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1
Aquilina, Kristian. "Animal models of intraventricular haemorrhage and post-haemorrhagic ventricular dilatation." Thesis, University of Bristol, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.574598.
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Continuing improvements in neonatal care have allowed significant progress in the clinical outcome of prematurity, with improvement t in both survival and neurological outcome. Although the incidence of intraventricular haemorrhage associated with prematurity has been lowered, it still represents a significant source of neurological morbidity. Several management strategies have attempted to reduce the neurological impact of IVH and its progression to post-haemorrhagic ventricular dilatation (PHVD). Studies have evaluated the impact of serial withdrawal of cerebrospinal fluid (CSD) by lumbar puncture, fontanelletap or through a ventricular access device, yet none of these interventions have reduced progression to PHVD. The use of agents that reduce production of CSF have actually led to worse clinical outcomes for unclear reasons. A new technique involving intraventricular fibrinolysis, drainage and irrigation, while not reducing the need for CSF diversion, has improved cognitive outcome at 2 years.
2
Samarasekera, Neshika Erangi. "Does lobar intracerebral haemorrhage differ from non-lobar intracerebral haemorrhage?" Thesis, University of Edinburgh, 2015. http://hdl.handle.net/1842/15836.
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Spontaneous (non-traumatic) intracerebral haemorrhage accounts for ~10% of all strokes in Western populations. Investigations may identify intracerebral haemorrhage (ICH) as ‘secondary’ to underlying causes such as tumours or aneurysms, but ~80% of ICHs which have no apparent underlying cause (so-called ‘primary’ ICH) tend to be attributed to small vessel vasculopathies such as arteriolosclerosis or cerebral amyloid angiopathy (CAA), on the basis of an adult’s risk factors and clinical and radiographic features of the ICH. The commonly accepted hypothesis is that CAA contributes to lobar ICH and arteriolosclerosis causes non-lobar ICH. In the following thesis, I set out to explore whether (a) the baseline demographic, clinical features and apolipoprotein E genotype of adults with lobar and non-lobar ICH differ, (b) the prognosis of adults with lobar and non-lobar ICH differ and (c) the neuroimaging correlates of small vessel disease in adults with lobar and non-lobar ICH differ since this might provide clues to the vasculopathies underlying lobar and non-lobar ICH. I explored (d) the strength of the association between CAA and ICH by systematically reviewing neuropathological case control studies and (e) the radiological and pathological features of lobar ICH to examine the nature of CAA in persons with lobar ICH and whether any computed tomography (CT) features of ICH are associated with CAA-related lobar ICH. I set up a prospective, community-based inception cohort study of adults with ICH in South East Scotland. Adults with spontaneous primary definite ICH had the opportunity to consent to participate in the Lothian Study of IntraCerebral Haemorrhage, Pathology, Imaging and Neurological Outcome (LINCHPIN), an ethically-approved, prospective community-based research study examining the causes of ICH using apolipoprotein E genotyping, brain MRI and research autopsy in case of death. Of 128 adults with first-ever spontaneous primary definite ICH diagnosed during 2010- 2011, age and pre-morbid hypertension did not differ by ICH location but a history of dementia was more common in adults with lobar ICH. The proportion of adults with one or more non-lobar brain microbleed (BMB) was significantly higher in adults with non-lobar ICH but I did not find any other differences in the severity or distribution of other neuroimaging correlates of small vessel disease between lobar and non-lobar ICH. The apolipoprotein e4 allele was more common in participants with lobar ICH in comparison to those with non-lobar ICH but the frequency of the e2 allele did not differ by ICH location. Adults with lobar ICH were significantly more likely to survive one year after their ICH in comparison to those with non-lobar ICH after adjustment for other known predictors of outcome. From a systematic review of neuropathological case control studies of CAA and ICH, stratified by ICH location, I found a significant association between CAA and lobar ICH but not with ICH in other locations. I examined the radiological and pathological features of 33 adults with first-ever lobar ICH. The presence of CAA or vasculopathy and the severity of CAA in a lobe affected by ICH was concordant with that of the corresponding contralateral unaffected lobe. Capillary CAA was associated with severe CAA. Subarachnoid extension of the ICH tended to be more frequent in those with CAA-related strictly lobar ICH. Having explored the incidence, risk factors and prognosis of lobar and non-lobar ICH, in future work I would aim to establish the strength of the association between CAA and ICH in different brain locations in a neuropathological case control study. Future work should examine the radiopathological features of lobar ICH in a larger cohort and the coexistence of other small vessel diseases, in particular arteriolosclerosis in persons with ICH.
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Sobowale, Oluwaseun. "Intracerebral haemorrhage and inflammation." Thesis, University of Manchester, 2018. https://www.research.manchester.ac.uk/portal/en/theses/intracerebral-haemorrhage-and-inflammation(7139560f-bd3c-4ff0-b628-f86ffc6477d2).html.
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Intracerebral haemorrhage (ICH) is a significant healthcare concern worldwide. Following ICH, primary injury occurs due to physical injury to neurones and glia as a result of mass effect from the haematoma. Secondary mechanisms of injury include haematoma expansion, toxic effects of the products of coagulation and blood breakdown products and sterile inflammation. Perihaematomal oedema can exacerbate mass effect in the acute and sub-acute phase of ICH. At present, the pathophysiology behind the secondary mechanisms of injury following ICH is not fully understood and this has led to inability to translate new treatments from bench to bedside. Haematoma expansion is a significant contributor to neurological deterioration in the acute phase; however, understanding of the factors leading to a third of patients developing haematoma expansion is limited. This thesis presents the results of work aiming to develop a reproducible model of haematoma expansion in preclinical ICH. Using this model we found that a systemic inflammatory stimulus failed to induce haematoma expansion in spontaneously hypertensive rats or their healthy controls. We gained further insight into factors that may contribute to haematoma expansion in ICH by studying the proteomic profile of patients in clinical ICH. We demonstrate the feasibility of multi-modality brain imaging in sub-acute ICH, which we propose will be a useful tool to monitor neuro-inflammation in the acute stages if the disease. Finally, we investigated the association between peripheral markers of inflammation (white blood cell count and C-reactive protein) and perihaematomal oedema at baseline and clinical outcome (mortality at 30 days). Our findings suggest that acute inflammation may drive acute perihaematomal oedema and interestingly, we found a negative association between C-reactive protein at baseline and 30-day mortality. Our findings are significant in the field of clinical ICH, and suggest that the inflammatory response is important. We will take our findings forward in future work with the goal of understanding why haematoma expansion occurs, with the aim of developing a test to identify patients at highest risk and interventions to improve outcome after ICH.
4
Garner, Jeffrey Philip. "Resuscitation after blast and haemorrhage." Thesis, University of Newcastle upon Tyne, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.440563.
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McEvoy, Andrew William. "Haemostatic studies in subarachnoid haemorrhage." Thesis, University College London (University of London), 2005. http://discovery.ucl.ac.uk/1444986/.
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Object. The primary objective of this thesis was to establish the pattern of change in haemostatic systems in patients following a subarachnoid haemorrhage (SAH). I hypothesise that following a SAH there is an undefined period of increasing hypercoagulability, which if present would predispose to ischaemic stroke. Methods. This was a prospective, observational study on 67 consecutive patients admitted with a primary diagnosis of SAH. There were 24 males, median age 47.5 years (25-75) and 43 females, median age 53 years (23- 80). Blood was taken at 4 time periods (<48hours, 4-5, 9-10 and 15-16 days) following the ictus depending on the day of hospital admission, and on regular intervals during the hospital stay. In addition, a sample was taken at 3 months from the ictus. A Thromboelastograph (TEG) profile performed at 37 C, and the routine coagulation studies, International Normalised Ratio (INR) and Activated Partial Thromboplastin Time Ratio (APTR) were obtained at each of these time points. In addition a full blood count, biochemical profile, and plasma for coagulation and fibrinolytic assays was also taken. Results. The results demonstrated that SAH patients were hypercoagulable immediately following the ictus, when compared with the blood sample taken 3 months later. In addition we observed the development of an increasingly hypercoagulable state for the first 21 days following the ictus. This increase in coagulation was demonstrated against a background of haemodilution during this time. Conclusions. This highly significant data demonstrates that SAH patients become increasingly hypercoagulable over time (maximum 21 days) following the ictus. This prothrombotic tendency has reversed by 3 months. This may provide a new direction in the treatment of symptomatic vasospasm. In addition, an in-vitro study using TEG has been performed in 20 volunteer subjects to assess whether haemodilution 'per se' has an intrinsic affect on coagulation specific to the dilutent itself. This study demonstrates that haemodilution does alter coagulation profiles measured using TEG. Different crystalloid and colloid fluids used to achieve haemodilution produce qualitatively consistent but quantitatively very different effects on coagulation in-vitro.
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Belachew, Johanna. "Retained Placenta and Postpartum Haemorrhage." Doctoral thesis, Uppsala universitet, Institutionen för kvinnors och barns hälsa, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-246185.
