MEDICINE

REVIEW ARTICLE

Coma After Acute Head Injury

Raimund Firsching

n 2014, 267 186 patients were admitted to German

SUMMARY
Background: Coma after acute head injury is always
I hospitals with an intracranial injury (1). Traumatic
brain injury is a common cause of death worldwide at all
alarming. Depending on the type of injury, immediate ages up to young adulthood (2, 3). This article is intended
treatment may be life-saving. About a quarter of a million
to provide an overview of the diagnosis, treatment, prog-
patients are treated for traumatic brain injury in Germany
nosis, and causative mechanisms of post-traumatic coma.
each year. Treatment recommendations must be updated
It is based on the current guideline on the treatment of
continually in the light of advancing knowledge.
head injury in adults that was issued in 2015 by the
Methods: This review of treatment recommendations, Association of the Scientific Medical Societies in Ger-
prognostic factors, and the pathophysiology of coma after many (Arbeitsgemeinschaft der Wissenschaftlichen
acute head injury is based on a 2015 German guideline for Medizinischen Fachgesellschaften [AWMF]) (4), pro-
the treatment of head injury in adults and on pertinent duced under the leadership of the German Neurosurgical
publications retrieved by a selective search in PubMed for Society (Deutsche Gesellschaft für Neurochirurgie) in
literature on post-traumatic coma. collaboration with the German societies for anesthesiol-
Results: As soon as the vital functions have been secured, ogy and intensive care, neurology, neuroradiology, and
patients with acute head injury should undergo cranial trauma surgery. Further information in this article is de-
computed tomography, which is the method of choice for rived from publications up to 2015 that were retrieved by
identifying intracranial injuries needing immediate treat- a selective literature search in PubMed for the key words
ment. Patients who have an intracranial hematoma with “unconsciousness,” “coma,” “traumatic brain injury,” and
mass effect should be taken to surgery at once. The “prognosis.” Most of the recommendations in the guide-
prognosis is significantly correlated with the patient’s age, line are not based on validated scientific evidence; many
the duration of coma, accompanying neurological mani- measures have been assigned a high recommendation
festations, and the site of brain injury. The case fatality level in the light of decades of consistent clinical experi-
rate of patients who have been comatose for 24 hours and ence, even though their efficacy cannot be demonstrated
who have accompanying lateralizing signs, a unilaterally in a clinical trial—for example, the recommendation that
absent pupillary light reflex, or hemiparesis lies between intracranial hematomas with mass effect in patients with
30% and 50%. This figure rises to 50-60% in patients with severe neurological deficits should be surgically evacu-
abnormal extensor reflexes and to over 90% in those with ated as soon as possible.
bilaterally absent pupillary light reflexes. Current neur-
opathological and neuroradiological studies indicate that The definition of unconsciousness
coma after acute head injury is due to reversible or The terms “unconsciousness” and “coma” are used
irreversible dysfunction of the brainstem. synonymously by international convention, regardless of
Conclusion: Brain tissue can tolerate ischemia and the duration of the condition (5). Both refer to a state of
elevated pressure only for a very limited time. Comatose absent perception of oneself and one’s environment,
head-injured patients must therefore be evaluated ur- from which one cannot be aroused. The Glasgow Coma
gently to determine whether they can be helped by the Scale (GCS) (6), first proposed in 1974, does not contain
surgical removal of a hematoma or by a decompressive a precise definition of coma. An international working
hemicraniectomy. group of the Neurotraumatology Committee of the
►Cite this as: World Federation of Neurological Surgeons
Firsching R: Coma after acute head injury. recommends the following clinical definition of coma:
Dtsch Arztebl Int 2017; 114: 313–20. the patient does not follow commands and does not open
DOI: 10.3238/arztebl.2017.0313 his or her eyes either spontaneously or in response to a
noxious stimulus. Spontaneous movements are
compatible with the definition of coma. In consideration
of pertinent neurological disturbances, four grades of
severity of coma have been proposed (Box 1) (7, 8).
Coma, by this definition, corresponds to a Glasgow
Universitätsklinik für Neurochirurgie, Magdeburg: Prof. Dr. med. Firsching Coma Score of 7 or less.

