic Dissection - Do NOT Miss This

• Tearing/ripping pain maximal at onset
• Radiates to back (between shoulder blades)
• BP differential > 20 mmHg between arms
• Pulse deficit
• New aortic regurgitation murmur
• Widened mediastinum on CXR
• Normal or non-specific ECG (but can involve coronary ostia)

• Heart rate control (IV labetalol or esmolol) → target HR < 60
• BP control → target SBP 100-120 mmHg
• Type A (ascending) → emergency surgery
• Type B (descending only) → medical management (TEVAR if complicated)

PART 7: SPECIAL SITUATIONS

Cocaine-Induced Chest Pain

• Cocaine causes coronary vasospasm AND accelerated atherosclerosis
• Avoid beta-blockers (unopposed alpha stimulation → worsens vasospasm and hypertension)
• Use benzodiazepines (reduces sympathomimetic drive), nitrates, calcium channel blockers
• Aspirin if ACS features present

Takotsubo (Stress) Cardiomyopathy

• Emotional or physical stress triggers catecholamine surge
• Apical ballooning of LV on echocardiography ("octopus pot" shape)
• Mimics STEMI - ST changes + troponin rise
• Typically in post-menopausal women after acute stress
• Coronary angiography is normal (no obstructive CAD)
• Treatment: supportive - ACEi, beta-blocker; usually recovers fully

Wellens Syndrome - Do Not Miss

• Deeply inverted (Type B) or biphasic (Type A) T-waves in V2-V3
• Patient is pain-free when the ECG is taken (easy to dismiss)
• Represents critical proximal LAD stenosis that is temporarily reperfused
• Patient is at very high risk of massive anterior MI
• Do NOT do stress test - can precipitate complete occlusion
• Urgent cardiology referral and angiography

PART 8: INTERVIEW QUESTIONS & MODEL ANSWERS

"Diabetic patients commonly present with atypical or silent myocardial infarction because autonomic neuropathy blunts the typical chest pain response. Jaw pain, nausea, epigastric discomfort, fatigue, and diaphoresis can all be ACS equivalents. My first action is a 12-lead ECG within 10 minutes of arrival - this is non-negotiable for any patient with a presentation that could possibly be cardiac. I take a detailed history - duration, onset, associated symptoms, risk factor burden. I check hs-troponin at 0 and 1 hour. I give aspirin 300mg immediately if ACS is suspected and there is no contraindication. Even with a normal ECG and initial troponin, I do not discharge this patient - I observe and repeat bloods. A high index of suspicion in diabetics is mandatory."

"The target is 90 minutes from first medical contact to balloon inflation for primary PCI in STEMI. For patients transferred from another facility, the target extends to 120 minutes. The reason it matters is the fundamental principle that time equals myocardium - every minute of complete coronary occlusion results in irreversible cardiomyocyte death. Studies consistently show that achieving door-to-balloon time under 90 minutes significantly reduces infarct size, preserves ejection fraction, and reduces 30-day and 1-year mortality. When PCI cannot be achieved within this window - for example in a rural setting - thrombolytics should be given within 30 minutes of arrival (door-to-needle time), followed by transfer for angiography within 3 to 24 hours."

"The HEART score is a five-variable risk stratification tool for chest pain patients in the ED - History, ECG, Age, Risk factors, and Troponin. Each is scored 0-2, giving a maximum of 10. A score of 0-3 is low risk - less than 2% chance of major adverse cardiac event at 6 weeks - and these patients can be safely discharged with outpatient follow-up. A score of 4-6 is intermediate and warrants observation, serial troponins, and consideration of stress testing or cardiology review. A score of 7-10 is high risk - over 50% MACE probability - and requires admission and early angiography. It is practical, validated across multiple studies, and is now embedded in most ED chest pain pathways."

"In a posterior MI the infarcting territory is on the back of the heart, so the standard leads V1 and V2 show a mirror image - not ST elevation but tall broad R waves and ST depression, which is the reciprocal change. To confirm, I apply right-sided posterior leads - V7, V8, and V9 - which are placed at the left posterior chest. ST elevation of ≥ 0.5mm in these leads confirms a posterior STEMI. The culprit vessel is usually the RCA or left circumflex. This is a true STEMI equivalent and should trigger cath lab activation exactly as a conventional STEMI would - it must not be missed just because the standard ECG does not show classic ST elevation."

"There are three situations where nitrates are contraindicated or dangerous in chest pain. First, right ventricular MI - which occurs in 30-50% of inferior STEMIs from proximal RCA occlusion. The RV is preload-dependent and nitrates cause venodilation, dropping preload catastrophically and causing profound hypotension. I always get right-sided leads in any inferior STEMI before giving nitrates. Second, if the patient has taken a phosphodiesterase-5 inhibitor such as sildenafil or tadalafil within 24-48 hours - the combination causes severe refractory hypotension. Third, if the patient is hypotensive - SBP below 90 mmHg - nitrates will worsen haemodynamic compromise."

QUICK REFERENCE - ACS DRUGS AT A GLANCE

DAY 7 PRACTICE CHECKLIST

• Draw the ECG territory table (inferior/anterior/lateral leads and arteries) from memory
• State STEMI criteria precisely (mm thresholds, number of leads, gender differences)
• Explain the 0h/1h troponin algorithm
• Name 5 causes of troponin rise other than ACS
• Calculate a HEART score for a sample patient
• State door-to-balloon time target: 90 minutes
• State three contraindications to nitrates in chest pain
• Describe Wellens syndrome and why stress testing is dangerous
• Practise the "diabetic with jaw pain" answer aloud

DAY 8 - Acute Dyspnoea

Complete Interview Preparation Guide

THE CORE CONCEPT

"Dyspnoea is a symptom, not a diagnosis. Your job is to identify the mechanism and treat it - fast."

• Stabilise first (oxygen, positioning, IV access, monitoring)
• Differentiate fast (clinical exam + bedside tools = diagnosis within minutes)
• Treat the mechanism (not just the symptom)

THE DIAGNOSTIC FRAMEWORK - THINK IN MECHANISMS

ACUTE DYSPNOEA
│
├── AIRWAY PROBLEM      → Obstruction (asthma, COPD, anaphylaxis, foreign body)
├── ALVEOLAR PROBLEM    → Fluid (pulmonary oedema), pus (pneumonia), collapse (atelectasis)
├── PLEURAL PROBLEM     → Pneumothorax, haemothorax, effusion
├── VASCULAR PROBLEM    → Pulmonary embolism
├── PUMP FAILURE        → Cardiogenic pulmonary oedema, tamponade
└── DRIVE PROBLEM       → Metabolic acidosis (Kussmaul), anxiety, neuromuscular

BEDSIDE DIFFERENTIATION - USE THESE TOOLS FAST

PART 1: ACUTE SEVERE ASTHMA

Severity Classification (British Thoracic Society / GINA)

Why a Normal PaCO2 in Acute Asthma Is a Warning Sign

• In acute asthma, patients hyperventilate due to hypoxia → PaCO2 is typically LOW (e.g., 3.5-4.5 kPa)
• A normal PaCO2 (5-6 kPa) means the patient is tiring - they can no longer maintain the hyperventilation needed to blow off CO2
• A raised PaCO2 (> 6 kPa) = near-fatal asthma - imminent respiratory arrest

Management - Stepwise

1. Oxygen - high flow, target SpO2 94-98% (not 100% - hyperoxia may worsen V/Q mismatch)
2. Sit upright
3. Continuous monitoring

• Intubating a severe asthmatic is dangerous (bronchospasm on laryngoscopy, dynamic hyperinflation, right heart failure, risk of barotrauma)
• Use ketamine for RSI (bronchodilator properties)
• Low RR (10-12/min), long expiratory time (I:E ratio 1:4 or 1:5)
• Allow permissive hypercapnia (accept PaCO2 up to 10 kPa) - "controlled hypoventilation"

