Bimodal distribution-> first- at teen age- accidental trauma with recreational activities, alcohol/ drug abuse Falls- m/c/c of TBI RTA- m/c/c of death from TBI Assaults S[prtomg injuries Industrial trauma NAI in children

TBI Flashcards by An Individual

What are the types of injuries in TBI?

=> Primary injury: Occurs at the time of initial insult due to-
Tissue trauma, hypoxia, ischemia
- May be focal or global

=> Secondary injury: Consequence of primary injury
-Can worsen outcomes significantly

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Initial assessment
Important history

from lecture series on CICM training

Timing
Mechanism- blunt/ penetrating/ speed of vehicle/ height of fall
=>Influencing factors-
* Toxins eg- alcohol
* Anticoagulation/ antiplatelets, reversibility of agents
* Age

=>Features-
* Seizures
* Other injures associated
* Tt given so far and response to Tt
* Allergies
* Pregnancy
* Family- how much do they know?

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M/C/C of TBI

Bimodal distribution-> first- at teen age- accidental trauma with recreational activities, alcohol/ drug abuse

Falls- m/c/c of TBI
RTA- m/c/c of death from TBI
Assaults
S[prtomg injuries
Industrial trauma
NAI in children

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Mechanisms of Primary injury

Contusion (coup/contrecoup)
Hematomas: extradural, subdural, subarachnoid, intracerebral
DAI (diffuse axonal injury)- due to shearing forces.

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What areas are commonly affected in DAI?

Corpus callosum
Parasagittal white matter in cerebral cortex
Axons in brainstem

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Focal Hypoxic injury- Importance

Surrounding the infarct is region of ischemic penumbra
Interventions are directed to preserve penumbra key to optimise outcomes

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Global Hypoxic / Ischemic Injury Cause
Prognosis
MRI findings

-> Caused by period of severe hypotension/ cardiac arrest
->Recovery depends upon rapid reversal of Primary cause
->MRI findings
Pathological white matter signal changes
* Frontal & occipital lobes
* Periventricular regions
( areas susceptible to ischemia/hypoxia)

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Outline the pathophys asso with Primary TBI

=> Loss of homeostasis:
i - Failure of ion pumps
→ cytotoxic edema
→↑ Intracellular Ca²⁺ and Na⁺
→↑ Glutamate (decreased uptake) → excitotoxicity → seizures

ii - Restriction of Oxygen use:
* Disruption of Cell membrane & Organelles → apoptosis

iii - Vasogenic Edema
* Due to mediator release
* BBB (blood-brain barrier) breakdown
* ↑ Capillary permeability → protein/fluid leakage into interstitial space

iv) Loss of autoregulation

Brain region vulnerability varies:
-Cell bodies & grey matter more vulnerable
- White matter more resilient

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Secondary Injury- What are the Mechanisms

Mechanisms of Secondary Injury:

I => Local factors:
i) Expansion of intracranial hematomas
ii) Cerebral edema:
-Compromised blood supply
- brain herniation
iii) Seizures

II =>Systemic insults:
* Hypoxia
* Hypo-/hypercarbia
* Hypotension
* Electrolyte disturbances
* Hyper-/hypoglycemia
* Hyperthermia
* Anemia

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Classification of TBI

=>Mild- GCs- 13-14, Headache, N/V, dizziness, agitation, emotonal lability
=>Moderate- GCS- 9-12
=>Severe->GCS- <8
Moderate and severe are the ones that req ICU & are asso with complications

=>Imp not to miss other injuries- esp- vertebral injuries( asso with TBI in upto 10% cases)
Secondary and tertiary surveys imp.

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Poor prognostic signs in TBI

Age > 60 years
– Associated with significantly worse outcomes.
Pupillary Abnormality
– 70–90% mortality if bilateral fixed pupils (absent light reflex).
GCS on Presentation
– 65% mortality if GCS = 3.
Severity of Primary and secondary injuries
Presence of Hypoxia
– Doubles the likelihood of poor neurological outcome.
Presence of Hypotension
– Doubles mortality.
CT Scan Abnormalities
– The more abnormal, the worse the outcome.
Presence of Extracranial injuries
Comorbidities
– Increase risk of poor outcomes.

BP, G,P increase mortality-> low BP, GCS and pupillary abn

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Scores available for prognostication

1)=> Based on MRC crash data- meant for high income countries- predicts unfavourable outcome @ 6months only.
2)=>Derived from CRASH -II trial data, includes CT findings, SBP and HR

None are ablsolute- predicting prognosis is very hard, scores act as a guide only.

