Relevant bibliographies by topics / Haemorrhage

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Haemorrhage'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "Haemorrhage"

1

Boertjes, Emma, Stefanie Hillebrand, Janneke Elisabeth Bins, and Laurien Oswald. "Pulmonary haemorrhage in Weil’s disease." BMJ Case Reports 13, no. 1 (January 2020): e227570. http://dx.doi.org/10.1136/bcr-2018-227570.

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Leptospirosisis a zoonosis caused by spirochaetes from the species Leptospira. The more severe form of leptospirosis, known as Weil’s disease, is characterised by the triad of jaundice, renal impairment and haemorrhages. Pulmonary involvement occurs in 20%–70% of the patients, with severity ranging from non-productive cough to respiratory failure mainly due to pulmonary haemorrhage. Recognition of Weil’s disease in patients presenting with pulmonary symptoms can be difficult. This case illustrates a classic case of pulmonary haemorrhagic involvement in Weil’s disease.
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Blanco, Alicia, Roberto Chuit, Susana Meschengieser, Ana Kempfer, Cristina Farías, María Lazzari, and Adriana Woods. "Major haemorrhage related to surgery in patients with type 1 and possible type 1 von Willebrand disease." Thrombosis and Haemostasis 100, no. 05 (2008): 797–802. http://dx.doi.org/10.1160/th-07-12-0757.

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SummaryPatients with von Willebrand disease (VWD) frequently bleed under a challenge. The aim of our study was to identify predictive markers of perioperative major haemorrhage in type 1 (VWF:RCo = 15–30 IU dl-1) and possible type 1 (VWF:RCo = 31–49 IU dl-1)VWD patients. We recorded perioperative bleeding complications previous to diagnosis and laboratory parameters in 311 patients with 498 surgical procedures. The patients were grouped according to the absence (A) or presence (B) of perioperative major haemorrhages. Eighty-one patients (26%) and 87 surgical procedures (17.5%) presented major haemorrhages associated with surgeries. There was no difference between the percentage of type 1 and possible type 1 VWD patients who had major haemorrhages (32.6% and 24.8% respectively; p=ns). No difference in the prevalence of O blood group, age, gender, positive family history and laboratory test results (FVIII and VWF) was observed, independent of the haemorrhagic tendency. Bleeding after tooth extraction was the most frequent clinical feature observed in patients with perioperative major haemorrhages. The bleeding score and the number of bleeding sites (≥3) were not predictors of major haemorrhage associated with surgery. Caesarean section and adenotonsillectomy showed the highest frequency of major haemorrhages (24.6% and 22.3%, respectively). In conclusion, type 1 and possible type 1VWD patients showed similar incidence of perioperative major haemorrhages. Laboratory tests and positive family history did not prove to be effective at predicting major haemorrhages in patients that had either type 1 or possible type 1 VWD. The history of bleeding after tooth extraction could define risk factors of major haemorrhage.
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Abdulla, M. C. "Spontaneous soft tissue haemorrhage in systemic lupus erythematosus." Reumatismo 68, no. 4 (December 31, 2016): 199. http://dx.doi.org/10.4081/reumatismo.2016.952.

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Diversity in clinical presentations and complications of systemic lupus erythematosus (SLE) make the diagnosis and management challenging. The mechanisms of haemorrhagic manifestations in SLE have not been well elucidated. A 47-year-old woman with no comorbidities was admitted after suffering fatigue and low grade fever for six months. She had bilateral soft tissue haemorrhage over the forearm and intra retinal haemorrhages. She was assessed and diagnosed as having SLE based on positive antinuclear antibody, strongly positive anti double stranded DNA, thrombocytopenia and low C3 and C4 levels. We describe a case of spontaneous bilateral soft tissue haemorrhage in SLE and discuss the various mechanisms causing bleeding in lupus.
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Ibrahim, Umma A., Sagir G. Ahmed, Modu B. Kagu, and Usman A. Abjah. "Impact of intestinal helminths on the risks of gastrointestinal haemorrhage and iron deficiency among haemophilia patients in northern Nigeria." Journal of Haemophilia Practice 4, no. 1 (January 26, 2017): 58–64. http://dx.doi.org/10.17225/jhp00097.

