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  1. Wafa SR, Jamsari S, Karis BM
    Med J Malaysia, 1999 Jun;54(2):273-6.
    PMID: 10972043
    We present a rare case of a patient diagnosed with probable dengue fever sustaining an intracranial haemorrhage after a trivial motor vehicle accident. From the literature reviewed, it was noted that there have been no reports of dengue fever presenting with an intracranial haemorrhage, and the association is more common in patients diagnosed with dengue hemorrhagic fever and/or dengue shock syndrome.
    Matched MeSH terms: Intracranial Hemorrhages/etiology*
  2. Fadzil F
    Med J Malaysia, 2011 Aug;66(3):261-3.
    PMID: 22111455
    Inherited factor VII (FVII) deficiency is a rare autosomal recessive hemorrhagic disorder. Clinical bleeding can vary widely and does not always correlate with the level of FVII coagulant activity measured in plasma. Most severe cases of factor VII (FVII) deficiency are diagnosed during childhood, often during the first 6 months of life. In infancy, the most common sites of bleeding occur in the gastrointestinal tract or CNS, accounting for 60-70% of bleeds in this age group. Recombinant factor VIIa (rFVIIa) is one such agent, which has been shown to prevent hematoma expansion and improve outcome in acute intracranial haemorrhages. The purpose of this case report is to share our experience regarding the usefulness of rFVIIa in the management of acute intracranial haemorrhage.
    Matched MeSH terms: Intracranial Hemorrhages/etiology*
  3. Abu Bakar I, Shuaib IL, Mohd Ariff AR, Naing NN, Abdullah JM
    Asian J Surg, 2005 Jan;28(1):1-6.
    PMID: 15691788
    OBJECTIVE: Spontaneous intracranial haemorrhage constitutes 18-40% of all stroke cases. Indications for cerebral angiography to find underlying potentially treatable vascular abnormalities are not clear. This study determined which intracranial haemorrhage patients need cerebral angiography by correlating computed tomography (CT) findings, age and hypertension history with cerebral angiography findings.

    METHODS: A total of 54 patients (8-79 years) with intracranial haemorrhage who underwent both CT examination and six-vessel cerebral angiography were studied over a 2-year period. Cerebral angiography was repeated within 6 weeks if the first angiogram was negative.

    RESULTS: Angiography detected vascular lesions in 50% of cases (aneurysm 38.9% and arteriovenous malformation, AVM, 11.1%). In the aneurysm group, angiographic yield was 34.3% whereas in the AVM group, it was 37.9%. Subarachnoid haemorrhage (SAH) combined with other types of haemorrhage (such as intracerebral haemorrhage, ICH) was not significantly correlated with the likelihood of finding a vascular lesion, both aneurysm and AVM (p = 0.157). Age less than 50 years had significant correlation (p = 0.021) in the AVM group as well as in the aneurysm group (p < 0.001). A history of hypertension was associated with both aneurysm (p = 0.039) and AVM (p = 0.008). No patients with deep intracerebral haematoma had vascular lesions. The presence of an intravascular haemorrhage (IVH) had significant correlation with aneurysm (p = 0.008) but not AVM. There was no significant difference in mean age between patients with and without a vascular lesion (p = 0.134).

    CONCLUSION: Cerebral angiography is justified in patients with ICH accompanied by pure SAH (p = 0.001). Other factors associated with finding a vascular lesion were a history of hypertension and the presence of IVH. Diagnostic cerebral angiography is indicated for patients with ICH and SAH and IVH with a history of hypertension, regardless of age.