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Principles of Mx of TBI

Aim is to prevent/ minimize secondary brain injury
=>Initial resuscitation and stabilization
=>Management of ICP and maintain CPP
=>Supportive Medical Mx
=>Surgical intervention if req.
=>Long term Neuro rehab

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Initial resusc

=>Primary survey:
* Identify and treat life threatening injuries
* Rapid assessment of pupils, GCS score, and motor function
* Airway control- RSI
* Avoid hypoxia,hyperoxia, hypo and hypercarbia-
(PaO2- 60-90, PaCO2- 35-40)
* Maintain MAP >80(assuming ICP-20)
* imaging of brain- ?mass lesions

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Secondary survey

=>Top to tail assessment
* Head- scalp lacerations, bleeding, skull #
* Associated trauma- Vertebral #s, extremity traua etc.
=>Invx:
* Imaging- Bony pathology, #es, ICH, Traumatic SAH, Carotic/ vertebral artery dissection
* Bloods- BGL, ABG, CBE- Platelets, Hb, coags
* Optic nerve sheath diameter- >6mm -asso with ⬆️ed ICP, often preceeds pappiloedema

Causes of HTN in severe TBI: Pain, Agitation, ⬆️ed ICP

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Management of Intracranial Pressure (ICP)

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Target: Keep ICP < 20–22 mmHg & CPP between 60–70 mmHg.
Bedside Measures: Head elevation, Neutral neck position, loose ETT ties, avoid IJ lines- unobstructed venous drainage
optimize sedation/pain relief.
Hyperosmolar Therapy: Hypertonic saline (3% or 23.4%) to treat elevated ICP.
CSF Drainage: EVD for continuous or intermittent drainage

Dose of 3%- 3ml/kg over 10 mins
SE- AKI, Pulmonary congestion in HF, oliguria

Mannitol suggested by BTF. Dose- 0.25-1gm/kg, Target osmolality- 300-330 mosm/L
SE- Repeated doses harmful- hypovolemia, hypotension, e disturbances.

Supportive ICU Mx

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Temperature Control: Aggressively treat fever (avoid > 39°C) to reduce metabolic demand.
Seizure Prophylaxis: anticonvulsants (phenytoin or levetiracetam) during the first 7 days, particularly for severe, penetrating, or high-risk injuries.
Sedation: Propofol / Midazolam to reduce oxygen demand, and manage ICP.
Nutrition: Start early enteral nutrition within 48 hours to 5 days, aiming to meet caloric requirements.
VTE Prophylaxis: Mechanical prophylaxis immediately, Pharmacological (LMWH or unfractionated heparin) starting within 2-3 days, provided the brain injury is stable

Surgical Intervention

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Evacuation of mass lesions: eg- epidural or subdural hematomas.
Decompressive Craniectomy: Used as a last-tier measure for refractory intracranial hypertension.
Compound/Open Wounds: Debridement and repair, often with antibiotic prophylaxis

When to involve neurosurgeons

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=>Depends upon Pathology, severity, comorbidities
1)* EDH- Mostly drained when blood vol >30ml, Midline shift, GCS<8, Pupillary abnormalities
2)* SDH- >10mm, Midline shift>5mm, GCS <8, ⬆️ in ICP persisting for >20min.
3)* SAH- Traumatic SAH- rarely req NSx intervention except when Dilated ventricles on CT-> for EVD
4)* ICH- Haematoma <1cm from cortex can be drained, draining deeper haematomas has not shown improvement in outcomes(STITCH -I & II)
* Intraventricular extension of ICH may need EVD
5)* Penetrating TBI
6)* Compound depressed skull #

Rehab/ long term care

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Multidisciplinary Team involvement- physiatrists, physical therapists, occupational therapists, and speech therapists to improve functional outcomes.
Neuropsychological Care: Evaluation for cognitive deficits and support for mood changes, agitation, or behavioral issues.

Management of TBI-
Apply Cerebroprotective strategies
i Airway
ii Fluids
iii CPP, ICP
iv Temp control
v Sedation, Analgesia
vi Seizure control

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Airway – Indications for Intubation
1. Loss of airway reflexes
2. GCS ≤ 8 or rapid deterioration
3. Hypoxia/hypercapnia
4. Hypoventilation, copious secretions, facial/jaw trauma
5. Transport safety
6. Seizures
7. Suspected ↑ICP (e.g., #base of skull)

Oxygenation
* Target SaO₂: 94–95%
* Avoid hypoxia
* Avoid hyperoxia (toxic effect)

⸻

PEEP
* PEEP may ↑ICP theoretically#
* Manage cautiously in raised ICP, especially if hypovolemic

⸻

CO₂ Control
* Target PaCO₂: 35–40 mmHg
* CBF ↑by 4mm hg for every 1mm hg ↑in CO2
* Avoid both hypo- and hypercapnia

