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The Epidural Hematoma

By: , Posted on: November 29, 2017

Epidural hematomas are a source of frustration. The texts of both Hippocrates (c. 460 BC – 370 BC) and Celsus (c. 25 BC – AD 50) indicate that these two giants of surgery in the classical world, were aware of the existence of collections of blood between the bone and the dura; the membrane covering the brain. Celsus moreover was aware that such a collection of blood could accumulate in the absence of an adjacent fracture. Yet epidural hematomas as a nosological entity were not recognized until the 19th century.

My book, Intracranial Epidural Bleeding: History, Management, and Pathophysiology, has three main purposes. Because epidural hematomas were not recognized as a separate entity, the first of these is to trace slowly evolving concepts of head injury management. The second is to trace the gradual discovery and nature of intracranial epidural hematomas as a separate nosological entity. The third is to present a modern account of the very special pathophysiology of the development of epidural hematomas.

Evolving Concepts of Head Injuries

Following the evolution of ideas on head injury management, two things become clear. Firstly, a number of individuals had glimpses of the truth but were ignored. Secondly, it is accepted that modern scientific medicine based on technological advances started in the nineteenth-century and is essential for our current understanding of epidural bleeding. Nonetheless, the understanding that symptoms following cranial trauma were the result of disturbances of the brain and not of any other tissue required no equipment that was not available from classical times.

Post-traumatic Symptoms

For the ancients, there was no intellectual framework which could relate the collection of such a hematoma to a clinical picture. Hippocrates understood that the brain was the seat of intellectual and emotional function. He made no clear comment on the relationship between trauma and changes in consciousness. His remarks on this topic are mixed together with comments of patients who have a secondary infection. On the other hand, Aulus Cornelius Celsus (ca 25BC – ca. 50 AD) attributed post traumatic symptoms concerning pain and changes in consciousness to injuries to the cranium or the meninges. This, had limited influence for a millennium after his time because he wrote in Latin which was considered inferior to Greek as a medium in which medical notions could be expressed. Thus, his writings were forgotten until 1426 when they were rediscovered. The invention of the printing press with moveable type meant that his De Medicina could be both produced and distributed. Published in 1478 the book was the first medical text to be published using the new method and it had great influence. It contains much good sense but unfortunately the attribution of post-traumatic symptoms to injuries of the bone and meninges was a source of confusion.

On the other hand, the most lasting influence in this regard is that of Galen (129 – 216). The location and nature of the soul and its relationship to the individual in which it was housed remained necessarily confused. From Galen onwards, physicians believed the soul to be located in the brain and disturbances of the soul could be reflected in changes in consciousness. It was not however believed that the brain had any function related to movement or sensation or that post-traumatic symptoms were related to disturbances of the brain.

Another source of the persisting error that the brain could not be the source of post-traumatic symptoms was a finding going back to Galen. The removal of substantial chunks of brain tissue can be consistent with normal intellectual, motor and sensory function. This was noted by amongst others Ambroise Paré (1510 – 1590) and Richard Wiseman (1621 – 1676). They argued from this that the brain could not be the source of symptoms.

Anatomical Errors

Galen for very strange reasons refused to believe that the dura was attached to the skull except at the sutures. This nonsense persisted up to the eighteenth-century. The concomitant teaching was that opening the skull at the sutures must be avoided because that would be the location where the dura would be most at risk. This teaching obviously must have limited the optimal location of trephination for nearly two millenia. Berengario Da Carpi (1460–1530) alone maintained that the dura was adherent all over the interior of the calvarium

From Hippocrates onwards, there was the believe that hematomas if trapped, for example under the skull, would putrefy with dangerous consequences. This was the basis for trephining skull fissures without any clear idea of how to distinguish patients with hematomas from those who were not so damaged.

Aretaeus in the second century AD understood that injury to one side of the brain produced paralysis on the opposite side. His insights were ignored. Subsequently, there were mediaeval surgeons who realized that injury on one side of the head produced paralysis on the other side. One of these was William of Saliceto (1210 – 1277) and once again Berengario Da Carpi demonstrated his superiority by noting that following trauma paralysis could be either ipsilateral or contralateral.