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BOX 1 removal of life-threatening intracranial hematomas,

the interval from the accident to the CT should be
less than one hour if possible, as hematomas can
Coma Classification of the World Federation expand over time (11, 12). There are scant evidence-
of Neurosurgical Societies* based recommendations about drugs to be given
● Grade I Coma without any of the neurological disturbances listed below during transport. The term “analgosedation”
(translation of the common German term Analgo-
● Grade II Coma with lateralizing signs, unilateral fixed and dilated pupil, sedierung) is misleading and not in general use
or hemiparesis internationally. The unconscious patient cannot per-
● Grade III Coma with pathological extensor responses ceive any internal or external stimuli and thus cannot
● Grade IV Coma with bilateral fixed and dilated pupils have pain, in the sense of a conscious, unpleasant
experience of noxious stimuli. Thus, counteracting
* Neurotraumatology Committee 1976 (7, 8) pain in coma with analgesic drugs makes little sense.
The respiratory-depressive effect of some potent
analgesic drugs can be exploited successfully in in-
dividual cases of comatose head-injured patients
who breathe against the ventilator.
Pre-hospital treatment at the scene There is no evidence from clinical trials that any
of the accident further sedation helps (4). In particular, medication
First aid for an unconscious trauma victim at the scene to reduce intracranial pressure has not been shown to
of the accident is directed toward securing the vital improve the outcome of treatment. The practical
functions (ABC = airway, breathing, circulation). disadvantage of sedation is that it impairs the
Manifest bleeding must be controlled. If the neurologi- physician’s ability to assess motor function and
cal examination reveals that the patient is comatose, a thereby detect a hemiparesis or pathological flexion
consensus of medical opinion holds that the patient and extension responses, which may indicate acute
should be intubated without delay (4, 9, 10), as clinical brainstem dysfunction. If the patient shows signs of
experience has shown that swallowing and breathing transtentorial herniation (increasing impairment of
are often impaired in comatose patients, and their air- consciousness leading to coma, fixed and dilated pu-
ways are in danger of inhalation of blood, secretions, or pils, pathological flexion and extension responses),
vomitus. The neurological examination, as described then the administration of osmodiuretics such as
below, is the basis for further interventions after arrival mannitol or hyperosmolar saline and/or hyperventi-
in the hospital. lation can acutely lower the intracranial pressure at
The Glasgow Coma Score alone is insufficient docu- the scene of the accident, during transport, or on the
mentation of the patient’s neurological condition. In an way to the CT scanner (13–15). A recommendation
unconscious patient, the pupillary responses must be to give glucocorticoids at the scene of the accident to
examined, as well as the motor function of all four patients in post-traumatic coma was issued in 1980
limbs (tested separately). The patient’s (lack of) spon- and remained in force for more than two decades; a
taneous movement, response to noxious stimuli, and study published in 2005 (16), however, showed that
any pathological flexion or extension responses are to this practice is contraindicated, as it is associated
be noted. These findings are crucially important, as with significantly higher mortality. 10% of comatose
they have a bearing on the differential diagnostic brain-injured patients also have cervical spine in-
considerations in patients with injuries of the brain and juries. It is thus recommended in many guidelines
spinal cord. Post-traumatic coma is often due to a brain from around the world (1982 to present) that the cer-
lesion, but it can also be due to an intoxication, vical spine of all patients found in a coma should be
endocrine or metabolic disturbances, hypoxia, brain immobilized prophylactically with a hard collar (4).
hemorrhage, or other causes (4).
In-hospital treatment of the comatose
Transport of the comatose patient head-injured patient
The comatose patient, when first seen, should be The method of choice for detecting intracranial
assumed to have a potentially life-threatening injuries is head CT. Spiral CT of the entire body is
dysfunction of the brain and should therefore be practical, as there is generally no other way to
transported immediately to a hospital in which exclude further, extracranial injuries in comatose
computerized tomography (CT) and neurosurgical patients (4). This study takes less time than conven-
treatment are available around the clock. Magnetic tional x-rays while giving more information.
resonance imaging (MRI) should also be available, The CT should be obtained as soon as the patient
because there may be an accompanying spinal cord arrives in the hospital, except when the vital signs,
injury, and MlRI should be possible for intubated circulation, or breathing require immediate life-
patients. If there is more than one suitable hospital in saving attention. The care of polytraumatized pa-
the area, the shortest transport time (not distance) tients should be interdisciplinary. The sequence of
determines the choice. For the timely and successful treatment of multiple injured organ systems is based

