Post-Extubation (Post-Intubation) Laryngospasm

Definition & Pathophysiology

• Contraction of the lateral cricoarytenoid muscle (adduction + medial rotation of arytenoids) via the recurrent laryngeal nerve
• Contraction of the thyroarytenoid muscle (vocal cord shortening and glottic closure) via the recurrent laryngeal nerve
• Contraction of the cricothyroid muscle (tensing of vocal cords) via the external branch of the SLN

• Barash Clinical Anesthesia 9e, p. 2535
• Miller's Anesthesia 10e, p. 11571

Incidence

• Overall incidence: 0.79% of all anesthetics (136,929 patients surveyed)
• Pediatric incidence: 0.4% to 10% during induction and emergence
• Most common in infants aged 1-3 months; almost 1 in 50 anesthetics in young children
• More common during emergence than induction

• Barash Clinical Anesthesia 9e, p. 2535-2536
• Morgan & Mikhail's Clinical Anesthesiology 7e, p. 1708

Timing

Causes & Risk Factors

Direct Triggers (Stimuli at the Larynx)

Patient-Related Risk Factors

• Pediatric age (especially < 6 months to 3 years) - narrow airway, more reactive reflexes
• Pre-existing reactive airway disease (asthma, bronchial hyperreactivity)
• Recent or active upper respiratory tract infection (URI) - airway hyperreactivity persists 4-6 weeks after URI
• Exposure to secondhand tobacco smoke in children
• Obstructive sleep apnea
• Patients with pre-existing upper airway pathology

Anesthesia-Related Risk Factors

• Extubation during the excitation phase (light anesthesia, not deeply asleep but not awake)
• Use of inhalational anesthesia vs. IV anesthesia (higher risk with volatiles)
• Inadequate depth of anesthesia during airway manipulation
• Care by less experienced providers (risk is lower with pediatric anesthesiologists)

• Morgan & Mikhail's Clinical Anesthesiology 7e, p. 1708
• Barash Clinical Anesthesia 9e, p. 2535, 2283-2287
• Miller's Anesthesia 10e, p. 11571

Clinical Recognition

Management - Step-by-Step

Step 1: Remove the Triggering Stimulus

• Suction secretions, blood, or vomitus from the pharynx
• Reposition the airway; remove any airway device that is stimulating the larynx

Step 2: Apply 100% Oxygen + CPAP with Jaw Thrust (Larson's Maneuver)

• Apply a well-fitting mask with 100% oxygen
• Apply CPAP up to 15-40 cmH2O (most sources cite 15-20 cmH2O in children, up to 40 cmH2O in adults)
• Simultaneously apply a firm jaw thrust (mandible lifted anteriorly into mask) - this both opens the upper airway and creates a painful stimulus that can break the spasm
• Larson's Maneuver: apply firm pressure at the "laryngospasm notch" - the area between the angle of the mandible, the mastoid process, and the base of the skull

Note: Aggressive positive pressure ventilation (PPV) alone is unreliable - a completely spasmed glottis can resist up to 140 mmHg. Forcing air in risks stomach insufflation, aspiration, and decreased functional residual capacity.

Step 3: Deepen Anesthesia

• IV Propofol (sub-anesthetic dose: 0.5-1 mg/kg) - depresses laryngeal reflexes
• IV Lidocaine (1-1.5 mg/kg IV) - reduces airway reactivity
• Call for help at this stage if not already done

Step 4: Neuromuscular Blockade (if Steps 1-3 fail)

• Succinylcholine (0.1 mg/kg "mini-dose") can break laryngospasm while preserving spontaneous respiration
• Full dose (1-2 mg/kg) used when desaturation and bradycardia develop
• IM succinylcholine (4-6 mg/kg) with atropine is acceptable when IV access is unavailable

Step 5: Emergency Intubation

• Administer a full induction dose of induction agent + intubating dose of muscle relaxant
• Proceed with emergent tracheal intubation
• Forcibly attempting to pass a tube through a closed glottis is contraindicated and risks laryngeal injury

