Die Epiphysioloyse des Dens axis im Kleinkindalter ist eine seltene Verletzung, die jedoch bei Pkw-Unfällen mit frontaler Krafteinwirkung und mittelhoher Geschwindigkeit sicher abgeklärt werden muss. Wir berichten über einen kleinen Patienten, der aufgrund eines Dezelerationstraumas im Kindersitz im Rahmen eines Verkehrsunfalls eine Epiphysiolyse des Dens axis erlitten hat, welche initial nicht diagnostiziert wurde. Das Vorliegen der Epiphysiolyse konnte mithilfe von konventionellen Röntgenaufnahmen, MRT und CT gesichert werden. Die aufgrund der Anamnese verzögerte konservative Ausbehandlung im Halofixateur erfolgte dann komplikationslos.
Epiphysiolysis of the dens axis at the infant age is a rare injury, which must be surely clarified at car accidents with frontal application of force at medium high speed. We report of a small patient sitting in a child seat, who suffered a epiphysiolysis of the dens axis, which was initially not diagnosed, due to a abrupt deceleration in the context of a car accident. The epiphysiolysis of the dens axis could be secured with the aid of conventional radiography, MRT and CT. The delayed conservative treatment due to the anamnesis was then complicationless.
Life-threatening complex pelvic fractures are commonly associated with vast peripelvine soft-tissue injuries and hemorrhage. Correct assessment and classification of the existing pelvic trauma and additional severe injuries present is required for accurate diagnosis and effective therapy. Treatment of the usually multiply injured patient is time-sensitive. The circulatory situation is the benchmark for diagnostic and therapeutic actions. Emergency stabilization of an initially unstable pelvic ring should be done first, followed by an extraperitoneal tamponade, if needed to control bleeding. The positive results of these actions can be measured by hemodynamic parameters. Delayed definitive internal stabilization of the anterior and/or posterior pelvic ring is then performed according to the fracture classification.
Lebensbedrohliche komplexe Beckenfrakturen weisen neben der knöchernen Verletzung einen häufig ausgedehnten peripelvinen Weichteilschaden mit Blutungskomplikationen auf. Im Rahmen der Notfallversorgung ist die korrekte Einschätzung und Klassifikation der vorliegenden Beckenverletzung, aber auch das Erkennen vorhandener schwerer Zusatzverletzungen Voraussetzung für eine zielgerichtete und effektive Diagnostik und Therapie. Die Versorgung der in der Regel polytraumatisierten Patienten ist zeitsensitiv. Als Richtgröße für das diagnostische und therapeutische Vorgehen ist die Kreislaufsituation des Verletzten entscheidend. Zunächst sollte eine Notfallversorgung des initial instabilen Beckenringes, gegebenenfalls mit nachfolgender extraperitonealer Tamponade zur Blutungskontrolle erfolgen. Die Erfolgskontrolle der ergriffenen Maßnahmen findet über die hämodynamischen Parameter statt. Zeitversetzt wird dann eine definitive interne ventrale und/oder dorsale Stabilisierung in Abhängigkeit von der Klassifikation durchgeführt.
A histoplasmose é uma doença fúngica causada pela inalação de esporos de Histoplasma capsulatum. A maioria dos indivíduos normais não apresenta doença após pequena inalação, porém exposições mais prolongadas podem levar ao desenvolvimento de infecção pulmonar aguda, crônica ou disseminada. Nos pacientes imunocomprometidos a infecção é disseminada e grave. Relatamos o caso de um paciente de treze anos, imunocompetente, com febre, tosse seca e dispnéia progressiva havia dois meses. O radiograma e a tomografia computadorizada de tórax evidenciavam infiltrado intersticial com micronódulos difusos. O paciente relatava contato intenso com pássaros em sua residência. Foi submetido a biópsia pulmonar a céu aberto, que evidenciou Histoplasma capsulatum em tecido pulmonar. A cultura do fragmento da biópsia confirmou a presença de Histoplasma capsulatum sp. O paciente foi tratado com anfotericina-B por 28 dias, seguida de itraconazol por seis meses, com resolução do quadro.
Traumatic brain injury (TBI) is characterized by a high mortality which is largely determined by the initial cerebral trauma, secondary brain injury or indirectly during a Multiple Organ Dysfunction Syndrome (MODS). Therefore, we analyzed IL-6, IL-8, and IL-10 in cerebrospinal fluid (CSF) and in plasma with respect to blood-brain barrier (BBB) integrity in 29 patients suffering from isolated TBI. IL-6 and IL-8 were significantly increased compared to baseline levels early after trauma in CSF and plasma. In all patients CSF IL-6 and IL-8 were found to be higher than corresponding plasma levels. IL-10 in plasma was significantly increased above control plasma values, however, without a significant difference to the corresponding CSF values. BBB dysfunction was temporary present in 23 patients. Significant correlations between BBB dysfunction and cytokines were not found. Thus, alterations of the BBB seems not to influence the distribution pattern of interleukines in CSF and plasma after trauma.