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The aim was to explore the possibility to diagnose retained placental tissue and other placental complications with 3D ultrasound and to investigate the impact of previous caesarean section on placentation in forthcoming pregnancies. 3D ultrasound was used to measure the volumes of the uterine body and cavity in 50 women with uncomplicated deliveries throughout the postpartum period. These volumes were then used as reference, to diagnose retained placental tissue in 25 women with secondary postpartum haemorrhage. All but three of the 25 women had retained placental tissue confirmed at histopathology. The volume of the uterine cavity in women with retained placental tissue was larger than the reference in most cases, but even cavities with no retained placental tissue were enlarged (Studies I and II). Women with their first and second birth, recorded in the Swedish medical birth register, were studied in order to find an association between previous caesarean section and retained placenta. The risk of retained placenta with heavy bleeding (>1,000 mL) and normal bleeding (≤1,000 mL) was estimated for 19,459 women with first caesarean section delivery, using 239,150 women with first vaginal delivery as controls. There was an increased risk of retained placenta with heavy bleeding in women with previous caesarean section (adjusted OR 1.61; 95% CI 1.44-1.79). There was no increased risk of retained placenta with normal bleeding (Study III). Placental location, myometrial thickness and Vascularisation Index were recorded on 400 women previously delivered by caesarean section. The outcome was retained placenta and postpartum haemorrhage (≥1,000 mL). There was a trend towards increased risk of postpartum haemorrhage for women with anterior placentae. Women with placenta praevia had an increased risk of retained placenta and postpartum haemorrhage. Vascularisation Index and myometrial thickness did not associate (Study IV). In conclusion: 3D ultrasound can be used to measure the volume of the uterine body and cavity postpartum, but does not increase the diagnostic accuracy of retained placental tissue. Previous caesarean section increases the risk of retained placenta in subsequent pregnancy, and placenta praevia in women with previous caesarean section increases the risk for retained placenta and postpartum haemorrhage.
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Krishnan, Kailash. "Outcomes after acute intracerebral haemorrhage." Thesis, University of Nottingham, 2017. http://eprints.nottingham.ac.uk/43228/.
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Primary Intracerebral haemorrhage is a severe form of stroke with poor prognosis attributed to haematoma characteristics. High blood pressure is present during the acute phase of intracerebral haemorrhage and associated with poor outcome in part through expansion of haematoma. Data from the ‘Efficacy of Nitric Oxide in Stroke trial’ (ENOS) was used to analyse the performance characteristics of qualitative and quantitative descriptors of intracerebral haematoma. The results showed that formal measurement of haemorrhage characteristics and visual estimates are reproducible. Intracerebral haemorrhage volumes measured using the modified ABC/2 formula were significantly lower compared to standard ABC/2 and computer assisted semi-automatic segmentation. In 629 patients with intracerebral haemorrhage presenting within 48 hours, the effect of blood pressure lowering with transdermal glyceryl trinitrate was assessed. Glyceryl trinitrate lowered blood pressure, was safe but did not improve functional outcome. In a small group of patients treated within 6 hours, glyceryl trinitrate improved functional outcome. Analysis of 246 patients with acute intracerebral haemorrhage from ENOS was undertaken to assess whether there were any differences in functional outcome among those who continued prior antihypertensive drugs during the immediate stroke period compared to those assigned to stop temporarily for 7 days. The results were neutral indicating that there was no benefit in those who continued treatment. Data of 1,011 patients with intracerebral haemorrhage in hyperacute trials from the VISTA collaboration showed differences in baseline characteristics and functional outcomes among patients from various ethnic backgrounds. A systematic review was updated to assess the effect of 26 randomised controlled trials that aimed to alter blood pressure within one week of acute stroke. The results showed that blood pressure reduction did not improve functional outcome irrespective of stroke type. When examined by time, treatment within 6 hours appeared to benefit but the number of patients were small and more studies are needed. The analysis also showed that continuing prestroke antihypertensive drugs in the immediate period after stroke did not benefit and might be harmful. In summary, this thesis provides new information on parameters used to estimate intracerebral haematoma, relationship between management of blood pressure and outcomes after haemorrhagic stroke. The work supports testing of whether very early blood pressure lowering after ictus is beneficial as is being undertaken in ongoing randomised controlled trials. Adjusting for ethnic differences may further identify patients in whom treatment may confer measurable advantage.
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Budohoski, Karol Paweł. "Cerebral autoregulation and subarachnoid haemorrhage." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648435.
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Lindgren, Cecilia. "Subarachnoid haemorrhage : clinical and epidemiological studies." Doctoral thesis, Umeå universitet, Anestesiologi och intensivvård, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-87553.
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Background: Subarachnoid haemorrhage (SAH) is a severe stroke that in 85% of all cases is caused by the rupture of a cerebral aneurysm. The median age at onset is 50-55 years and the overall mortality is approximately 45%.Sufficient cortisol levels are important for survival. After SAH hypothalamic/pituitary blood flow may be hampered this could result in inadequate secretion of cortisol. SAH is also associated with a substantial inflammatory response. Asymmetric dimethyl arginine (ADMA), an endogenous inhibitor of nitric oxide synthase, mediates vasoconstriction and increased ADMA levels may be involved in inflammation and endothelial dysfunction. Continuous electroencephalogram (EEG) monitoring can be used to detect non-convulsive seizures, leading to ischemic insults in sedated SAH patients. Elevated ADMA levels are risk factors for vascular diseases. Vascular disease has been linked to stress, inflammation and endothelial dysfunction. SAH possesses all those clinical features and theoretically SAH could thus induce vascular disease. Aims: 1. Assess cortisol levels after SAH, and evaluate associations between cortisol and clinical parameters. 2. Assess ADMA levels and arginine/ADMA ratios after SAH and evaluate associations between ADMA levels and arginine/ADMA ratios with severity of disease, co-morbidities, sex, age and clinical parameters. 3. Investigate occurrence of subclinical seizures in sedated SAH patients. 4. Evaluate if patients that survive a SAH ≥ one year have an increased risk of vascular causes of death compared to a normal population. Results: Continuous infusion of sedative drugs was the strongest predictor for a low (<200 nmol/L) serum cortisol. The odds ratio for a sedated patient to have a serum cortisol < 200 nmol/L was 18.0 times higher compared to an un-sedated patient (p < 0.001). Compared to admission values, 0-48 hours after SAH, CRP increased significantly already in the time-interval 49-72 hours (p<0.05), peaked in the time-interval 97-120 hours after SAH and thereafter decreased. ADMA started to increase in the time-interval 97-120 hours (p<0.05). ADMA and CRP levels were significantly higher, and arginine/ADMA ratios were significantly lower in patients with a more severe condition (p<0.05). Epileptic seizure activity, in sedated SAH patients, was recorded in 2/28 (7.1%) patients during 5/5468 (0.09%) hours of continuous EEG monitoring. Cerebrovascular disease was significantly more common as a cause of death in patients that had survived a SAH ≥ one year, compared to the population from the same area (p<0.0001). Conclusions: Continuous infusion of sedative drugs was associated with low (<200 nmol/L) cortisol levels. ADMA increased significantly after SAH, after CRP had peaked, indicating that endothelial dysfunction, with ADMA as a marker, is induced by a systemic inflammation. Patients with a more severe condition had significantly higher ADMA and CRP levels, and significantly lower arginine/ADMA ratio. Continuous sedation in sedated SAH patients seems to be beneficial in protecting from subclinical seizures. Cerebrovascular causes of death are more common in SAH survivors.Funding: The Swedish Society of Medicine, the Faculty of Medicine at Umeå University, The Kempe Foundations and The Stroke Foundation of Northern Sweden supported this study financially.
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Naumann, David Nathaniel. "Early microcirculatory dysfunction following traumatic haemorrhage." Thesis, University of Birmingham, 2018. http://etheses.bham.ac.uk//id/eprint/8351/.
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Traumatic haemorrhagic shock (THS) is the most frequent cause of preventable death after severe injury. Shock is characterised by inadequate provision of oxygen and substrates to tissues in relation to their requirements, and it is within the microcirculation that this process is regulated. Investigation of the microcirculation is therefore key to understanding the pathological processes following THS. In Part I, some mechanisms of microcirculatory dysfunction following trauma are presented. Endotheliopathy of trauma is associated with poor microcirculatory flow, and occurs within minutes of injury. It is also associated with higher levels of circulating cell-free DNA (cfDNA), supporting the hypothesis that cfDNA is an aetiological factor in this pathological response. Both endotheliopathy and elevated cfDNA and are related to poor clinical outcomes. In Part II, clinical implications of microcirculatory monitoring are discussed for patients in the early phase following THS. It is safe and feasible to monitor the microcirculation following THS, and a novel point-of-care grading system has performed well, suggesting that targeted fluid resuscitation towards microcirculatory flow after THS may be possible. The optimal fluid strategy in this context is unknown, but physical properties (e.g. oncotic potential and viscosity) as well as endothelial restorative properties appear to be as important as oxygen-carrying capacity. Potential therapeutic interventions aimed at microcirculatory and endothelial resuscitation open intriguing possibilities for improving outcomes after THS.
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Mjoli, Ntethelelo. "Brain arteriovenous malformations presenting with haemorrhage." Master's thesis, University of Cape Town, 2012. http://hdl.handle.net/11427/2886.
