Clinical assessment of head injury: The history

A quick and concise history is essential in the care of the patient with head injury. Necessary details include:
• Age
• Type of accident that caused the head injury and the events surrounding it
• Time of occurrence
• Details of rescue/transportation to the hospital
• Occurrence and details of

o Vomiting: may indicate raised ICP
o Convulsions (early/late post traumatic seizures)
o Bleeding (craniofacial orifices and others)
o CSF leaks
o Fever
o Loss of consciousness

• Allergies (avoid drugs of allergy)
• Last meal (stomach may need to be emptied before general anaesthesia)
• Details of pre-hospital care
• Co-morbidities

The history is obtained from a conscious patient while relations and bystanders at the site of the accident or from the ambulance officers are important informants for both the conscious and the unconscious .

Initial management of head injury

The initial management of head injury is very important to reduce the morbidity and mortality associated with the condition. The initial care impacts significantly on the eventual outcome and if not properly done, it may make nonsense of any eventual specialist neurosurgical care.

The key aspects in the management of patients following head injury involve:
• accurate clinical assessment of the neurological and other injuries
• determination of the pathological process involved
• accurate assessment of changes in the neurological status of the patient; this indicates an improvement, progression or change in the pathological processes.

At the injury site, immediate care involves careful extraction of the injured individual (e.g from a car wreck, collapsed building, gutters, etc), rapid restoration and maintenance of an adequate airway, protection of the cervical spine, ventilation, essential circulatory resuscitation, first aid treatment of other injuries and the urgent transfer of the patient to hospital.

It is essential to avoid hypoxia and hypotension as these will cause further brain
injury (secondary brain damage). The ‘ABC’ of resuscitation gives a good guide for the initial management of the head-injured patient like other trauma patients.

Clinical Features of Hydrocephalus

Clinical presentation of hydrocephalus depends on the age of the affected individual and the rate of CSF accumulation. In infants, the most striking feature is the abnormal increase in the size of the head whereas in adults, it commonly presents with features of raised intracranial pressure.

In young children, hydrocephalus could present with any combination of the following symptoms and signs:

• Abnormally large head; usually with the rate of growth of the cranium greater than that of the face (craniofacial disproportion)
• Irritability
• Poor neck/head control
• Poor developmental milestone attainment/loss of previously attained milestones such as social amile, neck control, sitting, walking and talking
• Nausea and vomiting
• Bulging fontanelle(s)
• Widening of the cranial sutures (sutural diastasis)
• Prominent, enlarged and engorged scalp veins
• ‘Setting sun sign’ or sunset appearance of the eye due to paralysis of upward gaze (Parinaud syndrome) from pressure of the accumulated CSf in the suprapineal recess on the tectum of the midbrain
• Sixth nerve (abduscens) palsy (due to its long intracranial course)
• Macewen’s sign: cracked pot sign on percussion of the skull
• Miscellaneous findings
o Hyperactive reflexes
o Irregular respirations with apneic spells

In older children/adults, it presents with features of increased ICP:
• Headache
• Nausea and vomiting
• Gait abnormalities
• Papilloedema
• Upward gaze palsy
• Sixth nerve palsy

If the ventricles enlarge slowly, the condition may initially be asymptomatic.
The classic triad of normal pressure hydrocephalus is:
• Dementia
• Urinary incontinence
• Gait ataxia

Causes of Hydrocephalus

The conditions causing hydrocephalus include the following:

• Excessive CSF production by the choroid plexuses
o Choroid plexus papilloma

• Blockage in the CSF circulation, either within the ventricle, or on the outside of them
o Aqueductal stenosis
o Tumours
o Chiari malformation especially types I and II
o Dandy-Walker malformation
o Intraventricular haemorrhage
o Meningitis
o Spinal tumour
o Myelomeningocoele

• Impairment of CSF absorption by the arachnoid villi.
o Meningitis
o Subarachnoid haemorrhage

The causes enumerated above could also be classified into congenital or acquired.

Hydrocephalus: Introduction

Hydrocephalus is a neurosurgical condition in which there is excessive accumulation of brain water (called cerebrospinal fluid) in the head. Hydro = water; cephalus = head. It is rare but certainly present in our community.

Many of the children, and alas! Adults that you see around with big heads suffer from this condition. Do not stigmatize the sufferer, it is definitely not his/her making.

The causes of the condition are many; some are congenital (occur before birth) while some others are acquired (contracted after birth). To properly understand the causes of hydrocephalus, you need to appreciate the formation and flow of the brain water. A simple overview of this is as follows:

• The brain has large spaces within it called the ventricle (four of them, called right lateral, left lateral, third & fourth)

• The ventricles communicate with a space surrounding the brain, called the subarachnoid space through openings (foramina in the 4th ventricle)

• The subarachnoid space in turn coomunicates with a similar space surrounding the spinal cord

• Cerebrospinal fluid (CSF) is produced by flower like structures in the ventricles called the choroid plexus

• The fuid circulate in the ventricle and into the subarachnoid space (around the brain and the spinal cord)

• The fluid get absorbed into the blood stream via finger-like structures called arachnoid villi located in the coverings of the brain

• CSF production is in dynamic balance with absorption to prevent its accumulation.

From the foregoing, you would probably have deduced that hydrocephalus can result from:
1. Excessive CSF production by the choroid plexuses
2. Blockage in the CSF circulation, either within the ventricle, or on the outside of them
3. Impairment of CSF absorption by the arachnoid villi.

Simple isn’t it? You don’t have to be a genius to understand this. Watchout for my updates on this topic. I will appreciate your feedback on how useful you think this introduction is. I will also make myself available on this site to answer any question that bothers you about this very important condition. In addition, I shall appreciate your comments on the topic.

Join this discussion.

The Glasgow Coma Scale

The Glasgow Coma Scale was introduced by Graham Teasdale and Lord Jennet in 1974. Till date, it is the most widely used and accepted measure of level of consciousness. The scale has 3 parameters as defined below. Obtainable scores are from 3 to 15 with scores below 15 indicating diminished levels of consciousness. A patient with a score of 8 or below is said to be in coma.

The scale is renowned for its simplicity, reproducibility and objectivity. It provides a fast means of patient assessment which can be used by various cadres of health workers including paramedics, nurses and physicians.

Parameter Numerical Value

Eye Opening
Spontaneous 4
To speech 3
To pain 2
None 1

Best Verbal Response
Orientated 5
Confused 4
Inappreopriate 3
Incomprehensible sounds 2
None 1

Best Motor Response
Obeys commands 6
Localizes pain 5
Flexion withdrawal 4
Abnormal flexion 3
Extension to pain 2
None 1

TOTAL 3-15