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Types of head injuries
All the different types of blunt and sharp injuries already discussed in study unit 5 can involve the scalp. A blow to the head with a blunt object can split the skin because the scalp is trapped between the blunt object and the underlying skull. These wounds can easily be confused with an incised wound. However, careful examination will reveal tissue bridges and a fine margin of abrasion.
The appearance of entrance gunshot wounds is discussed elsewhere.
If someone wears a protective cap or even just has a thick head of hair, the skin, but not necessarily the underlying brain, may be protected against injury. Absence of skin injuries or fractures does therefore not exclude brain injury.
Skull fractures can be classified as follows:
· Simple fractures: the overlying scalp is intact
· Open or compound fractures: the fracture and underlying tissue communicate through a skin defect with the external environment. These fractures can easily become infected.
· Comminuted fracture: the bone is broken into many separate pieces.
Skull fractures have certain unique features:
· Linear fractures are usually not associated with movement of the adjacent bone plates.
· Depressed fractures differ from the above. They are often more localised, and result from impact against a smaller object. Knobkieries often cause a depressed fracture.
· Contre-coup fractures are found diagonally opposite the point of impact. If someone falls on the back of his head, fractures may occur on the frontal aspect of the skull, especially of the thin and delicate bone overlying the orbital cavities (orbital plates).
· A ring fracture is present around the hole at the base of the skull (the foramen magnum). These fractures occur when someone lands forcefully on his feet and the weight of the head propels the skull downward on the spine.
· Hinge fractures are severe and may display extensive fractures involving the base of the skull. After removal of the cranial vault, the anterior and posterior aspects of the skull base can be moved relative to one another.
It must be remembered that the skull of an infant toddler may deform substantially without fracturing. Brain injuries could therefore occur without any fractures. However, the sutures between the bony plates may be damaged (diastasis).
Wherever the brain is brought forcefully into contact with the overlying bone or even the free edges of the dural folds (eg the inferior aspect of the falxcerebri, the dural fold dividing the brain in two halves), the tissue can become contused. If the force is sufficient, the brain surface may even tear (lacerate). As these lacerations are always surrounded by contusions, we often refer to them as contusions/lacerations.
As can be expected, these injuries will be located at the points of contact with the overlying bone. Contusions are therefore seen at the crest of the convolutions (gyri), and not in the depth of the grooves (sulci). Those parts of the brain in contact with rough and uneven bony elements are particularly prone to injury. This especially applies to the base of frontal lobe. If the contact between the brain and bone is severe, the brain lobe hitting the bone may burst. This usually involves the frontal and temporal lobes.
In the past much emphasis has been placed on the concepts coup and contre-coup (fig 7.14). The former is said to occur at the point of impact and the latter diagonally across from it. It was also said that the contre-coup injury tends to be more severe. This is not always true.
If someone is hit on the back of the head (occiput), movement of the under-surface of the frontal lobe over the rough bony surface of the anterior cranial fossa will cause a contre-coup injury of the base of the frontal lobe. However, the occipital lobe moving over the relatively smooth surface of the tentorium cerebelli will suffer less injury. In this case the contre-coup injury will be more severe than the coup injury.
If the blow is over the frontal aspect, the frontal lobe will still suffer more injury, for the same reasons. In this case the coup injury will be more severe than the contre-coup injury.
Diffuse axonal injury (DAI) is a condition which occurs at the moment of impact. Due to acceleration and deceleration forces in the brain tissue (often accompanied by rotational and angulation forces), a diffuse disruption of axons (nerve fibres) occurs due to shearing and traction.
DAI presents immediately at the moment of impact. Clinically it can present with a spectrum of different grades, varying from mild, which presents clinically as concussion, to severe. In the latter case the patient is immediately unconscious with no lucid interval. In these cases the coma usually lasts more than 6 hours.
Macroscopically (with the naked eye) or with certain radiological procedures (a CT scan or magnetic resonance (MR)) petechial haemorrhages are present in the corpus callosum (the fibres joining the two halves of the brain) and in the dorso-lateral aspects of the pons (a part of the brain stem). A tear of the septum pellucidum and fornixes may also be present. This results in haemorrhage in the two lateral ventricals of the brain (intraventricular haemorrhage). The petechial haemorrhages are the result of rupture of the small blood vessels running alongside the axons (nerve fibres) in the brain. As these vessels are also damaged by the shearing forces experienced during DAI, it is an indirect indicator of axonal injury, as the latter is not visible with the naked eye. In the corpus callosum and dorso-lateral aspects of the pons, the nerve fibres are more susceptible to damage as they are longer and are therefore more prone to damage by shearing forces.
