Description

Part 1: BIS and Density Spectral Array Interpretation Before Surgical Incision in a 64-Year-Old Male with Diffuse Axonal Injury and Subarachnoid Hemorrhage Undergoing ORIF Pelvis and L1 Fixation

Learning Focus

This section focuses on the pre-incision interpretation of BIS, SEF, MF, and DSA in a neurotrauma patient who received intravenous anesthetic agents but has not yet undergone surgical stimulation.
The aim is to help anesthesiologists recognize how pathologic EEG suppression from diffuse brain injury interacts with sedative drug effects before the first surgical stimulus.

1. Clinical Context

A 64-year-old male, 10 days post-traumatic subarachnoid hemorrhage (SAH) with diffuse axonal injury (DAI), presented for ORIF pelvis with L1 fixation.
He was E2M2, tracheostomized, and off sedation in the ICU.

Neuroimaging Summary

• Bilateral fronto-parieto-temporal SAH with intraventricular extension

• Multiple contusions (largest 11 mm right gangliocapsular)

• Thin bilateral subdural collections (8.7 mm left)

• No midline shift or mass effect

Physiological Parameters at OR Arrival

Drugs administered (pre-incision):

• Fentanyl 200 µg

• Midazolam 1 mg

• Dexmedetomidine 30 µg (over 5 min)

• Atracurium 40 mg

No volatile anesthetic or propofol infusion had begun.

2. BIS and DSA Observations

The BIS of 64, SEF 17 Hz, and MF 2 Hz indicate a slow, synchronized EEG pattern with low-frequency dominance — reflecting combined effects of underlying DAI–SAH and the administered sedatives.

Interpretation Summary

• The patient was already in a pathologically slow cortical state from DAI.

• Sedative drugs enhanced delta–theta synchronization, mimicking deep anesthesia.

• The BIS value (64) therefore does not indicate light anesthesia but reflects suppressed cortical function.

3. Neurophysiologic Mechanisms

3.1 Diffuse Axonal Injury

• Axonal shearing disconnects cortical neurons from subcortical relay centers, disrupting thalamocortical synchronization.

• EEG becomes delta-dominant (0.5–4 Hz) with reduced amplitude.

• This background slowing reduces BIS reliability because the algorithm assumes an intact cortical generator network.

3.2 Subarachnoid Hemorrhage

• SAH produces cortical irritation, ischemic spasm, and transient energy failure.

• Loss of high-frequency oscillations (alpha/beta) further lowers BIS coherence.

• The EEG shows slow–mixed delta-theta activity typical of post-SAH sedation states.

3.3 Pathologic–Pharmacologic Overlap

• Midazolam and dexmedetomidine potentiate the same thalamocortical inhibitory pathways injured by DAI, further slowing frequencies.

• Fentanyl, though not a direct cortical depressant, augments this synchronization.

Clinical Correlation

A BIS of 64 in this context represents a biologically depressed cortex, not a patient in danger of awareness.
Thus, the anesthesiologist must interpret BIS through the DSA spectrum, not through...