Surgical Treatment of Traumatic Brain Injury
Maliawan S, Golden N, Mahadewa T, Niryana W
Dept. of Neurosurgery, School of Medicine. University of Udayana. Sanglah Academic Hospital. Bali. Indonesia
Objective:The aim of this study is to analyze the surgical indications for the treatment of post-traumatic intracranial hematoma and to evaluate the role of external decompression in the management of post-traumatic intra-cranial hypertension.
Review: Conservative management of traumatic intra-cranial hematoma is still an important part of treatment, especially when during admission the surgical intervention is uncertain. Hematoma might evolve overtime, and surgical intervention might not necessary. Regular and periodical clinical evaluation would have to be conducted and that is to look for early surgical indications.
A significant number of patients, harboring small/ minimal epidural or subdural hematomas for instance with lesion thickness less than 10 mm or midline shift less than 5 mm, could be managed conservatively. The current neurosurgical practices had revealed that a large number of post-traumatic hematoma patients were operated on either within 24 hour for acute subdural hematoma as prevailing lesion, or later for parenchymal hematoma as the prevailing lesion. According to recent European Study, about one third of these patients (with minimal hematomas) had undergone surgical decompression as well, although the evidence base of this procedure in term of improving the outcomes, was still uncertain.
Summary: Surgical intervention is still a frequent treatment modality chosen in the management of post-traumatic intracranial hematoma, although it is barely supported by level 2 evidence base studies. Bone flap decompression should be considered, when other modalities of treatment to lower/ decrease intracranial pressure had failed.
Introduction
From 100 to 350 patients per 100 000 inhabitants per year are admitted to hospital care following a traumatic brain injury (TBI) all around the world [1]. About 80% of these patients are classified as mild head injury [Glasgow Coma Scale (GCS) 14 15], 10% as moderate (GCS 9 13) and 10% as severe head injuries (GCS <9). The development of an intracranial posttraumatic hematoma complicates 25 45% of severe TBI, 3 12% of moderate TBI and 1 3% of mild TBI. As many as 100 000 patients per year may require surgical management of a posttraumatic intracranial hematoma in the United States alone [2__]. The results of surgical management vary with the type of hematomas: already in 1982 it was reported that patients treated with an admission GCS from 3 to 5 have a mortality of 74% in the case of subdural hematoma, of 50% in the case of intraparenchymal lesions and of 36% in the case of epidural hematomas [3]. In the same years it was shown that with a good neurotrauma organization and with timely evacuation, mortality in epidural hematomas could have been zero in the future [4]. Unfortunately this was not the case and even contemporary reports from Europe show a mortality from 6% (pure epidural hematomas) to 33% (cases with associated lesions) [5]. Furthermore, observational studies show different attitudes toward indications for surgery and decompressive craniectomies in posttraumatic intracranial hematomas both in Europe [6__] and in the USA [7].
Background
no patients with large posttraumatic hematoma will be randomized to a nonsurgical arm in a level I study. Therefore, although ranking surgicalevacuation of large posttraumatic hematomas as an
option would be consistent with guidelines methodology, it may not be consistent with the best medical practice [10]. A multicenter observational study showed in fact that the current practice is emergency surgical evacuation in 93% of cases of large subdural hematomas [6__]. There are, however, uncertainties concerning surgical indications in small extracerebral hematomas and concerning any kind of posttraumatic intraparenchymal damage.
General considerations
series of 404 patients operated within 24 h from injury, acute subdural hematomas isolated or in combination with brain contusions still constituted 69% of all patients and 72% of patients with hematoma evacuation plus emergency bone decompression [6__]. Nevertheless patients with small hematomas (<10mm) and with midline shift under 5mm may be managed conservatively [17]. We have learned that with the increased availability of emergency care on the scene of accidents, patients are studied much earlier with CT being obtained in some within an hour from injury. In these circumstances a very early CT can show a hematoma in evolution. Differently from epidural hematomas, acute subdural can enlarge but also disappear [18]. In comatose patients with small subdural hematomas an intracranial pressure (ICP) monitoring can guide a careful conservative management [19].
Specific considerations for traumatic parenchymal lesions Data from the series already cited published from the European Brain Injury Consortium [6__] show how intraparenchymal posttraumatic hematomas constitute (in contrast to subdural hematomas) the lesion most frequently (73%) evacuated at some distance from injury.