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Abstract We predicted that haemophilia would create a prohaemorrhagic host-parasite relationship, which would make haemophiliacs very vulnerable to haemorrhagic effects of intestinal helminths in tropical countries like Nigeria. If our prediction is correct, the frequency and risks of gastrointestinal haemorrhage and iron deficiency will be higher among haemophiliacs infected by helminths in comparison with uninfected haemophiliacs. Frequency of gastrointestinal haemorrhages and iron deficiency among haemophiliacs with and without intestinal helminth infections were retrospectively obtained and analysed, and their relative risk determined by regression analysis. Haemophiliacs with intestinal helminths had significantly higher frequencies of gastrointestinal haemorrhage (73.3% vs. 18.5%, p<0.05) and iron deficiency (60% vs. 22.2%, p<0.05) in comparison with haemophiliacs without intestinal helminths. Haemophiliacs with intestinal helminths had significantly elevated relative risks (RR) of gastrointestinal haemorrhage (RR=3.4, CI95%: 2.4- 4.3, p=0.007) and iron deficiency (RR=2.5, CI95%: 1.7-3.3, p=0.009). These results showed that helminth infections were associated with increased risks of gastrointestinal haemorrhage and iron deficiency in haemophiliacs. This is thought to be due to a pro-haemorrhagic host-parasite relationship resulting from host haemostatic abnormality, coupled with the concurrent manipulation of the host haemostatic system by anticoagulants produced by some of the parasites. Haemophiliacs in tropical countries should be regularly screened and treated for intestinal helminths.
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Azeemuddin, Muhammad, Muhammad Awais, Fatima Mubarak, Abdul Rehman, and Noor Ul-Ain Baloch. "Prevalence of subarachnoid haemorrhage among patients with cranial venous sinus thrombosis in the presence and absence of venous infarcts." Neuroradiology Journal 31, no. 5 (June 12, 2018): 496–503. http://dx.doi.org/10.1177/1971400918783060.

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Introduction In patients with cranial venous sinus thrombosis, the occurrence of subarachnoid haemorrhage in association with haemorrhagic venous infarcts is a well described phenomenon. However, the presence of subarachnoid haemorrhage in patients with cranial venous sinus thrombosis in the absence of a haemorrhagic venous infarct is exceedingly rare. Methods We retrospectively reviewed charts and scans of all patients who had cranial venous sinus thrombosis confirmed by magnetic resonance venography at our hospital between September 2004 and May 2015. The presence of subarachnoid haemorrhage was ascertained on fluid-attenuated inversion recovery, susceptibility-weighted imaging and/or unenhanced computed tomography scans by a single experienced neuroradiologist. Statistical analysis was performed using the Statistical Package for Social Sciences version 20. Differences in the proportion of haemorrhagic venous infarcts among patients with subarachnoid haemorrhage versus those without subarachnoid haemorrhage were compared using the chi-square test. A P value of less than 0.05 was considered significant. Results A total of 138 patients who had cranial venous sinus thrombosis were included in the study. Seventy-three (52.9%) were women and the median age of subjects was 35 (interquartile range 22–47) years. Venous infarcts and haemorrhagic venous infarcts were noted in 20/138 (14.5%) and 62/138 (44.9%) cases, respectively. Subarachnoid haemorrhage was present in 15/138 (10.9%) cases and, in three cases, subarachnoid haemorrhage occurred in the absence of a venous infarct. Haemorrhagic venous infarcts were more prevalent ( P = 0.021) among patients with subarachnoid haemorrhage (11/15) than in those without subarachnoid haemorrhage (51/123). Conclusion In patients with cranial venous sinus thrombosis, subarachnoid haemorrhage can occur even in the absence of a haemorrhagic venous infarct. The recognition of cranial venous sinus thrombosis as the underlying cause of subarachnoid haemorrhage is important to avoid misdiagnosis and inappropriate management.
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Grysiewicz, Rebbeca, and Philip B. Gorelick. "Update on Amyloid-associated Intracerebral Haemorrhage." European Neurological Review 7, no. 1 (2012): 22. http://dx.doi.org/10.17925/enr.2012.07.01.22.