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Abid, Kamran. "Modulation of inflammation in intracerebral haemorrhage." Thesis, University of Manchester, 2015. https://www.research.manchester.ac.uk/portal/en/theses/modulation-of-inflammation-in-intracerebral-haemorrhage(1a1793e0-0013-4f6b-9e51-a5c15828a8a5).html.
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Intracerebral Haemorrhage (ICH) exhibits the worst mortality and morbidity of any stroke subtype. There are no efficacious treatments for this condition and little improvement in patient outcome has been noted despite advancements in medical science over the previous three decades. Furthermore, current available data is increasingly obsolete as the population suffering the disease burden rapidly ages and develops co-morbidities. It is thought that future therapies for this condition may be able to target neuroinflammatory response triggered by the formation of brain haemorrhage however there is little published evidence that has examined this aspect of ICH pathophysiology. This study therefore examines the current prognosis of a large cohort of patients with ICH to determine the key factors which result in mortality. We find that patients treated at a specialist centre have a surprising and significantly improved survival advantage. Since clinical practice in the United Kindgom is widely influential, the second part of the study focuses on whether the optimal cases are currently being transferred to these centres. The next part of the study then uses MRI/PET brain imaging for the first time in patients with ICH to establish an important link between the processes of neuroinflammation and Blood-Brain-Barrier breakdown. Finally, the concluding part of the thesis presents functional and radiological data from a rat model of ICH in which the inflammatory cascade has been modulated by the use of an antagonist against IL-1. The thesis thus presents a novel and important contribution in our present understanding of the preclinical and clinical disease process.
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Hales, Majella. "Postoperative antifibrinolytic drugs to control haemorrhage." Thesis, Queensland University of Technology, 2002.
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Church, Nicholas I. "Endoscopic therapy for major peptic ulcer haemorrhage." Thesis, University of Edinburgh, 2004. http://hdl.handle.net/1842/24456.
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This thesis is based on a randomized, placebo controlled trial comparing heater probe plus thrombin injection with heater probe plus placebo injection for the treatment of high-risk patients with peptic ulcer bleeding. Two hundred and fifty six patients were randomized. There were nine protocol violations, and these were excluded from the analysis. One hundred and twenty seven patients were treated with the heater probe plus thrombin injection; the remainder received heater probe plus placebo injection. Re-bleeding developed in 9 (15%) of thrombin plus heater probe and 17 (15%) of placebo plus heater probe patients. Emergency surgery was necessary in 16 (13%) and 13 (11%) patients respectively. Eight patients in the thrombin group had adverse events compared with four in the placebo group. Eight (6%) of thrombin plus heater probe patients and 14 (12%) of placebo plus heater probe patients and 14 (12%) of placebo plus heater probe patients died (p = 0.21). These results suggest that the combination of thrombin and the heater probe does not confer additional benefit over heater probe and placebo as endoscopic treatment for bleeding peptic ulcer. This trial does not support the use of this combination of haemostatic therapy. A detailed score was used to document the extent of comorbid disease in the trail patients. Outcome was closely related to overall score, higher scores being associated with re-bleeding, surgery and mortality. The impact of different comorbid conditions were assessed using logistic regression analysis. Neurological disease and malignancy were independently associated with re-bleeding. Surgery was required more commonly in patients with neurological and respiratory conditions, and neurological disease, respiratory conditions and renal failure were associated with death. It is a widespread view that endoscopy should be performed as soon as possible after resuscitation in patients with significant upper gastrointestinal bleeding. An analysis of outcomes of the trial patients according to timing of endoscopy showed that re-bleeding and surgery rates were higher in the group in whom endoscopy was performed early, but mortality was unaffected. Endoscopy performed outwith normal working hours was not associated with adverse outcomes. Re-bleeding rates of 15-20% can be expected after initially successful endoscopic therapy. Accurate prediction of those patients at highest risk and allow for better use of intensive monitoring.
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Nandra, Kiran Kaur. "Novel therapeutic approaches for experimental trauma-haemorrhage." Thesis, Queen Mary, University of London, 2013. http://qmro.qmul.ac.uk/xmlui/handle/123456789/8470.
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Haemorrhagic shock (HS) is commonly associated with trauma. Severe haemorrhage causes hypoperfusion of tissues resulting in a global ischaemic state, and resuscitation is performed to restore circulating volume. However, the return of oxygen to ischaemic tissues causes the induction of a systemic inflammatory response, which contributes to cell death leading to organ failure. In trauma patients, failure of more than four organs is linked to certain mortality, highlighting the need for interventions that may reduce or prevent the deterioration in organ function. The aim of this thesis was to investigate the effect of therapeutic approaches on the organ injury and dysfunction induced by HS. Briefly, male Wistar rats were subjected to haemorrhage by withdrawal of blood to reduce the mean arterial pressure to 35 ± 5 mmHg for 90 min. Followed by resuscitation with 20 ml/kg Ringer’s lactate for 10 min and 50% of the shed blood for 50 min. Organ function was determined 4 h after the onset of resuscitation. This model was used to investigate the effect of three different interventions on the organ injury and dysfunction induced. In the first study, administration of bone marrow-derived mononuclear cells (BMMNCs) upon resuscitation resulted in (1) significant attenuation of the organ injury and dysfunction associated with HS, and (2) restoration of the activation of the Akt pro-survival pathway. It is possible that these beneficial effects are mediated by paracrine mediators secreted by BMMNCs, which modulate this pathway, however injection of large numbers of cells is not practical in the acute setting of trauma. Therefore, in the next study erythropoietin (EPO) was used as a daily pre-treatment for three days prior to the induction of haemorrhage, as EPO is a known stimulus of endothelial progenitor cell (EPC) mobilisation. EPO pre-treatment resulted in (1) significant attenuation of the organ injury and dysfunction associated with HS, (2) mobilisation of EPCs (CD34+/flk-1+), and (3) activation of the Akt pro-survival pathway with enhanced activation of eNOS. However, when used clinically EPO is associated with an increased risk of thrombotic events, therefore in the final study a non-erythropoietic analogue of EPO was investigated. Treatment with pyroglutamate helix B surface peptide (pHBSP) resulted in (1) significant attenuation of the organ injury and dysfunction associated with HS, and (2) activation of the Akt pro-survival pathway with enhanced activation of both eNOS and STAT3. Additionally, late pHBSP treatment, up to 60 min after the onset of resuscitation, exerted the highest degree of protection. The findings of this thesis support the view that modulation of the Akt pro-survival pathway is a potential therapeutic target in the treatment of the ischaemia-reperfusion injury associated with severe haemorrhage and resuscitation.
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Morrison, Jonathan James. "Resuscitative endovascular haemorrhage control in wartime injury." Thesis, University of Glasgow, 2014. http://theses.gla.ac.uk/5669/.
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Non-compressible haemorrhage from within the torso and junctional regions constitutes the leading cause of potentially preventable death on the battlefield. It can be defined as haemorrhagic shock arising from injury to named torso vessels, pulmonary parenchyma, high grade solid organ injury and/or disruption of the bony pelvis. Data from the US Department of Defence Trauma Registry demonstrate a torso injury rate of 12.7% with 17.1% of casualties exhibiting torso injury and shock. The overall mortality is 18.7%, with major arterial injury and pulmonary injury identified as independent predictors of mortality on multivariate analysis. The UK Joint Theatre Trauma Registry reports similar findings with the greatest burden of mortality occurring prior to hospital admission (75.0%), a rate that has remained unchanged over a decade of war. Injury from improvised explosive devices (IEDs) in particular are associated with non-compressible haemorrhage, frequently causing traumatic lower extremity amputation in combination with torso injury. Contemporary surgical strategy relates to early operative haemorrhage control in patients presenting with shock. In patients sustaining a circulatory arrest, resuscitative thoracotomy and aortic cross clamping can be used to control inflow and increase cardiac afterload. The UK experience over 5 years at Camp Bastion demonstrated a mortality of 78.5%, with greatest survival observed in patients with the shortest time to thoracotomy. In patients sustaining lower extremity amputation following IED injury, 1 in 5 require a laparotomy for proximal vascular control, with less than half requiring further intra-abdominal intervention. There is a pressing need for a haemorrhage control and resuscitation adjunct in non-compressible haemorrhage that can be deployed prior to or as an adjunct to operative haemorrhage control. Resuscitative endovascular balloon occlusion of the aorta (REBOA) is a technique that can occlude the aorta without the need for an operating theatre. It is an experimental technique, so its effect on survival and physiology is unknown. In a porcine model of uncontrolled pelvic haemorrhage, infra-renal REBOA was shown to be as effective as chitosan gauze in the setting of normal coagulation. However, REBOA was associated with a significantly greater survival in a coagulopathic setting. Similar results were obtained when using a porcine model of abdominal haemorrhage in conjunction with thoracic REBOA. In both studies, balloon occlusion demonstrated a significant improvement in systolic blood pressure and other haemodynamic measures compared to the no-occlusion control groups. Having demonstrated a survival and haemodynamic benefit in uncontrolled haemorrhage models, the metabolic and inflammatory consequences of thoracic REBOA were characterised in further detail using a porcine model of controlled hypovolaemic shock. Occlusion for 30 and 90 minutes was associated with a significant lactate burden when compared to animals undergoing shock alone. However, following resuscitation with blood and intravenous fluid, normal physiology was restored within 6 hours. The inflammatory sequelae were studied following 30, 60 and 90 minutes of shock and occlusion. Increasing occlusion time resulted in an escalating release of interleukin-6 which manifest clinically as an increase in ARDS and need for vassopressor support. In order to develop a fluoroscopy free REBOA system, a series of human studies were undertaken to examine the relationship between an external measure of torso height and aortic length in order to guide insertion length. A retrospective examination of computed tomography in male trauma patients demonstrated a correlation between torso height and aortic length. This was confirmed by a prospective study which was also used linear regression to develop equations predictive of insertion length. Finally, the UK Joint Theatre Trauma Registry was used to determine the need for REBOA in a population of UK military personnel injured over 10 years of conflict. Of 1317 severely injured patients 70.2% had no indication, 11.2% had a contra-indication and 18.5% had an injury pattern indication for REBOA. Of those with an indication for REBOA, 66 (27.0%) patients died en-route to hospital and 29 (11.9%) died in-hospital. In conclusion, non-compressible haemorrhage constitutes a significant burden of potentially preventable battlefield mortality. REBOA is a technique that can be used in the thoracic or infra-renal aorta as a haemorrhage control and resuscitation adjunct, prior to operative haemorrhage control. While associated with a significant survival advantage in models of uncontrolled haemorrhage, it is associated with a significant metabolic penalty, although with resuscitation this can be ameliorated successfully.