Background. In injured brain tissue with a disrupted blood-brain barrier (BBB) catecholamines such as norepinephrine (NE) are known to enhance glucose consumption and cerebral blood flow but may lead to an energy depletion increasing the risk of ischemia. Therefore it is of great interest whether the exogenous administration of NE used mainly to maintain an adequate cerebral perfusion pressure influences CSF NE levels or not, and whether elevated plasma or CSF leves of NE can influence the actual clinical condition. We addressed this issue by measuring the levels of NE in CSF and plasma and correlating them with the actual clinical condition of the patients.
Zusammenfassung Das isolierte oder mit weiteren Verletzungen kombinierte Schädel-Hirn-Trauma (SHT) ist ein Hauptprognosefaktor für Morbidität und Mortalität nach einem Unfallereignis. Die Prognose des Patienten ist sowohl von der primären, mechanischen Hirnschädigung als auch von der Entwicklung sekundärer Hirnschäden abhängig. Als Ursachen einer sekundären Hirnschädigung werden neben der intrakraniellen Raumforderung aufgrund posttraumatischer Blutungen und Ödembildungen, sowie der daraus resultierenden Ischämie, Entzündungsprozesse diskutiert. Sowohl beim isolierten SHT als auch nach Polytrauma mit und ohne Hirnschädigung kann eine inflammatorische “Systemreaktion” (SIRS) unter der Beteiligung von Zytokinen und anderen Entzündungsmediatoren zu einem Ein- oder Multiorganversagen (MOF) führen. Dabei sind einzelne Verletzungskomponenten und Funktionsstörungen meistens überlebbar, können jedoch in Ihrer Kombination und Kumulation tödlich enden. Hypermetabolische Zustände nach einem SHT werden auch als Interaktionen des ZNS mit dem Gesamtorganismus unter Beteiligung der neuroendokrinen Achse aufgefaßt. Diesen Auswirkungen eines SHT auf den übrigen Organismus ist der Einfluß multipler Verletzungen eines polytraumatisierten Verletzten auf die Hirnfunktion gegenüberzustellen, wobei schockbedingte Perfusionsstörungen eine prognoselimitierende Hypoxie des Gehirns verursachen können. Darüber hinaus beeinflußt die generalisierte “Ganzkörperentzündungsreaktion” Blutgerinnung, Stoffwechsel und Frakturheilung. Die Kenntnisse der traumainduzierten, bidirektionalen, inflammatorischen Interaktionen zwischen Gehirn und Gesamtorganismus, sowie der Einfluß der derzeit angewendeten Therapiemaßnahmen sind bisher noch unzureichend und bedürfen weiterer Aufklärung. Letztendlich muß aus dieser Sicht auch die Wahl des richtigen Zeitpunktes für sekundäre Eingriffe, die nicht unmittelbar der Lebenserhaltung dienen und zu einer zusätzlichen Belastung des Patienten durch das Operationstrauma führen, überdacht werden. Diese Arbeit versucht wichtige Aspekte auf diesem Gebiet zusammenzufassen.
Isolated severe head trauma (SHT) or SHT in combination with multiple injuries are important factors for the prognosis of morbidity and mortality in patients suffering from the consequences of accidents. The prognosis mainly depends on the presence of primary mechanic brain injury and the development of secondary brain damage. Causes for the development of secondary brain damage are the intracranial space demand after traumatic injury and edema formation which may result in iscemia, as well as inflammatory processes. Both isolated SHT and polytrauma with or without brain damage may result in a systemic inflammatory response syndrome (SIRS) due to the synthesis of cytokines and other inflammatory mediators which may cause a single or multiple organ failure (MOF). Often the organism is able to survive isolated traumatic injuries and functional disturbances, but in combination or cumulation they may be lethal. The hypermetabolism after SHT is often regarded as an interaction between the central nervous system and the whole organism by the activation of the neuroendocrine axis. In contrast to the consequences of SHT for the whole organism, multiple injuries after polytrauma may affect brain functions, such as the shock dependent disturbance of the brain perfusion accompanied by brain hypoxia which may lead to an aggravated prognosis. Moreover, coagulation, metabolism and fracture healing are influenced by the onset of SIRS as well. Our knowledge about the bidirectional inflammatory interaction between brain and whole organism is still limited. In this context, the effects of secondary surgical interventions which may additionally, stress a traumatized body have to be considered and are the subject for actual clinical discussions and experimental studies. This article tries to summarize some important aspects on this topic.
