 |
|
||||
| Home | Login | |||||
| About | Editorial board | Articles
|
NSI Publications
|
Search | Instructions | Online Submission | Subscribe | Videos | Etcetera | Contact |
|
||||||||||||||||||||
|
|
|
Post-traumatic subarachnoid hemorrhage: A review
Correspondence Address: Source of Support: None, Conflict of Interest: None DOI: 10.4103/0028-3886.178030
Head injury has been the leading cause of death and disability in people younger than 40 years and the incidence is rising continuously. Anticipation of the pathological consequences of post-traumatic subarachnoid hemorrhage (tSAH) and an outcome-oriented management are very important in these cases. To encounter the complications pertaining to traumatic brain injury (TBI) and tSAH, various classifications have been proposed and goal-oriented screening strategies have been offered. The role of serial computed tomography (CT) scans, perfusion studies, transcranial Doppler, magnetic resonance imaging (MRI), and angiographic studies as diagnostic tools, has been described. Recently, MRI fluid-attenuated inversion recovery (FLAIR), gradient reversal echo (GRE), and susceptibility weighted imaging (SWI) have emerged as excellent complimentary MRI sequences, and the authors of this article have evaluated their role in the diagnosis and prognostication of patients with tSAH. Numerous studies have been conducted on the various complications associated with tSAH such as vasospasm, hydrocephalus, and electrolyte disturbances and their management. This article discusses these aspects of tSAH and their management nuances. Keywords: Diagnosis; epidemiology; management; pathogenesis; post-traumatic subarachnoid hemorrhage
Traumatic brain injury (TBI) is a daunting challenge faced by neurosurgeons from all over the world. Among the wide spectrum of injuries included in TBI, traumatic subarachnoid haemorrhage (tSAH) is one of the leading causes of morbidity and functional impairment.The incidence of tSAH varies from 26% to 53% in patients with TBI. [1] Road traffic accidents account for approximately 59% of TBIs, and it is estimated that with this trend, it will be the fifth leading cause of death in India by the year 2030. The incidence of head injury varies from 67 to 317 per 100,000 individuals, and the mortality rate ranges from approximately 4%-8% for moderate injury to approximately 50% for severe head injury. [2] Subarachnoid hemorrhage (SAH) is an integral component of TBI, and trauma is the most common cause of SAH. tSAH was first defined by Wilks as "sanguinous meningeal effusion" in 1859. [3] Eisenberg evaluated the CT scans of 753 patients with severe head injury. He discovered that the CT findings most often related to abnormal intracranial pressure (ICP) and to death were a significant midline shift, compression, or obliteration of the mesencephalic cisterns, and the presence of subarachnoid blood. [4] According to Greene et al., however, shift of the midline structures was not found to be a significant variable. [5] tSAH doubles the mortality rate in patients with TBI. Basal cisternal tSAH has a positive predictive value of 70% for a bad outcome. [1] Hence, one cannot deny the fact that tSAH, either in isolation or in combination with other brain injuries, contributes significantly to the final outcome. tSAH-induced vasospasm, dyselectrolemia, pituitary or hypothalamic dysfunction, and hydrocephalus may be the cause of poor outcome in these patients. Previous studies such as the Head Injury Trial (HIT) 1 and 2 and the Cochrane review (2003) found that patients with tSAH had a poorer prognosis and a worse outcome. They categorized the patients with tSAH into a separate category in HIT 3 and 4 to study the effects of tSAH on the final outcome, but the results of HIT 4 were only partially published. Therefore, neurosurgeons are faced with persistent diagnostic and prognostic challenges related to tSAH in their day-to-day clinical practice. Many large multicentric trials on tSAH have been conducted utilizing different clinical parameters. The factors responsible for a poor outcome still remain relatively undetermined. In the present study, we have attempted to review the previous trials and have also tried to study the predictive value of various clinical parameters and different MRI (FLAIR, diffusion weighted imaging [DWI], SWI, GRE) sequences in the prognostication of tSAH. It has been noted that even a small, isolated, sulcal SAH was associated with a poor Glasgow coma scale (GCS) score at presentation. A poor outcome following a diffuse SAH is understandable but when associated with a small sulcal SAH is difficult to explain. This study, therefore, attempts to review the unchartered territories associated with tSAH.