    Matched MeSH terms: Intracranial Hemorrhages/etiology
  4. Zamzuri I, Abdullah J, Madhavan M, Ariff AR
    Med J Malaysia, 2002 Mar;57(1):114-7.
    PMID: 14569729
    Epidermoid cysts of the central nervous system are described as rare, benign, slow growing lesions with a history of high rate of recurrence even after surgical removal. This lesion is rarely located at the cerebellopontine angle and is found to be composed of solid and cystic components with close adherence to vital neurovascular structures that might complicate its removal. We present a rare case of a twenty-five year old housewife with signs and symptoms of increased intracranial pressure due to the above pathology after multiple episodes of intra-tumoral bleeding. Microneurosurgical techniques were used for tumour dissection and excision. The patient recovered well after a three-year follow-up. This is the fourth example in the index medicus of bleeding seen in a histopathologically proven cerebellopontine angle intraepidermoid cyst.
    Matched MeSH terms: Intracranial Hemorrhages/etiology*
  5. Lim WK, Fong CY, Li L, Foo JC, Yap TY
    J Clin Neurosci, 2019 Jun;64:11-14.
    PMID: 30948308 DOI: 10.1016/j.jocn.2019.03.056
    We report a rare case of distinctive extensive punctate intracranial haemorrhage associated with acute lymphoblastic leukaemia with hyperleukocytosis. A 7-year-old girl presented with hyperleukocytosis (white cell count 788.7 × 109/L; 94% peripheral blasts) and laboratory tumour lysis syndrome. The diagnosis of T-cell acute lymphoblastic leukaemia was established and confirmed by immunophenotyping of peripheral blood and chemotherapy was commenced promptly. On day 3 of treatment, she developed progressive encephalopathy, left sided hemiparesis with left 6th and upper motor neuron 7th cranial nerve palsy. Brain MRI scan showed extensive punctate haemorrhages with perilesional oedema over the frontal, parietal, occipital, temporal, brainstem and cerebellar regions. The lesions were predominantly over the juxtacortical grey matter. She made a full neurological recovery after 3 months. Our report widens the neuroradiological features of intracranial haemorrhage associated with hyperleukocytosis and highlights the importance of prompt chemotherapy in these patients.
    Matched MeSH terms: Intracranial Hemorrhages/etiology*
  6. Abdullah JM, Husin A
    Acta Neurochir. Suppl., 2011;111:421-4.
    PMID: 21725794 DOI: 10.1007/978-3-7091-0693-8_72
    The use of intravascular hypothermia in the treatment of hemorrhagic stroke is currently still being researched. The exact therapeutic properties and effect of hypothermia on the natural progression of the disease are not known, and a only small number of papers has been published with results from these studies. Mild hypothermia at 34°C was induced in six patients with hemorrhagic stroke in the first 48 h after presentation, using an intravascular catheter placed in the inferior vena cava. The hypothermia was induced and maintained for 24 h followed by gradual rewarming. Another 18 patients with hemorrhagic stroke but not receiving hypothermia were then taken as the control group, and all patients were treated with standard stroke management. The patients were then followed up using the modified Rankin Scale (mRS) for 6 months and 1 year. There was a statistically significant improvement at 6 months and 1 year follow-up using the mRS score in the hypothermia group, indicating a possible beneficial effect of early therapeutic hypothermia in the management of acute hemorrhagic stroke. However, a larger study is needed in order to confirm our finding.
    Matched MeSH terms: Intracranial Hemorrhages/etiology*
  7. Ghani AR, Prakash RG, Abdullah J
    Med J Malaysia, 2006 Mar;61(1):100-2.
    PMID: 16708744 MyJurnal
    We report one case of posterior fossa intracranial haemorrhage in a full-term Malay baby boy following vacuum assisted delivery. The patient, a term baby boy was delivered by a vacuum extraction and later developed signs of increased intracranial pressure 72 hours after birth. Computed tomography (CT) of the brain showed a posterior fossa intracranial haemorrhage with acute obstructive hydrocephalus. He was initially treated with isolated ventricular shunting which later caused an upward cerebellar herniation. An immediate suboccipital craniectomy for evacuation of cerebellar haematoma was performed which resulted in a gradual recovery.
    Matched MeSH terms: Intracranial Hemorrhages/etiology*
  8. Nooraudah AR, Mohd Sham K, Zahari N, Fauziah K
    Med J Malaysia, 2004 Jun;59(2):160-5.
    PMID: 15559164
    Non-accidental head injury leading to massive intracranial trauma has been identified as a leading cause of death in small children. In a typical case, a child usually below the age of one year is violently shaken, leading to rupture of the connecting veins between the dura mater and the brain substance with variable degrees of bleeding into the subdural space resulting in increased intracranial pressure. The accompanying venous thrombosis affecting the vessels of the brain substance leads to cerebral hypoxia and cellular death. In this study conducted throughout the year 1999, all children below the age of 3 years who were admitted to Hospital Kuala Lumpur and had died due to non-accidental injuries were included. Postmortems, including histopathological studies, were conducted to determine the most likely mechanisms of the injuries. Ten cases were identified for the whole year. In 2 cases, both below one year of age, the features presented showed evidence of violent shaking of the infants. In 6 other cases whose average age was 13 (range 4-24) months, there were evidences of direct trauma and violent shaking. In the last two cases, aged 24 and 33 months respectively, there was only evidence of direct trauma on the heads without being shaken. This study shows that death due to intracranial trauma caused by shaking with or without direct impact is the most frequent cause of mortality in abused children. Death due to direct impact between the head and another object is a less frequent occurrence.
    Matched MeSH terms: Intracranial Hemorrhages/etiology
  9. Aziz ZA, Lee YY, Ngah BA, Sidek NN, Looi I, Hanip MR, et al.
    J Stroke Cerebrovasc Dis, 2015 Dec;24(12):2701-9.
    PMID: 26338106 DOI: 10.1016/j.jstrokecerebrovasdis.2015.07.025
    Stroke remains a major health burden worldwide. The incidence and prevalence rates of stroke are decreasing in developed countries, an opposite trend is taking place in the Asia Pacific, where an increasing number of patients are being diagnosed with acute stroke. The results of the present study on acute stroke in multi-ethnic Malaysia will significantly contribute to the global stroke epidemiological data. We aimed to present epidemiological data of stroke including incidence and prevalence rates as well as associated risk factors from a prospective nationwide hospital-based registry from 2010 to 2014.
    Matched MeSH terms: Intracranial Hemorrhages/etiology
  10. Pairan MS, Mohammad N, Abdul Halim S, Wan Ghazali WS
    BMJ Case Rep, 2018 Sep 10;2018.
    PMID: 30206067 DOI: 10.1136/bcr-2018-225265
    We present an interesting case of late-onset intracranial bleeding (ICB) as a complication of Streptococcus gordonii causing infective endocarditis. A previously healthy young woman was diagnosed with infective endocarditis. While she was already on treatment for 2 weeks, she had developed seizures with a localising neurological sign. An urgent non-contrasted CT brain showed massive left frontoparietal intraparenchymal bleeding. Although CT angiogram showed no evidence of active bleeding or contrast blush, massive ICB secondary to vascular complication of infective endocarditis was very likely. An urgent decompressive craniectomy with clot evacuation was done immediately to release the mass effect. She completed total 6 weeks of antibiotics and had postoperative uneventful hospital stay despite having a permanent global aphasia as a sequel of the ICB.
    Matched MeSH terms: Intracranial Hemorrhages/etiology*
  11. Mahmood A, Needham K, Shakur-Still H, Harris T, Jamaluddin SF, Davies D, et al.
    Emerg Med J, 2021 Apr;38(4):270-278.
    PMID: 33262252 DOI: 10.1136/emermed-2020-210424
    BACKGROUND: Early tranexamic acid (TXA) treatment reduces head injury deaths after traumatic brain injury (TBI). We used brain scans that were acquired as part of the routine clinical practice during the CRASH-3 trial (before unblinding) to examine the mechanism of action of TXA in TBI. Specifically, we explored the potential effects of TXA on intracranial haemorrhage and infarction.