Microscopically a diffuse disruption of the axons can be seen. Depending on the survival period certain changes will be evident, of which the first sign will be retraction balls due to axonal swelling. Damage to axons (and neurons, ie brain cells) is irreversible, and with time these damaged neurons disappear.
The method of injury (whether the brain decelerates or accelerates inside the cranial cavity) can cause certain associations with other, but separate, brain injuries. Gliding contusions occur almost in the midline of the brain (parasagittal region) where the surface of the brain is fixed by means of the arachnoid villi to the overlying dura mater. When movement of the brain occurs relative to these points of fixation, small haemorrhages occur at the interface between the white and grey matter as the latter is fixed by means of the arachnoid villi, and cannot move with the white matter.
There are sometimes also haematomas (localised haemorrhages) in die deep intra-cerebral matter, in the region of the basal ganglia. They are also known as intermediary coup lesions.
It is important to note that DAI has no or minimal association with other injuries which are normally the result of more localised impact, such as fractures of the skull, contusions or lacerations of the brain matter, and intracranial haemorrhages (other than those mentioned above). In addition DAI is seldom associated with an increase in the intracranial pressure.
To summarise: DAI is a common injury due to acceleration and deceleration of the brain, often concomitant with rotational and angulation forces. If severe enough, it can cause a vegetative state, where a patient is unconscious, but able to maintain his or her own vital functions (respiration and cardiovascular status)
· This is often the result of non-missile injury, such as a blow to the head.
· These haemorrhages are the most common cause of deterioration in a patient after a lucid (``awake'') period.
· More than 35 ml is a sufficient volume to act as a space-occupying lesion.
· These haemorrhages are often associated with fracture(s).
· There is often more than one type of haemorrhage.
· Although of primary origin, it often presents as a complication, in other words as a secondary phenomenon.
· extradural haemorrhage
· subdural haemorrhage
· subarachnoidal haemorrhage
· intracerebral haemorrhage
· intraventricular haemorrhage
This classification is limited to traumatic haemorrhages, and does not include spontaneous causes of haemorrhages, such as hypertensive haemorrhages or haemorrhages due to rupture of a berry aneurysm (defect in the blood-vessel wall).
Extradural haemorrhages are also known as epidural haemorrhages. These haemorrhages occur between the dura and the overlying skull. The dura is a relatively thick membrane which lines the inner surface of the skull. A number of arteries are present in the dura. They are often partially embedded in the overlying skull bone. One of these arteries is the middle meningeal artery which runs on the side of the head in the temporo-parietal region. This artery can be damaged with subsequent haemorhage if a fracture occurs in that region. Smaller fracture-associated extradural haemorrhages may also occur elsewhere.
A number of small veins run between the surface of the brain (arachnoid mater or leptomeninges) and the dura. With sudden acceleration or deceleration these small veins may rupture, with subsequent haemorrhage. A relatively small brain compared with the cranial cavity will predispose to such movement, and therefore injury with subsequent haermorrhage. This condition is therefore often found in alcoholics with brain atrophy. In addition, babies have relatively small brains compared with the cranial cavity.
The muscles of a baby's neck are also not well developed, and if you shake a baby, as is often seen in cases of child abuse, excessive movement of the brain can occur in the cranial cavity, with subsequent damage to these vessels.
Subdural haemorrhages can also occur in cases of burst lobe, where severe trauma to part of the brain will cause haemorrhage in the brain tissue (in a brain lobe), as well as outside (in the subdural space). This usually communicates via contusion/laceration. Subdural haemorrhage typically present after a period of time, as they are venous in origin and therefore take time to develop (longer compared with an extradural haemorrhage). These patients are often called ``walk-talk-and-die'' patients, as the patient will present to the trauma unit with a history of even relatively trivial trauma, and after examination the doctor will send the patient home. The next day or thereafter the patient presents in a comatose state and dies.
Subdural haemorrhages can be divided into acute, subacute and chronic haemorrhages. An acute haemorrhage will consist of clotted blood, while a chronic haemorrhage will consist of liquid blood. In addition there will often be signs of membrane formation encapsulating these haemorrhages. Subdural haemorrhages, like any other space-occupying lesion, will cause herniation of brain tissue if of sufficient volume.
These haemorrhages occur below the leptomeninges (arachnoid mater) in the subarachnoidal space, are quite common in head injuries, and can be diffuse or focal. Subarachnoidal haemorrhages are also seen when there is rupture of a berry aneurysm. Berry aneurysms occur because of weakening of the vasculature of the brain. At these points the wall of the blood vessel forms small balloons (aneurysms) which can rupture, with subsequent often fatal haemorrhage. It is important to remember that this is not a trauma-related haemorrhage.