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Cerebral congophilic or amyloid angiopathy (CAA) is a clinicopathological entity that is considered a common cause of primary non-traumatic brain haemorrhage in the elderly. CAA is frequently associated with Alzheimer’s disease (AD) and has become a primary focus of scientific inquiry. The spectrum of intracerebral haemorrhage (ICH) that may occur in CAA includes: cerebral lobar haemorrhages, deep haemorrhages, purely subarachnoid and subdural haemorrhages and cerebral microbleeds. CAA is also associated with microinfarcts, leukoencephalopathy and superficial siderosis. This brief article will provide an update on the advances in our understanding of CAA-associated ICH with a focus on the following topics: neuropathology and mechanism of CAA-related haemorrhage; epidemiology, including genetic and other possible risk factors; clinical presentation; diagnosis, including newer imaging modalities; and prospects for prevention and treatment.
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Patwary, ZP, MAR Faruk, and MM Ali. "Clinical and Histopathological Study of Important Air-Breathing Fishes." Progressive Agriculture 19, no. 1 (November 23, 2013): 69–78. http://dx.doi.org/10.3329/pa.v19i1.17109.

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A study was conducted to know the health and disease problems of three important air-breathing fishes viz. Shing (Heteropneustes fossilis), Magur (Clarias batrachus) and Thai Koi (Anabas testudineus) through clinical and histopathological technique from June 2007 to March 2008 collected from selected farms and from local markets. Generally, during December and January, acute pathologies were recorded. Clinical signs of Shing included haemorrhage, extended belly and ulceration. Histopathologically, partly missing and splitted epidermis and dermis, necrotic, vacuoled and ruptured myotomes of muscle with fungal granuloma were observed. Major gill pathologies included partly missing and highly hypertrophied, haemorrhagic gill lamellae, presence of monogenetic trematode and pyknotic cells. In liver, haemorrhagic areas, necrotic, vacuoled, hyperplasid hepatocytes, cell debris, pyknotic nuclei and plenty of inflammatory cells were evident. Haemorrhages, vacuolation, necrosis, missing and ruptured kidney tubules and pyknotic nuclei were the major pathologies of kidney. Clinically, dark red lesion, haemorrhage, necrosis and ulcer in body surface were seen in Magur. Histopathologically observed pathologies in Magur were almost similar to that of Shing. Clinical signs of Thai Koi included discoloration, loss of scales and fins, abnormal caudal fin, haemorrhage in gill and ulcer. Marked histopathology in the skin and muscle were observed such as totally lost epidermis, dermis separated from muscle, severely ruptured, degenerated and missing of myotomes in many places. In gills, hypertrophy, hyperplasia, telangiectasis, clubbing, haemorrhage and massive necrosis in both primary and secondary gill lamellae were found. Pathologies observed in liver and kidney were most alike to that of Shing. In the months of February and March, all the investigated organs of the three fish species were at a healing stage.DOI: http://dx.doi.org/10.3329/pa.v19i1.17109 Progress. Agric. 19(1): 69 - 78, 2008
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Klopfleisch, R., B. Kohn, S. Plog, C. Weingart, K. Nöckler, A. Mayer-Scholl, and A. D. Gruber. "An Emerging Pulmonary Haemorrhagic Syndrome in Dogs: Similar to the Human Leptospiral Pulmonary Haemorrhagic Syndrome?" Veterinary Medicine International 2010 (2010): 1–7. http://dx.doi.org/10.4061/2010/928541.

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Severe pulmonary haemorrhage is a rare necropsy finding in dogs but the leptospiral pulmonary haemorrhagic syndrome (LPHS) is a well recognized disease in humans. Here we report a pulmonary haemorrhagic syndrome in dogs that closely resembles the human disease. All 15 dogs had massive, pulmonary haemorrhage affecting all lung lobes while haemorrhage in other organs was minimal. Histologically, pulmonary lesions were characterized by acute, alveolar haemorrhage without identifiable vascular lesions. Seven dogs had mild alveolar wall necrosis with hyaline membranes and minimal intraalveolar fibrin. In addition, eight dogs had acute renal tubular necrosis. Six dogs had a clinical diagnosis of leptospirosis based on renal and hepatic failure, positive microscopic agglutination test (MAT) and/or positive blood/urineLeptospira-specific PCR.Leptospiracould not be cultured post mortem from the lungs or kidneys. However,Leptospira-specific PCR was positive in lung, liver or kidneys of three dogs. In summary, a novel pulmonary haemorrhagic syndrome was identified in dogs but the mechanism of the massive pulmonary erythrocyte extravasation remains elusive. The lack of a consistent post mortem identification ofLeptospiraspp. in dogs with pulmonary haemorrhage raise questions as to whether additional factors besidesLeptospiramay cause this as yet unrecognized entity in dogs.
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Pertiwi, Kartika, Allard van der Wal, Dara Pabittei, Claire Mackaaij, Marinus van Leeuwen, Xiaofei Li, and Onno de Boer. "Neutrophil Extracellular Traps Participate in All Different Types of Thrombotic and Haemorrhagic Complications of Coronary Atherosclerosis." Thrombosis and Haemostasis 118, no. 06 (April 19, 2018): 1078–87. http://dx.doi.org/10.1055/s-0038-1641749.

