Diss. (sammanfattning) Umeå : Umeå universitet, 2009. / Härtill 5 uppsatser.

Intracranial monitoring after severe traumatic brain injury offers the possibility for early detection and amelioration of physiological insults. In this thesis, I explore cerebral insults due raised intracranial pressure, decreased cerebral perfusion pressure and impaired cerebral pressure reactivity after traumatic brain injury. In chapter 2, the importance of intracranial pressure, cerebral perfusion pressure and pressure reactivity in regulating the cerebral circulation is elucidated along with a summary of the existing evidence supporting intracranial monitoring in traumatic brain injury. In chapter 4, intracranial pressure, cerebral perfusion pressure, and pressure reactivity insults are demonstrated to be common, prognostically important, and responsive to long-term changes in management policies. Further, while these insults often occur independently, coexisting insults portend worse prognosis. In chapter 5, I examine possible imaging antecedents of raised intracranial pressure and demonstrate that initial subarachnoid haemorrhage is associated with the subsequent development of elevated intracranial pressure. In addition, elevated glucose during the intensive care stay is associated with worse pressure reactivity. Cortical blood flow and brain tissue oxygenation are demonstrated to be sensitive to increases in intracranial pressure in chapter 6. In chapter 7, a method is proposed to estimate the cerebral perfusion pressure limits of reactivity in real-time, which may allow for more nuanced intensive care treatment. Finally, I explore a recently developed visualisation technique for intracranial physiological insults and apply it to the cerebral perfusion pressure limits of reactivity. Taken together, this thesis outlines the scope, risk factors and consequences of intracranial insults after severe traumatic brain injury. Novel signal processing applications are presented that may serve to facilitate a physiological, personalised and precision approach to patient therapy.

Made available in DSpace on 2014-06-11T19:31:09Z (GMT). No. of bitstreams: 0 Previous issue date: 2006-12-01Bitstream added on 2014-06-13T20:41:27Z : No. of bitstreams: 1 paula_dp_dr_jabo.pdf: 211399 bytes, checksum: 606341726183ad88b54ff88eee11d7a4 (MD5) / Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) / Objetivou-se com este estudo avaliar os efeitos da infusao continua de propofol ou de etomidato, em caes anestesiados, sobre a pressao intracraniana (PIC), pressao de perfusao cerebral (PPC), temperatura intracraniana (TIC), frequencia cardiaca (FC), pressoes arteriais sistolica (PAS), diastolica (PAD) e media (PAM), debito e indice cardiaco (DC e IC, respectivamente), pressao venosa central (PVC), volume e indice sistolico (VS e IS, respectivamente), temperatura corporal (TC). Foram utilizados 20 caes adultos, machos ou femeas, higidos, sem raca definida. Os caes foram distribuidos equitativamente em dois grupos, denominados GP e GE. Os animais do GP foram induzidos a anestesia geral por meio de administracao intravenosa de propofol, na dose de 10 mg/kg. Os caes foram intubados com sonda de Magill acoplada ao aparelho de anestesia inalatoria e iniciou-se ventilacao controlada, com amplitude e frequencia suficientes para permitir leitura de capnometria constante em 35 mmHg. Ato continuo, iniciou-se a infusao continua de propofol, por meio de bomba de infusao, na dose de 0,8 mg/kg/min. Aos animais do GE, o procedimento foi o mesmo realizado no GP, substituindo-se o propofol pelo etomidato, que foi utilizado na dose de 5 mg/kg para inducao anestesica e 0,5 mg/kg/min para a manutencao, sendo que apos 10 minutos reduziu-se a dose para 0,2 mg/kg/min. Os parametros foram mensurados decorridos 30 minutos da implantacao do cateter de pressao intracraniana (M1) e se repetiu a cada 20 minutos (M2, M3 e M4) apos M1. A avaliacao estatistica das variaveis foi efetuada pela Analise de Perfil (p<0,05). Observou-se diferencas entre os grupos na PIC, TIC, FC, DC, IC e TC, onde as medias do GP foram superiores ao do GE, e na PPC, PVC, RVS e IRVS, onde as medias de GP foram inferiores as do GE... / Continuous rate infusion (CRI) of propofol or etomidate in the intracranial pressure (ICP), cerebral perfusion pressure (CPP), intracranial temperature (ICT), heart rate (HR), systolic (SAP), diastolic (DAP), and mean arterial pressures (MAP), cardiac output (CO) and index (CI), central venous pressure (CVP), stroke volume (SV) and index (SI), rectal temperature (RT) were analyzed, in twenty adult healthy males or