Discharge Criteria for Asthma

• PEFR ≥ 75% predicted, sustained for 1 hour
• SpO2 ≥ 94% on air
• Symptoms resolved
• Inhaler technique checked
• Prednisolone prescription given (5-7 days)
• Follow-up arranged within 48 hours

PART 2: ACUTE COPD EXACERBATION

Definition

• Respiratory tract infection (viral 50%, bacterial 50%)
• Common bacterial organisms: Haemophilus influenzae, Streptococcus pneumoniae, Moraxella catarrhalis

Severity Assessment

The Oxygen Controversy in COPD

• Hypoxic drive is a minor component. The main concern is:
  • Haldane effect - oxygen displaces CO2 from haemoglobin → PaCO2 rises
  • V/Q mismatch worsening - oxygen dilates previously vasoconstricted vessels in under-ventilated areas
• Correct approach: Target SpO2 88-92% in COPD with known hypercapnia or at-risk patients
• This is NOT "withholding oxygen" - it is titrated controlled oxygen
• Start low (24-28% Venturi mask), titrate up, monitor with ABG

Management of COPD Exacerbation

1. Controlled oxygen - target SpO2 88-92%, Venturi mask 24-28%
2. Salbutamol - 2.5-5mg nebulised (driven by air, not pure O2 if at risk)
3. Ipratropium - 500mcg nebulised
4. Prednisolone - 30-40mg oral for 5 days (IV hydrocortisone if cannot swallow)
5. Antibiotics - if purulent sputum, consolidation on CXR, or clinical infection:
   • Amoxicillin 500mg TDS (first-line) OR Doxycycline 200mg loading
   • Co-amoxiclav or Azithromycin if moderate/severe or prior organisms
6. ABG - baseline and after 1 hour of treatment
7. NIV (BiPAP) - if pH < 7.35 and PaCO2 > 6 kPa despite medical treatment (see below)

Non-Invasive Ventilation (NIV / BiPAP) in COPD

• pH < 7.35 (acidosis) + PaCO2 > 6 kPa + RR > 23/min
• After maximal medical therapy for 1 hour

• IPAP (inspiratory positive airway pressure): 12-20 cmH2O (augments tidal volume)
• EPAP (expiratory): 4-5 cmH2O (prevents alveolar collapse)

• Vomiting / unable to protect airway
• Haemodynamic instability
• Undrained pneumothorax
• Recent upper GI / facial surgery
• Excessive secretions not managed by patient
• Decreased consciousness / agitation

PART 3: ACUTE PULMONARY OEDEMA (APO)

Cardiogenic vs Non-Cardiogenic

Management of Acute Cardiogenic Pulmonary Oedema

1. Sit upright (reduces venous return, reduces work of breathing)
2. High-flow oxygen - target SpO2 ≥ 94%
3. IV access + monitoring

• Reduces preload AND afterload - most effective agent in APO
• Hold if SBP < 90 mmHg

1. Furosemide (frusemide) - 40-80mg IV bolus (if not already on diuretics; higher doses if chronic use)
   • Immediate venodilation (within 5-15 min, before diuresis starts)
   • Diuresis peaks at 30-60 min
2. Morphine - 2-4mg IV (reduces anxiety, mild venodilation) - controversial, some evidence of harm; use cautiously if at all

• Recruits alveoli, reduces work of breathing, decreases preload and afterload
• Strong evidence - reduces need for intubation in cardiogenic APO
• Contraindicated: vomiting, undrained PTX, haemodynamic collapse

BNP / NT-proBNP in Dyspnoea

PART 4: PULMONARY EMBOLISM (PE)

Risk Stratification - Two Steps

• ≤ 4 = PE unlikely → D-dimer (if negative, PE excluded)

• 4 = PE likely → CT Pulmonary Angiography (CTPA) directly

ECG in PE - Know All the Signs

Management of PE

• Anticoagulation - LMWH (enoxaparin 1.5mg/kg SC daily) OR DOAC (rivaroxaban or apixaban - can start directly without prior LMWH)
• Rivaroxaban: 15mg BD for 21 days, then 20mg OD
• Apixaban: 10mg BD for 7 days, then 5mg BD
• Warfarin: if used, bridge with LMWH until INR therapeutic (2-3)

• Thrombolytics: Alteplase (tPA) 100mg IV over 2 hours (or 0.6mg/kg over 15 min if arresting)
• Immediate anticoagulation (UFH infusion)
• CPR if in arrest - continue for at least 60-90 min after thrombolytics
• Surgical embolectomy if thrombolytics contraindicated or failed

• Class I/II (low risk) → consider home treatment with DOAC
• Class III-V → admit

D-Dimer - Understanding Its Role

• High sensitivity, low specificity
• Useful only to RULE OUT PE in low pre-test probability patients
• A positive D-dimer does NOT diagnose PE - it just means more investigation needed
• D-dimer rises with: age, infection, surgery, malignancy, pregnancy, trauma, haematoma

• Example: 70-year-old: threshold = 700 mcg/L (not the standard 500)
• Increases specificity without reducing sensitivity

PART 5: PNEUMOTHORAX

Types and Context

Size and Treatment (BTS Guidelines)

• Rim < 2cm on CXR AND not breathless → discharge, observe, no intervention
• Rim ≥ 2cm OR breathless → needle aspiration (14-16G, 2nd ICS MCL)
  • Success (lung re-expands, SpO2 improves): discharge
  • Failure → small-bore chest drain (8-14F Seldinger technique)

• Any size → chest drain regardless

Chest Drain - Key Points

• 4th or 5th ICS, anterior axillary line (the "safe triangle")
• Safe triangle boundaries: anterior axillary line (lateral), lateral border of pectoralis major (medial), line of the nipple (inferior)
• Avoid: long thoracic nerve (medial), intercostal vessels (inferior rib margin)
• Drain over the superior border of the rib (vessels/nerves run under inferior border)
• Swing confirms intrapleural placement; bubbling confirms pneumothorax draining; drainage confirms haemothorax

Tension Pneumothorax - Recap

• Severe respiratory distress
• Absent breath sounds ipsilateral
• Tracheal deviation AWAY from affected side (late sign)
• Distended neck veins
• Hypotension + tachycardia

1. Needle decompression: 2nd ICS, midclavicular line, 14G needle
2. Rush of air = confirms diagnosis
3. Proceed to chest tube immediately after

PART 6: LUNG ULTRASOUND (POCUS) IN DYSPNOEA

• A-lines + sliding = normal lung / COPD / PE / asthma
• B-lines bilateral = pulmonary oedema
• B-lines unilateral = pneumonia
• A-lines + no sliding = pneumothorax

PART 7: ABG INTERPRETATION - RAPID APPROACH

Five-Step Method

• CO2 up → respiratory acidosis
• CO2 down → respiratory alkalosis

• HCO3 down → metabolic acidosis
• HCO3 up → metabolic alkalosis

Common ABG Patterns in Dyspnoea

PART 8: INTERVIEW QUESTIONS & MODEL ANSWERS

"This patient is in acute hypercapnic respiratory failure until proven otherwise. My immediate priorities are: controlled oxygen via 28% Venturi mask - targeting SpO2 88-92%, not higher - while I simultaneously nebulise salbutamol and ipratropium on air, not pure oxygen. I give IV or oral prednisolone and antibiotics if there is purulent sputum or consolidation on CXR. Crucially, I get an ABG within the first 30-60 minutes to assess pH and PaCO2. If the pH is below 7.35 and PaCO2 is above 6 kPa despite one hour of medical treatment, this patient needs NIV - BiPAP. I set the team up for NIV, ensure the patient is cooperative and able to tolerate the mask, and reassess with a repeat ABG after one hour on NIV. If he deteriorates further, I need to have an early conversation about ceilings of care and whether intubation and ICU admission are appropriate given his baseline."