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Curry, Nicola Suzanne. "The coagulopathy of trauma related major haemorrhage." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608299.
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Garden, O. James. "Prediction of outcome following acute variceal haemorrhage." Thesis, University of Edinburgh, 1986. http://hdl.handle.net/1842/18218.
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Between August 1979 and September 1982, acute variceal haemorrhage has been managed in the University Department of Surgery, Glasgow Royal Infirmary by a policy of oesophageal tamponade and injection sclerotherapy. Haemorrhage was controlled in 90% of admissions with an admission mortality of 28%. Recurrent haemorrhage occurred in half the patients surviving their first admission to hospital despite entering a programme of elective sclerotherapy. The results of this management policy are reviewed and the means of selecting patients for more aggressive therapy discussed. The deficiencies of a modified Child's classification in selection of patients are highlighted and overcome by the development of a prognostic index obtained by regression analysis on data collected on patients managed over this 3 year period. The admission prognostic index clearly defines 'high' and 'low' risk groups and 'predicts' outcome following admission in 90% of patients. The use of this index is validated in a further group of patients managed by a similar policy. Further regression analysis is used to obtain a prognostic index for alcohol cirrhotic patients alone and to determine the factors associated with one year survival. These indices are used to audit the management policy. Prothrombin, creatinine and encephalopathy are shown to have a clear association with outcome when measured at the time of variceal haemorrhage whereas other factors such as albumin and haemoglobin emerge as having prognostic value when measured one month following the acute episode. The possible applications of these prognostic indices are investigated in a prospective two centre study assessing the efficacy of propranolol in preventing recurrent variceal haemorrhage. It is shown that they can be used to exclude patients from entry into a study assessing the longterm benefit of propranolol when the prospects of short-term survival are limited. Their value in auditing management and their possible use in withdrawing treatment are shown. The prognostic indices are used to compare results of treatment at the two hospitals and are shown to be of value in analysing the results of the trial. These prognostic indices provide an objective means of evaluating patient management and may allow selection of patients for consideration of other treatment options.
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Tooth, Claire L. "Outcome following neurosurgical treatment of aneurysmal subarachnoid haemorrhage." Thesis, University of Sheffield, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.421001.
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Roos, Yvo Benjamin Walther Elisabeth Maria. "Fibrinolysis and antifibrinolytic treatment in aneurysmal subarachnoid haemorrhage." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2000. http://dare.uva.nl/document/55676.
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Wheatley, K. E. "Peptic ulcer haemorrhage : the role of intragastric fibrinolysis." Thesis, University of Newcastle Upon Tyne, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308741.
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Sinha, S. K. "Vitamin E and periventicular haemorrhage in preterm babies." Thesis, University of Manchester, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.234205.
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Tait, Matthew James. "The role of aquaporin-4 in subarachnoid haemorrhage." Thesis, University of Oxford, 2011. http://ora.ox.ac.uk/objects/uuid:9b50df6f-9949-4ac2-a920-c1f44872aeb1.
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Introduction. The glial cell water channel aquaporin-4 (AQP4) plays an important ro le in brain oedema, astrocyte migration and neuronal excitability. Current theories of AQP4 function are based largely on experiments using AQP4 -1- mice. These mice have only been partially characterized. I therefore undertook a detailed investigation of baseline brain properties in AQP4 -1- mice. In the second part of my experiments I investigated the role of AQP4 in brain oedema in a mouse model of subarachnoid haemorrhage. Method. Gross anatomical measurements included estimates of brain and ventricle size. Neurons, astrocytes and oligodendrocytes were assessed using the neuronal nuclear marker NeuN, the astrocyte marker GFAP, and the myelin stain Luxol Fast Blue. The blood brain barrier was studied by electron microscopy and the horseradish peroxidase extravasation technique. A mouse model in which 30~1 of autologous blood was injected into the basal cisterns was used to reproduce subarachnoid haemorrhage. Brain water content, intracranial pressure and neurological score were compared in wildtype and AQP4 -/- mice. I also measured blood brain barrier permeability and the osmotic permeability of the glia lim itans, one of the routes of oedema elimination.
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Fullarton, Grant M. "Studies on the pathophysiology of upper gastrointestinal haemorrhage." Thesis, University of Edinburgh, 1988. http://hdl.handle.net/1842/18895.
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Menezes, Kevin Gerard. "A computer model of acute haemorrhage and resuscitation." Thesis, University of Aberdeen, 1998. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU114245.
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Acute haemorrhage cases are extremely difficult to analyse using randomised experimental studies and are well suited to computer modelling. The two main areas of current research are whether intravenous fluids should be administered to patients at the scene of an accident or not and what type of fluid should be given. A computer model was designed which analyses the fluid volume compartments within the human body. The relationship between the blood volume and blood pressure was examined, as was the transcipillary refill effect and the mechanics of the bleeding site. The model was then validated by comparing simulated predictions with previously published animal experiments for different sets of bleeding parameters. The agreement between published and predicted values of blood pressure and haematocrit was good (1.1% and 1.4 respectively). The model was then used to analyse the behaviour of intravenous fluids in trauma resuscitation. It was shown that crystalloid solutions do not follow the established pattern of leakage out of the intravascular system but that the half varies according to the degree of under resuscitation of the patient. The model was also used to determine the efficiency of three different accident site treatment protocols: no treatment, crystalloid infusion and colloid infusion. It was found that for shorter transport time (10-30 minutes) crystalloid infusion had to be at a high rate to be more efficient than no treatment. At high transport times (30-50 minutes) colloid infusion was more efficient that crystalloid and no treatment for medium infusion rates only.
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Brooke, Nicholas S. R. "The study of human cerebral metabolism using 31-phosphorus magnetic resonance spectroscopy." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.364064.
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Lentsoane, Tiisotso Lenake. "Intraventricular haemorrhage in premature babies at Dr George Mukhari Hospital, Pretoria." Thesis, University of Limpopo (Medunsa Campus), 2011. http://hdl.handle.net/10386/670.
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Thesis MSc.(Med)(Virology)-- University of Limpopo, 2011Background: Intraventricular hemorrhage (IVH) is a known complication occurring in the first week of life in premature neonates. The exact time of its occurrence and the ideal time to perform diagnostic imaging investigation remain controversial. Objectives: 1. To determine the incidence of intraventicular hemorrhage in premature babies at Dr George Mukhari Hospital, Pretoria. 2. To determine the timing at which bleeding occurs. 3. To determine if the rate of diagnosing intraventicular hemorrhage improves when performing ultrasound via the posterior fontanelle. 4. To determine the risk factors for intraventricular haemorrhage Materials and methods: The study included 60 premature babies of gestational age of less than 32 weeks that were admitted to our neonatal Intensive Care Unit over a two months period and screened for IVH. They were grouped into three categories according to their weight at birth, and according to their gestational age. All babies had a cranial ultrasound on day 1, 3 and 7. Results: We found that the overall incidence of IVH among premature babies was 28%. Although it did not reach statistical significance, the incidence was found to be inversely related to the birth weight and gestational age. The majority of the bleeds occurred within the first day of life and were mostly grade I and II according to Papile’s classification. The use of inotropes was found to be significantly associated with development of IVH. We also found that scanning through the posterior fontanelle did not significantly increase the rate of diagnosis for IVH.
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Zetterling, Maria. "Clinical Studies in the Acute Phase of Subarachnoid Haemorrhage." Doctoral thesis, Uppsala universitet, Neurokirurgi, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-129160.
