|Year : 2020 | Volume
| Issue : 1 | Page : 58-60
Bilateral subdural haematomas secondary to spontaneous intracranial hypotension-A dilemma in management
Girish R Menon, Sandesh Onkarappa, RT Sanjeev, Saurabh Beedkar, Rajesh P Nair
Department of Neurosurgery, Kasturba Medical College, MAHE, Manipal, Karnataka, India
|Date of Submission||23-Aug-2020|
|Date of Acceptance||31-Aug-2020|
|Date of Web Publication||1-Oct-2020|
Dr. Sandesh Onkarappa
Department of Neurosurgery, Kasturba Medical College, MAHE, Manipal, Karnataka
Source of Support: None, Conflict of Interest: None
We present a case of bilateral subdural haematomas secondary to spontaneous intracranial hypotension. The diagnostic features and the management issues are discussed.
Keywords: Epidural blood patch, spontaneous intracranial hypotension, subdural haematoma
|How to cite this article:|
Menon GR, Onkarappa S, Sanjeev R T, Beedkar S, Nair RP. Bilateral subdural haematomas secondary to spontaneous intracranial hypotension-A dilemma in management. J Cerebrovasc Sci 2020;8:58-60
|How to cite this URL:|
Menon GR, Onkarappa S, Sanjeev R T, Beedkar S, Nair RP. Bilateral subdural haematomas secondary to spontaneous intracranial hypotension-A dilemma in management. J Cerebrovasc Sci [serial online] 2020 [cited 2021 Dec 7];8:58-60. Available from: http://www.jcvs.com/text.asp?2020/8/1/58/296923
| Introduction|| |
Spontaneous intracranial hypotension (SIH) is a treatable cause of postural headache which remains a grossly underdiagnosed clinical entity due to its relative infrequency. SIH has diverse clinical manifestations and can pose considerable management dilemmas. We report the case of a 30-year-old male who presented with bilateral subdural haematomas (SDHs) secondary to SIH.
| Case Report|| |
A 30 year old male patient presented with recent onset sub-occipital headache with a characteristic postural pattern. The headache would aggravate on standing and sitting and would get relieved on lying down. He gave no history of fever, altered sensorium, loss of consciousness, trauma, seizures or any focal deficits. On clinical examination, he had no neurological deficits and his fundus examination was unremarkable. Craniospinal magnetic resonance imaging (MRI) scan was performed which revealed evidence of bilateral fronto-temporoparietal subdural collection [Figure 1] and [Figure 2]. MRI also revealed certain characteristic features in the form of midbrain sagging (midbrain displaced below the level of dorsum sella) decreased pontomesencephalic angle (~30°), decreased pontomammillary distance (~4.1 mm), flattening of pons against clivus and caudal displacement of tonsils, distension of dural venous sinuses with outwards convex margins [Figure 1] and [Figure 3]. Thickened and enhancing dura along bilateral frontal, parietal and temporal lobes were also noted [Figure 2].
|Figure 1: Fluid signal intensity between the spinous processes of C1 and C2|
Click here to view
|Figure 2: Magnetic resonance imaging brain showing, distension of dural venous sinuses with thickened and enhancing dura along convexity with bilateral subdural collection|
Click here to view
|Figure 3: Midbrain sagging with midbrain displaced below the level of dorsum sellae, decreased pontomesencephalic angle, decreased pontomammillary distance, flattening of pons, caudal displacement of tonsils|
Click here to view
In spinal MRI Focal area of fluid signal intensity was noted between the spinous processes of C1 and C2 suggesting a probable site of cerebrospinal fluid (CSF) leak. In view of the above radiological features, a provisional diagnosis of SIH was made. He was managed conservatively with bed rest, hydration and analgesics. He initially had significant clinical improvement and was discharged, but presented after 1 month later with worsening headache associated with vomiting. Neurological examination revealed the presence of papilledema. Emergency computerised tomography (CT) brain showed the presence of bilateral fronto temporoparietal chronic SDH (cSDH) with significant mass effect [Figure 4]. The patient underwent bilateral parietal burr hole and evacuation of cSDH. This was followed by the administration of epidural blood patch (EBP). The patient had an uneventful recovery and was discharged within a week.
|Figure 4: Computerised tomography brain – showing bilateral fronto-temporoparietal subdural haematoma with mass effect|
Click here to view
| Discussion|| |
SIH is an uncommon yet curable cause of postural headache. Due to its relative infrequency, it is often underdiagnosed., The clinical manifestations can be vary from chronic headache to large bilateral SDHs with impending herniation as was seen in our case.