"The distinction matters because the treatments are almost opposite in some ways - heart failure needs diuretics and nitrates, COPD needs bronchodilators and possibly NIV with careful oxygen. I use a combination of history, examination, bedside tests, and POCUS. A patient with orthopnoea, paroxysmal nocturnal dyspnoea, bilateral ankle oedema, a history of IHD or AF, and an S3 gallop points to heart failure. A patient with a chronic smoking history, barrel chest, pursed-lip breathing, and previous COPD admissions points to COPD.

On the ECG I look for AF or ischaemic changes suggesting cardiac cause. CXR showing cardiomegaly, bilateral perihilar shadowing, and Kerley B lines suggests cardiogenic oedema. Lung POCUS showing bilateral B-lines in all zones is very specific for pulmonary oedema. BNP is very helpful - above 400 pg/mL strongly favours heart failure; below 100 makes it unlikely. ABG showing hypercapnia with compensated respiratory acidosis suggests COPD. In practice, both can coexist - 'cardiac COPD' overlap is common - and I may need to treat both simultaneously while the picture clarifies."

"A Wells score of 5 places her in the PE-likely group - I go directly to CTPA without waiting for D-dimer. While imaging is being arranged, I start anticoagulation - I do not wait for confirmation if clinical probability is high, unless there is a significant contraindication. My choice would be LMWH or a DOAC - apixaban or rivaroxaban can be started directly. I give oxygen to target SpO2 ≥ 94%. I get an ECG looking for sinus tachycardia or right heart strain, and basic bloods including troponin and BNP to assess severity. Once CTPA confirms PE, I use the PESI score to classify severity and guide disposition - low risk may be suitable for outpatient DOAC treatment, but with SpO2 of 93% and tachycardia this patient warrants at least a period of observation and assessment for submassive PE."

"The main contraindications to NIV are: inability to protect the airway - reduced consciousness or vomiting, which risks aspiration; haemodynamic instability where the patient needs immediate intubation rather than a trial of NIV; undrained pneumothorax, where positive pressure can tension a pneumothorax rapidly; facial trauma or recent upper GI surgery preventing mask placement; copious secretions the patient cannot clear, as NIV will not help and may worsen things; and significant agitation or non-compliance where the patient will not tolerate the mask. If any of these are present, the decision should be made early about intubation rather than delaying with NIV."

QUICK COMPARISON TABLE - ACUTE DYSPNOEA

DAY 8 PRACTICE CHECKLIST

• State the SpO2 target for COPD with hypercapnia (88-92%) and explain why
• Describe NIV settings in COPD (IPAP/EPAP) and 3 contraindications
• Explain why a normal PaCO2 in acute severe asthma is a danger sign
• State the Wells PE score criteria and the action at each threshold
• Describe the BLUE protocol lung ultrasound findings for 3 diagnoses
• State the immediate treatment for tension pneumothorax
• Name 3 differences between cardiogenic and non-cardiogenic pulmonary oedema
• Practise the "72-year-old COPD" answer aloud in under 90 seconds

DAY 9 - Abdominal Emergencies

Complete Interview Preparation Guide

THE CORE CONCEPT

"Abdominal pain is common. Missed abdominal emergencies kill. Your job is to identify the surgical abdomen before it becomes a dead abdomen."

1. Resuscitate - IV access, fluids, analgesia (do NOT withhold analgesia - it does not mask findings)
2. Localise and characterise - history + examination + targeted investigations
3. Identify: surgical vs medical - does this patient need an operation tonight?

THE FRAMEWORK - ANATOMY-BASED THINKING

RIGHT UPPER QUADRANT    → Biliary (cholecystitis, cholangitis), hepatic, duodenal
EPIGASTRIC              → PUD, pancreatitis, gastritis, early appendicitis, AAA
LEFT UPPER QUADRANT     → Splenic, gastric, pancreatitis
RIGHT LOWER QUADRANT    → Appendicitis, ovarian (R), Meckel's, ileitis, ectopic (R tube)
LEFT LOWER QUADRANT     → Diverticulitis, ovarian (L), ectopic (L tube), sigmoid
CENTRAL / PERIUMBILICAL → Early appendicitis, SBO, AAA, mesenteric ischaemia
DIFFUSE                 → Peritonitis (perforation), mesenteric ischaemia, DKA, SBO
LOIN TO GROIN           → Renal / ureteric colic

THE SURGICAL ABDOMEN - RECOGNISE THESE FEATURES

PART 1: APPENDICITIS

Pathophysiology

Classic Presentation

• Central / periumbilical pain migrating to right iliac fossa (RIF) over 12-24 hours
• Anorexia (very consistent - if patient is hungry, think twice)
• Nausea / vomiting (after pain onset, not before - bilious vomiting before pain suggests SBO)
• Low-grade fever (38-38.5°C - high fever suggests perforation)
• RIF tenderness at McBurney's point (1/3 of the way from ASIS to umbilicus)

Clinical Signs

Alvarado Score (MANTRELS)

Investigations

• Blood: FBC (leukocytosis + left shift), CRP (rises later - more useful at 12-24h), LFTs, amylase, BhCG (all women of reproductive age)
• Urine: Dipstick (haematuria ≠ rules out appendicitis - inflamed appendix near ureter causes microscopic haematuria)
• Imaging:
  • Ultrasound: First-line in children and women (no radiation) - non-compressible appendix > 6mm, periappendiceal fat stranding - sensitivity ~75-80%, highly operator-dependent
  • CT abdomen/pelvis (with IV contrast): Gold standard in adults - sensitivity > 95%. Shows appendix, perforation, abscess, alternative diagnoses
  • MRI: Preferred in pregnant women (avoids radiation, high sensitivity)

Management

• IV access, fluids, analgesia (IV morphine or paracetamol - do NOT withhold)
• NBM (nil by mouth)
• Surgical referral
• Uncomplicated appendicitis: Laparoscopic appendicectomy (gold standard)
• Complicated (perforated, abscess): Drainage ± delayed appendicectomy OR immediate surgery depending on presentation
• Non-operative management: Evidence supports antibiotics alone (Amoxicillin-clavulanate or Piperacillin-tazobactam) for uncomplicated appendicitis in selected patients - 70-80% success, but 20-30% recur within 1 year

Appendicitis in Special Groups

PART 2: GI PERFORATION

Causes of Perforation

Recognition of Perforation

• Sudden severe abdominal pain (often described as "tearing" or "like being stabbed")
• Peritonism (rigid, board-like abdomen, involuntary guarding, rebound)
• Signs of sepsis (fever, tachycardia, hypotension)

• Free air under the diaphragm (pneumoperitoneum) - visible in ~70% of perforations
• Right hemidiaphragm more commonly shows air (liver moves gas up)
• If CXR negative but perforation suspected → CT abdomen (much more sensitive)

Management of GI Perforation

1. Resuscitation: IV access × 2, aggressive fluid resuscitation, vasopressors if septic shock
2. NBM + NG tube (decompress stomach)
3. Analgesia - morphine IV
4. Broad-spectrum antibiotics: Co-amoxiclav + Metronidazole OR Piperacillin-tazobactam
5. Urinary catheter - monitor output
6. Surgical referral - urgent
7. Emergency laparotomy (most perforations) OR laparoscopic repair (selected stable patients with small DU perforation)

PART 3: ACUTE PANCREATITIS

Causes - "GET SMASHED"

Presentation

• Pain: Epigastric, constant, severe, radiates to the back ("boring" through to back), relieved by leaning forward
• Nausea and vomiting (persistent)
• Epigastric tenderness (may be surprisingly minimal in early/mild pancreatitis)
• Signs of severe disease: Tachycardia, hypotension, tachypnoea, fever, jaundice (if biliary)