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AbstractAcute coronary syndromes can be initiated by either atherosclerotic fibrous cap ruptures, superficial plaque erosions or intraplaque haemorrhages (IPHs). Since neutrophil extracellular traps (NETs) display pro-inflammatory and pro-thrombotic properties, we investigated the presence, extent and distribution of neutrophils and NETs in different types of plaque complications in relation to the age of overlying thrombus mass or haemorrhage. Sixty-four paraffin-embedded coronary plaque segments of 30 acute myocardial infarction patients were retrieved from the autopsy archives, which contained 44 complicated plaques (17 IPHs, 9 erosions and 18 ruptures) and 20 intact plaques. Complicated plaques were further categorized according to the histological age of thrombus or haemorrhage. Immunohistochemistry was performed to visualize neutrophils (anti-myeloperoxidase, anti-elastase and anti-CD177) and NETs (anti-citrullinated histone-3 and anti-peptidyl-arginine-deiminase-4). The results were scored semi-quantitatively. Neutrophils and NETs were abundantly present in all types of complicated, but not in intact, plaques (p < 0.05). They were found in thrombus, haemorrhages and at the thrombus–plaque interface, with no significant differences in extent between ruptures, erosions and IPHs. Interestingly, adjacent perivascular tissue of complicated, but not of intact plaques, also contained high numbers of neutrophils and NETs (p < 0.05). In thrombus and haemorrhage of different age, neutrophils and NETs were more frequently present in non-organized (fresh) thrombi and in on-going IPHs. In conclusion, netosis is a prominent pro-thrombotic participant in all distinct types of atherothrombosis, which may facilitate the progression of thrombotic or haemorrhagic complications and thus the onset of ensuing clinical coronary ischemic syndromes.
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Belenje, Akash, Rupali Bose, and Subhadra Jalali. "Rare case of Terson’s syndrome and viral retinitis due to dengue haemorrhagic fever in an infant." BMJ Case Reports 14, no. 5 (May 2021): e242274. http://dx.doi.org/10.1136/bcr-2021-242274.

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Dengue haemorrhagic fever with consequent thrombocytopaenia can lead to intracranial haemorrhage and Terson’s syndrome that can lead to visual problems. Simultaneously, the dengue virus can cause typical viral retinitis like picture in the eye. Early funduscopy and vision assessment is desirable in all dengue patients. In our case, an infant with dengue haemorrhagic fever and intracranial haemorrhage developed not only simultaneous bilateral vitreous and subinternal limiting membrane haemorrhage due to Terson’s syndrome from the indirect effect of thrombocytopaenia but also typical chorioretinitis possibly due to the direct effect of the virus on the retina. The vitreoretinal surgical outcome was satisfactory in this case.
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Dissertations / Theses on the topic "Haemorrhage"

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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.
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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.
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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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Books on the topic "Haemorrhage"

1

S, Hunt P., ed. Gastrointestinal haemorrhage. Edinburgh: Churchill Livingstone, 1986.

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W, Lindsay Kenneth, and Van Gijn J, eds. Subarachnoid haemorrhage. London: Saunders, 1992.

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1941-, McAllister V. L., ed. Subarachnoid haemorrhage. Berlin: Springer-Verlag, 1986.

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Sengupta, R. P., and V. L. McAllister. Subarachnoid Haemorrhage. London: Springer London, 1986. http://dx.doi.org/10.1007/978-1-4471-1383-6.

