Stab wounds to the neck with partial transsection of the spinal cord and penetrating injury to the esophagus.
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Adult↗
Biomedical subjects
Thomas Kossmann
Publications and source records attributed to Thomas Kossmann.
Detection of metallic implant-associated infections with FDG PET in patients with trauma: correlation with microbiologic results.
PURPOSE: To prospectively evaluate the value of positron emission tomography (PET) with fluorine 18 fluorodeoxyglucose (FDG) in the detection of metallic implant-associated infections in patients with trauma. MATERIALS AND METHODS: Twenty-nine partial-body FDG PET scans in 22 patients suspected of having metallic implant-associated infections were obtained prior to surgery. In two of the 22 patients, data were acquired with a combined PET-CT in-line system. Soft-tissue and bone infections were evaluated. PET scans were analyzed by two experienced nuclear medicine physicians first separately and then in consensus. Disease status was defined on the basis of the results of microbiologic evaluation of surgical specimens together with intraoperative findings. Sensitivities, specificities, accuracies, interobserver variability (determination of kappa values), and receiver operating characteristic curves were obtained. RESULTS: Of 29 PET scans, 14 were true-positive, 14 were true-negative, and one was false-positive. Sensitivity, specificity, and accuracy were 100%, 93.3%, and 97%, respectively, for all PET data; 100%, 100%, and 100%, respectively, for the central skeleton; and 100%, 87.5%, and 95%, respectively, for the peripheral skeleton. The degree of overall interobserver concordance was high (kappa = 0.96). CONCLUSION: FDG PET appears to be a sensitive and specific method for the detection of infectious foci due to metallic implants in patients with trauma.
Adolescent↗
Prolonged intrathecal release of soluble Fas following severe traumatic brain injury in humans.
The mechanisms underlying cell death following traumatic brain injury (TBI) are not fully understood. Apoptosis is believed to be one mechanism contributing to a marked and prolonged neuronal cell loss following TBI. Recent data suggest a role for Fas (APO-1, CD95), a type I transmembrane receptor glycoprotein of the nerve growth factor/tumor necrosis factor superfamily, and its ligand (Fas ligand, FasL) in apoptotic events in the central nervous system. A truncated form of the Fas receptor, soluble Fas (sFas) may indicate activation of the Fas/FasL system and act as a negative feedback mechanism, thereby inhibiting Fas mediated apoptosis. Soluble Fas was measured in cerebrospinal fluid (CSF) and serum of 10 patients with severe TBI (GCS< or =8) for up to 15 days post-trauma. No sFas was detected in CSF samples from patients without neurological pathologies. Conversely, after TBI 118 out of 120 CSF samples showed elevated sFas concentrations ranging from 56 to 4327 mU/ml. Paired serum samples showed above normal (8.5 U/ml) sFas concentrations in 5 of 10 patients. Serum levels of sFas were always higher than CSF levels. However, there was no correlation between concentrations measured in CSF and in serum (r(2)=0.078, p=0.02), suggesting that the concentrations in the two compartments are independently regulated. Also, no correlation was found between sFas in CSF and blood brain barrier (BBB) dysfunction as assessed by the albumin CSF/serum quotient (Q(A)), and concentrations of the cytotoxic cytokine tumor necrosis factor-alpha in CSF, respectively. Furthermore, there was no correlation with two markers of immune activation (soluble interleukin-2 receptor and neopterin) in CSF. Maximal CSF levels of sFas correlated significantly (r(2)=0.8191, p<0.001) with the early peaks of neuron-specific enolase in CSF (a marker for neuronal cell destruction), indicating that activation of the Fas mediated pathway of apoptosis may be in part the direct result of the initial trauma. However, the prolonged elevation of sFas in CSF may be caused by the ongoing inflammatory response to trauma and delayed apoptotic cell death.
Adolescent↗
The production of macrophage inflammatory protein-2 induced by soluble intercellular adhesion molecule-1 in mouse astrocytes is mediated by src tyrosine kinases and p42/44 mitogen-activated protein kinase.
Severe traumatic brain injury stimulates the release of soluble intercellular adhesion molecule-1 (sICAM-1) into CSF. Studies in cultured mouse astrocytes suggest that sICAM-1 induces the production of macrophage inflammatory protein-2 (MIP-2). In the present study, we investigated the underlying mechanisms for MIP-2 induction. sICAM-1 induced MIP-2 in astrocytes lacking membrane-bound ICAM-1, indicating that its action is due to heterophilic binding to an undescribed receptor rather than homophilic binding to surface ICAM-1. Signal transduction may be mediated by src tyrosine kinases, as the src tyrosine kinase inhibitors herbimycin A and PP2 abolished MIP-2 induction by sICAM-1. Phosphorylation of p42/44 mitogen-activated protein kinase (MAPK), but not of p38 MAPK, occurred further downstream, as evidenced by western blot analysis combined with the use of herbimycin A and specific MAPK inhibitors. By contrast, induction of MIP-2 by tumour necrosis factor-alpha (TNF-alpha) involved both p42/44 MAPK and p38 MAPK. Following stimulation with either sICAM-1 or TNF-alpha, astrocyte supernatants promoted chemotaxis of human neutrophils and incubation of these supernatants with anti-MIP-2 antibodies more efficiently suppressed the migration induced by sICAM-1 than by TNF-alpha. These results show that sICAM-1 induces the production of biologically active MIP-2 in astrocytes by heterophilic binding to an undefined receptor and activation of src tyrosine kinases and p42/44 MAPK.