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Patients admitted in similar clinical condition after spontaneous SAH can develop very different clinical courses. This could depend on the severity of the initial global ischemic brain injury at ictus. In the present study, we explored relations between clinical and radiological parameters at admission that indicate a more severe initial impact, and the following days hormone levels and brain metabolism. Early global cerebral oedema (GCE) on computed tomography occurred in 57 % of SAH patients and was associated with a more severe clinical condition. The brain’s glucose metabolism, measured with intracerebral microdialysis (MD), changed the first days. MD-glucose was initially high and MD-pyruvate low. MD-glucose gradually decreased and MD-pyruvate and MD-lactate increased, suggesting a transition to a hyperglycolytic state. This was more pronounced in patients with GCE. Similar patterns were seen for interstitial non-transmitter amino acids. From initial low concentrations, they gradually increased in parallel with MD-pyruvate. The amino acid concentrations were higher for patients admitted in better clinical condition. Insulin lowered MD-glucose and MD-pyruvate even when plasma glucose values remained high. P-ACTH and S-cortisol were elevated early after SAH. GCE was associated with higher S-cortisol acutely. Urine cortisol excretion, indicating levels of free cortisol, were higher in patients in a better clinical condition. Suppressed P-ACTH occurred in periods of brain ischemia. We suggest that GCE on the first CT scan is a warning sign indicating increased vulnerability if the patient is exposed to compromised energy supply or increased energy demand. Reduction of blood glucose after SAH should be done with caution. The temporal change of the glucose metabolism and the amino acid concentrations probably reflect activated repair mechanisms. This should be considered in the intensive care treatment of SAH patients. Finally, our results support earlier observations that the response of the hypothalamic-pituitary-adrenal system is important in critical care.
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Domingo, Zayne. "Ischaemia following subarachnoid haemorrhage : magnetic resonance spectroscopy and imaging." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360214.
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Jacobs, Neal. "Novel resuscitation strategies for casualties of blast and haemorrhage." Thesis, University of Newcastle Upon Tyne, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.556122.
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Blast injury is a dominant and increasing mode of battlefield injuries. The resulting complex injury pattern may include hypoxia due to primary blast lung injury and haemorrhage due to severe secondary and tertiary blast injuries. It has been previously shown that hypotensive resuscitation, as recommended by NICE for pre-hospital trauma resuscitation, is not compatible with survival over extended evacuation times following combined blast injury and haemorrhage, due to underlying inadequacy of systemic tissue oxygen delivery. This thesis investigates a hybrid resuscitation strategy, utilising a novel target blood pressure profile of hypotension (SBP 80 mmHg) for one hour followed by normotension (SBP 110 mmHg). This strategy, termed novel hybrid resuscitation (NH), was investigated with an in vivo model of terminally anesthetised pigs exposed to either a blast shock wave or sham blast, followed by severe controlled haemorrhage plus uncontrolled haemorrhage from a grade IV liver injury. In this model of survivable battlefield injury, NH resuscitation using 0.9% saline demonstrated superiority over hypotensive resuscitation for extended evacuation times (up to 8 hours), with significantly improved survival time after combined blast injury and haemorrhage (from 258 to 452 minutes, mean, p=0.0169) and a clinically significant improvement in physiological state after haemorrhage in the absence of blast. There was no evidence of increased re- bleeding associated with NH. The use of hypertonic saline dextran (HSD) as the initial resuscitation fluid in an NH strategy was also assessed. Although HSD did show some physiological benefit after haemorrhage in the absence of blast injury, survival time was Significantly shorter when animals were initially resuscitated with HSD after combined blast and haemorrhage (208 minutes, mean, p=0.04). The reason remains unclear. In conclusion, NH should be considered as an emergency measure when delayed casualty evacuation is enforced. However HSD should be contraindicated when significant primary blast injury complicates haemorrhage.
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McMahon, Catherine Jane. "Inflammation and delayed cerebral ischaemia induced byaneurysmal subarachnoid haemorrhage." Thesis, University of Manchester, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.491335.
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Stroke is a sudden, unpredictable, often devastating neurological event. The commonest cause of morbidity and mortality associated with subarachnoid haemorrhage (SAH) is delayed cerebral ischaemia (DCI). Ischaemic and haemorrhagic strokes are recognised to induce a significant peripheral and central inflammatory response. These responses may be important in the exacerbation of ischaemic damage and in the development and exacerbation of DCI after SAH. A number of studies have examined the potential contribution of pro-inflammatory cytokines, such as interleukin-l (IL-l) and interleukin-6 (IL-6), to damage caused by experimental ischaemia. Intracerebroventricular (ICV) injection of interleukin-lP(IL-l P) causes a marked exacerbation of ischaemic damage in experimental paradigms of cerebral ischaemia. Conversely, administration of the cytokine anatgonist, interleukin-l receptor antagonist (ILlRA), or other inhibitors of IL-l release and action confer neuroprotection; The aim of this work was to test two primary hypotheses, namely (1) circulating markers of inflammation, (specifically, C-reactive protein (CRP), IL-6 and IL-lRA) predict the development of DCI after SAH, and (2) that there is a direct relationship between peripheral and central inflammation. Clinicai predictors of any cerebrovascular event, and outcome after SAH, were also determined. In a prospective study of 179 aneurysmal SAH patients between January 2004 and August 2007, plasma samples (and in 25 patients CSF samples) were obtained over a period of 15 days after SAH. Levels of inflammatory markers and presence· or absence of DCI was determined. In case-control analysis of 159 patients, only rate of change of IL-6 (OR 2.3, CI 1.1 to 5, pO.03) was predictive of DCI. In a secondary analysis of Erythrocyte sedimentation rate (ESR) and WCC, initial ESR (OR 2.4, CI 1.3 to 4.6, pO.006) average ESR (OR 2.3, CI 1.3 to 4.2, pO.006), peak ESR (OR 2.1, CI 1.1 to 3.9, pO.02) and final ESR (OR 2.0, CI 1.2 to 3.3, pO.009) in addition to final WCC (OR 1.2, CI 1 to 1.3, pO.Ol) and rate of change of WCC (OR 1.3, CI 1 to 1.6, pO.OS) were significantly associated with the development of DCI. A direct relationship was not demonstrated between peripheral and central inflammation. In unifactorial analysis of the 179 patient cohort, female sex (HR 1.8, CI 1 to 3.1, pO.04) hypertension (HI3-Z-,_CL1)_J.Q__~:;?,. pO.OOS), statin use (HR 2, CI 1 to 3.8, pO.04), infection peri-study (HR 1.9, CI 1.2 to 3.0, pO.007), increasing WFNS grade (II & III, HR 2.5, CI 1.5 to 4.2, pO.OOO; IV & V, HR 3.8, CI 2to 7.3, p
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Estcourt, Lise Jane. "Risk factors for haemorrhage in patients with haematological malignancies." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:4efbd9b1-62e5-4536-a5ee-df5eea4620d0.
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Haematological malignancies and their treatment lead to prolonged periods of severe thrombocytopenia (platelet count ≤ 50 x 109/l). Despite the use of prophylactic platelet transfusions, haemorrhage remains an important complication during this thrombocytopenic period. Within a 30 day period up to 70% of patients have clinically significant haemorrhage (World Health Organization (WHO) grade 2 or above bleeding) and up to 10% have severe or life-threatening haemorrhage (WHO grade 3 or 4 bleeding). Hence our current management of these patients to prevent haemorrhage is sub-optimal. The aim of this thesis was to identify clinical and laboratory factors that may predict the risk of haemorrhage in patients with haematological malignancies and severe thrombocytopenia. This was achieved via several different study designs and assessed the effect of clinical and laboratory factors on any or clinically significant haemorrhage and their effect on intracranial haemorrhage. This thesis has demonstrated that there is no consensus on how bleeding is assessed and graded in this patient group. Also it showed that the absolute immature platelet number may be a better alternative to the total platelet count to guide administration of platelet transfusions. Female sex, a previous history of a fungal infection, a high C-reactive protein, a high white cell count, a low platelet count, anaemia, impaired renal function, and recent clinically significant haemorrhage were all found to be independent risk factors for haemorrhage. Patients who were in complete remission from their haematological malignancy had a much lower risk of bleeding.
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Wang, Xia. "Rapid blood pressure lowering treatment in acute intracerebral haemorrhage." Thesis, The University of Sydney, 2016. http://hdl.handle.net/2123/15431.
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Acute spontaneous intracerebral haemorrhage (ICH) occurs when a diseased blood vessel ruptures within the brain, allowing blood to track inside the brain to damage tissues and raise intracranial pressure from the mass effect of the resulting haematoma. ICH is less common than acute ischaemic stroke due to occlusion of an intracerebral vessel, accounting for between 10% and 35% of strokes according to the at-risk population. Temporal trends in the incidence of ICH appear stable and its prevalence is increasing in aging populations. The high burden of premature death and disability associated with ICH is well established and treatment options, either medical or surgical, are limited. The most common cause of ICH is elevated blood pressure (BP) and the hypertensive response at presentation also predicts a poor outcome. The INTEnsive Blood Pressure Reduction in Acute Cerebral Haemorrhage Trials (pilot [INTERACT1] and (main [INTERACT2] phases) were undertaken to determine whether early intensive lowering of BP would improve clinical outcomes, and were conducted over a 10-year period from 2006 to 2012. They included patients with spontaneous ICH within 6 hours of onset and associated high systolic BP (SBP) who were randomised to lower level (target SBP <140 mmHg within 1 hour) or contemporaneous guideline-recommended higher level (target SBP <180 mmHg) of routinely available BP lowering treatment. INTERACT2 was the largest randomised evaluation of a treatment in ICH, using a pragmatic design to establish the effectiveness of a potentially widely applicable treatment. The treatment effect on the primary outcome, according to the conventional binary analysis of death or major disability (i.e. scores of 3 to 6 on the modified Rankin scale [mRS]) at 90 days was not significant (P=0.06) at the conventional P <0.05 level. However, the key secondary outcome using an ordinal analysis across all grades on the mRS indicated significantly improved functional outcomes in patients who received intensive BP lowering. In this thesis, I undertook further analyses of the INTERACT datasets to provide further evidence to support the beneficial effects of early intensive BP lowering treatment in ICH. Specific sections of the thesis present different aspects of BP lowering treatment and ancillary management of patients.