In India, more than 1 million accidents occur every year that lead to more than 1,50,000 deaths per year (as per the 2011 statistics). The overall rate is one accident per minute and one death in every 4-5 minutes. Nearly 350 people die due to road traffic accidents in India per day. Per 1 million kilometers driven, there are six deaths in India. In total, 60% of all cases of head injury in India are caused by road traffic accidents. The fatality rate is 70 per 10,000 vehicles, which is 30 times higher than that in the United States. The incidence of alcohol related injuries constitutes 15%-20% of the total head injuries. Of the victims classified as "severely injured" in road traffic accidents, 76% have an associated head injury. [6] In the United Kingdom, approximately 1.4 million patients per year suffer from head injuries. In the United States, more than 1.7 million people present to the emergency department (ED) with TBIs each year. Approximately 52,000 people die, 275,000 are hospitalized, and 1.4 million are evaluated and discharged from the ED. [7]
The incidence of tSAH varies from 2.9% to 53% in different series. González Pérez et al., Mattioli et al., and Sinha et al., reported the incidence of SAH in head injury as being 53.06%, 61%, and 13.06%, respectively. Wong et al., stated an incidence of 61% in head injured patients admitted to intensive care units (ICUs). In the NIMHANS series, the incidence was 2.9% in their patients with a mild head injury [Table 1].
Specialized scores used to classify tSAH are as follows:
The etiology of tSAH is unknown but the possible mechanisms are as follows: (1) rotational acceleration causing short-lasting oscillatory movements of the brain; (2) vertebrobasilar artery stretch due to hyperextension; (3) sudden rise of intra-arterial pressure from a blow to the cervical carotid artery; (4) tearing of the bridging veins or pial vessels; and, (5) diffusion of blood from contusion into the subarachnoid space. Sometimes, no cause can be found. [3] SAH can be found associated with contusion and subdural hematoma, spreading outwards from lacerations and around penetrating injuries. tSAH can occur over the ventral surface of the brain stem (basilar SAH). After SAH, cerebrospinal fluid (CSF) shows a polymorphonuclear response within 24 hours, which becomes prominent by 48 hours. After 48 hours, lymphocytes and macrophages start replacing the polymorphonuclear leucocytes. Macrophages phagocytose red blood cells (RBCs), and such lipid-laden phagocytes may persist for years in the arachnoidal meninges and the Virchow-Robin spaces. tSAH may impair the absorption of CSF and may produce hydrocephalus. Post-traumatic vasospasm (PTV) is a significant secondary insult to the injured brain. It typically develops between 12 hours and 5 days after the injury and lasts between 12 hours and 30 days. It can also occur in a more delayed manner and may involve both anterior and posterior circulation arteries. Martin and colleagues have suggested three different circulatory stages after severe head injury: Phase I (hypoperfusion), phase II (hyperemia), and phase III (vasospasm). [15] Phase I: This stage occurs on the day of injury (day 0) and is defined by: (1) a low cerebral blood flow (CBF); (2) normal middle cerebral artery (MCA) velocity; (3) normal hemispheric index (ratio of MCA velocity to internal carotid artery velocity); and, (4) normal arteriovenous difference of oxygenation (AVDO). Phase II: This stage occurs between days 1-3: (1) the CBF increases; (2) the AVDO falls; (3) the MCA velocity rises; and, (4) the hemispheric index remains less than 3. Phase III: This stage occurs between days 4-15: (1) there is a fall in CBF; (2) there is further increase in MCA velocity; (3) there is a significant rise in the hemispheric index. [15] The mechanism of vasospasm is poorly understood. tSAH may occur at different sites and may have a varying time course as compared with aneurysmal SAH (aSAH). It may involve the supratentorial, convexity, sulcal, and interhemispheric spaces. In tSAH, PTV occurs early and resolves earlier than in an aSAH. PTV is not always associated with significant SAH and has been noted in patients with extra-axial hematomas or even without any radiographic evidence of SAHs. [2] Jung et al., concluded that after SAH, glutamate, glutamine, glycine, and histidine might be analysed in CSF as markers for arteriographic cerebral vasospasm. Serum S100B, but not neuron specific enolase, was associated with delayed cerebral ischemia, but did not correlate with angiographic vasospasm. These results need to be validated in a larger prospective cohort. [16]
