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

Management of Head Injury in the ICU and Factors Influencing Outcome of Severe Traumatic Brain Injury

Introduction

• Barash Clinical Anesthesia 9e, p. 4813
• Plum & Posner's Stupor and Coma, p. 581

I. Pathophysiology: Primary vs. Secondary Brain Injury

Primary Injury

• Caused by the mechanical force at the time of impact
• Results in: contusions (coup/contre-coup), diffuse axonal injury (DAI), epidural/subdural/intracerebral haematoma (EDH/SDH/ICH)
• Irreversible; not amenable to treatment after the fact
• ICH occurs in ~40% of cases (small/medium vessel tearing); EDH in <1% (meningeal artery rupture)

Secondary Brain Injury (the target of ICU management)

• Barash Clinical Anesthesia 9e, p. 4814
• Miller's Anesthesia 10e, p. 12005

II. Physiological Framework: Monro-Kellie Doctrine & CPP

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

CPP = MAP - ICP (Normal: 75-105 mmHg)

• Bailey & Love 28e, p. 382
• Morgan & Mikhail 7e, p. 1085
• Miller's Anesthesia 10e, p. 12005

III. Initial Assessment and Resuscitation

Primary Survey (A-B-C-D-E)

• Airway: Assume cervical spine instability in all trauma. Use in-line manual stabilisation - "chin-lift" and "head-tilt" are contraindicated. All patients with GCS ≤8 require intubation.
• Breathing: Exclude and treat tension pneumothorax, open pneumothorax. Target PaO2 80-120 mmHg, PaCO2 35-38 mmHg.
• Circulation: Haemorrhagic shock is the primary extracranial cause of poor outcome. Use equal-ratio blood product replacement (red cells:plasma:platelets = 1:1:1). Activate massive transfusion protocols when needed.
• Disability: GCS score, pupillary examination
• Exposure: Full physical examination

Airway Management Specifics

• Rapid Sequence Intubation (RSI) is mandatory (all trauma patients at high aspiration risk)
• Nasotracheal intubation: relatively contraindicated if skull base fracture suspected
• Target: GCS ≤8 → intubate and ventilate before CT scanning
• Succinylcholine may transiently increase ICP - use with caution; rocuronium is an alternative

Blood Pressure Targets (BTF 4th Edition)

• Plum & Posner, p. 577-578
• Barash Clinical Anesthesia 9e, p. 4813

IV. Classification of Head Injury

• All severe TBI patients must be managed in ICU and urgently evaluated by neurosurgery.

V. ICU Management of Severe TBI - A Tiered Approach

Tier 0: General ICU Measures (Universal)

• Head of bed elevation: 30 degrees (reduces ICP by improving venous drainage)
• Avoid neck rotation (obstructs jugular venous return)
• Avoid hypotonic IV fluids (worsen cerebral oedema)

• Continuous ICP monitoring (EVD or parenchymal probe)
• Target ICP <22 mmHg, CPP 60-70 mmHg
• Multimodal monitoring: brain tissue PO2 (PbrO2), transcranial Doppler (TCD), jugular venous oximetry (SjO2), cerebral microdialysis, continuous EEG
• Pupillary monitoring at least hourly

• Normocapnia: PaCO2 35-38 mmHg (standard target)
• Normoxia: PaO2 80-120 mmHg
• Lung-protective ventilation (risk: may increase PaCO2 and ICP - needs careful balance)
• Prolonged prophylactic hyperventilation (PaCO2 <30 mmHg) is contraindicated - causes cerebral vasoconstriction and ischaemia

• Maintain MAP to achieve CPP 60-70 mmHg
• Vasopressors (noradrenaline) if needed; avoid massive fluid therapy
• Short-acting antihypertensives (labetalol, nicardipine) for hypertensive surges

Tier 1: First-Line ICP-Lowering Therapies

• Preferred agents: Propofol (short context-sensitive half-life, facilitates daily neurological assessment, potent CMRO2 reducer)
• Propofol Infusion Syndrome: monitor for (lactic acidosis, rhabdomyolysis, renal failure) when high-dose propofol used >48h
• Opioids (fentanyl, sufentanil, remifentanil): no ICP effect provided MAP is maintained
• Dexmedetomidine: increasingly used - no respiratory depression, preserves neurological examination
• Benzodiazepines: longer half-life, less suitable for neuro-monitoring but acceptable
• Ketamine: previously contraindicated; in intubated/ventilated patients, no adverse ICP effect; has beneficial effects (reduces vasopressor and opioid need, preserves gut motility, bronchodilation)
• Muscle relaxants: acceptable; succinylcholine may transiently raise ICP
• Nitrous oxide and etomidate: should NOT be used in severe TBI

• External ventricular drain (EVD) placed in lateral ventricle
• Allows both ICP monitoring AND therapeutic CSF drainage
• Very effective first-line therapy when ventricles are still detectable