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Dawes, William John. "Neural stem cells as therapeutic targets in germinal matrix haemorrhage." Thesis, Queen Mary, University of London, 2017. http://qmro.qmul.ac.uk/xmlui/handle/123456789/24869.
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Haemorrhage within the germinal matrix with extension into the ventricle is commonly seen in very low birth weight babies. Outcome following severe haemorrhage, in particular when associated with post haemorrhagic hydrocephalus and congestive venous infarction is poor, whilst outcome following moderate degrees of haemorrhage remains variable. The Neural Stem Progenitor Cells (NSPC) within the GM have been shown to be exquisitely sensitive to micro-environmental cues, as such, haemorrhage within the GM is postulated to impact on neurological outcome through aberration of normal NSPC behaviour. Here we have developed a stereotactic model of autologous blood injection which recapitulates key features of Papile grade II/III Germinal Matrix Haemorrhage / Intraventricular Haemorrhage (GMH/IVH). This model demonstrates that GMH/IVH causes an activation of the NSPC within the wall of the lateral ventricle and increases the number of transient amplifying cells within the transcallosal pathway. Further to this RNA extraction from the NSPC (selected using a CD133 MACS protocol) revealed that GMH/IVH causes a significant down regulation of the transmembrane receptor Notch, a finding that was validated using Hes5 in situ hybridisation (ISH). Using a battery of behavioural tests including assessment of developmental landmarks, neuromotor and reflex development we found that GMH/IVH causes subtle but significant impacts on early neonatal development. GMH/IVH in transgenic mice overexpressing the polycomb group gene Bmi1 in NSC (Nestin+ve) revealed increased self-renewal and resistance to oxidative stress (properties of Bmi1 overexpression) reduced the impact of GMH on the oligodendrocyte population, it also revealed a unique behavioural phenotype. We propose that GMH/IVH down regulates Notch in the NSPC causing a burst of precocious proliferation and depleting the NSPC pool, which impacts on neurological outcome due to altered cortical architecture. Further we suggest that modulation of NSPC properties may play role in determining outcome and should be further explored for its therapeutic potential.
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Horne, Margaret Anne. "Investigating the risk of intracranial haemorrhage or focal neurological deficit in adults diagnosed with cerebral cavernous malformation." Thesis, University of Edinburgh, 2015. http://hdl.handle.net/1842/15879.
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Background A cerebral cavernous malformation (CCM) is a small cluster of thin-walled, dilated blood vessels within the brain which is prone to bleed. Although the quantity of blood leaking tends to be small, even a small intracranial haemorrhage (ICH) can result in a clinically significant neurological deficit. Because some focal neurological deficits (FND) may in fact be haemorrhages that were undetected by imaging, FND were also included in the analysis wherever possible. In Scotland, between 2006 and 2010, the annual CCM detection rate was 0.8 per 100,000 people. Since estimates of prognosis inform decisions about whether to treat CCM, it is crucial that the untreated clinical course of the disease is fully understood. Aim The aims of this thesis are (i) to quantify the risk of ICH (or ICH or FND, referred to as ‘clinical event’) for an untreated adult within five years of CCM diagnosis, (ii) to identify prognostic factors for ICH (clinical event), and (iii) to create a model to predict, at the time of diagnosis, an individual’s risk of a subsequent ICH (clinical event). Methods Initially, a literature review was undertaken. Then data from adults diagnosed with CCM in the Scottish Intracranial Vascular Malformation Study (SIVMS) were analysed. SIVMS is a prospective, population-based cohort study: it includes all adults resident in Scotland at the time of diagnosis of a first-ever intracranial vascular malformation during the two five-year periods 1999–2003 and 2006–2010. Time-to-event methods were employed to compare the estimated risk of ICH (clinical event) for those who experienced a first ICH (clinical event) during untreated five-year follow-up with those who experienced a second ICH (clinical event). A statistical challenge when analysing clinical outcomes from patients with CCM is that the outcome event of ICH or FND is comparatively rare; therefore a larger cohort of CCM patients was required to identify more robustly potential predictors of ICH (clinical event) and to create a prognostic model to predict, at the time of diagnosis, an individual’s risk of a subsequent ICH (clinical event). Three research groups agreed to contribute their data to enable an individual patient data meta-analysis (IPDMA) to be undertaken. Results In the two SIVMS cohorts, 136 (1999–2003) and 165 adults (2006–2010) were diagnosed with CCM. In the earlier cohort, the estimated risk of a first ICH within five years of presentation (2.4%, 95% CI 0.0% to 5.7%) was significantly lower (p < 0.0001) than the risk of a recurrent ICH (31.9%, 95% CI 4.5% to 59.3%), but the annual risk of a recurrence declined over the five-year period. In the same cohort, women had an increased risk of a second clinical event (log-rank χ2(1) = 6.2, p = 0.01). The IPDMA was based on 988 adults, 62 of whom suffered a first ICH within five years of CCM diagnosis. When the data were pooled, the estimated adjusted hazard ratio for first ICH for clinical presentation (ICH/FND vs other presentation) was 4.5 (95% CI 1.5 to 13.4) and for brainstem location (brainstem vs other location) the adjusted hazard ratio was 3.3 (95% CI 1.5 to 7.2); age, sex and CCM multiplicity did not add any additional prognostic information. Conclusion In this thesis two risk factors have been identified that are independently associated with increased likelihood of experiencing an ICH (or clinical event) within five years of diagnosis. A prognostic model has been built and evaluated, based on these factors. Other areas to be explored in the future include external validation of the model and investigating the effects of (i) antithrombotic therapy and (ii) pregnancy on the progression of the disease.
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Brookes, Zoe L. S. "The effects of haemorrhage on the microcirculation during intravenous anaesthesia." Thesis, University of Sheffield, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327629.
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Galea, James. "Pharmacokinetics of intravenous interleukin-1 receptor antagonist in subarachnoid haemorrhage." Thesis, University of Manchester, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.509780.
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Clarke, Samantha A. "Increased body temperature following subarachnoid haemorrhage : a retrospective correlational study." Thesis, Queensland University of Technology, 2009. https://eprints.qut.edu.au/26542/1/Samantha_Clarke_Thesis.pdf.
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Introduction: Nursing clinicians are primarily responsible for the monitoring and treatment of increased body temperature. The body temperature of patients during their acute care hospital stay is measured at regular repeated intervals. In the event a patient is assessed with an elevated temperature, a multitude of decisions are required. The action of instigating temperature reducing strategies is based upon the assumption that elevated temperature is harmful and that the strategy employed will have some beneficial effect.
Background and Significance: The potential harmful effects of increased body temperature (fever, hyperthermia) following neurological insult are well recognised. Although few studies have investigated this phenomenon in the diagnostic population of non-traumatic subarachnoid haemorrhage, it has been demonstrated that increased body temperature occurs in 41 to 72% of patients with poor clinical outcome. However, in the Australian context the frequency, or other characteristics of increased body temperature, as well as the association between increased body temperature with poor clinical outcome has not been established.
Design: This study used a correlational study design to: describe the frequency, duration and timing of increased body temperature; determine the association between increased body temperature and clinical outcome; and describe the clinical interventions used to manage increased body temperature in patients with non-traumatic subarachnoid haemorrhage. A retrospective clinical chart audit was conducted on 43 patients who met the inclusion criteria.
Findings: The major findings of this study were: increased body temperature occurred frequently; persisted for a long time; and onset did not occur until 20 hours after primary insult; increased body temperature was associated with death or dependent outcome; and no intervention was recorded in many instances.
Conclusion: This study has quantified in a non-traumatic subarachnoid haemorrhage patient population the characteristics of increased body temperature, established an association between increased body temperature with death or dependent outcome and described the current management of elevated temperatures in the Australian context to improve nursing practice, education and research.
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Clarke, Samantha A. "Increased body temperature following subarachnoid haemorrhage : a retrospective correlational study." Queensland University of Technology, 2009. http://eprints.qut.edu.au/26542/.
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Introduction: Nursing clinicians are primarily responsible for the monitoring and treatment of increased body temperature. The body temperature of patients during their acute care hospital stay is measured at regular repeated intervals. In the event a patient is assessed with an elevated temperature, a multitude of decisions are required. The action of instigating temperature reducing strategies is based upon the assumption that elevated temperature is harmful and that the strategy employed will have some beneficial effect.
