|Year : 2022 | Volume
| Issue : 1 | Page : 44-48
Bilateral putaminal haemorrhages – unearthing a myth, lessons learnt
Rajesh Parameshwaran Nair1, Lakshman I Kongwad2, Vinod Kumar3, Ajay Hegde1, Raghavendra Nayak1, R Girish Menon1
1 Department of Neurosurgery, Kasturba Medical College, Manipal University, Manipal, Karnataka, India
2 Department of Neurosurgery, BGS Hospital, Bengaluru, Karnataka, India
3 Department of Neurosurgery, High Tech Hospital, Udupi, Karnataka, India
|Date of Submission||19-Jul-2022|
|Date of Decision||16-Aug-2022|
|Date of Acceptance||20-Aug-2022|
|Date of Web Publication||22-Sep-2022|
Source of Support: None, Conflict of Interest: None
Primary multiple spontaneous intracerebral haemorrhages (MSICHs) are a cryptic entity that is very less understood since they are sparsely encountered in clinical practice. MSICH has been deciphered and defined as 'two discrete primary intracerebral haemorrhage occurring simultaneously or within 24 h since the first identified intracerebral haemorrhage. Primary MSICH is sporadic and has a reported incidence varying from 0.75% to 3% of all spontaneous intracerebral haemorrhage; however, the trigger for such bleeds is yet to be ascertained. We present our clinical experience with six cases of MSICHs. A retrospective analysis of data from the Medical Records Department of Kasturba Medical College, Manipal (KMC, Manipal), spanning from 2016 to 2017 and collecting the data of all the patients with the diagnosis of bilateral putaminal haemorrhages who have been treated/operated in KMC, Manipal. SPSS software was used to analyse the data and determines the correlation between the variables. Simultaneous bilateral basal ganglionic bleeds are rare but carry a grave prognosis. The exact pathophysiology is unknown but is probably related to long-standing hypertension. The treatment essentially involves primary prevention with strict control of hypertension and minimising the risk factors. SICH are very rare forms of intracranial bleeds and are often associated with high morbidity and mortality. Often seen in the basal ganglia or thalamus, the mechanism and predisposing factors still remain elusive. The varied clinical presentation and uncertainty in ideal treatment still leave a lot to subjective protocols of individual surgeons. The jury is still out in this matter.
Keywords: Basal ganglia haematoma, bilateral putaminal haemorrhage, hydrocephalus, hypertensive bleeds, multiple spontaneous intracerebral haemorrhages
|How to cite this article:|
Nair RP, Kongwad LI, Kumar V, Hegde A, Nayak R, Menon R G. Bilateral putaminal haemorrhages – unearthing a myth, lessons learnt. J Cerebrovasc Sci 2022;10:44-8
|How to cite this URL:|
Nair RP, Kongwad LI, Kumar V, Hegde A, Nayak R, Menon R G. Bilateral putaminal haemorrhages – unearthing a myth, lessons learnt. J Cerebrovasc Sci [serial online] 2022 [cited 2023 Jan 30];10:44-8. Available from: http://www.jcvs.in/text.asp?2022/10/1/44/356696
| Introduction|| |
Bilateral primary hypertensive simultaneous putaminal haemorrhages constitute an extremely rare subgroup of primary spontaneous intracerebral haematomas. We report a series of six cases of bilateral primary hypertensive simultaneous putaminal haemorrhages (one postoperative case) and attempt to discuss the pathophysiology of this rare entity.
| Patients and Methods|| |
We present our clinical experience with six cases of multiple spontaneous intracerebral haemorrhages (MSICHs). We discuss the various presentations, clinical spectrum, probable pathophysiology and the varied outcome in such patients and the treatment dilemma associated with such cases. A retrospective analysis of data from the Medical Records Department of Kasturba Medical College, Manipal (KMC, Manipal), spanning from 2016 to 2017 and collecting the data of all the patients with the diagnosis of bilateral putaminal haemorrhages who have been treated/operated in KMC, Manipal. SPSS software (SPSS software IBM SPSS Statistics for Windows, version 26, IBM Corp., Armonk, N.Y.) was used to analyse the data and determines the correlation between the variables.
| Case Reports|| |
A 28-year-old male with no previous comorbidities presented to the emergency centre of our hospital with a sudden drop in sensorium. On arrival, he was comatose and had a Glasgow Coma Scale (GCS) of 4 (eye-opening one, verbal response one and motor response two). Pupils were bilateral 2 mm and nonreactive. His blood pressure on admission was 190/100 mmHg and his pulse rate was 54/min. Computed tomography (CT) of the brain revealed bilateral ganglia haematoma, the volume being larger on the right side [Figure 1]a and [Figure 1]b. His laboratory investigation reports were unremarkable. He was intubated, ventilated and managed conservatively with anti-oedema measures. He continued to deteriorate and succumbed within 48 h of admission.