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a b
Figure 1: Head CT and MRI in patients with traumatic brain injury.
a) This 42-year-old woman (physician) was comatose 3 hours after
an accident, with acute pathological extensor responses. The CT
shows an epidural hematoma. She awakened promptly after
surgical removal of the hematoma.
b) This 20-year-old man fell, remained mentally lucid, and went
home; a few hours later, he was found unconscious in bed with
fixed and dilated pupils. The CT shows an epidural hematoma,
which was removed immediately, like the one in (a).
c) After surgery, he remained comatose and his pupils remained
fixed and dilated. The MRI shows increased signal intensity
throughout the brainstem, evidently reflecting a pathological
abnormality that arose secondarily, after the lucid interval, as a
result of sustained pressure on the brainstem arising from the
epidural hematoma. The superiority of MRI to CT in this case is
clear, as the lethal brainstem injury cannot be seen in the CT in
(b), just as the CT in (a) cannot show the absence of a brainstem
lesion.
c

on urgency; more than one operation can be There has not yet been any documentation of
performed at the same time if necessary. better outcomes from treatment guided by ICP or
The current literature does not indicate that any CPP measurement, compared to treatment guided by
further sedating or intracranial-pressure-lowering clinical neurological surveillance without any ICP or
drugs given to the unconscious patient improve the CPP measurement (19–21). A consensus holds that
outcome. Barbiturate coma was said to do so (17), intracranial hematomas with mass effect should be
but this was not confirmed by a comprehensive surgically evacuated without delay (4). For penetrat-
analysis (18). Sedation to secure the airway may be ing injuries, and injuries of the frontal skull base with
needed for practical reasons. CSF leakage, it may be advisable not to proceed to
Invasive intracranial pressure (ICP) monitoring surgical repair immediately, as acute post-traumatic
can provide a useful early warning of rising ICP; if it brain edema increases the operative risk. The most
is performed via an intraventricular catheter, the ICP effective way to lower ICP is decompressive hemi-
can be lowered by drainage of cerebrospinal fluid craniectomy (22). Even though the utility of this
(CSF). Maintenance of the cerebral perfusion measure with respect to outcome is debated, and
pressure (CPP, defined as the difference between sequelae after reimplantation of the skull flap are not
mean arterial blood pressure and intracranial uncommon, there is nonetheless convincing evidence
pressure [ABP – ICP]) in the normal range is ef- in its favor from observations made in individual
fected mainly by avoiding arterial hypotension, cases.
rather than by lowering the ICP with drugs. In criti- Surgery for accompanying injuries that are not
cal situations, drugs often do not suffice to lower the life-threatening should be deferred until the patient
ICP adequately. has recovered sufficiently from the head injury to be