Algorithm Summary

Laryngospasm recognized
        ↓
1. Remove stimulus + suction
        ↓
2. 100% O₂ + CPAP + Jaw thrust (Larson's maneuver)
        ↓ (fails)
3. Deepen anesthesia: IV Propofol ± IV Lidocaine — Call for help
        ↓ (fails / desaturation + bradycardia developing)
4. Succinylcholine IV (0.1–1 mg/kg) or IM (4–6 mg/kg)
        ↓ (fails)
5. Full induction + intubating dose NMB → Emergent intubation

Complications if Untreated

• Severe hypoxemia - PaO2 <50 mmHg inhibits spasm eventually, but at the cost of hypoxic injury
• Negative-pressure pulmonary edema (NPPE) - results from forceful inspiratory effort against a closed glottis, generating extreme negative intrathoracic pressure
• Bradycardia - vagal response to hypoxia, especially in children
• Cardiac arrest - terminal event in unrecognized/untreated complete laryngospasm

Prevention

• Extubate either fully awake (eyes open, purposeful movement) or deeply anesthetized (spontaneously breathing, not swallowing/coughing) - the dangerous "in-between" period should be minimized
• Suction the oropharynx gently before extubation
• Avoid extubation in patients with active URI if elective surgery
• Lateral position for somnolent pediatric patients in recovery - allows oral secretions to drain away from the vocal cords
• IV lidocaine (1-1.5 mg/kg) before extubation reduces airway reactivity
• Allow parents at bedside in children (reduces anxiety, lowers catecholamine-driven reflex activity)

• Miller's Anesthesia 10e, p. 11571
• Barash Clinical Anesthesia 9e, p. 2535-2536
• Morgan & Mikhail's Clinical Anesthesiology 7e, p. 1708
• Barash Clinical Anesthesia 9e (Pediatric section), p. 3756

1. Introduction + Epidemiology - sets the context with numbers
2. Pathophysiology - Primary vs Secondary injury (foundational concept)
3. Physiological framework - Monro-Kellie, CPP = MAP - ICP (always expected)
4. Classification - GCS-based severity table
5. Initial Resuscitation - primary survey, RSI, BP targets (BTF 4th edition figures)
6. ICU Management - Tiered Approach - this is the core of the answer:
   • Tier 0: universal measures (positioning, monitoring, ventilation, haemodynamics)
   • Tier 1: first-line ICP therapies (sedation, EVD, osmotherapy)
   • Tier 2: rescue therapies (hyperventilation, barbiturates, decompressive craniectomy)
   • What NOT to do (steroids, prophylactic hyperventilation - with trial evidence)
7. Additional ICU care - nutrition, transfusion, DVT, seizures, electrolytes
8. Surgical interventions - by lesion type
9. Factors influencing outcome - categorized A to F (non-modifiable, clinical, physiological, CT, process, biomarkers)
10. Neuromonitoring table
11. ICP checklist (directly from Miller's/BTF guidelines)
12. Outcome prediction tools (IMPACT, CRASH)
13. Conclusion - synthesizes the key message

• ICP treatment threshold: >22 mmHg (BTF 4th edition change from >20)
• CPP target: 60-70 mmHg
• Normocapnia: PaCO2 35-38 mmHg
• Mannitol osmolality limit: <320 mOsm/L
• Transfusion trigger (TBI): Hb <9 g/dL (liberal strategy)
• CRASH trial: steroids = higher mortality in TBI - absolute contraindication
• Decompressive craniectomy: only for late refractory ICP (not early)

1. Introduction & Epidemiology
2. Pathophysiology - Primary vs Secondary brain injury with all secondary insult mechanisms
3. Monro-Kellie Doctrine & CPP physiology
4. Classification - GCS-based severity table
5. Initial Resuscitation - Primary survey, RSI, BTF 4th edition BP targets
6. ICU Management - Tiered Approach (Tier 0 → Tier 1 → Tier 2 → Contraindicated therapies)
7. Additional ICU care - nutrition, transfusion, DVT, seizures, electrolytes
8. Surgical Interventions by lesion type
9. Factors Influencing Outcome - categorized into non-modifiable, clinical, physiological, CT/Marshall grading, process-of-care, and biomarker factors
10. Neuromonitoring table with targets
11. ICP Management Checklist (BTF/Miller's)
12. IMPACT & CRASH prognostic tools
13. Conclusion