Background The generation of iron-dependent toxic oxygen radicals during the initial resuscitation from hemorrhagic shock was shown to be a relevant factor for the initiation of the inflammatory cascade. Therefore, this experimental study was designed to evaluate the effects of a deferoxamine-conjugated hydroxyethyl-starch solution (HES-DFO) on oxygen radical induced injury and microcirculatory alterations in the rat liver compared with resuscitation with regular hydroxyethyl-starch, lactated Ringer's solution (RL), or a gelatin-based solution. Methods After hemorrhage and random assignment to 1 hour of blood-free resuscitation with the aforementioned solutions, hepatic microcirculation and leukocyte adhesion characteristics were assessed by intravital fluorescence microscopy in anesthetized rats. Oxygen radical activity was estimated by determination of glutathione levels in liver homogenate and determination of thiobarbituric acid-reactive substances in plasma as markers of lipid peroxidation. Results Resuscitation by HES-DFO resulted in restoration of hemodynamic parameters compared with gelatin-based solution and HES. The hepatic microcirculation was severely altered 1 hour after resuscitation from shock in all groups indicated by sinusoidal narrowing and reduced sinusoidal blood flow. HES-DFO, however, attenuated leukocyte adhesion and improved velocity index in sinusoids as well as sinusoidal perfusion. The shock-associated generation of oxygen radicals during resuscitation was prevented by HES-DFO as indicated by restored glutathione and reduced thiobarbituric acid-reactive substances. Conclusion The results suggest that HES-DFO effectively reduces oxygen radical formation during the initial resuscitation period, thus, attenuating pathologically enhanced leukocyte adhesion and improving hepatic microcirculation.
Holanda, M.; Rose, S.; Marzi, I.; Hahne, M.; Wiercinski, A.; Mutschler, W. Author Information
Extended hemodynamic monitoring during arterialized rat liver transplantation procedure and the effects of resuscitation with albumin, starch-desferrioxamine-conjugated hydroxyethyl starch (HES-DFO), or hydroxyethyl starch (HES) on hemodynamics are presented. Livers from SPRD rats were stored for 20 hr in ice-cold UW solution and were orthotopically transplanted with reconstruction of the hepatic artery under hemodynamical monitoring applying invasive measurement of mean arterial blood pressure (MAP) and cardiac output (CO). Comparable amounts of albumin, HES-DFO, and HES were given in a randomized and blinded fashion after transplantation. Ringer's solution was given additionally when blood pressure was below 65 mmHg. Fifteen, 60, and 90 min after surgical procedure blood samples were taken to determine acid base status, blood gases, and blood cell count. Oxygen radical-induced reperfusion injury was determined by thiobarbituric acid reactive substances (TBARS) in serum and total glutathione in liver tissue 90 min after surgery. During the anhepatic period CO was reduced to 20% of baseline and MAP to 40 mmHg. In all groups, declamping led to a transient recovery of hemodynamic situation, whereas during further reperfusion, CO and MAP were significantly reduced in the HES- and HES-DFO-treated group in contrast to the group receiving albumin. Animals of the HES group required significantly more Ringer's solution to maintain blood pressure (2.6 +/- 0.9 ml; 4 of 6 animals needed additional resuscitation) than animals given albumin (0.4 +/- 0.3 ml, P < 0.05, 2/9 needed further supplementation) or HES-DFO (1.2 +/- 0.5 ml; 5/10 required additional resuscitation), respectively. Animals treated with HES or HES-DFO failed to restore base excess and serum lactate in contrast to resuscitation with albumin. However, TBARS was mitigated by resuscitation with HES-DFO compared to albumin and HES, whereas no significant differences were observed in respect to tissue glutathione of transplanted livers. In conclusion the model described allows intensive monitoring of hemodynamic parameters and metabolic status during arterialized rat liver transplantation procedure. Moreover, the results indicate that resuscitation with albumin could maintain central hemodynamics and restore homeostasis during the early reperfusion period after transplantation in contrast to resuscitation with HES or HES-DFO, respectively. Although resuscitation with HES-DFO resulted in mitigation of lipid peroxides determined by TBARS, no significant improvement of hemodynamics and homeostasis could be observed during reperfusion as it can be observed with albumin.
Rose, S.; Holanda, M.; Pizanis, A.; Dike, J.; Bauer, M.; Ziegenfu, T.ß; Marzi, I.; Bühren, V. Author Information