• Mannitol (20%): 0.25-1 g/kg IV bolus; reduces ICP by osmotic dehydration; also reduces blood viscosity improving CBF; maintain serum osmolality <320 mOsm/L; avoid if hypovolaemic
• Hypertonic Saline (3-23.4%): likely equally effective to mannitol; preferred in haemodynamically unstable patients and hyponatraemia; no nephrotoxicity concern; given as bolus ONLY (never prophylactic)
• Never give osmotherapy prophylactically - only for documented/suspected ICP elevation

Tier 2: Second-Line / Rescue Therapies

• Use only as a temporizing emergent measure for acute ICP crisis (herniation)
• Target: PaCO2 30-35 mmHg (short-term)
• Mechanism: cerebral vasoconstriction → reduces CBV → reduces ICP
• Duration: shortest possible; prolonged use causes cerebral ischaemia (vasoconstriction without adequate O2 delivery)
• Complete CI: PaCO2 <28 mmHg

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

• BTF Guidelines: recommend only for late refractory ICP elevation, NOT early refractory ICP
• Evidence (DECRA trial): decompressive craniectomy increases the number of patients surviving in a vegetative state or with severe disability despite lowering ICP
• RESCUEicp trial: improved survival but increased severe disability/vegetative state
• Still has a role in select patients as a last resort

• Maintain normothermia (36-37°C) aggressively - fever significantly worsens outcome
• Antipyretics (paracetamol), surface cooling, endovascular cooling
• Prophylactic mild hypothermia: NOT beneficial in prospective multicentre trials (failed to show superiority over normothermia)
• Therapeutic hypothermia (33-35°C): may reduce ICP but has not improved outcome

What NOT to Do (Contraindicated Therapies)

VI. Additional ICU Care

Nutrition

• Enteral nutrition: start as early as possible (aim day 1-2; minimum by day 5-7)
• Transgastric jejunal tube preferred
• Greater energy/protein deficits = prolonged ICU stay
• Glucose target: 110-150 mg/dL (max 180 mg/dL); avoid both hyperglycaemia and hypoglycaemia

Transfusion

• Liberal transfusion strategy: trigger at Hb <9 g/dL (superior to restrictive Hb <7 g/dL in severe TBI)
• Red blood cell transfusion guided by individual cerebral physiological triggers where possible

DVT Prophylaxis

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

Seizure Prophylaxis

• Phenytoin (or levetiracetam): reduces early post-traumatic seizures (within first 7 days)
• Does not reduce late seizures
• Not obligatory but widely used in severe TBI

Electrolyte Management

• Target eunatraemia - hyponatraemia worsens cerebral oedema
• Watch for Syndrome of Inappropriate ADH (SIADH) and Cerebral Salt Wasting (CSW)
• Correct aggressively

VII. Surgical Interventions

VIII. Factors Influencing Outcome of Severe TBI

A. Non-Modifiable (Premorbid / Anatomical) Factors

B. Clinical / Neurological Factors

C. Physiological / Secondary Insult Factors

D. Radiological / CT Factors (Marshall CT Classification)

E. Process-of-Care / System Factors

F. Serum Biomarkers (Emerging)

• S100B protein: marker of astrocyte/glial injury; elevated levels correlate with severity and poor outcome
• NSE (Neuron-Specific Enolase): neuronal injury marker; prognostic value in TBI
• GFAP (Glial Fibrillary Acidic Protein): increasingly used in outcome prediction
• UCH-L1 (Ubiquitin C-terminal hydrolase L1): FDA-approved blood biomarker for TBI

IX. Neuromonitoring in the ICU

X. Summary of ICP Management Checklist (Miller's Anesthesia, BTF Guidelines)

1. Keep all physiological variables normal (normotension, normocapnia, normoxia, normothermia, normoglycaemia, normovolaemia)
2. Head 30° elevation; avoid head rotation
3. Target CPP 60-70 mmHg; avoid massive fluids or high-dose vasoconstrictors
4. Normocapnia (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, not prophylactic)
8. Barbiturate therapy (under EEG monitoring) for refractory ICP
9. Aggressive fever control
10. Surgical evacuation of mass lesions without delay

XI. Outcome Prediction Tools

• IMPACT Calculator (www.tbi-impact.org): uses age, GCS, pupillary reactivity, CT characteristics, systemic insults, and laboratory variables to estimate 6-month outcomes
• CRASH prognostic model: developed from >10,000 patients; includes age, GCS, pupil reactivity, presence of major extracranial injury, and CT findings

Conclusion

• Barash Clinical Anesthesia 9e, pp. 4813-4816
• Miller's Anesthesia 10e, pp. 12005-12009
• Morgan & Mikhail's Clinical Anesthesiology 7e, pp. 1085-1087
• Plum & Posner's Diagnosis and Treatment of Stupor and Coma, pp. 577-582
• Bailey & Love's Short Practice of Surgery 28e, pp. 382-383
• Brain Trauma Foundation Guidelines for Management of Severe TBI, 4th Edition
• SYNAPSE-ICU: ICP monitoring in acute brain injury (Lancet Neurol, 2021) [PMID: 34146513]
• Yen et al., Early progressive mobilisation in moderate-to-severe TBI: RCT (Crit Care, 2024) [PMID: 38778416]This is a complete, exam-ready long answer for MD Anaesthesia. Here is a quick orientation to the structure:

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