Diffuse Axonal Injury

Also known as: DAI

Diffuse axonal injury results from rotational acceleration and deceleration producing widespread shear and stretch injury to axons.

The damage concentrates at junctions between tissues of different density.

Common sites include:

Grey white matter junction
Corpus callosum
Dorsolateral upper brainstem
Internal capsule
Cerebellar peduncles

A patient can remain deeply unconscious despite a CT showing little haemorrhage because DAI is primarily microscopic.

Adams pathological grading

Grade I

Diffuse axonal injury in cerebral white matter, particularly at the grey white junction.

Grade II

Grade I injury plus corpus callosum involvement.

Grade III

Grade II injury plus brainstem involvement.

Grade III disease carries the greatest risk of prolonged coma and severe disability.

The classic presentation is immediate prolonged unconsciousness after high energy trauma.

Findings can include:

Coma disproportionate to CT findings
Abnormal posturing
Autonomic instability
Pupillary abnormalities with associated brainstem injury
Prolonged impaired consciousness

A patient does not need to be permanently comatose to have DAI. Mild and moderate axonal injury can produce persistent cognitive and behavioural impairment.

CT can be normal or show only:

Tiny haemorrhagic foci
Mild cerebral swelling
Small intraventricular haemorrhage

MRI: investigation of choice when DAI is suspected.

Useful sequences include:

Diffusion weighted imaging
Susceptibility weighted imaging
T2 and FLAIR

MRI identifies small lesions within:

Corpus callosum
Brainstem
White matter

MRI severity can inform prognosis but must not be used alone to declare neurological recovery impossible.

There is no operation that directly repairs diffuse axonal injury.

Management focuses on preventing secondary damage.

Use severe TBI principles:

Avoid hypoxaemia
Avoid hypotension
Treat ICP above 22 mmHg when monitored
Maintain CPP 60 to 70 mmHg
Treat seizures
Maintain normothermia
Provide early nutrition
Prevent VTE
Begin rehabilitation when stable

Surgery is required only for associated treatable lesions such as:

EDH
SDH
Large contusion
Hydrocephalus
Refractory intracranial hypertension requiring decompression

Prognosis

Recovery can continue for months.

Poor prognostic features include:

Brainstem DAI
Persistent fixed pupils
Severe hypoxic or hypotensive secondary injury
Prolonged unresponsive state

Do not use absence of early awakening after sedation withdrawal as a sole reason to assume futility.

Clinical toolsCalculators

BMI GCS EDD Parkland Formula

Corrected Sodium Corrected Calcium Anion Gap Creatinine Clearance Insulin Calculations qSOFA Wells PE Wells DVT CHA₂DS₂-VASc HAS-BLED CURB-65 Centor/McIsaac

Acute Subdural Haematoma

Also known as: Acute SDH

Acute subdural haematoma is accumulation of acute blood between dura and arachnoid, usually from:

Torn bridging veins
Cortical vessel injury
Lacerated brain associated with high energy trauma

Unlike EDH, acute SDH frequently accompanies major underlying parenchymal injury.

CT classically demonstrates a crescentic collection that can cross cranial sutures but is limited by dural reflections such as the falx and tentorium.

Outcome depends not only on haematoma size but also on:

Primary brain injury
Age
GCS
Pupillary status
Hypotension
Associated contusions

Reverse anticoagulation

For life threatening intracranial bleeding, reverse anticoagulation rapidly.

Warfarin

Give:

4 factor prothrombin complex concentrate according to INR and body weight

plus:

Vitamin K 10 mg IV

Dabigatran

Use:

Idarucizumab 5 g IV

Apixaban or rivaroxaban

Use:

Andexanet alfa where available and appropriate, or 4 factor PCC according to institutional emergency reversal protocol.

Do not delay life saving surgery waiting for complete laboratory normalisation when reversal has been initiated and neurological deterioration is ongoing.

Surgical thresholds

Evacuate an acute SDH when:

Thickness is greater than 10 mm

Midline shift is greater than 5 mm

regardless of GCS.

A comatose patient with:

GCS below 9
SDH thickness below 10 mm
Shift below 5 mm

still requires surgery when one or more of the following occur:

GCS has fallen by at least 2 points
New asymmetric or fixed dilated pupils
ICP is persistently elevated.

Severe TBI patients with acute SDH and coma require ICP focused monitoring and treatment.

Procedure

Perform a large trauma craniotomy.

Evacuate clot.

Control:

Cortical bleeding
Bridging veins where accessible
Contused bleeding surfaces

Inspect for significant underlying parenchymal injury.

If the brain remains swollen beyond the inner table or ICP remains dangerously high, leave the bone flap off and perform decompressive craniectomy with duraplasty.

The decompression should be large rather than a small restrictive window.

Nonoperative management

A small SDH without significant shift or neurological deficit can be observed with:

Frequent examination
Repeat CT
Correction of coagulopathy
ICP surveillance in severe injury

Any deterioration requires immediate reassessment.

Seizures

Use 7 day early seizure prophylaxis in significant acute SDH unless there is a specific contraindication.

Do not continue prophylaxis long term unless a seizure occurs or another indication develops.

Diffuse Axonal Injury

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management