Intracerebral haemorrhages may either be present in a lobe of the brain (lobar haematoma), or in the basal ganglia region, as seen in cases of diffuse axonal injury.
Intraventricular haemorrhages occur in the lateral ventricles of the brain.
They are often the result of rupture of the septum pellucidum or fornix.
These haemorrhages therefore occur in cases of diffuse axonal injury.
The volume of the cranial cavity is fixed. The intracranial contents consist of 70% brain tissue, 15% blood and 15% cerebrospinal fluid. If there is an increase in the volume occupied by the brain or blood, the cerebrospinal fluid will decrease in volume to accommodate this. However, when this volume is exceeded, the intracranial pressure will rise. Increased intracranial pressure is almost always associated with herniations (figure 7.15).
The intracranial cavity is divided by dural folds into three compartments. The tentorium cerebelli is the membrane fold separating the cerebrum (brain) and cerebellum (hind brain). The space below it is also called the infratentorial space and is found in the posterior cranial fossa. The supratentorial space above the tentorium is divided by the falxcerebri into two halves/ hemispheres.
Herniations are brain tissue which is forced from one part of the intracranial cavity to another. As the brain tissue is pushed over the free edges of the dural folds it can become contused and damaged. In addition, the general direction of herniation is downwards towards the foramen magnum, and with increasing pressure in the posterior cranial fossa, the vital centres controlling respiration and the vasomotor systems will become depressed, ultimately leading to death.
The following herniations may occur see (fig 7.15). As herniation is a dynamic process, more than one is often present, as it creates a domino effect.
· Subfalx herniation. The medial aspect of the one cerebral hemisphere is forced below (sub) the falxcerebri (falx) to the opposite side. As this is located above the corpus callosum it is also called a supra-callosal herniation. (The falxcerebri is the fold between the cerebral hemispheres. Herniation means the abnormal protrusion of a body structure through a defect in a membrane, muscle or bone.)
· Central herniation. The central aspect of the brain is forced downwards onto the brain stem. This may cause secondary haemorrhages in the brain stem, with damage to the vital centres, and death.
· Parahippocampalgyrus herniation. The medial aspect of the temporal lobe (the parahippocampalgyrus) is forced over the free edge of the opening in the tentorium cerebelli (incisura) into the posterior cranial fossa. Traction and compression may cause damage to nerves and blood vessels - the latter with infarction of brain tissue.
· Tonsillar herniation. This is also known as coning. The cerebellum (cerebellar tonsils) is forced downwards through the foramen magnum. As this is a risk in cases of raised intracranial pressure, it is contra-indicated to perform a lumbar puncture in patients expected to suffer from raised intracranial pressure, as it lowers the pressure in the spinal colum.
All these are internal herniations. External herniations occur when brain tissue herniate through a defect in the skull. It appears as a mushroom of brain tissue protruding from the head.
Brain swelling is an increase in the size of the brain or parts thereof. It can be due to an increase in the blood volume, ie perfusion swelling; the blood (and therefore fluid) is still intravascular (in the vessels). This condition occurs in two situations: in young children after brain trauma, and in the brain on the same side as a subdural haemorrhage. It is the result of collapse of the system which controls blood-flow in the brain.
If the fluid accumulates outside the vessels (extravascular) it is also called cerebral oedema. There are different types of oedema.
Tumors and brain abscesses are often surrounded by new, immature blood vessels. The walls leak, and fluid accumulates in the surrounding tissue. This surrounding rim of oedema is called vasogenic oedema, and increases the size of the tumor or abscess significantly.
The other important type of cerebral oedema is cytotoxic oedema. This is caused by damage to cells, which then swell due to loss of the normal energy-dependant fluid control of the cells. It is often seen in an infarction, where loss of oxygen supply causes the energy-dependant processes to stop. Sodium will then accumulate in the cell, it will attract water due to the osmotic pressure, with concomitant swelling.
As a matter of interest it must be noted that both types of oedema are often seen in an infarction. The central aspect shows cytotoxic oedema, and the more peripheral aspect, where the blood vessel walls have been damaged by the hypoxia, exhibits vasogenic oedema.
There are also other types of oedema, for example in cases of hypertension (hydrostatic oedema) or due to rehydration after a period of diabetic coma or hypertonic dehydration (osmotic oedema). These, however, fall beyond the scope of this study guide.
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