Neurological examination should evaluate the level of consciousness, pupillary size and reaction, motor responses, and reflexes. Trauma to the spinal cord, chest, and abdomen should be ruled out. [17] It should be followed by immediate radiological and essential blood investigations. The most frequently used diagnostic test is non-contrast CT scan of the brain. Radiation hazards and beam hardening effects are some of the disadvantages of the CT scan. [18] In the author's study, tSAH was found maximum in a mixed pattern involving the cerebral hemispheres and the basal cisterns (39.31%), the cortical sulci (33.33%), followed by the interhemispheric space (11.96%). [10] The maximally affected population was composed of patients aged between 21-30 years, especially male patients (90.56%), with the most common etiopathogenetic factor being road traffic accidents. [11] Functional imaging Positron emission tomography, MRI, and magnetic resonance spectroscopy are able to assess both perfusion and cerebral metabolism. These are helpful in defining the extent of injury and ischemia, and in predicting outcome. [18] Fluid attenuated inversion recovery (FLAIR)/gradient reversal echo (GRE)/susceptibility weighted imaging (SWI) sequences of MRI have a good sensitivity for the detection of acute SAH in the first 48 hours, and are complimentary to the CT scans [11] ; however, they are not suitable for a rapid assessment of head injuries. SAH can be diagnosed by SWI sequences by its dark signal intensity, surrounded by the CSF signal intensity. It is better than a CT scan in detecting intraventricular hemorrhage and a very small amount of SAH [Figure 1], [Figure 2], [Figure 3] and [Figure 4]. [19] The authors of this article are currently studying the prognostic value of different sequences of MRI in tSAH. The preliminary findings have suggested a better delineation of tSAH in the sulcal and tentorial regions (76.62%) using an MRI (FLAIR and GRE sequences) when compared with a non-contrast CT scan of the head (50.65% and 41.56%, respectively). These observations have been more pronounced in the presence of an intraventricular haemorrhage (IVH) and tSAH in the basal cisterns, where MRI was significantly better than the CT scan (22.08% vs. 9.09% and 31.17% vs. 12.99%, respectively) for diagnosing these entities. SWI sequences have been recently added to the study protocol of Agrawal et al., on seeing its benefits in the detection of tSAH. [11] Very rarely, spontaneous resolution of SAH has also been noted. [20]
The patient should be managed in a specialized neurosurgical center. Bladder catheterization, early enteral nutrition, analgesia, and antiemetic and antiepileptic medication are essential in the initial part of the treatment. [17] The general intensive care includes keeping the patient's head elevated, avoiding compression of the neck veins, frequent turning of the patient, physiotherapy, and mouth, bowel, and bladder care. [21] According to Bullock et al., management of tSAH should be targeted at avoiding secondary injury, [2] maintainance of cerebral perfusion pressure, optimizing cerebral oxygenation, and multimodality monitoring to achieve therapeutic targets. [7] Apart from baseline monitoring, the intensive care unit care should include intracranial pressure, jugular bulb venous oxygen saturation, and brain tissue oxygen tension monitoring; cerebral microdialysis; transcranial Doppler ultrasonography; mechanical ventilation; hemodynamic support; hyperosmolar therapy; Lund therapy; stress ulcer prophylaxis; and rarely, barbiturate coma for control of the raised intracranial pressure.
