Does Traumatic Donor Cause of Death Influence Outcome after Lung Transplantation? A Single-Centre Analysis

2015 ◽  
Vol 65 (05) ◽  
pp. 395-402 ◽  
Author(s):  
Jens Heckmann ◽  
Henning Carstens ◽  
Jura Lubarski ◽  
Heinz Jakob ◽  
Nikolaus Pizanis ◽  
...  

Background Owing to the shortage of donor organs in lung transplantation (LuTX), liberalization of donor selection criteria has been proposed. However, some studies suggested that donor traumatic brain damage might influence posttransplantation allograft function. This article aimed to investigate the association of donor cause of death (DCD) and outcome after LuTX. Methods A retrospective analysis of 186 consecutive double LuTXs at our institution from January 2000 to December 2008 was performed. DCD was categorized into traumatic brain injury (TBI) and nontraumatic brain injury (NTBI). In addition, NTBI was sub classified as spontaneous intracerebral bleeding (B), hypoxic brain damage (H), and intracerebral neoplasia (N). Results DCD was classified as TBI in 50 patients (26.9%) and NTBI in 136 patients (73.1%): B in 112 patients (60.2%), H in 21 patients (11.3%), and N in 3 patients (1.6%). Young male donors predominated in group TBI (mean age 36.0 ± 14.5 vs. 42.8 ± 10.7, p < 0.01; 29 males in the TBI group [58.0%] vs. 48 males in the NTBI group [35.3%], p < 0.01). Groups of DCD did not differ significantly by recipient age or gender, recipient diagnosis, donor ventilation time, or paO2/FiO2 before harvesting. TBI donors received significantly more blood (3.4 ± 3.8 vs. 1.8 ± 1.9, p = 0.03). A chest trauma was evident only in group T (n = 7 [3.7%] vs. 0 [0%], p < 0.001). Mode of donor death did not affect the following indices of graft function: length of postoperative ventilation, paO2/FiO2 ratio up to 48 hours, and lung function up to 36 months. One- and three-year survival was comparable with 84.4 and 70.4% for TBI donors versus 89.4% and 69.2% for NTBI donors. Five-year survival tended to be lower in the TBI group but did not reach statistical significance (43.4 vs. 53.9%). Conclusion This study indicates that traumatic DCD does not affect outcome after LuTX. These results can be achieved with an ideal donor management combined with an individual case-to-case evaluation by an experienced LuTX surgeon.

2017 ◽  
Vol 41 (3) ◽  
Author(s):  
Anil Yalcin ◽  
Ahmet Baydin ◽  
Özgür Korhan Tuncel ◽  
Ali Kemal Erenler ◽  
Cengiz Çokluk ◽  
...  

AbstractBackground:The primary aim of this study was to investigate the diagnostic values of serum S100 calcium-binding protein B (S100B) and proenkephalin (P-ENK) levels in brain damage caused by traumatic brain injury (TBI).Methods:We prospectively collected serum blood samples of 58 adult patients admitted to our emergency department due to TBI. Serum S100B and P-ENK levels were measured and compared according to clinical findings and outcomes of the patients.Results:When patients with brain injury were compared to controls, statistical significance was determined in both S100B and P-ENK levels. According to the receiver operating characteristic (ROC) analysis, cut-off values for serum S100B and P-ENK levels for the differential diagnosis of patients with and without brain damage were found to be 785.944 ng/mL and 2.445 ng/mL, respectively. There was a statistical significance in both S100B and P-ENK levels when patients who were discharged and those who died were compared.Conclusions:Serum S100B and P-ENK levels are found to be elevated in patients with TBI when compared to controls. Additionally, serum levels of both markers are found to be elevated in patients with multiple lesions when compared to patients with a single lesion. Serum S100B and P-ENK levels may also be used as predictors of mortality in patients with TBI.