females mongrel dogs allotted in GP and GE groups. In GP anesthesia was induced by administration of propofol (10 mg/kg IV) followed intracheal intubation to proceed controlled ventilation to mantain PaCO2 at 35 mmHg. Propofol CRI started subsequently at rate of 0.8mg/kg/min. For GE does etomidate (5 mg/kg IV) was used to induce and for maintenanceanesthesia, 0.5 mg/kg/min. After 10 minutes, the etomidato CRI was reduced to 0.2 mg/kg/min. Thirty minutes of intracranial catheter implantated (M1), and repeated at each 20 minutes (M2, M3, and M4). Statistical analysis was evaluated through ANOVA (P<0.05). Differences between groups were observed in ICP, ICT, HR, CO, CI, and RT when GP means were higher than GE. CPP and CVP were lower in GP when compared with GE. All parameters remained stable in each group during the study, except to ICT and RT that reduced gradually during the experimental period in GE animals. Continuous infusion of etomidate or propofol in dogs maintains cerebral perfusion, cerebral auto-regulation, and cardiovascular parameters in normal values. Dogs submitted to anesthesia with continuous infusion of etomidate demonstrated gradual reduction in rectal and intracranial temperature with severe hemolisys and myoclonus.

Submitted by Paloma do Espirito Santo Silva null (paloma_ess@yahoo.com.br) on 2017-10-19T01:38:19Z No. of bitstreams: 1 defesa tese.pdf: 2855357 bytes, checksum: e8f0b261e67e91cf6ecfe4e9dfbb7b81 (MD5) / Approved for entry into archive by Luiz Galeffi (luizgaleffi@gmail.com) on 2017-10-23T13:29:39Z (GMT) No. of bitstreams: 1 silva_pes_dr_jabo.pdf: 2855357 bytes, checksum: e8f0b261e67e91cf6ecfe4e9dfbb7b81 (MD5) / Made available in DSpace on 2017-10-23T13:29:39Z (GMT). No. of bitstreams: 1 silva_pes_dr_jabo.pdf: 2855357 bytes, checksum: e8f0b261e67e91cf6ecfe4e9dfbb7b81 (MD5) Previous issue date: 2017-09-18 / Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) / A anestesia intravenosa com propofol é amplamente utilizada em Medicina Veterinária, entretanto, apesar de ser um bom hipnótico e apresentar indução e recuperação rápidas, esse fármaco não possui efeito analgésico. A fim de proporcionar aos suínos, espécie largamente utilizada na experimentação animal, uma anestesia multimodal, foi proposto nesse estudo a avaliação da associação de propofol ao óxido nitroso (N2O), o qual produz analgesia. Além disso, buscou-se definir as concentrações mais adequadas de oxigênio e N2O a serem fornecidas durante a anestesia. Para tal, foram utilizados 48 leitões em fase de creche, pré-medicados com azaperone, induzidos à anestesia com propofol e mantidos em infusão contínua deste agente sob ventilação espontânea. Os animais foram distribuídos em 6 grupos, que receberam as concentrações de 10, 30 e 50% de N2O (GN10, GN30 e GN50) ou ar comprimido (GA10, GA30 e GA50), associadas às frações inspiradas de oxigênio (FiO2) de 0,9, 0,7 e 0,5, respectivamente. Foi estudada a hemogasometria arterial e venosa mista, além da dinâmica cardiovascular, dinâmica respiratória e parâmetros intracranianos. A coleta de dados teve início 40 minutos após a indução anestésica e repetidas a cada 15 minutos, durante 60 minutos. Para a análise estatística dos resultados foi feita a análise de variância de duas vias para comparação entre grupos e de uma via para comparação de momentos, ambas seguidas pelo teste de Bonferroni. A dinâmica cardiovascular não apresentou diferença entre os grupos para frquência cardíaca (FC), pressão arterial sistólica (PAS), média (PAM) e diastólica (PAD), pressão venosa central (PVC) e índice cardíaco (IC), porém, os resultados ficaram abaixo do fisiológico para a espécie. Além disso, não houve diferenças para frequência respiratória (f), pressão de perfusão cerebral (PPC), temperatura intracraniana (TIC) e temperatura corporal (TC). Todos os animais apresentaram hipercapnia, redução do pH e déficit de bases (DB), sugerindo que o protocolo experimental determinou acidose respiratória devido à formação de shunt pulmonar e metabólica devido à hipoperfusão tecidual. O emprego de FiO2 de 0,9 ou a adição de N2O à mistura gasosa, determinaram alterações mais graves na dinâmica respiratória e no shunt pulmonar. Houve aumento de pressão intracraniana (PIC) em todos os grupos, com diferenças pontuais, de modo que o N2O não interferiu diretamente nesse parâmetro. A ventilação espontânea não foi adequada para suínos anestesiados com propofol em cirurgias acima de 40 minutos, sendo que o GA30 (FiO2 de 0,7 associada ao ar comprimido) foi o menos prejudicial aos animais. / Intravenous anesthesia with propofol is common practice in Veterinary