In the absence of well accepted guidelines [13], the surgical decisions are based on the appearance of clinical deterioration, of CT evolution or rise in ICP. In contemporary practice such events are usually awaited before a decision is made [6__]. The occurrence of a clinical [20] and radiological [12] worsening has a negative impact on outcome and it could be of utmost importance to identify patients at risk in an earlier stage. Three recent papers [21_,22,23_] addressed the question of enlargement of brain contusions. Most of the patients (>70%) showing radiological deterioration are admitted in a clinical condition of mild moderate head injury [21_,23_]. The presence of traumatic subarachnoid hemorrhage on an admission CT is a powerful predictor of contusional evolution as well as the contusional volume on admission [21_,23_] with the highest risk in lesions between 5 and 25 cm3 [21_]. Older age, sex (men) and coagulation disorders seem also to be related to lesion evolution [22]. Conclusions on surgery of posttraumatic hematomas In spite of the absence of class I paper, guidelines have been published [2__] about surgical management of TBI. A conservative management of selected cases is possible but only when patients with uncertain surgical indications are admitted to neurosurgical centers. The hematomas may evolve over time and the indication for surgery is a dynamic process that can also change over time. This implies, at least in Europe, a new discussion about patients centralization. A recent British paper[24__]demonstrated worse outcomes in TBI patients admitted to non-neurosurgical
This selection must contain all possible surgical candidates. The lesson learned recently is that neither a good clinical status on admission nor a small hematoma on the first obtained CT scan can exclude subsequent surgical indications. Decompressive craniectomy for treating high intracranial pressure ICP is the most frequent cause of death and disability after severe TBI. When high ICP is not related to evacuable mass lesions, such as in patients with massive unilateral or bilateral brain swelling (diffuse brain injury type III and IV of the Marshall classification), medical treatment is frequently ineffective in controlling ICP.
The treatment of increased ICP is generally based on the algorithm proposed by the Brain Trauma Foundation Guidelines (BTFG). In summary, a set of general maneuvers are used (head elevation, normothermia, volume resuscitation, sedation) [26]. If these general maneuvers fail, first line therapeutic measures are started. These measures include cerebrospinal fluid drainage, moderate hypocapnia (PCO2 30 35mmHg) and osmotic therapies. When these first line measures fail to control ICP, only a few therapeutic options are available unless potentially evacuable mass lesions are found in the CT scan. In this situation, second tier measures should be considered.
These include high dose barbiturates, intense hyperventilation (PCO2 <30mmHg), hypertensive management, mild or moderate hypothermia and decompressive craniectomy. Of these only barbiturates have reached the level of guideline [26] while the remaining second level therapies are considered options, defined by the BTFG as strategies for patient management for which there is unclear clinical certainty about their use [27].
Background
rationale for decompressive craniotomy is that by removing a variable amount of bone we are able to convert the skull from a closed box with a finite volume into an open one [29].
craniotomy, with dura opening and large duraplasty, is the best way to achieve this goal. Yoo et al. [38] evaluated the efficacy of bone decompression alone in a cohort of 22 patients who underwent bilateral decompressive craniotomy to treat high ICP after either TBI or stroke. In this study the authors monitored ICP before surgery, after bone decompression and after opening the duramater. They clearly showed that the maximum ICP reduction was achieved only after opening the duramater [38]. This pivotal study quantified ICP reduction and therefore provides evidence to support opening the duramater in patients undergoing decompressive surgery. Large bone decompression without opening the duramater has to be considered suboptimal. Although this type of procedure might work in children, we do not recommend it. Duraplasty may be carried out with autologous fascia, heterologous tissue or any other material. Despite that we do not have evidence to prove the superiority of any of these materials in particular, we prefer to use lyophilized heterologous grafts. The removed bone flap should be stored frozen at _808C in sterile conditions. This is a much better option than storing it in the subcutaneous abdominal fat. In our opinion the bone flap should be replaced as early as possible after decompression to avoid the trephine syndrome and to permit early rehabilitation in order to maximize the possibilities of a favorable outcome. Complications of decompressive craniectomy Doubts about the benefits of decompressive craniectomy are influenced by its potential adverse effects, such as increased brain edema, subdural collections, cerebrospinal fluid leakage, hydrocephalus or brain infarctions that might occur early after surgery and the much more frequent complications observed at the time of bone flap replacement. In a recent study, Skoglund et al. [37_] reported that half the patients who underwent decompressive craniectomy had some complications, most of them after bone replacement. It is important to remember that repositioning of the bone flap in these fragile patients has a number of complications that have been underreported, such as epidural collections, local infections, hydrocephalus, cerebrospinal fluid leakage or bone flap resorption. Among them, the most important is infection of the bone flap, requiring its removal and repeated cranioplasty [39].
Conclusion
patients with a devastating neurological injury and predictable poor outcome, such as patients with radiological signs of brainstem damage or very severe diffuse axonal injury.
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