• Grey Turner's sign - flank bruising (retroperitoneal haemorrhage)
• Cullen's sign - periumbilical bruising (haemoperitoneum)

Investigations

• Serum amylase / lipase: > 3× upper limit of normal = diagnostic. Lipase is more sensitive and specific than amylase (amylase rises in many other conditions)
• LFTs: ALT > 3× upper limit = gallstone aetiology likely
• FBC, CRP, calcium, glucose, LDH: Used in scoring
• USS: Gallstones, biliary dilation (common bile duct > 6mm = obstruction), NOT for pancreatic imaging in acute phase (bowel gas obscures)
• CT abdomen with IV contrast: Gold standard for severity assessment - do at 48-72 hours (not immediately unless diagnosis unclear)
• MRCP: Better than CT for biliary system, no radiation

Severity Scoring - Modified Glasgow (Imrie) Score

Management of Acute Pancreatitis

1. Aggressive IV fluid resuscitation - Lactated Ringer's preferred over 0.9% NaCl (reduces SIRS) - 250-500 mL/hr in first 12-24 hours
2. Analgesia - IV morphine or paracetamol (opioids are safe and appropriate)
3. NBM initially → restart oral fluids/soft diet as soon as tolerated (early oral feeding improves outcomes)
4. Monitor: fluid balance, urine output (target > 0.5 mL/kg/hr), glucose, calcium

• Pancreatic necrosis (CT at 48-72h) - sterile vs infected
• Pseudocyst (fluid collection >4 weeks) - drainage if symptomatic
• Haemorrhage - eroded pancreatic vessels
• ARDS, AKI, DIC - systemic SIRS response

PART 4: BILIARY COLIC & ACUTE CHOLECYSTITIS

Spectrum of Biliary Disease

Gallstones (Cholelithiasis)
        │
        ├── Stone in cystic duct → BILIARY COLIC
        │
        ├── Obstructed cystic duct + inflammation → ACUTE CHOLECYSTITIS
        │
        ├── Stone in CBD → CHOLEDOCHOLITHIASIS
        │
        └── CBD obstruction + infection → CHOLANGITIS (SEPSIS)

Biliary Colic

• Pain: Severe, episodic RUQ pain radiating to right shoulder/scapula, onset 30-60 min after fatty meal, lasts 1-6 hours, resolves completely
• Examination: RUQ tenderness, no fever, no Murphy's sign
• Murphy's sign: Arrest of inspiration on palpation of RUQ - specific for cholecystitis (not biliary colic)
• Investigations: LFTs normal (or mildly raised if stone in CBD), USS shows gallstones
• Management: Analgesia (NSAIDs - ketorolac or diclofenac are highly effective for biliary colic; opioids also used), elective laparoscopic cholecystectomy outpatient

Acute Cholecystitis

• Pain: RUQ, constant (unlike biliary colic), fever, Murphy's sign positive
• Bloods: Leukocytosis, raised CRP, LFTs may be mildly abnormal
• USS: Gallstones + thickened gallbladder wall (> 3mm) + pericholecystic fluid + USS Murphy's sign

• NBM, IV fluids, analgesia
• Antibiotics: Co-amoxiclav OR Cefuroxime + Metronidazole
• Laparoscopic cholecystectomy: within 72 hours if fit (early is better than delayed - shorter hospital stay, less complications)

Acute Cholangitis - Charcot's Triad and Reynolds Pentad

1. RUQ pain
2. Fever + rigors
3. Jaundice

• IV antibiotics (Piperacillin-tazobactam)
• Aggressive resuscitation
• Urgent ERCP (within 12-24 hours) to drain the biliary tree - this is life-saving

PART 5: ECTOPIC PREGNANCY

Why This Is an EM Emergency

A ruptured ectopic pregnancy can kill a young woman in minutes from intra-abdominal haemorrhage. Every woman of reproductive age with abdominal pain MUST have a pregnancy test.

Risk Factors

• Previous ectopic pregnancy (greatest risk - 10-15× increased)
• Previous PID or STI (Chlamydia / gonorrhoea)
• Previous tubal surgery
• IUD in situ (does not prevent ectopic, just intrauterine)
• Assisted reproduction / IVF
• Smoking
• Endometriosis

Presentation

Investigations

1. Urine βhCG (pregnancy test) - FIRST, ALWAYS, in every woman of reproductive age with abdominal pain
2. Serum βhCG: Quantitative level
   • βhCG > 1500-2000 mIU/mL = discriminatory zone: if no intrauterine sac visible on transvaginal USS at this level → ectopic or failed intrauterine pregnancy
   • Rising βhCG (> 66% rise in 48h) = viable pregnancy; slower rise = abnormal (ectopic or miscarriage)
3. Transvaginal ultrasound (TVUSS): More sensitive than transabdominal for early ectopic
   • Intrauterine sac visible = likely not ectopic (but heterotopic pregnancy is rare exception)
   • Adnexal mass + free fluid + no IUP = ectopic until proven otherwise
4. FBC, blood group & crossmatch (all cases)
5. Free fluid in pouch of Douglas on USS = haemoperitoneum

Management

• This is a Category 1 surgical emergency
• 2 large-bore IVs, activate MTP, call gynaecology and theatre immediately
• Do NOT delay surgery for imaging if haemodynamically compromised
• Emergency laparoscopy (or laparotomy if unstable) - salpingectomy
• Rhesus-negative patients: Give Anti-D immunoglobulin

PART 6: OTHER KEY ABDOMINAL EMERGENCIES

Mesenteric Ischaemia - "The Great Masquerader"

• Acute mesenteric arterial embolism (SMA embolus from AF - most common, 50%)
• Acute mesenteric arterial thrombosis (atherosclerosis)
• Non-occlusive mesenteric ischaemia (NOMI - low flow states)
• Mesenteric venous thrombosis

• Metabolic acidosis + raised lactate (late - suggests bowel death)
• CT angiography - gold standard for diagnosis
• WBC raised, but often lags behind severity

• Immediate surgical and vascular surgery referral
• IV heparin anticoagulation
• Emergency surgical revascularisation or embolectomy
• Bowel resection if necrosis

Abdominal Aortic Aneurysm (AAA) - Ruptured

1. Severe tearing abdominal/back pain
2. Pulsatile abdominal mass
3. Haemodynamic shock

• Two large-bore IVs, MTP activation, O-negative blood
• Permissive hypotension - target SBP 50-70 mmHg (controversial but widely used) until surgery - aggressive resuscitation dislodges clot and worsens bleeding
• Immediate vascular surgery referral
• EVAR (endovascular repair) if anatomically suitable, or open repair
• Do NOT send a haemodynamically unstable patient to CT scan

Bowel Obstruction

• SBO: Central dilated loops (valvulae conniventes - herringbone pattern), > 3cm
• LBO: Peripheral dilated loops (haustrations - incomplete across bowel), > 6cm (colon), > 9cm (caecum)

• NBM, NG tube (drip and suck), IV fluids
• Monitor electrolytes (vomiting causes metabolic alkalosis + hypokalaemia)
• CT abdomen for diagnosis and to identify transition point / cause
• Surgery: strangulation, closed-loop obstruction, perforation, failure to resolve

PART 7: INTERVIEW QUESTIONS & MODEL ANSWERS

"The single most important first step is a urine pregnancy test - immediately, before any other investigation or management decision. This must be done in every woman of reproductive age presenting with abdominal pain or vaginal bleeding, without exception. If positive, I am dealing with a pregnancy-related emergency - the differential includes ectopic pregnancy, threatened or incomplete miscarriage, or gestational trophoblastic disease. If she is haemodynamically unstable with a positive test, my immediate concern is ruptured ectopic pregnancy - a surgical emergency. I call gynaecology, get IV access and crossmatch, and do a bedside FAST scan to look for free fluid. I do not wait for a formal ultrasound if she is shocked."

