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🧫 Tetanus — Crisp Study Notes (MBBS Level)

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1. Organism & Pathophysiology

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2. Clinical Types

• Short incubation = severe disease and poor prognosis

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3. Clinical Features — Progression (High-Yield)

Trismus (lockjaw)  →  Risus sardonicus  →  Dysphagia  →
Neck stiffness  →  Opisthotonos  →  Generalized spasms

• Autonomic dysfunction (2nd week of severe disease): labile BP, tachycardia, profuse sweating, hyperpyrexia, high catecholamines
• Mental status is NORMAL — important differentiator
• Death causes: laryngospasm (most common early) → respiratory failure; later: cardiovascular events from autonomic dysfunction

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4. Ablett Severity Classification (Memorize!)

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5. Diagnosis

• Clinical diagnosis — no confirmatory lab test required
• Culture of C. tetani from wound is not diagnostic (can colonize without disease)
• Serum antitetanus IgG ≥0.1 IU/mL = protective (argues against tetanus)

Differential Diagnosis

• Strychnine poisoning ← most important mimic (also causes generalized spasms)
• Dystonic reaction (phenothiazines, metoclopramide)
• Neuroleptic malignant syndrome
• Serotonin syndrome
• Stiff-person syndrome
• Hypocalcemic tetany
• Peritonitis (abdominal rigidity)

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6. MANAGEMENT — The Core (MBBS Must-Know)

A) Immediate Goals

Neutralize unbound toxin → Control spasms → Airway protection → Treat autonomic instability → Wound care → Antibiotics

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B) Airway & Ventilation

• Early intubation / tracheostomy for Grade III–IV or any laryngospasm
• Mechanical ventilation may be needed for weeks

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C) Control of Spasms

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D) Passive Immunization — Human Tetanus Immunoglobulin (HTIG)

• 3,000–6,000 units IM (some sources: 3,000–10,000 units)
• Neutralizes unbound circulating toxin (cannot reverse bound toxin)
• Give before wound debridement (debridement may release more toxin)
• Intrathecal HTIG (500 units) may be used adjunctively in severe cases
• If HTIG unavailable: equine antitoxin (higher anaphylaxis risk — test sensitivity first)

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E) Antibiotics

Note: Penicillin G is a GABA antagonist (like tetanospasmin) — some sources prefer metronidazole for this reason

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F) Wound Management

• Surgical debridement of necrotic tissue and foreign bodies
• Eliminate anaerobic environment → kills vegetative bacteria
• Debride after HTIG is given

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G) Autonomic Dysfunction (Grade IV)

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H) Active Immunization After Recovery

• Tetanus does NOT confer immunity (toxin dose insufficient to mount immune response)
• Start/complete vaccination after recovery: 3 doses of Td/TT spaced ≥2 weeks apart

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7. Wound Prophylaxis (Exam Favorite!)

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8. Summary Drug Card

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9. Prognosis

• Grade III–IV: hospitalization for 3–6 weeks
• Overall mortality: 20–25% with generalized tetanus despite optimal care
• Short incubation (<7 days) = worse prognosis
• Recovery = axonal nerve terminal sprouting (takes months)
• Most deaths in patients >55 years (due to waning immunity)

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10. One-Line High-Yield Mnemonics

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What's inside the card (2-page A4):

Tetanus Management — Crisp, Concise & Conceptual

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The Core Concept First

Tetanospasmin has already bound to nerves by the time symptoms appear. You cannot reverse what's done — you can only stop more toxin from binding, control the consequences, and keep the patient alive until the toxin wears off (4–6 weeks).

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The 6-Pillar Framework

STOP MORE TOXIN         →  HTIG + Wound debridement + Antibiotics
CONTROL THE AIRWAY      →  Intubation / Tracheostomy
CONTROL SPASMS          →  Benzodiazepines ± Mg²⁺ ± NMB
CONTROL AUTONOMIC STORM →  Labetalol + Mg²⁺
ACTIVE IMMUNIZATION     →  Toxoid (disease ≠ immunity)
SUPPORTIVE CARE         →  ICU, nutrition, DVT prophylaxis

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Pillar 1 — Stop More Toxin Binding

Why?