Medicine. However, despite being a good hypnotic and provides fast anesthetic induction and recovery, has no analgesic effect. In order to provide pigs with a multimodal anesthetic protocol, it was proposed to evaluate the association of propofol with nitrous oxide (N2O), due to its analgesic properties. Moreover, the aim of this study was to define the most appropriate concentrations of oxygen and N2O to be provided during anesthesia. To that purposes, a total of 48 pigs in nursery phase were used. They were premedicated with azaperone and anesthetized with propofol, which was also used during anesthesia maintenance. The animals were assigned into 6 groups, as follows concentrations of 10, 30 and 50% N2O (GN10, GN30 and GN50) or compressed air (GA10, GA30 and GA50) associated with fraction of inspired oxygen (FiO2) of 0.9, 0.7 and 0.5, respectively. It was studied the arterial and mixed venous blood gas analysis, as well as cardiovascular dynamics, respiratory dynamics and intracranial parameters. Data collection began 40 minutes after the induction and it was repeated every 15 minutes for 60 minutes. The statistical analysis of results was performed by two-way analysis of variance for comparison between groups and one-way for times comparison, both followed by the Bonferroni test. Cardiovascular dynamics showed no difference between groups for heart rate (HR), systolic arterial pressure (SAP), diastolic arterial pressure (DAP), mean arterial pressure (MAP), central venous pressure (CVP) e cardiac index (CI), although the results were below the physiological for this species. Also, there is no difference for respiratory rate (RR), cerebral perfusion pressure (CPP), intracranial temperature (ICT) and esophageal temperature (Tes). All animals presented hypercapnia, pH reduction and base excess (BE), suggesting that the experimental protocol determined respiratory and metabolic acidosis due to ventilation-perfusion mismatch. The use of FiO2 of 0.9 or the addition of N2O to the gas mixture determined more severe changes in respiratory dynamics and pulmonary shunt. There was an increase in intracranial pressure (ICP) in all groups, with few differences, so that N2O did not interfere directly with this parameter. The spontaneous ventilation was not adequate for pigs anesthetized with propofol in surgeries over 40 minutes, and the GA30 (FiO2 of 0.7 associated with compressed air) was the least harmful to the animals. / FAPESP: 2013/25655-0

The topic of this thesis is ?Nursing care for patients with craniocerebral trauma?. Three goals were set. We tried to find what the specifics of nursing care for patients with craniocerebral trauma are. We also examined whether nurses were aware of the specifics of nursing care for patients with craniocerebral trauma. The last goal was to find out whether nurses used basal stimulation in these patients. The research was based on a non-standardized interview. The interviews were performed with twelve nurses caring about these patients in the České Budějovice Hospital and the Faculty Hospital Královské Vinohrady. Three research questions were set. 1: What are the specifics of nursing care for patients with craniocerebral trauma? The research has shown that elevated head position, monitoring of GCS, pupil state and response, administering of bolus analgosedation doses in some nursing activities, ensuring detention administration and list of valuables are the specifics. We have also included CT examination, pre-operation preparation, care of invasive inputs, drains, operation wounds, careful handling with patients, constipation problems, care of a disturbed or aggressive patient and special approach to communication with these patients. 2: Are nurses aware of the specifics of nursing care for patients with craniocerebral trauma? We found that respondents knew the above mentioned specifics. However we found two drawbacks. The first one was in the unawareness of the possibility to increase ICP during defecation among the respondents, the other one was in communication with disturbed or aggressive patients. 3: Do nurses use basal stimulation in patients with craniocerebral trauma? The research has shown that the respondents do apply the concept of basal stimulation, but they only use some of the stimulation elements. This thesis may serve as study material for new nurses starting at the department, where they will care about these patients. The research results and the Standard nursing procedure of Basal stimulation elaborated by us will be offered to managers of both the hospitals where the interviews with nurses were performed.