#Upto 15cm h20 used safely in refractory hypoxia

Management of TBI-cont
Cerebral Perfusion Pressure (CPP) Targets

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CPP = MAP − ICP
- Maintain CPP > 60 mmHg
- If ICP ↑ → need higher MAP to maintain CPP
- In ischemic stroke: BP goal prior to thrombolysis = SBP < 185 mmHg / DBP < 110 mmHg
- For post-TBI, maintain MAP ≥ 80 mmHg (if assuming ICP ≈ 20 mmHg)

Management of TBI- cont
Fluids

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Use isotonic crystalloids (0.9% saline)
Avoid hypotonic fluids
Options:
- Albumin (avoid in TBI per SAFE-TBI)
- Plasmalyte / 0.9% saline
- Consider hyperosmolar therapy if ↑ICP
- Mannitol 0.25–1g/kg IV (short-term use only if neurologically deteriorating)- onset- minutes, duration around 3hrs

Management of TBI- cont
Head Positioning

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Elevate HOB 30°
Keep neck neutral, avoid jugular compression
In spinal injury: whole bed tilt instead of HOB elevation

Management of TBI- cont Temperature Control

* Avoid fever – maintain normothermia * Post-TBI: fever may reflect central dysregulation * Avoid hypothermia; may worsen outcome

Management of TBI- cont Sedation & Analgesia

* Adequate dosing required for ICP control * Propofol & fentanyl commonly used * Avoid excessive opioid use

Management of TBI- cont Seizure Control Risk factors

=> Risk highest in first 7 days -> Consider prophylaxis if: * GCS ≤ 10 * Seizure at presentation * Depressed skull fracture * Subdural/epidural/parenchymal hemorrhage * Post-traumatic amnesia >30 min * Age >65 * Alcoholism

**Post-Traumatic Epilepsy Definition Recommendation for antiepileptics**

->Defined as recurrent seizures occurring >7 days post-injury * BTF Recommendation: Use phenytoin only if risk of seizures outweighs the risks * Prevents early seizures, not late epilepsy

**Intracerebral Hemorrhage (ICH) Risk factors for Seizures Recommendation for Tt**

* Most important risk factor for seizure = cortical location * AHA: Treat only if clinical seizure * Avoid hypoglycemia * Maintain BGL between 4.5–10 mmol/L

**DAI Grading system**

**BTF guidelines** * DC * CSF drainage * Osmotherapy

=> 1. Decompressive Craniectomy * Not recommended to improve functional outcomes. * Associated with: -Longer ICU stay - Fewer ICP-targeted interventions => 2. CSF Drainage * Continuous drainage is preferred over intermittent. => 3. Osmotherapy * Mannitol: -Reserve for patients with herniation signs. * Hypertonic saline: - Not enough evidence for a firm recommendation.

**BTF guidelines cont..** * Hyperventilation * Sedation * Nutrition

=> 4. Hyperventilation * Avoid prophylactic hyperventilation, especially in the first 12–24h. * If used, target PaCO₂ ≥35 mmHg. * Only use in life-threatening raised ICP with neurological deterioration. => 5. Sedation * Barbiturates may be used in refractory intracranial hypertension. * Not recommended for routine ICP control. => 6. Nutrition * Aim to achieve goal nutrition by day 5–7.

**BTF guidelines cont..** * Prophylactic Hypothermia * DVT prophylaxis * Seizure control

=> 7. Prophylactic Hypothermia * Not recommended – does not improve outcomes. => 8. DVT Prophylaxis * All stable TBI patients should receive: * Heparin/enoxaparin * TED stockings => 9. Seizure Prophylaxis * Phenytoin for 7 days recommended.

**BTF guidelines cont**.. * Prophylactic antibiotics * ICP monitoring

=> 10. Prophylactic Antibiotics * Not indicated. * Use VAP (ventilator-associated pneumonia) bundle for prevention. => 11. ICP Monitoring =>Indications: GCS ≤ 8 and Abnormal CT OR - Normal CT plus ≥2 of the following: -> Age > 40 -> SBP < 90 mm Hg -> Motor posturing * Threshold for treatment: ICP ≥ 22 mmHg

****BTF guidelines cont.. * Target CPP * Advanced cerebral monitoring * SBP targets

=> 13. CPP Monitoring * Target CPP: 60–70 mmHg =>14. Advanced Cerebral Monitoring * No guideline support * Jugular bulb monitoring may be used to guide decisions, but not routinely recommended. => 15. SBP (Systolic Blood Pressure) Targets * For age 18–50: maintain SBP ≥ 100 mmHg * For age 51–70: maintain SBP ≥ 110 mmHg => 16. Steroids * Not recommended – associated with worse outcomes

TBI Flashcards

(35 cards)