"Severity assessment in acute pancreatitis uses clinical scoring systems combined with imaging. I use the Modified Glasgow score - also called the Imrie score - which looks at 8 parameters within 48 hours of onset: PaO2, age, white cell count, calcium, urea, LDH, albumin, and blood glucose. A score of 3 or more indicates severe pancreatitis requiring HDU or ICU admission. CRP above 150 mg/L at 48 hours is also a reliable marker of severity. For imaging, I perform a contrast-enhanced CT at 48-72 hours - not at presentation - to assess for pancreatic necrosis and its extent, which drives management decisions about enteral nutrition, antibiotics, and intervention. Early clinical signs that concern me include tachycardia, hypoxia, oliguria, and rising creatinine - these suggest end-organ dysfunction from SIRS."

"Charcot's triad describes the classic presentation of acute cholangitis: RUQ pain, fever with rigors, and jaundice. The pathophysiology is obstruction of the common bile duct - usually by a gallstone - causing bile stasis and ascending bacterial infection. Reynolds pentad adds two more features that indicate severe septic cholangitis: hypotension and altered mental status. When a patient has the full pentad, they are in septic shock from biliary sepsis and require urgent resuscitation and emergency biliary decompression by ERCP within 12-24 hours. Without draining the obstructed biliary system, antibiotics alone will not control the source and mortality is high."

"This combination - severe pain out of proportion to examination findings in a patient with AF - is the classic presentation of acute mesenteric ischaemia. In AF, atrial thrombus can embolise to the superior mesenteric artery, causing acute bowel ischaemia. The pain is visceral and intense, but the peritoneum is not yet involved so the abdomen remains soft and non-tender early on. The danger is that by the time the abdomen becomes peritonitic, the bowel is already necrotic and mortality approaches 80%. I treat this as a vascular emergency: IV access, blood tests including lactate and ABG looking for metabolic acidosis, and urgent CT angiography. I alert the vascular surgery team immediately and start IV heparin once the diagnosis is suspected. Time to revascularisation is the most important determinant of outcome."

QUICK REFERENCE - ABDOMINAL EMERGENCIES

DAY 9 PRACTICE CHECKLIST

• State the GET SMASHED mnemonic for pancreatitis causes
• Describe the Modified Glasgow score parameters (PAWCREAS) and the threshold for severe pancreatitis
• Draw the biliary spectrum: colic → cholecystitis → choledocholithiasis → cholangitis
• State Charcot's triad and Reynolds pentad
• Explain why pregnancy test is the FIRST step in any woman with abdominal pain
• Describe how βhCG level determines ectopic pregnancy management
• State the classic presentation of mesenteric ischaemia ("pain out of proportion")
• Practise the "lower abdominal pain + vaginal bleeding" answer - aim for 60 seconds

DAY 10 - Infectious Emergencies

Complete Interview Preparation Guide

THE CORE CONCEPT

"Sepsis is a time-critical emergency. Every hour of delay in antibiotics increases mortality by 7-10%. Think of sepsis like STEMI - the clock starts at recognition."

PART 1: SEPSIS AND SEPTIC SHOCK

Definitions (Sepsis-3, 2016 - Current Standard)

Organ Dysfunction - SOFA Score

Quick SOFA (qSOFA) - Bedside Screening Tool

Surviving Sepsis Campaign (SSC) - Hour-1 Bundle (2018)

Within the FIRST HOUR of recognition:
│
├── 1. MEASURE LACTATE
│      If lactate > 2 mmol/L = tissue hypoperfusion (even if BP normal)
│      If lactate > 4 mmol/L = high mortality → aggressive resuscitation
│
├── 2. BLOOD CULTURES × 2 (before antibiotics if possible)
│      At least 2 sets from 2 different sites
│      Do NOT delay antibiotics > 45 minutes to get cultures
│
├── 3. BROAD-SPECTRUM ANTIBIOTICS
│      Give WITHIN 1 HOUR of sepsis recognition
│      Earlier = better; every hour of delay ↑ mortality
│
├── 4. IV FLUID RESUSCITATION
│      30 mL/kg crystalloid (0.9% NaCl or Lactated Ringer's)
│      for hypotension OR lactate ≥ 4 mmol/L
│      Give as rapid bolus (over 30 minutes or faster)
│
└── 5. VASOPRESSORS (if hypotensive during/after fluids)
       Target MAP ≥ 65 mmHg
       Norepinephrine = FIRST-LINE vasopressor

Antibiotic Choice in Sepsis (Know Common Regimens)

Vasopressors in Septic Shock

Source Control in Sepsis

Corticosteroids in Septic Shock

• Indication: Refractory septic shock - vasopressor requirement persists despite adequate fluid resuscitation
• Drug: Hydrocortisone 200mg IV daily (continuous infusion or 50mg QID)
• Rationale: Relative adrenal insufficiency in critical illness - steroids restore vascular responsiveness
• Not recommended for sepsis without shock

PART 2: BACTERIAL MENINGITIS

Causative Organisms by Age

Clinical Features

1. Fever
2. Neck stiffness (nuchal rigidity)
3. Altered consciousness

• Severe headache ("worst of life")
• Photophobia / phonophobia
• Vomiting
• Petechial / purpuric rash (meningococcal - non-blanching = medical emergency)
• Kernig's sign: unable to extend knee with hip flexed 90°
• Brudzinski's sign: passive neck flexion causes involuntary hip/knee flexion

Management of Suspected Bacterial Meningitis

SUSPECTED BACTERIAL MENINGITIS
│
├── Petechial rash OR haemodynamically unstable?
│   YES → Give IV antibiotics IMMEDIATELY (do not wait for LP)
│         Ceftriaxone 2g IV + Dexamethasone 0.15 mg/kg IV
│
├── NO → Can LP be done safely?
│         Check: GCS, focal neurology, papilloedema, seizure
│         If ANY present → CT head first (herniation risk)
│         If all clear → LP immediately
│
├── LP findings (see below)
│
└── ALL CASES:
    Ceftriaxone 2g IV 12-hourly
    + Dexamethasone 0.15 mg/kg QID × 4 days (before or with 1st dose antibiotics)
    + If age > 50 / pregnant / immunocompromised → add Amoxicillin 2g IV (covers Listeria)

CSF Analysis in Meningitis

Dexamethasone in Meningitis - Why and When

• Reduces inflammation in subarachnoid space → reduces neurological complications
• Proven to reduce hearing loss and mortality in pneumococcal meningitis
• Must be given before or with the first dose of antibiotics
• If given after first dose → no benefit
• Continue for 4 days (stop early if not bacterial meningitis on LP)

PART 3: MALARIA

India-Specific Epidemiology

• India accounts for approximately 2% of global malaria burden
• Two main species in India:
  • Plasmodium vivax (60-65%) - relapsing, rarely fatal
  • Plasmodium falciparum (35-40%) - causes severe/complicated malaria, higher mortality
• High-burden states: Odisha, Jharkhand, Chhattisgarh, Meghalaya
• Tamil Nadu: Lower burden but still present, particularly in forested districts

Clinical Features

• Classic fever cycles:
  • P. vivax: every 48 hours (tertian fever - spikes on days 1, 3, 5...)
  • P. falciparum: irregular (every 36-48h) or continuous
• Rigors, sweating, headache, myalgia
• Splenomegaly (chronic/recurrent)
• Anaemia

Diagnosis

1. Thick and thin blood films - gold standard; identifies species and parasite density
2. Rapid Diagnostic Tests (RDTs): PfHRP2 (falciparum-specific) - quick bedside test
3. If films negative but high suspicion: Repeat films every 12-24 hours × 3

Treatment

• Artemisinin-based Combination Therapy (ACT):
  • Artemether + Lumefantrine (AL) - 6-dose regimen over 3 days
  • OR Artesunate + Sulfadoxine-Pyrimethamine (ASSP)