A) Human Tetanus Immunoglobulin (HTIG)

• 3,000–6,000 units IM in multiple sites
• Neutralizes circulating free toxin before it binds neurons
• Give before wound debridement — debridement releases trapped toxin into circulation
• Intrathecal HTIG 500 units (adjunct in severe cases — bypasses transport barrier)

B) Wound Debridement

• Remove devitalized tissue and foreign bodies
• Destroys the anaerobic niche where C. tetani vegetative form lives and produces toxin
• Give HTIG first, then debride

C) Antibiotics

Concept: Antibiotics kill the bacteria (stop new toxin production), but they don't affect toxin already in nerves. They are adjuncts, not the treatment.

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Pillar 2 — Protect the Airway

Why?

• Grade I–II: Monitor, prepare for early intubation
• Grade III–IV: Tracheostomy preferred over endotracheal intubation
  • Safer with ongoing spasms + trismus
  • Long-term ventilation anticipated (weeks)
• Have suction and emergency airway equipment bedside at all times

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Pillar 3 — Control Spasms

Why?

Concept: Benzodiazepines directly replace what tetanospasmin stole — they restore GABA-ergic inhibition pharmacologically. This is why diazepam is logically the first drug of choice.

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Pillar 4 — Control Autonomic Storm

When?

Concept: Use combined α+β blockade — pure β-blockade leaves α-receptors unopposed, crashing BP. Magnesium is elegant here because it controls both spasms AND autonomic instability simultaneously.

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Pillar 5 — Active Immunization Post-Recovery

Tetanus does NOT confer immunity. The toxin dose causing disease is sub-immunogenic.

• Start tetanus toxoid (Td/TT) during recovery
• Complete 3 doses spaced ≥2 weeks apart
• This is mandatory — survivors are fully susceptible to a second attack

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Pillar 6 — Supportive Care (ICU)

• Quiet, dark, isolated room — minimize sensory stimuli that trigger spasms
• NG tube feeding (early nutrition — high caloric demand from spasms)
• Urinary catheter (urinary retention from autonomic dysfunction)
• DVT prophylaxis (prolonged bed rest)
• Regular chest physiotherapy (aspiration pneumonia in 50–70%)
• Serum electrolytes monitoring (Mg²⁺ toxicity if using Mg sulphate infusion)

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Wound Prophylaxis — The Decision Tree

Any wound  →  Is vaccination history known?
                    │
        ┌───────────┴───────────┐
   < 3 doses / unknown      ≥ 3 doses
        │                       │
   Give TT + HTIG           Last booster?
   (for tetanus-prone)       ├── < 5 yr → Nothing
                             ├── 5–10 yr → TT only
                             └── > 10 yr → TT + HTIG

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Why Each Drug in One Line

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Prognosis Anchors

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Bottom line: Tetanus management is a race against time — intercept free toxin fast, secure the airway early, sedate aggressively, support the autonomic system, and wait for the bound toxin to degrade. Every step is mechanistically justified.

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Burn Wound Treatment — Crisp, Conceptual & Concise

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The Central Concept

A burn wound is a dynamic wound. Depth determines destiny — whether it heals on its own or needs surgery. Your job is to assess depth accurately, protect the wound from infection and dehydration, replace what's lost systemically, and close the wound as fast as possible.

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Step 0 — The ABCDEFs (Immediate Priorities)

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Step 1 — Assess Burn Depth (Determines Everything)

Key concept: The challenge is the indeterminate (deep partial-thickness) wound — even burn experts are only 60–80% accurate in assessing it. Management depends on whether it will declare itself as healing or non-healing within a short observation window.

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Step 2 — Estimate Burn Size (TBSA)

Head & Neck     = 9%
Each Arm        = 9%    (×2 = 18%)
Chest (front)   = 18%
Back            = 18%
Each Leg        = 18%   (×2 = 36%)
Perineum        = 1%

• Lund & Browder chart — more accurate, especially in children (head is proportionally larger)
• Palm rule: patient's palm + fingers = ~1% TBSA (for irregular burns)

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Step 3 — Fluid Resuscitation (Systemic Priority)

Why fluid?