Background and Significance: The potential harmful effects of increased body temperature (fever, hyperthermia) following neurological insult are well recognised. Although few studies have investigated this phenomenon in the diagnostic population of non-traumatic subarachnoid haemorrhage, it has been demonstrated that increased body temperature occurs in 41 to 72% of patients with poor clinical outcome. However, in the Australian context the frequency, or other characteristics of increased body temperature, as well as the association between increased body temperature with poor clinical outcome has not been established.
Design: This study used a correlational study design to: describe the frequency, duration and timing of increased body temperature; determine the association between increased body temperature and clinical outcome; and describe the clinical interventions used to manage increased body temperature in patients with non-traumatic subarachnoid haemorrhage. A retrospective clinical chart audit was conducted on 43 patients who met the inclusion criteria.
Findings: The major findings of this study were: increased body temperature occurred frequently; persisted for a long time; and onset did not occur until 20 hours after primary insult; increased body temperature was associated with death or dependent outcome; and no intervention was recorded in many instances.
Conclusion: This study has quantified in a non-traumatic subarachnoid haemorrhage patient population the characteristics of increased body temperature, established an association between increased body temperature with death or dependent outcome and described the current management of elevated temperatures in the Australian context to improve nursing practice, education and research.
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Dreier, Jens P. "Cortical spreading ischaemia and delayed ischaemic neurological deficits after subarachnoid haemorrhage." Doctoral thesis, [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=970109342.
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Gill, Navjot. "Long-term functional and neuropsychological outcomes of subarachnoid haemorrhage (SAH) survivors." Thesis, University of Auckland, 2011. http://hdl.handle.net/2292/6879.
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Stroke is the second commonest cause of death worldwide and the most frequent cause of disability in adults. Although Subarachnoid Haemorrhage (SAH) accounts for a small percentage of stroke, it impacts people at a younger age and with debilitating consequences, in the areas of mood, functioning and cognitive deficits which may persist for years after the SAH. However, very little research has been done to examine the long-term (beyond 1-3 years) outcomes of SAH. Furthermore, previous studies have not been population based, nor have they examined the impact of long-term cognitive outcomes using a battery of neuropsychological tests. The current population based study examined long-term neuropsychological and functional outcomes of SAH survivors (n=27). A control group (n=26) matched on age, gender and ethnicity was used to compare the mood, functional (i.e., disability, handicap, quality of life) and neuropsychological outcomes (i.e., verbal memory, visual memory, executive functioning, language, processing speed and visuoperceptual abilities) of SAH survivors. As compared to the controls, the SAH group was more depressed and was significantly impaired in the areas of disability, handicap, quality of life; particularly in the areas of mental health with females reporting poor mental health than males within the SAH group. Furthermore, the SAH group had significant deficits across cognitive domains (i.e., language, memory, visuoperceptual abilities, executive functioning/attention and information processing) when compared to controls. Although impairments were noted at 5-years post-SAH, over time (i.e., from acute stage) significant improvement had occurred in the areas of functioning (i.e., disability, health related quality of life and well-being) of SAH survivors. Depressed mood and baseline functioning were related to worse functional outcomes at 5-years post-SAH. Whilst poor cognitive functioning impacted the long-term functional outcomes of SAH survivors only, visual memory and language were found to independently relate to worse functional outcomes of SAH-survivors. The finding that long-term neuropsychological impairment in SAH-survivors is independently associated with the functional outcomes at 5-years post-SAH provides a new direction for the rehabilitation efforts which have traditionally focussed on physical functioning and activities of daily living. Thus, these findings are of relevance to clinicians to help them understand the expected cognitive deficits and their potential to impact on wider functional outcomes of SAH survivors, thereby allowing the clinicians to plan appropriate interventions for rehabilitations.
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Dinh, The Trung. "Pathogenesis of haemorrhage associated with dengue infection in adults in Vietnam." Thesis, Open University, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.576668.
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Clinical experience suggests that adults with dengue manifest a pattern of complications different from those observed in children, but direct comparisons among populations experiencing the same exposure have rarely been published. I conducted a large prospective descriptive study of dengue across all age-groups presenting to a single institution in an endemic country during a defined time-period. Vascular leakage was more severe in the paediatric patients and DSS developed much more frequently in this age-group. In contrast haemorrhagic manifestations and severe organ involvement were more common in adults. Similar to the established findings in children, typical coagulation abnormalities were apparent in the adults .. - i.e. prolonged APTT with reduced fibrinogen levels but without evidence of true disseminated intravascular coagulation. However thrombocytopenia was significantly worse among the adults throughout the evolution of the disease, even after adjusting for the higher rate of secondary infections in this group, and platelet counts after recovery remained lower than in the children. Clinically severe liver involvement was seen only in adults and was infrequent but usually resulted in I severe bleeding. Chronic hepatitis B co-infection was associated with modestly but significantly increased levels of alanine aminotransferase, but did not otherwise impact the clinical picture. To investigate the mechanisms underlying the increase in APTT I carried out APTT Mixing Studies confirming that deficiency of coagulation factors is a major contributory factor. Since there is little evidence for procoagulant activation the most likely mechanism for this would be leakage of coagulation proteins, many of which are of a similar size to albumin. An additional explanation for the increased APTT could be the presence of a circulating anticoagulant - I found very high levels of heparan sulfate (HS) in the dengue plasma, but was not able to show that the HS exerts an anticoagulant effect. I also used FACS analysis to demonstrate that circulating endothelial cells (CECs) are increased during dengue infections and that percentage CECs correlate with the severity of the coagulopathy and with bleeding. Parallel. increases in both CECs and HS levels support the theory that disruption of the endothelial cell/glycocalyx complex occurs during dengue infections - i.e. CECs appear to be shed from the endothelial layer while HS may be shed from the surface glycocalyx. These disruptions likely affect the function of the complex and could contribute to the pathogenesis of the systemic vascular leak syndrome.
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Morris, Paul Graham. "Long-term neuropsychological outcome following subarachnoid haemorrhage or traumatic brain injury." Thesis, University of Stirling, 2001. http://hdl.handle.net/1893/1877.
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Purpose: The principal aim of this project was to investigate the influence of clinical indices of injury severity and polymorphism of the apolipoprotein E gene upon the long-term physical, cognitive and emotional sequelae of traumatic brain injury and spontaneous subarachnoid haemorrhage. It was also intended to determine the extent to which changes occur in these sequelae beyond the initial six months post injury. Method: Sixty-two brain injury patients who had previously taken part in a neuropsychological assessment at six months post injury were traced and participated in a follow-up assessmens some 6-9 years subsequent to their injury. Separately, a group of 70 subarachnoid patients drawn from a consecutive series of neurosurgical admissions participated in a neuropsychological assessment at 14 months subsequent to their haemorrhage. In both studies, the assessment comprised a semi-structured interview and a battery of cognitive measures focusing principally upon memory and executive function tasks. A questionnaire including a range of standardised measures of anxiety, depression and quality of life was left with patients to be returned by post. Results: The ApoE e4 allele did not appear to influence recovery amongst these brain injury survivors, though there are suggestions that it may have an influence upon subgroups of patients. Amongst traumatic brain injury survivors, post-traumatic amnesia was a better predictor of functional or emotional outcome than consciousness based measures. However, consciousness based measures were more predictive of cognitive sequelae and low admission Glasgow Coma Scale was associated with continued improvement on information processing tasks. Other than on these tasks, there was little evidence of change between 6 months and 6-9 years post injury. Amongst the subarachnoid haemorrhage patients, Fisher Grade was found to be more predictive of subsequent Glasgow Outcome Scale and cognitive function than WFNS Grade or other clinical indices. Surviving aneurysmal patients had comparable levels of recovery to patients who had a negative angiogram. In both studies emotional sequelae, in particular anxiety-related difficulties, were found to be a principal factor in the functional outcome of some 40% of patients. Conclusions: Greater emphasis should be placed upon measures of post-traumatic amnesia as predictors of functional recovery in surviving patients. The use of an amnesia measure may also be warranted in studies of outcome following subarachnoid haemorrhage or other stroke. The ApoE e4 allele does not appear to have a strong influence upon functional recovery after brain injury across all patients, though it is possible that it interacts with other factors to influence recovery in subgroups. Greater emphasis should be placed upon the prevention and/or detection and treatment of mood disorders following brain injury. In the absence of intensive rehabilitative interventions, survivors of serious brain injury are more likely to deteriorate than to continue to recover beyond six months post injury.
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Doran, Catherine Margaret. "Effect of resuscitation strategies on coagulation following haemorrhage and blast exposure." Thesis, University of Newcastle upon Tyne, 2013. http://hdl.handle.net/10443/1868.