All medical students are taught about the contribution of Andreas Vesalius (1514 – 1564) to anatomy. We were also taught that Vesalius’ work debunked Galen’s errors. This is misleading. Vesalius in fact persisted at least two of Galen’s errors. His table of vascular anatomy shows the presence of a rete mirabile under the brain which is not present in humans. His drawing of the base of the brain is almost indistinguishable from that of Galen and greatly inferior to that of Thomas Willis.

Dawning of the Truth

The understanding that the brain was the source of post-traumatic disturbances of consciousness was expressed by Henri-François Le Dran (1685 – 1770) and Sir Percival Pott (1714 – 1788). Le Dran wrote as follows. “Must the Loss of Sense, which happened at the Moment the Blow was given, be looked upon as a Symptom of the Fracture? No because it continued only Half-a-quarter of an hour, the Fracture remaining in the same Condition for the space of a whole Day, without being dressed. Is it a Symptom of the Dura Mater’s being lacerated? It is not, for the same Reason. Therefore, this Symptom can only be attributed to a Concussion of the Brain.”. Pott tightened the argument with the following statement, “What are the symptoms of a fractured cranium? is often asked; and there is hardly any one who does not, from the authority of writers, both antient and modern, answer, vomiting, giddiness, loss of sense, speech, and voluntary motion…..This is the doctrine of Celsus.” He continues that such symptoms “can only be the consequence of an affection of the brain as the common sensorium. They may be produced by its having been violently shaken, by a derangement of its medullary structure, or by unnatural pressure made by a fluid extravasated on its surface or within its ventricles“. Neither of these statements required any more equipment than had been available at the time of Hippocrates. However, by the eighteenth century the time was right.

The Gradual Definition of Epidural Hematomas as a Nosological Entity

A number of eighteen-century surgeons published case reports of patients with an epidural hematoma. The components of the clinical picture came to be described bit by bit. James Hill (1703 – 1776) of Dumfries realized that a lesion on one side gave a contralateral hemiparesis. John Abernethy (1764 – 1831) was similarly aware. Benjamin Bell (1749 – 1806) from Edinburgh mentioned fixed dilated pupils without understanding how they came about. James Hill introduced elements of management which showed an instinct for managing raised intracranial pressure, without being in a position to understand the underlying processes. Thus, he avoided compressive bandages and where there was a cerebral hernia through a defect in the dura, he shaved it.

Sir John Erichsen (1818 – 1896) stated in 1857 in the second edition of his text book on surgery that the only certain clinical feature of extravasation was a progressively deteriorating level of consciousness. He described the clinical picture of initial unconsciousness, latent interval followed by increasing loss of consciousness which he attributed to what he called meningeal extravasation, due to a ruptured meningeal blood vessel. Hemiparesis or general paralysis would develop with dilated pupils. He also mentioned the variability of the clinical course. He did not mention the side of the dilated pupil. He emphasized a time frame of some hours. He was a highly successful amiable Dane who worked in London. His prestige and that of his book suggests that this information would have been widely available. He suggested the treatment was trepanation but that it was rare as he’d only seen a single case in fifteen years

The final definitive description of the clinical picture of an epidural hematoma should be credited to Sir Jonathan Hutchinson (1828 – 1913). “The importance of an interval of immunity between the accident and the occurrence of symptoms has long been recognized as the chief indication of a ruptured meningeal artery; and it is to this, almost exclusively, that we must still give attention, if we wish to diagnose these cases”. He went on to specify that the hemiparesis would be contralateral and the dilated pupil ipsilateral due to compression of the oculomotor nerve. This was an amazing achievement made at a time when the modern techniques of examining the central nervous system had not been invented.

There was one other development evolving through the early part of the nineteenth century. It began with the work of Franz Joseph Gall (1758 – 1828) who developed a theoretical type of brain localization called phrenology. It was nonsense, but it helped to stimulate the study of the existence of cerebral localization. There were those who believed in it and those who didn’t. The matter was finally settled at the great Seventh International Medical Congress in London in 1881, where the basis of modern cerebral localization was described.