Parkland Formula (most widely used)

First 24 hours:
  Lactated Ringer's:  4 mL × kg × % TBSA burn

  → Give FIRST HALF in first 8 hours (from TIME OF BURN, not time of admission)
  → Give SECOND HALF over next 16 hours

Second 24 hours:
  Colloid 0.5 mL/kg/% TBSA burn  +  2,000 mL 5% dextrose water

• Adults: 0.5–1 mL/kg/hr
• Children: 1 mL/kg/hr

Concept: Crystalloid replaces the water/electrolytes lost into the interstitium. Colloid in the second 24 hours is added once capillary integrity starts returning — it stays intravascular better after the leak slows.

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Step 4 — Wound Care (The Local Treatment)

3 Phases: Assess → Manage → Rehabilitate

What a good dressing must do:

1. Protect damaged epithelium
2. Minimize bacterial/fungal colonization
3. Reduce evaporative heat loss (prevents hypothermia)
4. Maintain moist wound environment → faster healing
5. Provide comfort

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Topical Antimicrobials — Who, When, Where

Concept: Topical agents don't heal the wound — they prevent infection from turning a partial-thickness wound (which could heal) into a full-thickness one (which won't). Infection is the enemy of wound healing.

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Systemic Antibiotics

• NOT given prophylactically for the burn wound
• Used only for diagnosed infections (pneumonia, wound sepsis)
• Cover MRSA + Pseudomonas (most common burn pathogens) when treating empirically

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Step 5 — Surgical Management (When Dressings Aren't Enough)

Indication for Surgery

• Deep partial-thickness wounds that won't heal in 3 weeks
• All full-thickness burns
• 4th degree burns

Timing

• Stabilize first (24–48 hours)
• Early excision and grafting within 2–4 days of injury reduces wound infection, systemic mediator release, and mortality

Tangential Excision

• Shave necrotic layers sequentially with guarded blade until healthy, bleeding tissue is reached
• Preserves maximum viable tissue

Graft Options

Autograft (gold standard)
  └── Split-thickness skin graft (STSG): epidermis + thin dermis
       → less donor morbidity, best graft take
       → meshed 4:1 to cover large areas
  └── Full-thickness skin graft (FTSG): for hands, face, joints
       → less contracture, better colour match
       → NOT meshed
       
Allograft (cadaveric skin)
  → Temporary cover when donor sites insufficient
  → Tests wound bed quality (if allograft "takes," autograft will too)
  
Skin substitutes (e.g. Integra, Biobrane)
  → For massive burns, staged reconstruction

Concept: Thin grafts take better than thick ones — easier vascular ingrowth. But function areas (hands, feet, face) need thick or full-thickness grafts to prevent contracture, which would otherwise destroy function.

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Step 6 — Nutritional Support (Often Underestimated)

• Supraphysiological cardiac output, elevated catecholamines, glucagon, cortisol
• Skeletal muscle catabolism to fuel gluconeogenesis

Caloric needs (Curreri formula):

25 kcal/kg + (40 × % TBSA burn) = daily calories
+ 1.5–2 g/kg/day protein

• Oxandrolone 0.1 mg/kg q12h — testosterone analogue; improves lean body mass; monitor LFTs weekly
• Propranolol (non-selective β-blocker) — blunts catecholamine-driven catabolism
• Glutamine supplementation — shown to benefit burn + trauma patients

Concept: Every unhealed burn wound is a metabolic drain. Closing the wound quickly AND providing adequate anabolic nutrition are two sides of the same coin — both reduce hypermetabolism.

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Step 7 — Escharotomy / Fasciotomy (When the Burn Tightens)

• Full-thickness circumferential burns create unyielding eschar → compartment syndrome
• Chest eschar → restricts respiration → chest escharotomy
• Limb eschar → vascular compromise → limb escharotomy (longitudinal incisions through eschar)
• If deep to fascia → fasciotomy

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Step 8 — Criteria for Burn Centre Referral

• Partial-thickness burns >10% TBSA
• Any full-thickness burn
• Burns to face, hands, feet, genitalia, perineum, major joints
• Electrical / chemical burns
• Inhalation injury
• Circumferential burns of limb or chest
• Burns with pre-existing conditions (DM, immunosuppression)
• Children in hospitals without paediatric burn capability

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Complications to Know

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One-Line Conceptual Summary per Step

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