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BOX 2 grade II, and more than 3 weeks for grade III. This
grading system has been found to be prognostically
relevant, particularly with respect to the return to
Classification of traumatic brain injury according to work, but it is retrospective and thus not applicable
MRI findings* in the acute phase.
● Grade I Exclusively supratentorial injury without any brainstem injury. The ultimate outcome of patients who are coma-
tose after a traumatic brain injury is significantly
● Grade II Unilateral brainstem injury at any level, with or without an additional correlated with their additional neurological
grade I injury. disturbances in the first 24 hours. Mortality is over
● Grade III Bilateral midbrain injury with or without an additional grade II injury. 90% if both pupils are fixed and dilated, 50–60 % if
● Grade IV Bilateral pontine injury with or without an additional grade III injury. there are pathological extensor responses, 30–50% if
a single pupil is fixed and dilated, and 5–10% if
* from Firsching et al. (32); MRI, magnetic resonance imaging none of these are the case (11). The duration of coma
can be determined reliably only if sedating drugs are
given in no higher doses than needed for the patient
to tolerate mechanical ventilation. Under these
circumstances, long-term follow-up studies have
shown that a 20-year-old patient who has been
TABLE unconscious for 18 days has the same low chance of
Classification of traumatic brain injury according to CT findings*
survival (5%) as a 75-year-old patient who has been
unconscious for only 5 days. Thus, age (e3) and the
Grade CT findings duration of coma are of major prognostic signifi-
Diffuse injury, grade I normal cance. An initially comatose patient who regains
Diffuse injury, grade II cisterns preserved, midline shift <6 mm,
consciousness once an epidural hematoma has been
contusions <25 cm2 removed has a much better prognosis than a patient
in persistent coma.
Diffuse injury, grade III cisterns narrowed
Marshall et al. 1991 (e4) proposed a classification of
Diffuse injury, grade IV midline shift >5 mm, surgically evacuated posttraumatic CT findings for use in prognostication
hematoma, or hematoma >25 cm2
(Table), yet no clear correlation has been found be-
* modified from (15); CT, computerized tomography tween the CT findings of initially comatose patients
and the outcome of their treatment (Figure 1). There is
likewise no clear correlation between the extent of
brain contusions seen in CT and the outcome (28, 29).
considered stable (23). Induced hypothermia as a Somatosensory evoked potentials (SSEPs) are
treatment for patients with traumatic brain injury prognostically significant: if the SSEPs are
has been studied repeatedly over the past five bilaterally absent, the mortality is 80–90% (e5–e7).
decades, but no benefit has ever been convincingly Pioneer studies performed decades ago already
shown (24, e1). There is likewise insufficient suggested that the ICP was of lesser prognostic sig-
evidence supporting the utility of hyperbaric nificance than the patient’s clinical condition (30).
oxygen therapy (e2). Multiple studies performed since then have not modi-
fied this conclusion. No clear correlation has been
The prognosis of patients with post-traumatic found between mildly or moderately elevated ICP
coma values and the ultimate morbidity or mortality of
In the early phase after traumatic brain injury, the brain-injured patients. It is true, however, that
patient’s emergence from coma is just as unpredict- persistently and markedly elevated, life-threatening
able as a sudden worsening of consciousness from ICP that cannot be pharmacologically lowered is
fully alert to comatose. As a rule, it is not possible to correlated with increased mortality (31).
prognosticate reliably on clinical grounds alone in MRI reveals traumatic lesions in the brain
the first 24 hours after injury. An early clinical (particularly the brainstem) in much greater detail
classification of traumatic brain injury as mild, than CT (Figure 1) and is thus more useful for
moderate, or severe, determined on the basis of the prognostication (32). It is more time-consuming,
Glasgow Coma Score at the time of the accident or however, and it is no better than CT at showing the
at variable times thereafter (6, 12, or 24 hours), is bony and intracranial traumatic lesions that require
internationally in widespread use but has not been surgical treatment (4).
found to be adequately correlated with outcomes and It has only become clear since the advent of MRI
therefore provides no practical help (25, 26). that brainstem lesions are of major prognostic
In Germany, traumatic brain injury is commonly significance with respect to mortality, as well as
classified as grade I, II, or III (27) on the basis of the morbidity in surviving patients (32) (Box 2). The
duration of the post-traumatic neurological distur- MRI findings can be used for a four-level classifi-
bance: up to 4 days for grade I, up to 3 weeks for cation of the severity of traumatic brain injury:

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a b
Figure 2: Head CT and MRI scans of a 12-year-old girl who was
struck by an automobile while crossing the street and was imme-
diately rendered unconscious, with a fixed and dilated right pupil.
a) This CT scan was obtained within 2 hours of the injury: at this time,
both pupils were fixed and dilated. There is a right frontotemporal
subdural hematoma of the same width as the calvaria, as well as a
small right temporal hemorrhagic contusion and very marked right-
to-left shift of the midline structures, mainly due to swelling of the
right hemisphere. These findings would be classified as grade IV in
the scheme of Marshall et al. 1991 (e4). A short time after this image
was taken, an extensive right hemicraniectomy was performed,
along with removal of the acute subdural hematoma.
b) and c) MRI on day 2 shows a large right temporal contusion, but
no brainstem injury.
c

● grade I (no brainstem lesion) hematoma can be followed by a lucid interval and then
– seen in 39% of comatose patients by acute coma that resolves when the hematoma is
– mortality, 4.5% removed (33) has been explained as reflecting
● grade II (unilateral brainstem lesion) reversible brainstem dysfunction due to compression
– seen in 22% of comatose patients (34). Another concept of the organic cause of coma
– mortality, 15.9% arose from the histopathological observation of
● grade III (bilateral midbrain lesions) massive neuronal injury, with axonal lesions extending
– seen in 19 % of patients far into the white matter of the cerebral hemispheres.
– mortality, 23.5% From 1982 onward, diffuse axonal injury was consid-
● grade IV (bilateral pontine lesions) ered to be the cause of post-traumatic coma, when the CT
– seen in 20% of comatose patients showed no hematoma exerting a mass effect, and the
– mortality, 97.3%. patient remained comatose for 6 hours or more after the
69% of patients with a grade I injury survived with- trauma. It was concluded from multiple histopathological
out functional impairment, while only 25% of patients case reports that brainstem injury was rare and not the
with a grade II injury did. Not one patient with a grade cause of coma (35, 36). Coma was attributed to damage of
III or grade IV injury survived without functional im- neural pathways that ascend from the brainstem in the set-
pairment. ting of diffuse axonal injury to the hemispheric white
matter. With this concept maintaining the upper hand, the
The pathophysiology of coma contrary notion that coma, pupillary areflexia, and
Experts disagree little with regard to the diagnostic pathological extensor responses are signs of brainstem
evaluation, treatment, and prognosis of comatose head- damage was vehemently disputed as recently as 2002 (the
injured patients, yet much controversy surrounds the “brainstem damage saga”) (37).
question, “Which brain structures are responsible for Other teams of researchers, however, reported
coma?” The longstanding observation that an epidural neuropathological findings that conflicted with this

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d e

f g
Continuation of Figure 2:
d) and e) Two weeks later, follow-up CTs show persistent brain swelling, with incipient resorption of the hemorrhagic contusion.
f) and g) Six months later, before the skull flap was surgically reinserted, follow-up MRI shows a large right temporo-occipital tissue defect.
At this time, the patient has a moderately severe left visual field defect, but no other neurological deficits. She is back at school in her
Gymnasium (academically-oriented German secondary school): she is reportedly doing poorly in mathematics and has difficulty with spatial
processing, but her language ability is above average. Coma and pupillary areflexia at the time of the injury are best explained as reflecting
acute, but reversible brainstem dysfunction, due to the pressure that was exerted mainly by the swelling of the brain contusion and, to a
lesser extent, by the subdural hematoma. The mass effect was rapidly and successfully reduced by hemicraniectomy, preventing
irreversible structural damage to the brainstem.