Fluids and electrolytes Electrolyte disturbances are frequently seen in the presence of tSAH. The hypothalamic-pituitary axis damage is a major contributing factor. The goal is to maintain euvolemia to moderate hypervolemia. Normal saline (NS) is the recommended solution. Hypotonic solutions, such as ½ NS, ¼ NS, 5% dextrose in water (D5% W), D5% ½ NS, D5% ¼ NS, or Ringer's lactate, should be avoided. In severe TBI patients with increased ICP or brain edema, a serum sodium (Na + ) level of up to 150-155 mEq/L may be acceptable. Hyponatremia is a major secondary systemic brain insult as it leads to exacerbation of brain edema. It is usually secondary to cerebral salt wasting syndrome, or to the syndrome of inappropriate antidiuretic hormone secretion. In the former, both volume and sodium correction are the essential components, whereas in the latter, fluid restriction usually suffices, with or without sodium correction. Hence, central venous pressure monitoring, renal function tests, and a periodic estimation of electrolytes are of paramount importance. Vasospasm Traumatic vasospasm ranges from 19% to 68%, but the exact incidence remains unknown. Zubkov et al., noted an increased incidence of vasospasm (measured by a transcranial Doppler [TCD] study) in traumatic epidural and subdural hematomas, but not with intracerebral or intraventricular hemorrhage. Gaetani et al., did not find any correlation between the Fisher grading and the initial presentation, and stated that the presence of vasospasm was predictive of the Glasgow outcome score at 6 months. Only 3.9%-16.6% of patients with tSAH with delayed radiographic or TCD-diagnosed cerebral vasospasm develop referable neurological deficits, compared with 17%-40% of patients with vasospasm secondary to aSAH. Hypertension and hypervolemia, the mainstays of treatment of vasospasm associated with aSAH, must be rationally used in tSAH. These agents may be dangerous in tSAH and can worsen cerebral edema, which is a more significant issue in TBI than in aSAH. [22] Calcium channel blockers have shown some promise in decreasing the mortality or severe disability in patients with tSAH, but their mechanism of action has not been completely established. [23] The usual dose is 60 mg every 4 hourly for 21 days. A 2003 Cochrane review reported an improved outcome with nimodipine in these patients; however, because the results of Head Injury Trial (HIT) 4 were only partly presented, there is still controversy regarding whether or not patients with tSAH should be treated with this drug. The findings by Vergouwen et al., do not lend support to the finding of a beneficial effect of nimodipine on the outcome in patients with tSAH. [24] Hydrocephalus The incidence of post-traumatic hydrocephalus is approximately 0.7%-29%. Among patients who develop secondary hydrocephalus, contusion (73.6%) and tSAH (50%) were the most common findings. [25] Tian et al., noted a 11.96% incidence of hydrocephalus in tSAH. The important factors influencing the development of hydrocephalus were an increasing age, a low GCS score at admission, as well as the presence of an intraventricular hemorrhage and/or severe tSAH. [24] Hydrocephalus is usually of the communicating type and is managed by ventriculoperitoneal shunting. [26] In our study of tSAH, hydrocephalus was not observed in any of the patients. [11]
tSAH is a commonly encountered entity in TBI. It is one of the important factors influencing the overall outcome in head injured patients. [20] Evidence has shown that tSAH has a significant effect on the outcome of head injury that is much more than was originally realized. [15] It is well known to be detrimental to the clinical progress of patients. Recording a detailed history is one of the key factors in differentiating aSAH from tSAH. Although MRI is not the investigation of choice for TBI, its specific sequences like the FLAIR, GRE, and susceptibility weighted imaging play a useful role in the diagnosis of tSAH. Cases with isolated tSAH are treated conservatively. The management protocol remains more or less the same as in TBI. The goal should be to prevent complications like dyselectrolytemia, vasospasm, and hydrocephalus. Patients with tSAH should be offered nimodipine for 3 weeks. The GCS score remains the most important parameter for assessing the neurological outcome. As tSAH is one of the important contributory factors in the prognosis of TBI, its pathophysiology and anticipated complications must be properly understood. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.
[Figure 1], [Figure 2], [Figure 3], [Figure 4]
[Table 1], [Table 2], [Table 3], [Table 4]
|
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
|||||