This was relevant for the monograph by W.H.A. Jacobson published only five years after the London medical congress. Diagrams in that paper were taken from the papers of contemporary colleagues to illustrate the relevance of the new cerebral localization to the clinical picture in the patients with epidural hemorrhage which Jacobson described. He presented 70 cases of whom 13 survived. His choice of patients and the statistics used are slightly eccentric. However, the important message he got across was that patients with epidural hematomas could survive if treated early enough.

Since Jacobson’s time there have been a number of developments. Firstly, clinical neurological examination became systematized. X-rays were discovered in 1905. Cerebral angiography was invented in 1927. It permitted the visualization of changes in the cerebral arteries specific for an epidural hematoma. Computerized tomography introduced in 1973 – 74 permitted the direct visualization of these hematomas and sometimes could show if active bleeding was persisting. In addition, a clinical observations scale was introduced which greatly facilitated the early diagnosis of deterioration and thereby the need for emergency surgery. Further improvements in the management of epidural bleeding will mostly need to concentrate on the correct selection of patients to send to a neurosurgical contre and accelerating the transfer.

The Pathophysiology of Intracranial Epidural Hemorrhage Physiology of Intracranial Hematoma Formation

It is necessary to consider a number of interacting factors which result in the production of an epidural hematoma.

Any intracranial hematoma is produced when an opening is made in the wall of an intracranial blood vessel. The force generating such a hematoma is called the bleeding pressure. It consists of the pressure difference between the arterial pressure and the intracranial pressure.

As a hematoma is produced while the arterial pressure remains unchanged the presence of the generated hematoma results in a rise in intracranial pressure. A consequence of this rise is a reduction in the bleeding pressure.

The process in nature which results in the cessation of bleeding is called thrombosis. The factors which affect thrombosis are the stickiness of the blood, the smoothness of the blood vessels’ lining and the speed of blood flow. With a fall in the bleeding pressure the speed of the bleed causing an intracranial hematoma falls facilitating the formation of a thrombus which will stop the bleeding.

Thus, the formation of an intracranial hematoma is a rapid self-limiting process due to the rise in intracranial pressure secondary to the formation of a hematoma

Intracranial Epidural Hematoma Formation

The formation of an epidural hematoma is different. It occurs into a space which is not present in nature; the epidural space. This space is formed by separating the dura from the skull to which it is normally attached. Thus, it is necessary to show that the processes involved include dura separation. The possibility of such separation was first shown by Sir Charles Bell at the beginning of the 19th century. He showed that it was possible to generate dura separation by applying a blow to the skull.

The next question is whether or not, persistent meningeal artery bleeding could generate enough pressure to produce further separation of the dura after the initial injury. Animal research has demonstrated that this can happen provided the initial dura separation occurs over an adequate area. Moreover, a pulsatile pressure such as would arise from an injured artery is more efficient for separating the dura than a steady pressure. There is also substantial evidence to show that when the intracranial pressure is normal at the time of epidural bleeding, venous hemorrhage lacks the pressure to be able to produce further separation of the dura. However, the veins could at least notionally produce dura separation if the intracranial pressure has been artificially lowered as could happen during air ventriculography or more recently ventricular shunting.

The next interesting point is that it appears that when bleeding occurs into a post-traumatic epidural space there is a considerable capacity to allow the blood to leave the epidural space via veins which are torn during the process of dura separation. This shunting of blood out of the epidural space slows down the rise in intracranial pressure, occurring during intracranial hematoma formation which could account for the lucid interval so characteristic of epidural bleeding.

Finally, it could be demonstrated in lethal epidural bleeding that after the initial rise in pressure there was a period of steady state following the cessation of bleeding. This in turn was followed by a secondary rise in intracranial pressure leading to death. It would appear that this rise is due to the development of hydrocephalus secondary to the occlusion of the aqueduct in the midbrain.

To order a copy

Neurosurgeons, neurologists, surgical trainees, trauma surgeons, and medical historians will be interested in this book. It is available in print and e-book via the Elsevier store at up to 30% off the list price and free global shipping through the end of 2017. To order visit the Elsevier Store here and apply discount code STC317 at checkout.

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