|Figure 1: Computed tomographic scan of the brain (CT brain) axial (a) and coronal section (b) showing bilateral basal ganglia bleed, right > left with mild midline shift to the left. CT: Computed tomography|
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An 86-year-old female presented to the triage with sudden-onset loss of consciousness and elevated blood pressure. It was at a record high of 210/110 mmHg and she had bradycardia, Bilateral Bleeds [Figure 2]a and [Figure 2]b, right larger than left with intraventricular extension and mass effect and midline shift. In view of poor GCS, the relatives deferred any form of intervention and she was managed conservatively. She deteriorated after 48 h of admission and after all attempts at resuscitation failed, she was declared dead.
|Figure 2: CT Brain, axial (a) and coronal (b) section, showing large right basal ganglia bleed with intraventricular extension, mass effect and midline shift with concurrent left basal ganglia bleed. CT: Computed tomography|
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A 45-year-old male, non-compliant hypertensive with chronic alcoholism, presented with a history of sudden-onset decreased sensorium and right-sided weakness. On neurological examination, he was drowsy, opening eyes to the pain and localising with his upper limbs. Pupils were equal and reacted to light. CT brain revealed a large left basal ganglia haematoma [Figure 3]a. The patient underwent an emergency craniotomy and evacuation of haematoma; postoperatively, he recovered well and was extubated [Figure 3]b. On the 3rd post-operative day, he seemed to be neurologically obtunded and a repeat CT scan was ordered. A repeat scan of the brain revealed a left-side rebleed with a right-sided basal ganglia haematoma [Figure 3]c and [Figure 3]d. He was managed conservatively with anticonvulsants and decongestants. In view of poor prognosis, the family deferred further treatment and had the patient discharged against medical advice.
|Figure 3: Preoperative CT brain, axial (a) section showing left basal ganglia bleed with intraventricular extension and mass effect and midline shift. Postoperative CT axial section (b) showing residual blood with no obvious bleed in the right basal ganglia region. Axial CT brain axial section (c and d) showing a spontaneous rebleed in the right basal ganglia and residual within the left basal ganglia region. CT: Computed tomography|
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A 65-year-old patient presented with right-sided weakness and altered sensorium of 2 days duration. He was managed conservatively with antihypertensive and physiotherapy. He improved neurologically and was discharged. He presented 3 months later with a history of altered sensorium and left-sided weakness. CT brain was done which revealed bilateral basal ganglia bleeds [Figure 4]a and [Figure 4]b and he was managed conservatively. He persisted to have dysarthria but the left-sided weakness gradually improved. He is on regular follow-up and well preserved.
|Figure 4: CT brain, axial (a) and coronal (b) showing bilateral moderate-sized basal ganglia bleed, left > right with no significant mass effect or shift or intraventricular extension. CT: Computed tomography|
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A 55-year-old patient presented to the triage with uncontrolled hypertension on irregular treatment. His GCS was poor (E1M1V1) on presentation to the triage and the prognosis was explained to the relatives. Blood pressure was recorded at 210/110 mmHg and pulse of 112/min. A CT brain was done which showed bilateral basal ganglia bleeding with brain stem and intraventricular extension and acute hydrocephalus [Figure 5]a and [Figure 5]b. Despite all resuscitative measures, the patient was declared dead the following day.
|Figure 5: CT brain, axial (a) and coronal (b) section showing bilateral basal ganglia bleed with brain stem and intraventricular extension and acute hydrocephalus. CT: Computed tomography|
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A 62-year-old patient presented to us with a headache and altered sensorium of 2 days duration. He was opening eyes to the pain and was only flexing his arms to central pain. A CT brain revealed bilateral moderately sized basal ganglia haematoma [Figure 6]a and [Figure 6]b. He was managed conservatively; however, he aspirated and had to be intubated and ventilated in view of aspiration pneumonia. His respiratory parameters did not improve and he was planned for a tracheostomy. Post-tracheostomy, his respiratory parameters improved and he was shifted to the ward. He was discharged 2 weeks later on a tracheostomy. On a telephonic follow-up call, it was found out that he passed away 3 days after discharge.
|Figure 6: CT brain, axial (a) and coronal (b) showing bilateral moderate-sized basal ganglia bleed, left > right with no significant mass effect or shift or intraventricular extension. CT: Computed tomography|
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| Discussion|| |
Spontaneous intracerebral haemorrhage (ICH) accounts for 15%–20% of all strokes in Asia and the majority of them are associated with hypertension. These bleeds commonly occur at the putamen, thalamus, pons and cerebellum, the first two being the most common sites. Hypertensive bleeds are generally solitary and seldom recur at the same site. Multiple hypertensive bleeds are rare and constitute 14.7% of all spontaneous ICH. Simultaneous bilateral putaminal hypertensive bleeds are extremely rare with <50 reported cases in the literature. A comprehensive list of our patient series has been tabulated in [Table 1].