• IV Artesunate - drug of choice (superior to IV quinine - SEAQUAMAT trial)
• IV Artesunate 2.4 mg/kg at 0, 12, 24h then daily until oral possible
• Supportive care: IV fluids, glucose monitoring, seizure management, RRT if AKI

• Chloroquine 25 mg/kg over 3 days (still sensitive in most of India)
• PLUS Primaquine 0.25 mg/kg/day × 14 days (to eliminate liver hypnozoites - radical cure)
• Check G6PD status before primaquine - causes haemolysis in G6PD deficiency

PART 4: DENGUE FEVER

India-Specific Context

• Dengue is endemic across India, with major outbreaks in Tamil Nadu
• 4 serotypes (DENV 1-4) - infection with one serotype provides lifelong immunity to that serotype but increases risk of severe dengue on second infection with different serotype
• Transmitted by Aedes aegypti mosquito - daytime biter

Clinical Phases

WHO Dengue Classification

Warning Signs of Dengue (Must Know)

• Abdominal pain or tenderness
• Persistent vomiting (≥ 3 episodes in 24h)
• Clinical fluid accumulation (ascites, pleural effusion)
• Mucosal bleeding (gum bleed, epistaxis, melaena)
• Lethargy / restlessness
• Liver enlargement > 2cm
• Rapid fall in platelets with rise in haematocrit (Hct rise > 20% = plasma leakage)

Dengue Investigations

• FBC: Leukopenia + thrombocytopenia (platelet < 100,000 = warning; < 20,000 = severe)
• Haematocrit: Rising Hct indicates plasma leakage
• NS1 antigen: Positive days 1-5 (early)
• IgM antibody: Positive from day 5 (primary infection)
• IgG antibody: Previous infection / secondary infection
• LFTs: Elevated transaminases (dengue hepatitis)

Dengue Management

• Oral rehydration, paracetamol (NOT aspirin or ibuprofen - platelet dysfunction + Reye's risk)
• Return precautions: warning signs listed above
• Daily FBC monitoring

• Admit, IV isotonic crystalloids
• Fluid rate guided by Hct, clinical status
• Platelet transfusion: only if active bleeding OR platelet < 10,000

• Rapid IV crystalloid: 10-20 mL/kg over 15-30 min
• Reassess every 15-30 min
• If Hct rising despite fluids → consider colloid
• If Hct falling despite deterioration → bleeding (give blood products)

PART 5: OTHER IMPORTANT INFECTIOUS EMERGENCIES

Leptospirosis (Highly Relevant in India - Post-Monsoon)

• Zoonosis - Leptospira species via water/soil contaminated with animal (rat) urine
• Entry through skin abrasions or mucous membranes
• High-risk groups: Farmers, sewage workers, flood victims, Tamil Nadu post-monsoon

• Jaundice + AKI + bleeding (Weil's triad)
• Uveitis (late complication)
• Pulmonary haemorrhage

Scrub Typhus (Endemic in South India)

• Caused by Orientia tsutsugamushi, transmitted by larval mite (chigger) bite
• Eschar (painless black scab at bite site) - pathognomonic but present in only 50-60%
• Fever + headache + rash (maculopapular, trunk) + lymphadenopathy
• Complications: encephalitis, myocarditis, AKI, ARDS

PART 6: INTERVIEW QUESTIONS & MODEL ANSWERS

"This patient has septic shock - I apply the Sepsis-3 definition: organ dysfunction (confusion = neurological dysfunction) plus haemodynamic compromise requiring vasopressor support. I start the SSC Hour-1 bundle immediately.

First, I draw blood cultures - two sets from two sites - and send lactate. I do not delay for cultures beyond a few minutes. I start broad-spectrum IV antibiotics within the first hour - I choose Piperacillin-tazobactam empirically covering gram-positives and gram-negatives while I determine the source. Simultaneously, I give 30 mL/kg isotonic crystalloid as a rapid bolus.

If his BP does not respond to fluids - and it may not in distributive shock - I start norepinephrine via the largest peripheral IV available while establishing central access, targeting MAP ≥ 65 mmHg. I measure repeat lactate at 2 hours to assess response.

Throughout, I am working to identify the source: chest X-ray, urine dipstick, abdominal examination, skin inspection for wounds or rashes. Source control is as important as antibiotics - I cannot treat ongoing contamination with drugs alone. If lactate remains above 4 despite resuscitation, or organ dysfunction is worsening, I escalate to ICU early."

"Non-blanching petechial rash with fever is meningococcal septicaemia until proven otherwise. This is one of the true medical emergencies where I give antibiotics before anything else - before LP, before CT, before anything. I give Ceftriaxone 2g IV immediately, plus Dexamethasone 0.15 mg/kg IV with the first dose of antibiotics.

I assess for signs of meningism - neck stiffness, Kernig's, Brudzinski's. I check GCS, pupils, and look for any focal neurology. If he is haemodynamically compromised - which meningococcal septicaemia can cause rapidly - I resuscitate aggressively with IV fluids and vasopressors.

If GCS is normal, no focal neurology, and no papilloedema - LP can follow, but only after antibiotics are in. If he is deteriorating or has any neurological signs, LP is deferred entirely and he goes to ICU. The LP can wait. The antibiotics cannot."

"Dengue with warning signs identifies patients at risk of progression and who require hospital admission and close monitoring. The warning signs include abdominal pain or tenderness, persistent vomiting, clinical fluid accumulation such as ascites or pleural effusion, mucosal bleeding, lethargy, liver enlargement, and the key laboratory finding of a rising haematocrit with a rapid fall in platelet count - which together indicate ongoing plasma leakage. These patients need IV fluids and hourly monitoring.

Severe dengue is the next stage - it involves actual end-organ damage: severe plasma leakage causing dengue shock syndrome or respiratory distress, severe bleeding that is clinically significant, and severe organ impairment affecting the liver, CNS, heart, or kidneys. These patients need ICU management. The critical distinction in dengue is that the period of fever defervescence - days 4 to 6 - is when patients who appear to be improving are actually at their highest risk of plasma leakage and shock. Falling temperature is a warning, not reassurance."

"qSOFA - quick SOFA - is a bedside screening tool introduced with Sepsis-3 to identify patients outside the ICU who may have sepsis. It uses three criteria: altered mental status defined as GCS below 15, respiratory rate of 22 or above, and systolic BP of 100 or below. A score of 2 or more triggers a full sepsis assessment with SOFA scoring and lactate measurement.

Its limitations are important to understand. First, it is a screening tool - not diagnostic. A qSOFA of 2 does not confirm sepsis, and a qSOFA below 2 does not exclude it. Second, it has lower sensitivity than SIRS criteria for detecting sepsis early, meaning patients can be seriously septic with a qSOFA of 0 or 1. Third, in settings like India where SOFA scoring may not always be practical in the first hour, clinical judgement combined with lactate measurement is the most pragmatic approach. I use qSOFA as a quick doorway assessment to prioritise patients, not as a final determination."

QUICK REFERENCE - INFECTIOUS EMERGENCIES

DAY 10 PRACTICE CHECKLIST

• State the SSC Hour-1 Bundle - all 5 components in order
• Define sepsis and septic shock using Sepsis-3 criteria
• State qSOFA criteria (3 parameters) and name one limitation
• Describe the empirical antibiotic choice for unknown-source septic shock
• State the first action in a patient with petechial rash and fever (antibiotics BEFORE LP)
• Explain why dengue fever defervescence is actually a danger sign
• Name the drug for severe P. falciparum and why quinine is no longer preferred (SEAQUAMAT)
• State what to check before prescribing primaquine for P. vivax (G6PD status)
• Practise the "fever + confusion + hypotension" answer aloud - aim for 90 seconds

DAY 11 - Toxicology & Overdose

Complete Interview Preparation Guide

THE CORE CONCEPT

"In toxicology, the antidote is not always the answer. Resuscitation, decontamination, and supportive care save more lives than specific antidotes."