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Kakarieka, Algirdas. Traumatic Subarachnoid Haemorrhage. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60379-2.

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Kakarieka, A. Traumatic subarachnoid haemorrhage. Berlin: Springer, 1997.

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Langmoen, Iver A., Tryggve Lundar, Rune Aaslid, and Hans-J. Reulen, eds. Neurosurgical Management of Aneurysmal Subarachnoid Haemorrhage. Vienna: Springer Vienna, 1999. http://dx.doi.org/10.1007/978-3-7091-6377-1.

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Govaert, Paul. Cranial haemorrhage in the term newborn infant. Cambridge: Cambridge University Press, 1993.

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Cranial haemorrhage in the term newborn infant. London: Mac Keith Press, 1993.

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Salami, Ayobami T. Space applications and ecological haemorrhage: The Nigerian experience. Ile-Ife: Obafemi Awolowo University Press, 2009.

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Book chapters on the topic "Haemorrhage"

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Allkemper, T. "Haemorrhage." In Clinical MR Imaging, 65–76. Berlin, Heidelberg: Springer Berlin Heidelberg, 2006. http://dx.doi.org/10.1007/3-540-31555-1_3.

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Boyle, Maureen, and Judy Bothamley. "Haemorrhage." In Critical Care Assessment by Midwives, 70–85. New York, NY : Routledge, 2018.: Routledge, 2018. http://dx.doi.org/10.4324/9781315183657-6.

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Sengupta, R. P., and V. L. McAllister. "Historical Review." In Subarachnoid Haemorrhage, 1–8. London: Springer London, 1986. http://dx.doi.org/10.1007/978-1-4471-1383-6_1.

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Sengupta, R. P., and V. L. McAllister. "Basic Principles of Surgical Treatment of Intracranial Aneurysms." In Subarachnoid Haemorrhage, 193–235. London: Springer London, 1986. http://dx.doi.org/10.1007/978-1-4471-1383-6_10.

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Kolluri, V. R. Sastry. "Results of Surgical Treatment of Intracranial Aneurysms." In Subarachnoid Haemorrhage, 237–67. London: Springer London, 1986. http://dx.doi.org/10.1007/978-1-4471-1383-6_11.

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Sengupta, R. P., and V. L. McAllister. "Vasospasm." In Subarachnoid Haemorrhage, 269–81. London: Springer London, 1986. http://dx.doi.org/10.1007/978-1-4471-1383-6_12.

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Sengupta, R. P., and V. L. McAllister. "Arteriovenous Malformations." In Subarachnoid Haemorrhage, 283–313. London: Springer London, 1986. http://dx.doi.org/10.1007/978-1-4471-1383-6_13.

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Sengupta, R. P., and V. L. McAllister. "Subarachnoid Haemorrhage in Pregnancy." In Subarachnoid Haemorrhage, 315–23. London: Springer London, 1986. http://dx.doi.org/10.1007/978-1-4471-1383-6_14.

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Sengupta, R. P., and V. L. McAllister. "Subarachnoid Haemorrhage in Infancy, Childhood and Adolescence." In Subarachnoid Haemorrhage, 325–42. London: Springer London, 1986. http://dx.doi.org/10.1007/978-1-4471-1383-6_15.

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Sengupta, R. P., and V. L. McAllister. "Spinal Subarachnoid Haemorrhage." In Subarachnoid Haemorrhage, 343–56. London: Springer London, 1986. http://dx.doi.org/10.1007/978-1-4471-1383-6_16.

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Conference papers on the topic "Haemorrhage"

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Soni, A., N. Badiani, F. Gawecki, H. Finnamore, and C. Shovlin. "P121 Haemorrhage adjusted iron-requirements and exercise capacity in hereditary haemorrhagic telangiectasia patients." In British Thoracic Society Winter Meeting 2019, QEII Centre, Broad Sanctuary, Westminster, London SW1P 3EE, 4 to 6 December 2019, Programme and Abstracts. BMJ Publishing Group Ltd and British Thoracic Society, 2019. http://dx.doi.org/10.1136/thorax-2019-btsabstracts2019.264.