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Approximately one-third of trauma patients are coagulopathic on arrival to the emergency department. Acute traumatic coagulopathy and systemic inflammatory responses are serious secondary consequences of severe trauma and are linked to increased morbidity and mortality. Early tissue hypoxia is a major component in the aetiology of both complications. New resuscitation strategies are aimed at improving tissue oxygenation in the pre-hospital phase, and may attenuate coagulopathy and inflammatory sequelae. This is of particular importance in military personnel who suffer complex injuries, often from blast exposure, and may have extended evacuation times. This thesis evaluates the effect of a novel hybrid (NH) resuscitation strategy on coagulation and inflammation. Terminally anaesthetised pigs were randomised to one of two injury strands of haemorrhage +/- blast injury; initially resuscitated with 0.9% Saline to a hypotensive systolic blood pressure of 80mmHg for one hour. This was followed by either a return to a normotensive pressure (110mmHg) (NH) or a continuation at the hypotensive level. Over both injury strands NH significantly reduced Prothrombin Time, PT (mean proportion of baseline: 1.40±0.05 vs. 1.80±0.09; p=0.001) and interleukin-6 (IL6) levels (mean 1106±153 vs. 429±79 pg/ml; p=0.001) compared to the hypotensive groups. PT was positively correlated with IL6 (p=0.002) and base deficit (p=0.0004). These findings indicate that improving tissue oxygenation reduces the coagulation derangement and the pro-inflammatory response. No difference in coagulopathy was found between injury strands although blast did cause greater inflammation. Early identification of coagulopathic casualties is essential and a separate feasibility field study was preformed to assess the use of thromboelastometry in a deployed military hospital, evaluating the degree of coagulopathy in battlefield casualties and to monitor the coagulation status during the resuscitation process. In conclusion, NH attenuated the acute traumatic coagulopathy and inflammatory responses and therefore should be considered when an extended casualty evacuation is enforced.
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Charidimou, A. "Applied clinical neuroimaging in cerebral amyloid angiopathy and spontaneous intracerebral haemorrhage." Thesis, University College London (University of London), 2015. http://discovery.ucl.ac.uk/1461023/.
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Sporadic cerebral amyloid angiopathy is a common small vessel disease that preferentially involves small cortical and leptomeningeal arteries due to progressive amyloid-β deposition in their walls. Cerebral amyloid angiopathy occurs frequently in elderly people, and is a common and important cause of symptomatic lobar intracerebral haemorrhage and cognitive impairment. There is currently a growing interest in cerebral amyloid angiopathy, at least partly thanks neuroimaging, which now allows an unprecedented ability to investigate the disease dynamics in vivo using MRI to reveal complex patterns of cerebral bleeding and ischaemia. The detection of CAA during life is becoming an increasingly important challenge, since approaches of prevention or treatment (disease-modification) are now emerging as realistic possibilities. Determining the most promising treatments requires development of reliable biomarkers, the goal of my research. The main objective of this PhD thesis is to provide new insights into potential clinical and applied clinical neuroimaging biomarkers in patients with cerebral amyloid angiopathy. This is accomplished by a portfolio of research studies investigating: (a) the clinical and radiological spectrum of transient focal neurological episodes as a potential clinical clue for cerebral amyloid angiopathy; (b) cortical superficial siderosis, a distinct pattern on bleeding in the brain, as both a diagnostic and a prognostic marker of cerebral amyloid angiopathy; (c) MRI-visible perivascular spaces topography, as a new marker of small vessel disease and cerebral amyloid angiopathy; (d) potential pathological, neuroimaging and genetic differences in patients with pathology-proven CAA with and without intracerebral haemorrhage and presents evidence for different disease phenotypes; (e) the evidence whether the presence and burden of cerebral microbleeds on MRI scans is associated with an increased risk of recurrent spontaneous ICH, and if this risk is different according to MRI-defined microangiopathy subtype, in a meta-analysis.
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Zarros, Apostolos. "Development and assessment of in vitro simulation approaches to intracerebral haemorrhage." Thesis, University of Glasgow, 2017. http://theses.gla.ac.uk/8119/.
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This current PhD Thesis in Neuropathology focuses on the development and assessment of in vitro simulation approaches to intracerebral haemorrhage. The PhD Thesis provides a clinical and experimental neuropathological overview of intracerebral haemorrhage as well as an account of the in vitro simulation approaches to the disease, before proceeding to the presentation of the experimental work designed and performed by the author. The development of the herein presented in vitro simulation approaches to intracerebral haemorrhage was based on the use of an immortalized embryonic murine hippocampal cell-line (mHippoE-14) and its response to oligomycin-A and ferrum or haemin under appropriately selected conditions (aiming to simulate the natural history of the disease in a more reliable manner). The PhD Thesis provides a characterization of the mHippoE-14 cell-line (through a real-time cellular response analysis and a cytomorphological characterization), before proceeding to the actual experimental justification of the conditions chosen for the development of the herein presented in vitro simulation approaches to intracerebral haemorrhage, and their assessment. The latter was performed through the undertaking of: (a) real-time cellular response analysis, (b) cytomorphological assessment, (c) profiling of neuronal markers’ expression, (d) neurochemical assessment, and (e) proteomic profiling. All experiments were performed at the University of Glasgow. The current PhD Thesis also provides a critical appraisal of: (a) the utility, novelty and limitations of the developed in vitro simulation approaches, and (b) the positioning of the developed in vitro simulation approaches within the neuropathopoietic context.
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Hreash, Fatma. "The cardiovascular effects of vasopressin following acute haemorrhage in anaesthetized rats." Thesis, Imperial College London, 1988. http://hdl.handle.net/10044/1/47113.
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Hellawell, Deborah Jane. "Cognitive and funtional outcome following traumatic brain injury or subarachnoid haemorrhage." Thesis, University of Edinburgh, 1998. http://hdl.handle.net/1842/21299.
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The present study was designed to investigate the outcome of 100 surviving patients who were admitted consecutively to a regional neurosurgical unit with a diagnosis of either moderate or severe TBI. An additional group of 44 SAH patients was recruited to enable tentative comparisons to be drawn between groups with acute brain injury arising from these different causes. At intervals of 6, 12 and 24 months post-injury, global outcome was estimated using the Glasgow Outcome Scale (GOS) and patients were assessed using a battery of neuropsychological tests. Information concerning the extent of the patient's recovery was also collected at each time point. Poorer GOS outcome was associated with greater severity of initial injury. However, complications arising at the acute stage of treatment also influenced outcome. Because of the limited sensitivity of the GOS, a more detailed outcome scale, the Edinburgh Extended Glasgow Outcome Scale (EEGOS), was devised and applied. Results of the neuropsychological assessment in the TBI patient groups showed that severe cognitive impairment was typically associated with more severe initial injury. These results are in agreement with those of Rimel et al. (1982) in suggesting that patients with moderate TBI experience a level of morbidity intermediate between those with severe and those with minor TBI, and contrast with those of Anderson et al. (1994) for reasons which are discussed. Despite the relationship between severity of injury and cognitive impairment, functional problems were reported to a similar extent by relatives of both the severe and moderate TBI patients. The results suggest that the brain injury impacts on everyday life to a greater extent and in many more patients than might be expected on the basis of formal cognitive assessment. Comparisons between the TBI and SAH groups were heavily influenced by a difference in the estimated severity of initial brain injury, but there were similarities in outcome between groups. Formal assessment of cognitive function is useful and informative in the conditions studied, but that other measures provide important supplementary information about the ways in which acute brain injury influences the lives of patients.
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Chaudery, Muzzafer. "A reflection of pre-hospital imaging on traumatic intra-abdominal haemorrhage." Thesis, Imperial College London, 2016. http://hdl.handle.net/10044/1/47965.
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Torso haemorrhage remains one of the leading causes of preventable morbidity and mortality from trauma particularly in the prehospital setting. Early identification of the haemorrhage source is essential in order to improve outcomes and an effective imaging modality may help to establish the diagnosis. This thesis examines how to improve abdominal haemorrhage identification in the prehospital setting in order to achieve rapid haemorrhage control. The current literature is appraised and a national questionnaire distributed to frontline trauma care physicians. For haemorrhage identification research into ultrasound is recommended and for haemorrhage control novel procedures such as Resuscitative endovascular balloon occlusion of the Aorta (REBOA) are valued. FAST (Focused abdominal sonography for trauma) is considered the most appropriate modality for haemorrhage identification in the prehospital setting but it is associated with a steep learning curve. In order to improve training, a face, content and construct validation of a FAST simulator model is undertaken. Furthermore to better understand an ideal performance, an ergonomic analysis of experts’ workspace and force during a FAST scan is conducted. From this, an expert set of metrics is derived of the ideal ultrasound probe position and force for each FAST region. A learning curve study is implemented to assess two randomised groups of novices one trained with the expert metrics and the other trained using a standardised curriculum. The expert metrics group are faster and more accurate at performing a FAST scan than the control. This is also the case in a prospective validity study. REBOA is being investigated as a novel technique for prehospital haemorrhage control. Accurate inflation of the balloon catheter within the correct zone is critical to gain control of bleeding and prevent adverse effects, particularly in the prehospital setting. A feasibility study identifies that ultrasound guidance and balloon insufflation with contrast agent enhances catheter placement within Zone III. Subsequently, two groups of physicians are randomised to perform REBOA with and without ultrasound guidance. The former are faster and more precise than the latter group hence supporting the robustness of the ultrasound imaging technique. Overall this thesis enhances prehospital abdominal haemorrhage identification by improving FAST training and augments haemorrhage control through accurate REBOA placement with the use of ultrasound and contrast agent.
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Abdul-Kadir, Rezan Ahmed. "Inherited bleeding disorders in obstetrics and gynaecology." Thesis, University of London, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.391628.
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