RESUSCITATE → RECOGNISE THE TOXIDROME → DECONTAMINATE → SPECIFIC ANTIDOTE → SUPPORTIVE CARE

THE TOXIDROMES - RECOGNISE THE PATTERN

"Blind as a bat, dry as a bone, hot as a hare, red as a beet, mad as a hatter, full as a flask" (Mydriasis, dry skin, hyperthermia, flushing, delirium, urinary retention)

PART 1: PARACETAMOL (ACETAMINOPHEN) OVERDOSE

Why It Matters

• Most common intentional overdose in India and worldwide
• Deceptively benign at presentation - patient feels well in first 24 hours
• Untreated, causes fatal fulminant hepatic failure by day 3-4
• Highly treatable if antidote given early

Mechanism of Toxicity

Paracetamol → 95% sulphation/glucuronidation → harmless metabolites
             → 5% CYP2E1 → NAPQI (toxic metabolite)
             → NAPQI + Glutathione → harmless

Paracetamol (large dose) → Glutathione DEPLETED
→ NAPQI accumulates
→ Binds hepatocyte proteins → Centrilobular necrosis
→ Hepatic failure → Coagulopathy → Encephalopathy → Death

Clinical Stages of Paracetamol Toxicity

The Rumack-Matthew Nomogram

• Plots serum paracetamol level against time since ingestion
• Treatment line: if level falls above the line → give N-acetylcysteine (NAC)
• Only valid for single acute ingestions (not staggered or chronic)
• Must know time of ingestion accurately
• Draw serum paracetamol level at minimum 4 hours post-ingestion (earlier levels unreliable)

N-Acetylcysteine (NAC) - The Antidote

• Paracetamol level above treatment line on nomogram
• Ingestion of > 150 mg/kg (or > 7.5g in adults) AND cannot get level within 8 hours
• Staggered overdose → treat empirically
• Presentation > 8 hours after ingestion → treat empirically while awaiting level
• Any patient with hepatotoxicity (raised LFTs, coagulopathy) regardless of time

Loading dose: 150 mg/kg IV in 200 mL 5% dextrose over 1 HOUR
Second dose:  50 mg/kg IV in 500 mL 5% dextrose over 4 HOURS
Third dose:   100 mg/kg IV in 1000 mL 5% dextrose over 16 HOURS
Total: 21-hour regimen

King's College Criteria - Liver Transplant Referral

• pH < 7.30 (after resuscitation), regardless of other criteria
• OR all three of: INR > 6.5 + Creatinine > 300 µmol/L + Grade III-IV hepatic encephalopathy

PART 2: ORGANOPHOSPHATE POISONING

Relevance in India

• Organophosphate (OP) and carbamate pesticides are the leading cause of poisoning death in rural India
• Intentional ingestion (self-harm) is far more common than occupational exposure
• High mortality if not recognised and treated immediately

Mechanism

• Muscarinic receptors (parasympathetic - glands, smooth muscle, heart)
• Nicotinic receptors (neuromuscular junction, autonomic ganglia)
• CNS (brain)

Clinical Features - SLUDGE (Muscarinic) + Nicotinic + CNS

• Muscle fasciculations
• Weakness → paralysis (respiratory muscles - cause of death)
• Tachycardia (nicotinic > muscarinic at NMJ)

• Anxiety, agitation
• Seizures
• Coma

Severity Classification

Management - The Three Pillars

• Remove patient from exposure (staff must protect themselves - gown, gloves, mask)
• Remove all clothing (80% of pesticide is on clothes)
• Wash skin copiously with soap and water
• Gastric lavage if within 1 hour of ingestion (intubate first if airway compromised)
• Activated charcoal 50g if alert and airway protected (within 1-2 hours)

Atropine 2-4 mg IV bolus immediately
Repeat EVERY 5-10 MINUTES until secretions dry up
(Bronchorrhoea and bronchospasm are the endpoint - NOT heart rate or pupil size)

Total doses can reach 20-100 mg in severe cases - do NOT stop if secretions remain

• Reactivates acetylcholinesterase if given before "ageing" (irreversible binding)
• Most effective within 24-48 hours of exposure
• After ageing (>48h for most OPs), pralidoxime has no effect
• Dose: 1-2g IV over 15-30 min, then 500mg/hr infusion

• Intubate early if bronchorrhoea + respiratory failure (most deaths are from respiratory failure)
• Use succinylcholine ONLY ONCE in OP poisoning - cholinesterase is inhibited, causing prolonged paralysis. Prefer rocuronium for RSI.
• Ventilate in ICU until cholinesterase recovers

Intermediate Syndrome

• Occurs 24-96 hours AFTER recovery from acute cholinergic crisis
• Proximal limb weakness, neck flexor weakness, respiratory muscle weakness
• Can cause sudden respiratory arrest after apparent recovery
• Management: ICU monitoring and ventilatory support

PART 3: SNAKE BITE

India Context

• India has ~50,000 snake bite deaths per year (highest in the world)
• "Big Four" of India:
  1. Russell's viper (Daboia russelii) - most common cause of death
  2. Common krait (Bungarus caeruleus)
  3. Spectacled cobra (Naja naja)
  4. Saw-scaled viper (Echis carinatus)
• Tamil Nadu: All four species present

Venom Types and Effects

Clinical Assessment

• Fang marks (may be absent in krait bites)
• Swelling, erythema, blistering, necrosis (cytotoxic)
• Lymphadenopathy

• Haemotoxic: Spontaneous bleeding (gum bleed, epistaxis, haematuria, haematemesis), 20-minute whole blood clotting test (20WBCT) positive
• Neurotoxic: Ptosis (early), ophthalmoplegia, bulbar palsy (dysphagia, dysphonia), respiratory failure (late)
• Nephrotoxic: Russell's viper - AKI within 24-48 hours
• Systemic: Hypotension, shock (Russell's viper)

• Bedside test for coagulopathy
• Place 2mL blood in a clean glass tube, leave 20 minutes
• Blood that does not clot = venom-induced consumption coagulopathy (VICC)
• VICC = give antivenom immediately

Antivenom (AVS - Polyvalent Anti-Snake Venom Serum)

• 20WBCT positive (blood not clotting)
• Neurotoxicity (ptosis, respiratory compromise)
• Haemodynamic instability
• Significant local swelling progressing rapidly
• AKI

• Indian polyvalent ASV covers all Big Four
• Initial: 8-10 vials IV (diluted in 500mL saline over 1 hour)
• Repeat: If 20WBCT still positive at 6 hours → give another 8-10 vials
• Repeat: Neuro signs not improving → repeat doses

• Adrenaline 0.25mg SC (reduces anaphylaxis incidence)
• IV antihistamine + hydrocortisone (some protocols)
• Monitor for anaphylaxis during infusion

• Neostigmine 0.01mg/kg IV + Atropine 0.6mg IV (prevents muscarinic side effects)
• Try in cobra/krait envenomation with neurotoxicity

PART 4: SCORPION STING

India Context

• Mesobuthus tamulus (Indian red scorpion) - most dangerous species in India
• Highest incidence in Maharashtra, Tamil Nadu (Villupuram, Cuddalore, Salem districts)
• Venom releases massive catecholamine surge (autonomic storm)

Clinical Features

• Local pain, burning at sting site
• Autonomic storm: tachycardia, hypertension, diaphoresis, hypersalivation

• Pulmonary oedema (catecholamine-induced myocardial dysfunction + capillary leak)
• Myocarditis (ventricular dysfunction, ECG changes)
• Cardiovascular collapse
• Priapism (males)
• Limb ischaemia