The primary pathology is leak of CSF due to an anatomical weakness or traumatic/iatrogenic discontinuity in the dura. The common site of leak is either at the cervicothoracic junction or the thoraco lumbar region of spine. The size of the leak can vary from a small leak during a Valsalva manoeuvre, to a large amount leaking spontaneously. SIH can be divided into three general subgroups, based on the primary pathology: (A) Leak due to a nerve root sleeve diverticulum, (2) Leak due to an osteophyte spur and (3) CSF to venous fistula. Age-related degenerative disc disease may also puncture dura and result in SIH. Imaging the spinal cord using MRI, CT or MRI myelography, or cisternography is mandatory to isolate the site of the suspected leak. In patients with suspicion of a SIH, CT myelography is the recommended first line of investigation which can be further aided with MRI and MRI myelography. However, in case of slow leaks, MRI myelography appears to be more sensitive than CT myelograms. In spite of all these modalities, visualisation of the CSF leak and determining the anatomic leak site remain challenging. The site of leak in our patient was at the cervicothoracic region but the exact aetiology remains uncertain.
The diagnosis of SIH depends on a combination of clinical symptoms and signs and characteristic findings on brain imaging. The hallmark triad of SIH is orthostatic headache, diffuse pachymeningeal enhancement on MRI and low CSF opening pressure. The postural headache is the most common presenting feature seen in patients with SIH. This headache usually aggravates within 15 min of upright position and resolves within 30 min of lying down. SIH is usually defined by a CSF pressure of 6 cmH2O or less in a patient when measured in the lateral decubitus position. Diffuse pachymeningeal enhancement is the most commonly seen radiological feature in cranial MRI. Other characteristic radiological findings include 'descent', 'sinking' or 'sagging' of the brain characterised by (a) low lying cerebellar tonsils/tonsillar descent; (b) brainstem and mesencephalon descent; (c) distortion of brainstem, mesencephalon and diencephalon, (d) flattening of anterior pons; (e) Obliteration of prepontine, perichiasmatic cisterns (f) flattening of the optic chiasm; (g) Crowding of posterior fossa engorgement of venous sinuses; (h) subdural collections; (i) enhancement of pachymeninges without enhancement of leptomeninges; (j) engorgement of pituitary and (k) ventricular collapse., Our patient had almost all of the above radiological features as depicted in [Figure 1], [Figure 2], [Figure 3].
Patients with mild symptoms improve with rest, caffeine and adequate hydration. Those with significant symptoms improve by the administration of EBP at the site of leak. EBP often needs to be administered multiple times in some patients. The optimal amount of autologous blood to be injected is debatable and ranges from 10 to 40 ml through the interlaminar approach if the target is not specific. The common surgical policy is to inject the highest volume possible to allow the best spread of epidural blood to adjacent levels and maximise the chance of success. If the site of leak is definite a smaller volume of 1–5 ml would suffice.
The ideal treatment approach for SIH complicated by SDH is uncertain. The dilemma is whether the treating the dural defect alone should be enough and whether evacuation of the hematoma is required. Probably in patients with mild symptoms and small collections without mass effect, blood patch administration alone may provide relief of symptoms. In our patient, probably the application of EBP on first admission would have prevented increase of the SDH collection.
| Conclusion|| |
SIH should be considered as a potential aetiological cause in all patients with bilateral subdural collection, especially those who are young and give no history of trauma. The primary aim of the treatment should aim to address the CSF leak.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
We convey our regards to all the staff of our Department of Neurosurgery, KMC, Manipal, for their support and encouragement.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Schievink WI. Spontaneous spinal cerebrospinal fluid leaks and intracranial hypotension. JAMA 2006;295:2286-96.
Kranz PG, Tanpitukpongse TP, Choudhury KR, Amrhein TJ, Gray L. Imaging signs in spontaneous intracranial hypotension: Prevalence and relationship to CSF pressure. AJNR Am. J Neuroradiol 2016;37:1374-8.
Lin JP, Zhang SD, He FF, Liu MJ, Ma XX. The status of diagnosis and treatment to intracranial hypotension, including SIH. J Headache Pain 2017;18:4.
Schievink WI, Maya MM, Jean-Pierre S, Nuño M, Prasad RS, Moser FG. A classification system of spontaneous spinal CSF leaks. Neurology 2016;87:673-9.
Kranz PG, Luetmer PH, Diehn FE, Amrhein TJ, Tanpitukpongse TP, Gray L. Myelographic techniques for the detection of spinal CSF leaks in spontaneous intracranial hypotension, AJR Am J Roentgenol 2016;206:8-19.
Ferrante E, Wetzl R, Savino A, Citterio A, Protti A. Spontaneous cerebrospinal fluid leak syndrome: Report of 18 cases. Neurol Sci 2004;3:293-5.
Schievink WI. Spontaneous spinal cerebrospinal fluid leaks. Cephalalgia 2008;28:1347-56.
Chuang YS, Ju DT, Chiu TH, Huang YH, Cherng CH, Wu ZF. Thoracic epidural blood patch with high volume blood for cerebrospinal fluid leakage of cervical spine (C2-3) complicated with spontaneous intracranial hypotension, Acta Anaesthesiol Taiwanica 2015;53:112-3.
[Figure 1], [Figure 2], [Figure 3], [Figure 4]