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Hixson, Thomas, Annika Tihverainen, Sanjay Raina, and Mahvash Rastegari. "P133 Adrenal haemorrhage following birth trauma." In 8th Europaediatrics Congress jointly held with, The 13th National Congress of Romanian Pediatrics Society, 7–10 June 2017, Palace of Parliament, Romania, Paediatrics building bridges across Europe. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2017. http://dx.doi.org/10.1136/archdischild-2017-313273.221.

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Sphoorthy, T. M., and Vidya Patil. "Management of Atonic Postpartum Haemorrhage with Haemorrhagic Shock and Impending Cardiac Arrest for Emergency Peripartum Hysterectomy." In ISACON KARNATAKA 2017 33rd Annual Conference of Indian Society of Anaesthesiologists (ISA), Karnataka State Chapter. Indian Society of Anaesthesiologists (ISA), 2017. http://dx.doi.org/10.18311/isacon-karnataka/2017/ep042.

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Blare, S., C. N. McCollum, and R. M. Greenhalgh. "THE MECHANISM OF THE HYPERCOAGULABLE RESPONSE TO HAEMORRHAGE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643179.

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Gastrointestinal haemorrhage causes a hypercoagulable state and early blood transfusion increases both rebleeding and transfusion requirements [1]. The role of x- and B-adreno-receptors in the mechanism of this hypercoagulable state and the effects of infusions have been studied in NZW rabbits.Haemorrhage was simulated by aspirating 20% of the blood volume from the median ear artery. Coagulation was measured before haemorrhage and at 30-minute intervals using the Biobridge Impedance Clotting Time (ICT). Three different groups of rabbits were used: (a) normal controls, (b) B-blocked with propranolol 1mg/kg, and (c) x- and B-blocked with phentolamine 3mg/kg and propranolol 1mg/kg. Equal volumes of (i) Haemaccel, (ii) fresh blood or (iii) stored blood were then given 30 minutes after haemorrhage.Mean ± sem ICT was 6.0±0.15 minutes before haemorrhage, with no difference between the groups, suggesting that x- and B-blocking drugs have no effect on baseline coagulation. Haemorrhage produced a hypercoagulable state with the mean ICT shortened from 6.1±0.2 to 2,2±0.2 minutes (p<0.01). This response was significantly reduced to 5.2±0.4 and 5.1±0.2 minutes by both B-blockade and combined x- and B-blockade respectively.Haemaccel had no significant effect on the hypercoagulable state, with the ICT going from 2.6±0.2 to 2.8±0.3 minutes. However, fresh and stored blood both reversed hypercoagulability with ICT increasing from 2.6±0.3 to 4.6+0.2 and 5.1±0.1 minutes respectively.In this model the hypercoagulable response to haemorrhage appears to be mainly B- mediated and is partially reversed by both fresh and stored blood, but not by Haemaccel.1. Blair SD, Janvrin SB, McCollum CN, Greenhalgh RM (1986). Br J Surg 73: 783-785.
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Holgado, S., A. Olivé, M. Gumà, V. Ortiz-Santamaría, M. Valls, A. Lafont, E. Casado, and X. Tena. "AB0080 Treatment failure pulmonary haemorrhage of sistemic lupus." In Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.125.

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Azimee, M., A. Chakravarty, and S. Anand. "Subarachnoid haemorrhage and paraplegia in coarctation of aorta." In 18th Annual Conference of Indian Society of Neuroanaesthesiology and Critical Care (ISNACC 2017). Thieme Medical and Scientific Publishers Private Ltd., 2017. http://dx.doi.org/10.1055/s-0038-1646203.

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Waters, A. H., R. Ireland, R. S. Mibashan, M. F. Murphy, D. S. Millar, J. F. Chapman, P. Metcalfe, L. S. de Vries, C. H. Rodeck, and K. H. Nicolaides. "FETAL PLATELET TRASFUSIONS IN THE MANAGEMENT OF ALLOIMMUNE THROMBOCYTOPENIA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643977.