Cerebral malaria is a common encephalopathy in African children, but the cause of death and neurological sequelae are unknown. This dissertation examines the hypothesis that raised intracranial pressure (ICP) is a determinant of poor outcome in Kenyan children with cerebral malaria. The opening cerebrospinal fluid pressure was raised in all 26 children in whom it was measured on admission and 92% of 35 children in whom it was measured after admission. Brain stem signs, particularly an abnormal respiratory pattern, absent pupillary responses and a lack of spontaneous eye movement were associated with a death. In 33 children who died with cerebral malaria, at least 18-42% had clinical features of transtentorial herniation, according to the criteria used. Intracranial pressure monitoring was performed in 18 children with severe CM, of whom 14 had computerised tomography (CT) and in 10 the basal cranial arteries were monitored with transcranial Doppler (TCD) sonography. Three children with severe intracranial hypertension (maximum ICP > 60 mmHg and minimum cerebral perfusion pressure (CPP) < 40 mmHg) had a poor outcome despite aggressive therapy with mannitol. One child with a maximum ICP of 151 mmHg died with the signs of uncal and medullary stages of herniation. In the other 2 children, middle cerebral artery velocity and vascular resistance monitored with TCD sonography changed with ICP and CPP. Both of these children had diffuse brain swelling associated with generalised hypodensity on their acute CT scans. These children survived° with cerebral atrophy on their convalescent scans and severe neurological deficits. In the 8 children with intermediate intracranial hypertension (maximum ICP 20-60 mmHg and CPP < 50 mmHg) mannitol was effective in controlling the intracranial hypertension. TCD was not reliable in detecting changes in ICP or CPP. Two of these children had acute brain swelling, but the tomographic density was normal and the swelling had resolved when the repeat scans were performed 12-24 days later. All the children with intermediate intracranial hypertension survived without major neurological sequelae. In the remaining 7 children who had ICP monitoring, the maximum ICP was <20 mmHg and mannitol was not administered. None of the CT scans showed brain swelling and the children survived without severe sequelae. In a further 9 children with severe malaria (6 with CM) the agonal stages were monitored with TCD. Three children with CM had sonographic features of progressive intracranial hypertension associated with signs of herniation, whilst the other children (including 3 with CM) did not have these sonographic features, although one had evidence of brainstem compromise before dying. Thus raised ICP is a feature of CM in Kenyan children. Severe intracranial hypertension is associated with a poor outcome and could be responsible for at least a third of the children dying from CM. Mannitol reduces the ICP, but does not prevent nor control severe intracranial hypertension.

Traumatic brain injuries (TBIs) are a major public health problem worldwide where the symptoms can be anything from mild concussion to severe swelling of the brain tissue. As a result of TBI the intracranial pressure (ICP) can elevate to pathological levels with severe consequences such as hypoxia, ischemia and brain hemorrhage. TBI and the subsequent ICP increase could hence lead to disability or in worst cases death. Therefore to understand the severity of a head injury and the path regarding further treatments, monitoring of a patient's ICP is crucial in the intensive care units (ICU) environment. Invasive methods of ICP monitoring are at this present date the standard in ICU because of the accuracy when compared to non-invasive methods. All invasive ICP monitoring methods come with a risk to the patient and require the presence of a neurosurgeon. The thesis's objective was to develop a gradually increasing ICP testbed for a new non-invasive microwave based skin patch sensor. The aim with this project was to verify if a dependence in the resonance characteristic of the NASA SansEC microwave sensor with respect to ICP exists as suggested by previous works in a novel testbed and to provide a correlation model based on the testbed experiment. The developed testbed simulate increasing ICP by increasing volume of an artificial cerebro-spinal fluid (aCSF) liquid, a liquid emulating the CSF. The microwave sensor's resonance frequency is due to the permittivity changes caused by the change (increasing) in the fluid volume, which for this setup is directly correlated to the pressure change as well. Trials with different aCSF samples were made to ensure that the used aCSF in the testbed had the same dielectric properties as human CSF. The developed testbed had a simple structure made with several plastic containers of rectangular shape which were found to be well suited for the purpose of the experiment. For the microwave sensor trials an Fieldfox microwave analyzer was used and the sensor was evaluated around 1 - 4 GHz. The testbed pressure was increasing from 0 - 47 mmHg covering most useful ICP ranges. Larger pressures were also possible but limited by the height of the work room and the increase of complexity in the testbed design. The results from the trials showed a total resonance frequency shift of 76 MHz from 4 - 30 mmHg with an linear correlation of R2 = 0,91. The sensor measurements above 30 mmHg showed a saturation where the first principal frequencies were stable at 1,368 GHz. The linear relationship obtained for 4-30 mmHg is a reassurance that the Nasa SansEC sensor should be studied further. Future work should include new trials with modifications to the testbed setup and sensor design.

