What is the management of diffuse axonal injury?

Management of Diffuse Axonal Injury

Management of diffuse axonal injury focuses on preventing secondary brain injury through aggressive physiological stabilization and supportive care, as there is no specific treatment for the primary axonal damage itself. 1, 2

Immediate Diagnostic Approach

Non-contrast CT is the mandatory first-line imaging in acute moderate to severe traumatic brain injury and should be performed without delay 1, 2. However, CT has significant limitations—microhemorrhages associated with axonal injury are frequently invisible on conventional CT, leading to underdiagnosis 1, 2.

MRI is indicated when CT results are normal but persistent unexplained neurologic findings are present (class I recommendation) 1, 2. The optimal MRI sequences for detecting diffuse axonal injury include:

• T2-weighted gradient-echo (GRE) imaging* for detecting microhemorrhages in acute, early subacute, and chronic stages (evidence level II) 1
• Susceptibility-weighted imaging (SWI), which is 3-6 times more sensitive than T2* GRE in detecting hemorrhagic axonal injuries (evidence level II) 1
• Diffusion-weighted imaging (DWI) to visualize axonal injuries not easily appreciated on other sequences 1
• Gadolinium-based contrast agents are not necessary for conventional MRI in traumatic brain injury (class IIb recommendation) 1

Acute Physiological Management

Hemodynamic Stabilization

Maintain systolic blood pressure >110 mmHg to ensure adequate cerebral perfusion 2, 3. Rapidly correct arterial hypotension using vasopressors such as phenylephrine and norepinephrine when needed 2.

Ventilation Management

Control ventilation through tracheal intubation and mechanical ventilation with end-tidal CO2 monitoring 2, 3. Prevent hypocapnia, which causes cerebral vasoconstriction and increases the risk of brain ischemia 2, 3. This is a critical pitfall—overzealous hyperventilation can worsen outcomes.

Intracranial Pressure Management

ICP monitoring is recommended for patients with severe traumatic brain injury to detect intracranial hypertension 4, 2. The threshold for intervention is typically ICP >20 mmHg, as pressures of 20-40 mmHg are associated with a 3.95-fold increased risk of mortality and poor neurological outcome 4.

External ventricular drainage should be used for persistent intracranial hypertension despite sedation and correction of secondary brain insults 2. Decompressive craniectomy may be considered for refractory intracranial hypertension 2, though this must be weighed against the risk of increased survival with severe disability 4.

Sedation and Analgesia

Apart from treating intracranial hypertension and convulsive status epilepticus, sedation management should follow standard ICU guidelines 4. No single sedative or opioid agent has proven superior in traumatic brain injury patients 4. Avoid bolus administration of midazolam or opioids due to risk of arterial hypotension 4.

Management of Neurostorming (Paroxysmal Sympathetic Hyperactivity)

Diffuse axonal injury commonly triggers neurostorming, characterized by episodes of tachycardia, hypertension, tachypnea, hyperthermia, diaphoresis, and posturing 3. These episodes occur in a paroxysmal pattern with periods of relative normalcy between episodes and can be triggered by external stimuli such as repositioning or suctioning 3.

Management focuses on symptom control regardless of underlying etiology 3:

• Maintain adequate cerebral perfusion with systolic BP >110 mmHg 3
• Control ventilation through intubation and mechanical ventilation when necessary 3
• Prevent secondary brain injury through avoidance of hypocapnia 3
• Initiate early physical therapy to prevent contractures 3

Rehabilitation and Long-term Management

Early physical therapy and rehabilitation are essential to prevent joint contractures and muscle atrophy 2, 5, 6. Specific interventions include:

• Proper positioning and frequent repositioning to prevent pressure sores and contractures 2
• Range of motion exercises should be initiated as soon as the patient is stabilized 2
• Splinting may be necessary to maintain proper joint alignment and prevent contracture formation 2
• Task-oriented approaches, passive stretching, and bowel-bladder retraining exercises have demonstrated benefit 5, 6

Consistency in performing physiotherapy exercises is the most crucial component for achieving maximum functional independence 5, 6.

Prognostic Assessment and Follow-up

The location and extent of diffuse axonal injury lesions correlate with clinical outcomes 1, 2. DAI Stage 3 (dorsolateral brain stem lesions) is associated with poor outcomes 1. The presence of both a contusion and >4 foci of hemorrhagic axonal injury on MRI is an independent prognostic predictor 1, 2.

Regular neurological assessments are necessary to detect clinical deterioration 2. Follow-up imaging is indicated with neurological deterioration rather than on a routine basis 2.

Survivors require long-term hospitalization and rehabilitation to improve their chances of recovery 7. At 3 months post-injury, mortality rates can reach 25.6%, with satisfactory outcomes observed in approximately 48% of patients 7.

Multidisciplinary Considerations

Regular multidisciplinary case reviews are recommended for patients with severe diffuse axonal injury 1, 2. For patients with perceived devastating brain injury, early communication with regional neuroscience centers is essential 4. Advanced communication training for healthcare providers managing patients with limited prospect of recovery is advisable 1.

Establish patient values and preferences early to guide end-of-life care planning if needed 4. Honest and realistic discussions of the most likely outcome should occur at admission rather than delayed until a decision to withdraw life-sustaining therapy is considered 4.

Critical Pitfalls to Avoid

• Do not rely solely on CT imaging—diffuse axonal injury is frequently missed on conventional CT 1, 2
• Do not hyperventilate aggressively—hypocapnia worsens cerebral ischemia 2, 3
• Do not delay rehabilitation—early physical therapy prevents contractures that significantly impact long-term functional outcomes 2, 5, 6
• The number of microhemorrhages, while helpful for diagnosis, does not directly correlate with injury severity or outcomes (evidence level II) 1, 2