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Intracranial haemorrhage is the most serious complication of alloimmune neonatal thrombocytopenia (ANT). It has generally been assumed that this occurs during delivery, but evidence is accumulating that intracranial haemorrhage may have already occurred in utero. Management of the pregnancy at risk is therefore more exacting, and it has been suggested that intrauterine platelet transfusions may be of benefit (Daffos et al, Lancet, Li, 632. 1984). We have used this approach in two pregnancies in PlA1 negative mothers with PlA1 positive fetuses affected by ANT. Both were second pregnancies, the first in each case having produced a brain damaged infant due to CNS haemorrhage. First patient (CW): Ultrasound scans of the fetal head at 10,22,28 and 32 weeks were all normal. She was admitted at 35 weeks for fetal sampling and platelet transfusion. Ultrasonography showed dilated ventricles and a left anterior cerebral haematoma. The fetal platelet count was 12 × 109/1,rising after transfusion of PlA1negative platelets to 139 x 109/1. The baby was delivered by Caesarean section and the cord blood platelet count was 126 × 109/1.Subsequent clinical assessment by CT scanning and NMR indicated both recent (1-2 weeks) and older (>4weeks) cerebral haemorrhages (de Vries et al, in press). Second patient (CR): Platelet transfusions were started earlier in this pregnancy. At 26 weeks the fetal platelet count was 32 × 109/1, rising to 160 × 109/1 after platelet transfusion. This was repeated at 27 wk (25 to 280 × 109/1), 29 weeks (5 to 320 × 109/1) and regularly until birth. Before the third platelet transfusion, the mother received intravenous IgG 0.4 g/Kg/d for 5 days, which had no effect on the fetal platelet count. These cases illustrate the potential value of ultrasound-guided intravascular, umbilical cord transfusions of compatible platelets in raising the fetal platelet count in ANT, but emphasise the short duration of this effect (<1 week). As the procedure is so labour intensive, further studies are needed to identify the high risk pregnancies, to determine the optimal time for intervention and to assess the success of this approach.
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Eadie, Leila, Luke Regan, Ashish MacAden, and Philip Wilson. "Supporting Novice Prehospital Transcranial Ultrasound Scanning for Brain Haemorrhage." In 3rd International Conference on Bioimaging. SCITEPRESS - Science and Technology Publications, 2016. http://dx.doi.org/10.5220/0005789901180123.

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Tishkov, I., P. Karagyozov, I. Boeva, V. Gelev, I. Zheleva, and V. Mitova. "HEMOSUCCUS PANCREATICUS: A INFREQUENT CAUSE OF LIFE-THREATENING HAEMORRHAGE." In ESGE Days. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1704591.

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Costa, Poliane Cruz, Maria Lara Picolo, Henrique Luiz Staub, Karina Gatz Capobianco, and Marcelo Wainberg Jeffman. "Polyarteritis Nodosa Presenting As Non-Aneurysmal Medullary Subarachnoid Haemorrhage." In XXXIX Congresso Brasileiro de Reumatologia. Sociedade Brasileiro de Reumatologia, 2022. http://dx.doi.org/10.47660/cbr.2022.1926.

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Reports on the topic "Haemorrhage"

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Mulaku, Mercy N. Do non-clinical interventions reduce unnecessary caesarean section rates? SUPPORT, 2016. http://dx.doi.org/10.30846/1612112.

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There has been an increase in caesarean section rates globally. As much as caesarean sections might be life saving, some are unnecessary, they predispose the mother to potential harms, such as haemorrhage, and they have high costs. Non clinical interventions may reduce unnecessary caesarean section. This includes interventions such as providing education to health pro-fessionals and mothers, mandatory second opinions, financial in-terventions, and other guideline implementation strategies.
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Baston, Emma, and Andrew Thompson. Medical and surgical management of haemorrhagic cystitis. BJUI Knowledge, June 2022. http://dx.doi.org/10.18591/bjuik.0411.v2.

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Wang, M., C. Rossi, and C. S. Schmaljohn. Expression of Non-Conserved Regions of the S Genome Segments of Three Hantaviruses: Evaluation of the Expressed Polypeptides for Diagnosis of Haemorrhagic Fever with Renal Syndrome. Fort Belvoir, VA: Defense Technical Information Center, January 1993. http://dx.doi.org/10.21236/ada269774.

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Medical and surgical management of haemorrhagic cystitis. BJUI Knowledge, February 2017. http://dx.doi.org/10.18591/bjuik.0411.

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Role of hyperbaric oxygen in radiation induced haemorrhagic cystitis. BJUI Knowledge, April 2017. http://dx.doi.org/10.18591/bjuik.0412.

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