|Table 1: Demographics of the cases with bilateral putaminal haemorrhages|
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MSICH refers to two discrete primary intracerebral haemorrhages occurring simultaneously or within 24 h since the first identified intracerebral haemorrhage MSICH can be primary or secondary. Secondary MSICH are uncommon and are usually secondary to venous sinus thrombosis, coagulopathy, vasculitis, malignancy, etc. Primary MSICH is usually secondary to hypertension and rarely due to cerebral amyloid angiopathy. Although the incidence of MSICH is around 5.1%, primary MSCIH is rare with incidence varying from 0.7% to 3.04% which is much lower than secondary MSICH (4.5%–13.6%). Significant knowledge on this rare entity was available only in the past decade subsequent to the publication of two meta-analyses by Laiwattana et al. and Kono and Terada, et al. While Laiwattana et al. analysed all 105 patients with primary MSICH reported so far, Kono and Terada restricted their search to bilateral thalamic and putaminal haemorrhages.
Primary MSICH more commonly occurs in elderly males and in their meta-analysis of 105 patients, Laiwattana et al. observed that bilateral primary MSICHs were most commonly found in the basal ganglia (35 cases, 33.33%), followed by bilateral thalamic haemorrhages (19 cases, 18.1%). In Kono and Terada series of 41 cases, there were 18 bilateral putaminal and 12 bilateral thalamic haemorrhage cases. The exact pathophysiology of primary MSICH is unknown, but it has been observed in all reported cases that all the patients gave a prolonged history of hypertension and most of them have associated risk factors such as smoking, alcoholism and hyperlipidaemia. The duration of hypertension was longer and the percentage of the previous stroke was found to be higher in patients with these patients. The predilection for basal ganglia is unknown but is probably related to long-standing hypertensive changes making the lenticulostriate vessels fragile and susceptible to aneurysm formation and subsequent rupture. One of the possible mechanisms for bilateral simultaneous bleeds could be the rupture of bilateral microaneurysms simultaneously, an extremely rare phenomenon. The second postulate is that the initial haemorrhage increases Intracranial tension (ICT) and blood pressure, which may result in the rupture of the most vulnerable vessels at other sites. In patients with chronic hypertension, widespread degeneration with impaired autoregulation already exists and in the event of an initial rupture, there is an increase in hypertension with loss of cerebral autoregulation resulting in rupture of other vulnerable sites. A third mechanism postulates that the pain induced following the first bleed and the corresponding release of catecholamine causes worsening of hypertension, thereby causing additional areas of haemorrhage. Few cases of brain stem bleed in primary MSICH could be secondary to the raised intracranial pressure and herniation caused by a large putaminal or thalamic bleed. Yen, et al. found that hypertension was the only risk factor for the development of MSICH. Indirect evidence for the role of amyloid angiopathy in the development of MSICH has also been reported.
The management of primary MSICH is essentially conservative. A difference between MSICH and SICH has been enumerated in [Table 2]. Primary MSICH carries a poor prognosis, primary bilateral basal ganglionic bleeds more so, with a very high risk of mortality in Laiwattana et al. series (60%; 21 of 35 cases of putaminal bleeds and 31.58%; 6 of 19 cases of thalamic bleeds).
|Table 2: Differences between spontaneous intracerebral haemorrhage and multiple spontaneous intracerebral haemorrhage - an overview|
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| Conclusion|| |
Simultaneous bilateral basal ganglionic bleeds are rare but carry a grave prognosis. The exact pathophysiology is unknown but is probably related to long-standing hypertension. The treatment essentially involves primary prevention with strict control of hypertension and minimising the risk factors.
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Conflicts of interest
There are no conflicts of interest.
| References|| |
Kono K, Terada T. Simultaneous bilateral hypertensive putaminal or thalamic hemorrhage: Case report and systematic review of the literature. Turk Neurosurg 2014;24:434-7.
Laiwattana D, Sangsawang B, Sangsawang N. Primary multiple simultaneous intracerebral hemorrhages between 1950 and 2013: Analysis of data on age, sex and outcome. Cerebrovasc Dis Extra 2014;4:102-14.
Takeuchi S, Takasato Y, Masaoka H, Hayakawa T, Yatsushige H, Sugawara T. Simultaneous multiple hypertensive intracranial hemorrhages. J Clin Neurosci 2011;18:1215-8.
Yen CP, Lin CL, Kwan AL, Lieu AS, Hwang SL, Lin CN, et al.
Simultaneous multiple hypertensive intracerebral haemorrhages. Acta Neurochir (Wien) 2005;147:393-9.
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6]
[Table 1], [Table 2]