Animals↗
Elevated intracranial IL-18 in humans and mice after traumatic brain injury and evidence of neuroprotective effects of IL-18-binding protein after experimental closed head injury.
Proinflammatory cytokines are important mediators of neuroinflammation after traumatic brain injury. The role of interleukin (IL)-18, a new member of the IL-1 family, in brain trauma has not been reported to date. The authors investigated the posttraumatic release of IL-18 in murine brains following experimental closed head injury (CHI) and in CSF of CHI patients. In the mouse model, intracerebral IL-18 was induced within 24 hours by ether anesthesia and sham operation. Significantly elevated levels of IL-18 were detected at 7 days after CHI and in human CSF up to 10 days after trauma. Published data imply that IL-18 may play a pathophysiological role in inflammatory CNS diseases; therefore its inhibition may ameliorate outcome after CHI. To evaluate the functional aspects of IL-18 in the injured brain, mice were injected systemically with IL-18-binding protein (IL-18BP), a specific inhibitor of IL-18, 1 hour after trauma. IL-18BP-treated mice showed a significantly improved neurological recovery by 7 days, accompanied by attenuated intracerebral IL-18 levels. This demonstrates that inhibition of IL-18 is associated with improved recovery. However, brain edema at 24 hours was not influenced by IL-18BP, suggesting that inflammatory mediators other than IL-18 induce the early detrimental effects of intracerebral inflammation.
Adult↗
Inflammatory response in acute traumatic brain injury: a double-edged sword.
Inflammation is an important part of the pathophysiology of traumatic brain injury. Although the central nervous system differs from the other organs because of the almost complete isolation from the blood stream mediated by the blood-brain barrier, the main steps characterizing the immune activation within the brain follow a scenario similar to that in other organs. The key players in these processes are the numerous immune mediators released within minutes of the primary injury. They guide a sequence of events including expression of adhesion molecules, cellular infiltration, and additional secretion of inflammatory molecules and growth factors, resulting in either regeneration or cell death. The question is this: to what extent is inflammation beneficial for the injured brain tissue, and how does it contribute to secondary brain damage and progressive neuronal loss? This review briefly reports recent evidence supporting the dual, the beneficial, or the deleterious role of neuroinflammation after traumatic brain injury.
Animals↗
Definitive management of acute cardiac tamponade secondary to blunt trauma.
Blunt cardiac injuries are a leading cause of fatalities following motor-vehicle accidents. Injury to the heart is involved in 20% of road traffic deaths. Structural cardiac injuries (i.e. chamber rupture or perforation) carry a high mortality rate and patients rarely survive long enough to reach hospital. Chamber rupture is present at autopsy in 36-65% of death from blunt cardiac trauma, whereas in clinical series it is present in 0.3-0.9% of cases and is an uncommon clinical finding. Patients with large ruptures or perforations usually die at the scene or in transit--the rupture of a cardiac cavity, coronary artery or intrapericardial portion of a major vein or artery is usually instantly fatal because of acute tamponade. The small, rare, remaining group of patients who survive to hospital presentation usually have tears in a cavity under low pressure and prompt diagnosis and surgery can now lead to a survival rate of 70-80% in experienced trauma centres. As regional trauma systems evolve, patients with severe, but potentially survivable cardiac injury are surviving to ED. Two distinct syndromes are apparent--haemorrhagic shock and cardiac tamponade. Any patient with severe chest trauma, hypotension disproportionate to estimated loss of blood or with an inadequate response to fluid administration should be suspected of having a cardiac cause of shock. For patients with severe hypotension or in extremis, the treatment of choice is resuscitative thoracotomy with pericardotomy. Closed chest cardiopulmonary resuscitation is ineffective in these circumstances. Blunt traumatic cardiac injury presenting with shock is associated with a poor prognosis. The majority of survivors of blunt or penetrating cardiac injury present to the ED/trauma centre with vital signs. The main pathophysiologic determinant for most survivors is acute pericardial tamponade. The presence of normal clinical signs or normal ECG studies does not exclude tamponade. In recent years the widespread availability and use of ultrasound for the initial assessment of severely injured patients has facilitated the early diagnosis of cardiac tamponade and associated cardiac injuries. Two cases of survival from blunt traumatic cardiac trauma are described in the present paper to demonstrate survivability in the context of rapid assessment and intervention.
Acute Disease↗
Is the Australian hospital system adequately prepared for terrorism?
Australian hospitals need to be prepared to deal with mass casualties from terrorist strikes, including bomb blasts and chemical, biological and radiation injury. Injuries from bomb explosions are more severe than those commonly seen in Australian hospitals. In disasters involving mass casualties in urban areas, many of the injured make their own way to hospital, often arriving before the more seriously injured casualties. Major hospitals in Australia should plan for large numbers of undifferentiated and potentially contaminated casualties arriving with minimal warning. It is critical that experienced and trained senior medical officers perform the triage of casualties in emergency departments, with frequent reassessment to detect missed injuries (especially pulmonary blast injury). Hospitals require well developed standard operating procedures for mass casualty events, reinforced by regular drills. Preparing for a major event includes training staff in major incident management, setting up an operational/control unit, nominating key personnel, ensuring there is an efficient intra-hospital communication system, and enhancing links with other emergency services and hospitals.
Australia↗