What Sir William Battle Found: Observations Beyond his Sign

Eponyms remind us of a singular finding and, incidentally, honor the physicians who figured it out for us, typically without benefit of the diagnostic tools available today. As they say, an eponym is here to stay when it no longer presumes first-hand knowledge of the scientist’s work. However, “eponymization” may reduce the entire body of an academic practitioner’s work to a single observation. One such example may be the Battle sign. Few know he was a surgeon or that the eponym has nothing to do with battle trauma.

William Henry Battle (1855–1936) became known by his eponym, which indicates a retroauricular ecchymosis resulting from a basal skull fracture (Fig. 1). Battle also earned two other eponyms, Battle incision, which is used in appendectomies, and Battle operation, for femoral hernia repair. However, his major contribution was in traumatic brain injury (TBI), and few are aware of his key lectures entitled “Three Lectures on Some Points Relating to Injuries to the Head” [1,2,3]. He delivered these lectures at the Royal College of Surgeons of England. At the time, he was Hunterian Professor of Surgery and Pathology in the Royal College of Surgeons and Assistant Surgeon to the Royal Free Hospital.

Fig. 1

Battle sign in patient with traumatic brain injury

His first lecture involved the description and explanation of bloody, watery discharge from the ear and external bruises following TBI. The second lecture discussed cranial nerve involvement with basal skull fractures. The third lecture focused on changes in temperature and the rise of temperature, which he noted, for the first time, was a red flag for intracranial contusions. What can be learned from these observations today?

Battle’s Observations

Battle’s lectures [1,2,3] were published in three subsequent issues of the British Medical Journal (Fig. 2). The first lecture showed the position of fractures involving the middle fossa and some that were unaccompanied by bleeding from the ear (Fig. 3). This lecture concerned the sign that became one of his best-known eponyms in TBI. In his description of mastoid ecchymosis, Battle found that the bruise became apparent 3 to 14 days after the traumatic head injury, and his subsequent autopsy research discovered that extravasated blood could move from the suboccipital region to the more superficial tissue:

I must ask you to consider this sign somewhat fully, for I consider it under certain circumstances, to be a most important indication that the posterior fossa of the skull is of the fracture [2].

Fig. 2

The three lectures by Battle (1890)

Fig. 3

Middle fossa fractures

In his personal series, he noted a large proportion of patients dying from injury to the brain (more than half of the total number), and he felt it necessary to comment that the 11 cases in which fracture of the base was strictly limited to the posterior fossa also had a contused brain, with hemorrhage as the cause of death. He emphasized that hemorrhaging from the ears was the most important sign of fracture of the middle fossa, particularly when bleeding was copious and sustained:

In the main these observations confirm the opinion that immediate profuse and continued bleeding from the ear is an important sign of fracture of the middle fossa, and of a fracture passing through the tympanum associated with a rupture of the membrana tympani; also that that fracture has lacerated some of the vascular channels round the petrous bone.

He also noted hemorrhage from the eyes, and he thought this might have possibly escaped from the lachrymal canals. The patients who presented this symptom were both severely injured. At autopsy, one had a fracture in the posterior and middle fossa in the side opposite to the eye with the hemorrhage.

However, in the second lecture, Battle more clearly described signs of fracture of the anterior fossa, where effusion blood was limited to the eyelid at first and then spread to the ocular conjunctiva and the retroorbital ecchymosis. He emphasized that watery discharge appeared later and said the following:

I am of the opinion that more reliance should be placed on the chemical analysis of watery discharges. If these show on examination the presence of a large amount of chlorides, and give the sugar reaction to Fehling’s solution, then we may say that there is a fracture and communication with the subarachnoid space through a tear in the tubular prolongation of the membranes which surround the facial and auditory nerves; and this applies although there be some albumen from admixture with serum, blood, or secretion from the ear [2].

Of his three lectures, the third lecture has been infrequently cited; however, it has important new observations. In this lecture, Battle described temperatures following cases of injury to the brain. When there was only fracture of the posterior fossa, he found no evidence of temperature changes; temperatures remained normal or were mildly decreased. However, a later spike in temperature was associated with a fatal outcome and often preceded the patient lapsing into a coma. These temperature charts were shown in great detail (a representative one is Fig. 4), and he emphasized that temperature could be an important sign of contusions to the frontal and temporal lobes. He concluded the following:

I would submit to your judgment the following propositions, which express my ideas somewhat differently. If within three days after an injury to the head a patient passes from a condition of unconsciousness or semi-consciousness to one of increasing coma, or after a period of return of consciousness a similar condition of coma supervenes and with the coma there be a rise of temperature of or above 103°, the condition is the result of cerebral contusion with some laceration.… Rarely do we find acute meningitis developing and running its course to a fatal termination within 24 hours, with coma and unequal pupils [3].

Fig. 4

Temperature chart in patient with a developing brain contusion

He specifically noted that in the single case in which meningitis was diagnosed after TBI, the patient had no rise in temperature.

Man of Many Parts

Battle made more observations than the ones that have survived as eponyms. As a surgeon, he collected records of many patients with traumatic head injury and continually searched for early clinical signs predictive of deterioration. Remarkably, he managed to synthesize this information in the late 1800s without the confirmatory tests available today, relying exclusively on the physician’s detailed examination. The Battle sign is typically overlooked because it requires flipping the earlobe. Later, the ecchymosis may descend further down the neck, and only then is it noted.

Secondary deterioration after traumatic contusions is well known in the modern world of neurointensive care. We have forgotten to observe temperature courses. Knowing that hyperthermia occurs in the setting of cerebral vasospasm, new persistent spikes weeks after a traumatic head injury could certainly indicate the presence of meningitis or, after craniotomy, the appearance of an epidural empyema. But an early rise in temperature seems to indicate more than a skull fracture and increased probability of a contusional lesion. In their retrospective study, Meythaler and Stinson [4] noted an increased risk of “neurogenic fever” among patients with severe TBI who had experienced either diffuse axonal or frontal lobe contusions. Thompson et al. [5] noted similar findings. Because the frontal lobe has no major thermoregulatory centers, frontal lobe injury possibly indicates hypothalamic injury. Skull fracture does not independently predict development of fever; however, it has previously been associated with other indicators of hypothalamic injury following TBI, such as diabetes insipidus. Additionally, patients with TBI are at risk of secondary injury from fever; every 1-°C rise in body temperature substantially increases the metabolic rate. This burdens the stressed energy reserves of the severely brain-injured, catabolic patient.

When the central nervous system effects of hyperthermia following both global cerebral ischemia and fluid-percussion trauma were examined in rodent models, hyperthermia significantly increases mortality and cellular damage [6, 7]. This temperature course should be differentiated from dysautonomic storming, another important overlooked observation that came more than 75 years later [8].

William Battle was an astute clinical observer, and we should be grateful for his observations, including the subtle ones that we seem to have forgotten. He frequently closed his lectures with a few words on management:

When we regard the large number of patients who die from cerebral injury with hemorrhage from the part of the brain lacerated, the question presents itself most strongly for answer as to the advisability of using the trephine more often in an attempt to relieve them.… The operator must be guided by his knowledge of the effect of these injuries on the brain substance, and recollect that the fatal hemorrhage will usually be over that part of the brain directly opposite to the part struck, and not immediately underneath it.

That statement rings true today.