Management of Head Injury in the ICU & Factors Influencing Outcome of Severe TBI

1. Introduction

2. Classification of Head Injury

3. Pathophysiology: Primary vs Secondary Brain Injury

Primary Injury

• Caused by the direct mechanical force at time of impact
• Results in: contusions (coup/contre-coup), diffuse axonal injury (DAI), EDH/SDH/ICH
• ICH in ~40% (small vessel tearing), EDH in <1% (meningeal artery)
• Irreversible - not amenable to treatment

Secondary Brain Injury (the target of all ICU management)

4. Physiological Framework

Monro-Kellie Doctrine

1. Displacement of CSF from cranial to spinal compartment
2. Increased CSF absorption
3. Decreased CSF production
4. Reduction in cerebral venous blood volume

CPP Formula

CPP = MAP - ICP Normal CPP: 75-105 mmHg | Normal ICP: 5-15 mmHg

5. Initial Resuscitation (Primary Survey)

Airway

• Assume cervical spine instability in all trauma - use in-line manual stabilisation
• "Chin-lift" and "head-tilt" manoeuvres are contraindicated
• All GCS ≤8 patients require intubation before CT scanning
• Rapid Sequence Intubation (RSI) is mandatory (high aspiration risk)
• Nasotracheal intubation: relatively contraindicated if skull base fracture suspected
• Succinylcholine may transiently raise ICP; rocuronium is a suitable alternative

Breathing

• Exclude tension pneumothorax, open pneumothorax
• Target: PaO2 80-120 mmHg, PaCO2 35-38 mmHg

Circulation (BTF 4th Edition Blood Pressure Targets)

• Haemorrhagic shock: replace with equal-ratio blood products (RBC:FFP:Platelets = 1:1:1)
• Activate massive transfusion protocol when needed
• Crystalloid resuscitation for initial haemodynamic support

Disability

• GCS score documentation (use post-resuscitation GCS - most accurate)
• Pupillary examination (size, symmetry, reactivity)

6. ICU Management - Tiered Approach

Tier 0: Universal / General Measures

• Head of bed at 30 degrees - reduces ICP by improving venous drainage
• Avoid head rotation - obstructs jugular venous return
• Avoid hypotonic IV fluids - worsen cerebral oedema

• Continuous ICP monitoring (EVD - external ventricular drain, or parenchymal bolt)
• Target ICP <22 mmHg and CPP 60-70 mmHg
• Multimodal monitoring: brain tissue PO2 (PbrO2 >20 mmHg), transcranial Doppler (TCD), jugular venous oximetry (SjO2 55-75%), cerebral microdialysis (L/P ratio <25), continuous EEG
• Pupillary monitoring at least hourly

• Normocapnia: PaCO2 35-38 mmHg (standard target)
• Normoxia: PaO2 80-120 mmHg
• Lung-protective ventilation can be used, with monitoring for rising PaCO2
• Prolonged prophylactic hyperventilation (PaCO2 <30 mmHg) is absolutely contraindicated - causes cerebral vasoconstriction and ischaemia

• Vasopressors (noradrenaline preferred) to maintain MAP/CPP targets
• Short-acting antihypertensives (labetalol, nicardipine) for hypertensive surges
• Avoid massive fluid therapy or high-dose vasoconstrictors (risk of pulmonary oedema)

Tier 1: First-Line ICP-Lowering Therapies

• EVD placed in lateral ventricle allows both ICP monitoring AND therapeutic CSF drainage
• Highly effective first-line therapy; most efficient when ventricles still detectable

Tier 2: Second-Line / Rescue Therapies

• Use only as a temporising emergent measure for acute ICP crisis (signs of herniation)
• Target: PaCO2 30-35 mmHg short-term only
• Mechanism: cerebral vasoconstriction → reduced CBV → reduced ICP
• Duration: as short as possible; prolonged use causes cerebral ischaemia
• Hard limit: PaCO2 <28 mmHg is absolutely contraindicated