    METHODS: This is a prospective substudy nested within the CRASH-3 trial, a randomised placebo-controlled trial of TXA (loading dose 1 g over 10 min, then 1 g infusion over 8 hours) in patients with isolated head injury. CRASH-3 trial patients were recruited between July 2012 and January 2019. Participants in the current substudy were a subset of trial patients enrolled at 10 hospitals in the UK and 4 in Malaysia, who had at least one CT head scan performed as part of the routine clinical practice within 28 days of randomisation. The primary outcome was the volume of intraparenchymal haemorrhage (ie, contusion) measured on a CT scan done after randomisation. Secondary outcomes were progressive intracranial haemorrhage (post-randomisation CT shows >25% of volume seen on pre-randomisation CT), new intracranial haemorrhage (any haemorrhage seen on post-randomisation CT but not on pre-randomisation CT), cerebral infarction (any infarction seen on any type of brain scan done post-randomisation, excluding infarction seen pre-randomisation) and intracranial haemorrhage volume (intraparenchymal + intraventricular + subdural + epidural) in those who underwent neurosurgical haemorrhage evacuation. We planned to conduct sensitivity analyses excluding patients who were severely injured at baseline. Dichotomous outcomes were analysed using relative risks (RR) or hazard ratios (HR), and continuous outcomes using a linear mixed model.

    RESULTS: 1767 patients were included in this substudy. One-third of the patients had a baseline GCS (Glasgow Coma Score) of 3 (n=579) and 24% had unilateral or bilateral unreactive pupils. 46% of patients were scanned pre-randomisation and post-randomisation (n=812/1767), 19% were scanned only pre-randomisation (n=341/1767) and 35% were scanned only post-randomisation (n=614/1767). In all patients, there was no evidence that TXA prevents intraparenchymal haemorrhage expansion (estimate=1.09, 95% CI 0.81 to 1.45) or intracranial haemorrhage expansion in patients who underwent neurosurgical haemorrhage evacuation (n=363) (estimate=0.79, 95% CI 0.57 to 1.11). In patients scanned pre-randomisation and post-randomisation (n=812), there was no evidence that TXA reduces progressive haemorrhage (adjusted RR=0.91, 95% CI 0.74 to 1.13) and new haemorrhage (adjusted RR=0.85, 95% CI 0.72 to 1.01). When patients with unreactive pupils at baseline were excluded, there was evidence that TXA prevents new haemorrhage (adjusted RR=0.80, 95% CI 0.66 to 0.98). In patients scanned post-randomisation (n=1431), there was no evidence of an increase in infarction with TXA (adjusted HR=1.28, 95% CI 0.93 to 1.76). A larger proportion of patients without (vs with) a post-randomisation scan died from head injury (38% vs 19%: RR=1.97, 95% CI 1.66 to 2.34, p<0.0001).