Management

• Analgesia (local anaesthetic infiltration or IV morphine)
• Observation 4-6 hours

• Prazosin - alpha-1 blocker - first-line for autonomic storm
  • 250 mcg (child) to 500 mcg (adult) oral/SL every 3 hours
  • Reduces hypertension, pulmonary oedema, and mortality
• Dobutamine - if myocardial dysfunction / cardiogenic shock
• GTN - for pulmonary oedema
• Scorpion antivenom - available at select government centres; most effective within 1 hour; evidence base limited compared to ASV for snakes
• ICU admission for respiratory failure / shock

PART 5: ALCOHOL WITHDRAWAL

Why It Is Life-Threatening

• GABA receptor downregulation
• NMDA receptor upregulation

Timeline of Alcohol Withdrawal

Delirium Tremens - The Emergency

• Global confusion / delirium
• Severe tremor
• Autonomic hyperactivity: HR > 120, BP > 150, fever, diaphoresis
• Visual hallucinations (classically bugs/insects)
• Agitation

CIWA-Ar Scale (Clinical Institute Withdrawal Assessment for Alcohol)

• Nausea/vomiting, tremor, diaphoresis, anxiety, agitation, perceptual disturbances, headache, orientation, tactile/visual/auditory disturbances

Management of Alcohol Withdrawal

• Thiamine (Vitamin B1) 100-200mg IV BEFORE any dextrose - prevents Wernicke's encephalopathy
  • Wernicke's triad: Confusion + ophthalmoplegia + ataxia
  • Give thiamine before glucose in ANY alcoholic - always
• IV fluids (dehydrated, electrolyte depleted)
• Correct hypomagnesaemia, hypokalaemia, hypophosphataemia
• Anticonvulsants: benzodiazepines treat seizures; phenytoin is NOT effective for alcohol withdrawal seizures

• Phenobarbitone 10mg/kg IV (GABA agonist)
• Propofol infusion (ICU)
• Ketamine (NMDA antagonist - emerging evidence)
• Dexmedetomidine (adjunct - reduces autonomic storm)

PART 6: OTHER IMPORTANT TOXICOLOGICAL EMERGENCIES

Tricyclic Antidepressant (TCA) Overdose

1. QRS widening > 100ms → ventricular arrhythmia (VF)
2. QTc prolongation → Torsades de Pointes
3. Seizures (lower seizure threshold)

• Sodium bicarbonate - 1-2 mEq/kg IV bolus → narrows QRS (increases pH, reverses Na+ channel blockade), repeat until QRS < 100ms
• Benzodiazepines for seizures
• Avoid physostigmine, flumazenil (worsen seizures)
• Target serum pH 7.45-7.55 (alkaline environment protects Na+ channels)

Opioid Overdose

• 0.4-2mg IV/IM/IN, repeat every 2-3 minutes
• Duration of naloxone (30-90 min) < duration of most opioids → patient can re-sedate
• Observe for minimum 4-6 hours after last naloxone dose
• Infusion needed for long-acting opioids (methadone, sustained-release morphine)
• Do NOT precipitate acute withdrawal with large naloxone doses in dependent patients - use small titrated doses

Benzodiazepine Overdose

• Rarely fatal in isolation
• Supportive care (airway, positioning)
• Flumazenil - benzodiazepine antagonist - use cautiously:
  • Contraindicated if mixed with TCAs (lowers seizure threshold)
  • Contraindicated if chronic BZD use (precipitates withdrawal seizures)
  • Short-acting - re-sedation can occur

Carbon Monoxide (CO) Poisoning

• Colourless, odourless - "silent killer"
• Sources: faulty heaters, generators in enclosed spaces, fires
• Multiple victims from same household = CO until proven otherwise

• 100% oxygen via tight-fitting non-rebreather mask (reduces CO half-life from 4-5h to 60-90 min)
• Hyperbaric oxygen (HBO): COHb > 25%, neurological symptoms, cardiac compromise, pregnancy - reduces CO half-life to 20-30 min, reduces delayed neurological sequelae

PART 7: GENERAL DECONTAMINATION PRINCIPLES

PART 8: INTERVIEW QUESTIONS & MODEL ANSWERS

"This is organophosphate poisoning until proven otherwise - the combination of altered consciousness, miosis, and copious secretions fits the cholinergic toxidrome. My immediate priorities are: protect myself and the team - gown, gloves, mask before touching the patient. Remove all clothing and wash the skin with soap and water to stop ongoing absorption.

Airway is my immediate concern - copious bronchorrhoea and bronchospasm will kill this patient faster than anything else. I intubate early if he cannot maintain his airway - using rocuronium, NOT succinylcholine, because acetylcholinesterase inhibition will prolong succinylcholine paralysis unpredictably.

Atropine is the antidote for muscarinic effects - I give 2-4mg IV immediately and repeat every 5-10 minutes until the lungs are dry. My endpoint is dried secretions and improved air entry - not heart rate, not pupil size. In severe OP poisoning, doses of 20-100mg of atropine may be needed. I give pralidoxime 1-2g IV over 30 minutes to reactivate acetylcholinesterase - effective only if given within 48 hours before ageing occurs. He will need ICU admission and ventilation, and close monitoring for intermediate syndrome between days 1 and 4."

"Absolutely. The deceptive clinical well-being in the first 24 hours is exactly what makes paracetamol overdose so dangerous. Hepatocellular necrosis from NAPQI accumulation peaks at 72-96 hours - by which time it is often too late to prevent liver failure.

I take a detailed history: exact dose, exact time, any co-ingestants, any alcohol use or malnutrition - all of which increase risk. I draw serum paracetamol at a minimum 4 hours post-ingestion and plot it on the Rumack-Matthew nomogram. At 6 hours, the level is valid. If it falls above the treatment line, I start N-acetylcysteine immediately - 150mg/kg over 1 hour, then 50mg/kg over 4 hours, then 100mg/kg over 16 hours. Even if she has taken 30 tablets and the time is uncertain, I would start NAC empirically while awaiting the level. I do not wait to see how she feels. I also do baseline LFTs, INR, and creatinine. If her INR is already rising at 6 hours, the ingestion was likely earlier than reported and she is at high risk of hepatic failure."

"Wernicke's encephalopathy is an acute neurological emergency caused by thiamine (Vitamin B1) deficiency, most commonly in chronic alcohol users. The classic triad is confusion, ophthalmoplegia - particularly lateral rectus palsy and nystagmus - and ataxia. In practice the full triad is present in less than a third of cases, so I have a very low threshold for treatment.

The critical prevention point is this: thiamine MUST be given before any glucose - whether as IV dextrose or food - in any patient with suspected alcohol use or malnutrition. Glucose loads precipitate Wernicke's by consuming the last remaining thiamine in the cell. I give Thiamine 200mg IV before any dextrose-containing fluid in every alcoholic patient. If Wernicke's is suspected, the dose is 500mg IV three times daily for 3-5 days. Untreated Wernicke's progresses to Korsakoff's syndrome - irreversible anterograde amnesia and confabulation - which is preventable."

QUICK REFERENCE - ANTIDOTES

DAY 11 PRACTICE CHECKLIST

• Recite the 6 toxidromes with key signs (HR, pupils, skin, consciousness)
• State the anticholinergic mnemonic ("blind as a bat...")
• Describe NAC regimen for paracetamol (3 doses, times, amounts)
• State the endpoint of atropine therapy in OP poisoning (DRY LUNGS, not tachycardia)
• Explain why succinylcholine is avoided in OP poisoning RSI
• State the 20WBCT test and what a positive result means
• Describe the timeline of alcohol withdrawal (6h → 12-48h → 48-96h)
• State Wernicke's triad and the rule about thiamine and glucose
• State why QRS > 100ms in TCA overdose is dangerous and how to treat it
• Practise the "unconscious farmer with secretions" answer aloud