12.10.19 Head injury
Mechanisms
Penetrating
Generally minimal brain injury
e.g. Pool cue boy
Crush
Tends to damage base of skull
=> Cranial nerve injury
Acceleration/Deceleration
Rotational forces magnify the effect
Damage to olfactory nerve
Damage to pituitary stalk
=> e.g. diabetes insipidus
Missile
Damage proportional to velocity squared
Secondary damage
Raised ICP
Normal ICP ~10 mmHg
CPP = BP - ICP = Normally 100 mmHg
CPP <60 mmHg => Unconscious
Fits
Especially common in children
Causes hypoxic injury
Stop breathing
Raised cerebral oxygen demands
Easy to miss if sedated and intubated!
Consider prophylactic meds
Infection
e.g. Gardener scythe man
Check for dura breech
Loss of CSF
Cushing's Sign
Traditionally hypertension, bradycardia, and irregular respiration
Alternatively widened pulse pressure, irregular respiration, and bradycardia
Elevated systolic BP and a either decreased or normal diastolic BP
Watch out for:
Hypertension
Bradycardia
e.g. Kid kicked in the head
Indications for CT scan
GCS < 13 when first assessed in emergency department
GCS < 15 when assessed in emergency department 2 hours after the injury
Suspected open or depressed skull fracture
Sign of fracture at skull base
Haemotympanum
‘Panda’ eyes
Cerebrospinal fluid leakage from ears or nose
Battle’s sign
Post-traumatic seizure
Focal neurological deficit
> 1 episode of vomiting
Amnesia of events > 30 minutes before impact
Indications for admission
New, clinically significant abnormalities on imaging
Not returned to GCS 15 after imaging, regardless of the imaging results
Criteria for CT scanning fulfilled, but scan not done within appropriate period, either because CT not available or because patient not sufficiently co-operative to allow scanning
Continuing worrying signs
For example, persistent vomiting, severe headaches
Other sources of concern
For example, drug or alcohol intoxication, other injuries, shock, suspected non-accidental injury, meningism, cerebrospinal fluid leak
Indications for review during observation period
Agitation or abnormal behaviour developed
GCS dropped by 1 point and lasted for at least 30 minutes
Give greater weight to a drop of 1 point in the motor response score
Any drop of 3 or more points in the eye-opening or verbal response scores, or 2 or more points in the motor response score
Severe or increasing headache developed or persistent vomiting
New or evolving neurological symptoms or signs, such as pupil inequality or asymmetry of limb or facial movement
Discharge
In general, only discharge when certain there is somebody suitable at home to supervise the patient
CSF Leakage
Look at nose and ears
If unsure what it is, check [glucose]
Distinguishes nasal CSF from snot
Wallerian degeneration
Results when a nerve fiber is cut or crushed
Distal axon degenerates
Known as anterograde or orthograde degeneration
Due to a failure to deliver sufficient quantities of the essential axonal protein NMNAT2
Occurs after axonal injury in both the PNS and CNS
Usually begins within 24–36 hours of a lesion
Axonal skeleton disintegrates
Axonal membrane breaks apart
Axonal degeneration is followed by degradation of the myelin sheath and infiltration by macrophages
Neurolemma does not degenerate and remains as a hollow tube
Sprouts are sent out towards those tubes and these sprouts are attracted by growth factors produced by Schwann cells in the tubes
If a sprout reaches the tube, it grows into it and advances about 1 mm per day, eventually reaching and reinnervating the target tissue
If the sprouts cannot reach the tube, for instance because the gap is too wide or scar tissue has formed, surgery can help to guide the sprouts into the tubes
Types of peripheral nerve injury
Neurapraxia (Class I)
Temporary interruption of conduction without loss of axonal continuity
Physiologic block
Endoneurium, perineurium, and the epineurium are intact
There is no wallerian degeneration
Conduction is intact in the distal segment and proximal segment, but no conduction occurs across the area of injury
Recovery of nerve conduction deficit is full,and requires days to weeks
EMG shows lack of fibrillation potentials (FP) and positive sharp waves
Axonotmesis (Class II)
Loss of the relative continuity of the axon and its covering of myelin, but preservation of the connective tissue framework of the nerve
Wallerian degeneration occurs below to the site of injury
There are sensory and motor deficits distal to the site of lesion
There is no nerve conduction distal to the site of injury (3 to 4 days after injury)
EMG shows fibrillation potentials (FP),and positive sharp waves (2 to 3 weeks postinjury)
Axonal regeneration occurs and recovery is possible without surgical treatment
Sometimes surgical intervention because of scar tissue formation is required
Neurotmesis (Class III)
Total severance or disruption of the entire nerve fiber
Wallerian degeneration occurs below to the site of injury
There is connective tissue lesion that may be partial or complete
Sensory-motor problems and autonomic function defect are severe
There is not nerve conduction distal to the site of injury (3 to 4 days after lesion)
EMG and NCV findings are as axonotmesis
Because of lack of nerve repair, surgical intervention is necessary
Notes
GCS cutoff is LESS THAN OR EQUAL TO 8
Peripheral nerve structure
Neurone
Myelin
Endoneurium
Perineurium
Epineurium
Panda Eye bruise
Limited by orbital fascia
c.f. Black eye
=> Anterior skull fracture
Bruising around ear
=> Posterior skull fracture
Aim for pCO2 of 3.5 kPa
=> Cerebral vasoconstriction => Lowered ICP