• Pentobarbital/thiopentone for refractory ICP (all above measures failed)
• Mechanism: reduces CMRO2 and CBF
• Monitor with continuous EEG (target: burst-suppression pattern)
• Side effects: hypotension (frequent), immunosuppression, paralytic ileus
• Prophylactic barbiturates: contraindicated - worse outcome

• BTF Guidelines: only for late refractory ICP elevation, NOT early refractory ICP
• DECRA Trial: lowered ICP but increased vegetative state/severe disability
• RESCUEicp Trial: improved survival but higher rates of vegetative state and severe disability
• Role: last-resort salvage in select patients with late refractory intracranial hypertension

Absolute Contraindications in Severe TBI

7. Additional ICU Care

Nutrition

• Start enteral nutrition as early as possible (aim day 1-2; mandatory by day 5-7)
• Transgastric jejunal tube preferred
• Greater energy/protein deficits = prolonged ICU stay and more complications
• Glucose target: 110-150 mg/dL (maximum upper limit 180 mg/dL)
• Avoid both hyperglycaemia AND hypoglycaemia

Transfusion

• Liberal strategy: transfuse at Hb <9 g/dL (superior to restrictive Hb <7 g/dL trigger in severe TBI)
• Ideally guided by individual cerebral physiological triggers (PbrO2, SjO2)

DVT Prophylaxis

• Up to 25% of TBI patients develop DVT
• Use LMWH + mechanical compression despite increased risk of haematoma expansion
• Parkland Protocol helps stratify optimal timing of chemical prophylaxis initiation

Seizure Prophylaxis

• Phenytoin (or levetiracetam): reduces early post-traumatic seizures (first 7 days)
• Does NOT reduce late seizures; prophylaxis is therefore not obligatory long-term
• Continuous EEG to detect non-convulsive status epilepticus

Electrolyte Management

• Target eunatraemia - hyponatraemia worsens cerebral oedema
• Watch for SIADH and Cerebral Salt Wasting (CSW) - both cause hyponatraemia but managed differently
• Replace aggressively with hypertonic saline when indicated

Temperature Management

• Normothermia (36-37°C): actively maintain - fever significantly worsens outcome
• Use paracetamol, surface cooling, endovascular cooling
• Treat fever as a neurological emergency in TBI

8. Surgical Interventions

9. Factors Influencing Outcome of Severe TBI

• GOS 1: Death | GOS 2: Vegetative state | GOS 3: Severe disability | GOS 4: Moderate disability | GOS 5: Good recovery

A. Non-Modifiable Factors

B. Clinical / Neurological Factors

C. Physiological / Secondary Insult Factors

D. Radiological / CT Factors (Marshall CT Classification)

• Midline shift >5mm
• Compression/obliteration of basal cisterns
• Presence of subarachnoid blood
• Diffuse axonal injury pattern

E. Process-of-Care / System Factors

F. Emerging Biomarkers

10. Neuromonitoring in the ICU

11. ICP Management Checklist (BTF Guidelines / Miller's Anesthesia)

1. Maintain normotension, normocapnia, normoxia, normothermia, normoglycaemia, normovolaemia
2. Head of bed 30°; avoid head rotation
3. CPP 60-70 mmHg; avoid massive fluids or high-dose vasoconstrictors
4. PaCO2 35-38 mmHg; short-term hyperventilation (PaCO2 30-35 mmHg) only if ICP >20-25 mmHg
5. Adequate sedation (propofol preferred)
6. CSF drainage via EVD
7. Mannitol or hypertonic saline (bolus only, never prophylactic)
8. Barbiturate therapy (under continuous EEG) for refractory ICP
9. Aggressive fever control
10. Prompt surgical evacuation of mass lesions

12. Outcome Prediction Tools

• IMPACT Calculator (www.tbi-impact.org): uses age, GCS, pupillary reactivity, CT findings, hypotension, hypoxia, and lab values to estimate 6-month outcomes
• CRASH Prognostic Model: derived from >10,000 patients; includes age, GCS, pupil reactivity, CT findings, and major extracranial injury

13. Conclusion