    CONCLUSION: TXA may prevent new haemorrhage in patients with reactive pupils at baseline. This is consistent with the results of the CRASH-3 trial which found that TXA reduced head injury death in patients with at least one reactive pupil at baseline. However, the large number of patients without post-randomisation scans and the possibility that the availability of scan data depends on whether a patient received TXA, challenges the validity of inferences made using routinely collected scan data. This study highlights the limitations of using routinely collected scan data to examine the effects of TBI treatments.

    TRIAL REGISTRATION NUMBER: ISRCTN15088122.

    Matched MeSH terms: Intracranial Hemorrhages/etiology*
  12. Lim SY, Hodaie M, Fallis M, Poon YY, Mazzella F, Moro E
    Arch. Neurol., 2010 May;67(5):584-8.
    PMID: 20457958 DOI: 10.1001/archneurol.2010.69
    Gamma knife thalamotomy (GKT) has been used as a therapeutic option for patients with disabling tremor refractory to medications. Impressive improvement of tremor has been reported in the neurosurgical literature, but the reliability of such data has been questioned.
    Matched MeSH terms: Intracranial Hemorrhages/etiology
  13. Forouzanfar MH, Liu P, Roth GA, Ng M, Biryukov S, Marczak L, et al.
    JAMA, 2017 01 10;317(2):165-182.
    PMID: 28097354 DOI: 10.1001/jama.2016.19043
    Importance: Elevated systolic blood (SBP) pressure is a leading global health risk. Quantifying the levels of SBP is important to guide prevention policies and interventions.

    Objective: To estimate the association between SBP of at least 110 to 115 mm Hg and SBP of 140 mm Hg or higher and the burden of different causes of death and disability by age and sex for 195 countries and territories, 1990-2015.

    Design: A comparative risk assessment of health loss related to SBP. Estimated distribution of SBP was based on 844 studies from 154 countries (published 1980-2015) of 8.69 million participants. Spatiotemporal Gaussian process regression was used to generate estimates of mean SBP and adjusted variance for each age, sex, country, and year. Diseases with sufficient evidence for a causal relationship with high SBP (eg, ischemic heart disease, ischemic stroke, and hemorrhagic stroke) were included in the primary analysis.

    Main Outcomes and Measures: Mean SBP level, cause-specific deaths, and health burden related to SBP (≥110-115 mm Hg and also ≥140 mm Hg) by age, sex, country, and year.

    Results: Between 1990-2015, the rate of SBP of at least 110 to 115 mm Hg increased from 73 119 (95% uncertainty interval [UI], 67 949-78 241) to 81 373 (95% UI, 76 814-85 770) per 100 000, and SBP of 140 mm Hg or higher increased from 17 307 (95% UI, 17 117-17 492) to 20 526 (95% UI, 20 283-20 746) per 100 000. The estimated annual death rate per 100 000 associated with SBP of at least 110 to 115 mm Hg increased from 135.6 (95% UI, 122.4-148.1) to 145.2 (95% UI 130.3-159.9) and the rate for SBP of 140 mm Hg or higher increased from 97.9 (95% UI, 87.5-108.1) to 106.3 (95% UI, 94.6-118.1). For loss of DALYs associated with systolic blood pressure of 140 mm Hg or higher, the loss increased from 95.9 million (95% uncertainty interval [UI], 87.0-104.9 million) to 143.0 million (95% UI, 130.2-157.0 million) [corrected], and for SBP of 140 mm Hg or higher, the loss increased from 5.2 million (95% UI, 4.6-5.7 million) to 7.8 million (95% UI, 7.0-8.7 million). The largest numbers of SBP-related deaths were caused by ischemic heart disease (4.9 million [95% UI, 4.0-5.7 million]; 54.5%), hemorrhagic stroke (2.0 million [95% UI, 1.6-2.3 million]; 58.3%), and ischemic stroke (1.5 million [95% UI, 1.2-1.8 million]; 50.0%). In 2015, China, India, Russia, Indonesia, and the United States accounted for more than half of the global DALYs related to SBP of at least 110 to 115 mm Hg.

    Conclusions and Relevance: In international surveys, although there is uncertainty in some estimates, the rate of elevated SBP (≥110-115 and ≥140 mm Hg) increased substantially between 1990 and 2015, and DALYs and deaths associated with elevated SBP also increased. Projections based on this sample suggest that in 2015, an estimated 3.5 billion adults had SBP of at least 110 to 115 mm Hg and 874 million adults had SBP of 140 mm Hg or higher.

    Matched MeSH terms: Intracranial Hemorrhages/etiology
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