Background: Previously, we had shown that elevation of cerebral perfusion pressure, using pressors, improved short-term outcomes after traumatic brain injury and hemorrhagic shock in swine. The current study evaluates outcomes after resuscitation with diaspirin cross-linked hemoglobin (DCLHb)-a hemoglobin-based oxygen carrier with pressor activity-in the same swine model of traumatic brain injury and hemorrhagic shock. Methods: Anesthetized and ventilated swine received traumatic brain injury via cortical fluid percussion (6-8 atm) followed by 45% blood volume hemorrhage. One hour later, animals were randomized to either a control group (SAL) resuscitated with normal saline equal to three times shed blood volume or to one of two experimental groups resuscitated with DCLHb. The two experimental groups consisted of a low-dose group, resuscitated with 250 mL of DCLHb (Hb1), and a high-dose group, resuscitated with 500 mL of DCLHb (Hb2). Animals were observed for 210 minutes postresuscitation. Outcomes evaluated were cerebral oxygenation by measuring partial pressure and saturation of oxygen in cerebrovenous blood; cerebral function by evaluating the preservation and magnitude of cerebrovascular carbon dioxide reactivity; and brain structural damage by semiquantitatively assessing beta amyloid precursor protein positive axons. Results: Postresuscitation, cerebral perfusion pressure was higher in the DCLHb groups (p < 0.05, Hb1 and Hb2 vs. SAL), and intracranial pressure was lower in the Hb2 group (p < 0.05 vs. SAL). Cerebrovenous oxygen level was similar in all groups (p > 0.05). At baseline, 5% carbon dioxide evoked a 16 ± 1% increase in cerebrovenous oxygen saturation, indicating vasodilatation. At 210 minutes, this response was nearly absent in SAL (4 ± 4%) (p < 0.05 vs. baseline) and Hb1 (1 ± 5%), but was partially preserved in Hb2 (9 ± 5%). There was no intergroup difference in beta amyloid precursor protein positive axons. Five of 20 SAL and 0 of 13 DCLHb animals developed brain death (flat electroencephalogram) (p = 0.05, SAL vs. DCLhb). Postresuscitation, DCLHb animals maintained higher mean pulmonary arterial pressure (28 ± 1 mm Hg, SAL; 42 ± mm Hg, Hb1; 45 ± 1 mm Hg, Hb2) (p < 0.05, Hb1 and Hb2 vs. SAL) and lower cardiac output (3.9 ± 1.6 L/min, SAL; 2.6 ± 0.1 L/min, Hb1; 2.7 ± 0.1 L/min, Hb2) (p < 0.05, Hb1 and Hb2 vs. SAL). Three Hb2 animals died as a result of cardiac failure, and one SAL animal died as a result of irreversible shock. Conclusion: In this swine model of traumatic brain injury and hemorrhagic shock, resuscitation with DCLHb maintained a higher cerebral perfusion pressure. Low-dose DCLHb (minimal increase in oxygen carriage) failed to significantly improve short-term outcome. With high-dose DCLHb (significant improvement in oxygen carriage), intracranial pressure was lower and cerebrovascular carbon dioxide reactivity was partially preserved; however, this was at the cost of poorer cardiac performance secondary to high afterload.

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