interpretation (38), including findings from patients who of brainstem dysfunction) were indeed significantly
had remained comatose from the time of the accident until correlated with structural brainstem lesions seen on MRI.
death: all, without exception, had brainstem injuries (39). Thus, current evidence suggests that post-traumatic
This histological evidence was further supported by a coma is due to brainstem dysfunction rather than
prospective study involving serial MRI scans in comatose hemispheric axonal disruption (40). This conclusion is of
patients (32). A statistically significant correlation was practical significance: there is no way to reconnect torn
found between coma and brainstem lesions in the first 8 axons, but brainstem compression can be counteracted by
days. All patients who did not emerge from coma within 8 lowering the ICP (Figure 2). If needed, a far more effective
days had structural brainstem damage on MRI. An associ- way to lower ICP than any drug treatment is the surgical
ation of bilateral pontine injury with especially high evacuation of a hematoma that is exerting a mass effect,
mortality (over 90%) was described for the first time. and/or an extensive decompressive hemicraniectomy.
Moreover, pupillary areflexia and pathological flexor and These options should be available to all patients who are
extensor responses (traditionally considered clinical signs comatose after an acute traumatic brain injury.

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10. Maryglothling J, Duane T, Gibbs M, et al.: Emergency tracheal intubation

KEY MESSAGES
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dysfunction and should therefore be taken immediately subdural hematomas. Neurol Res 1997; 19: 257–60.
to a hospital where computerized tomography (CT) and 13. Bulger EM, May S, Brasel KJ, et al.: Out-of-hospital hypertonic resusci-
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tient’s emergence from coma is just as unpredictable as equiosmolar doses of mannitol and hypertonic saline on cerebral blood
a sudden worsening of consciousness that may put him flow and metabolism in traumatic brain injury. J Neurotrauma 2011;
28: 2003–12.
or her back in coma.
15. Wakai A, McCabe A, Roberts I, Schierhout G: Mannitol for acute
● The most effective way to lower elevated intracranial traumatic brain injury. Cochrane Database Syst Rev 2013; 8:
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Acknowledgement Cochrane Database Syst Rev 2012; 12: CD000033.
I am very grateful to Professor Skalej, chief of neuroradiology, for generously 19. Chesnut RM, Temkin N, Carney N, et al.: Trial of intracranial-pressure
supplying the impressive radiological images reproduced here and for his monitoring in traumatic brain injury. N Engl J Med 2012; 367: 2471–81.
scientific assistance in our clinical work.
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Dedication CD002043.
This article is dedicated to Professor Frowein, emeritus chief of neurosurgery
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indicating that bilateral brainstem injury rather than widespread www.aerzteblatt-international.de/ref1817

CLINICAL SNAPSHOT
Periungual Fibroma
An 86-year-old woman presented with a slowly growing,
painless, smoothsurfaced mass on the left third toe,
measuring ca. 1.0 × 0.5 × 0.5 cm). The mass was surgically
resected. Histological examination revealed a storiform
dermal tumor (i.e., one with a rope-like or whorled
configuration) consisting of spindle cells without atypia or
mitoses. This a periungual fibroma, a benign mesenchymal
Periungual fibroma of the left third toe. tumor. Multiple periungual fibromas may be a sign of the
tuberous sclerosis complex (TSC), which is due to a
mutation in the TSC1 or TSC2 gene. TSC is an autosomal dominant disease whose major symptom is epilepsy due to
lesions in the brain. Our patient had no such lesions.

Prof. Dr. med. Uwe Wollina, Klinik für Dermatologie und Allergologie, Krankenhaus Dresden-Friedrichstadt, Städtisches Klinikum,
Akademisches Lehrkrankenhaus der TU Dresden

Conflict of interest statement: The author states that he has no conflict of interest.

Cite this as: Wollina U: Periungual fibroma. Dtsch Arztebl Int 2017; 114: 320. DOI: 10.3238/arztebl.2017.0320

Translated from the original German by Ethan Taub, M.D.

320 Deutsches Ärzteblatt International | Dtsch Arztebl Int 2017; 114: 313–20
 MEDICINE

Supplementary material to:

Coma after Acute Head Injury
Raimund Firsching
Dtsch Arztebl Int 2017; 114: 313–20. DOI: 10.3238/arztebl.2017.0313

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