2004 ◽  
Vol 31 (S 1) ◽  
Author(s):  
E Kockelmann ◽  
CE Elger ◽  
C Helmstaedter

Author(s):  
Gopal Krishna ◽  
Varun Aggarwal ◽  
Ishwar Singh

Abstract Introduction Traumatic brain injury (TBI) affects the coagulation pathway in a distinct way than does extracranial trauma. The extent of coagulation abnormalities varies from bleeding diathesis to disseminated thrombosis. Design Prospective study. Methods The study included 50 patients of isolated TBI with cohorts of moderate (MHI) and severe head injury (SHI). Coagulopathy was graded according to the values of parameters in single laboratory. The incidence of coagulopathy according to the severity of TBI and correlation with disseminated intravascular coagulation (DIC) score, platelets, prothrombin time (PT), activated partial thromboplastin time (APTT), D-dimer, and fibrinogen was observed. The comparison was also made between expired and discharged patients within each group. It also compared coagulation derailments with clinical presentation (Glasgow Coma Scale [GCS]) and outcome (Glasgow Outcome Scale [GOS]). Results Road traffic accident was the primary (72%) mode of injury. Fifty-two percent had MHI and rest had SHI. Eighty-four percent of cases were managed conservatively. The mean GCS was 12.23 and 5.75 in MHI and SHI, respectively. Sixty-two percent of MHI and 96% of the patients with SHI had coagulation abnormalities. On statistical analysis, DIC score (p < 0.001) strongly correlated with the severity of head injury and GOS. PT and APTT were also significantly associated with the severity of TBI. In patients with moderate TBI, D-dimer and platelet counts showed association with clinical outcome. Fibrinogen levels did not show any statistical significance. The mean platelet counts remained normal in both the groups of TBI. The mean GOS was 1.54 and 4.62 in SHI and MHI, respectively. Conclusion Coagulopathy is common in isolated TBI. The basic laboratory parameters are reliable predictors of coagulation abnormalities in TBI. Coagulopathy is directly associated with the severity of TBI, GCS, and poor outcome.


2012 ◽  
Vol 33 (2) ◽  
pp. 311-318 ◽  
Author(s):  
Nicole A Terpolilli ◽  
Seong-Woong Kim ◽  
Serge C Thal ◽  
Wolfgang M Kuebler ◽  
Nikolaus Plesnila

Ischemia, especially pericontusional ischemia, is one of the leading causes of secondary brain damage after traumatic brain injury (TBI). So far efforts to improve cerebral blood flow (CBF) after TBI were not successful because of various reasons. We previously showed that nitric oxide (NO) applied by inhalation after experimental ischemic stroke is transported to the brain and induces vasodilatation in hypoxic brain regions, thus improving regional ischemia, thereby improving brain damage and neurological outcome. As regional ischemia in the traumatic penumbra is a key mechanism determining secondary posttraumatic brain damage, the aim of the current study was to evaluate the effect of NO inhalation after experimental TBI. NO inhalation significantly improved CBF and reduced intracranial pressure after TBI in male C57 Bl/6 mice. Long-term application (24 hours NO inhalation) resulted in reduced lesion volume, reduced brain edema formation and less blood–brain barrier disruption, as well as improved neurological function. No adverse effects, e.g., on cerebral auto-regulation, systemic blood pressure, or oxidative damage were observed. NO inhalation might therefore be a safe and effective treatment option for TBI patients.


1970 ◽  
Vol 33 (5) ◽  
pp. 498-505 ◽  
Author(s):  
R. Zupping

✓ Acid-base and gas parameters of CSF, jugular venous and arterial blood were measured in 45 patients with brain injury in the first 12 days after trauma or operation. CSF metabolic acidosis together with respiratory alkalosis and hypoxemia in the cerebral venous and arterial blood were the most characteristic findings. A close correlation between the severity of brain damage and the intensity of the CSF metabolic acidosis and arterial hypocapnia was revealed. It was concluded that brain hypoxia and acidosis play an important role in the development of cerebral edema and permanent brain damage.


2021 ◽  
Vol 19 ◽  
Author(s):  
Denise Battaglini ◽  
Dorota Siwicka-Gieroba ◽  
Patricia RM Rocco ◽  
Fernanda Ferreira Cruz ◽  
Pedro Leme Silva ◽  
...  

: Traumatic brain injury (TBI) is a major cause of disability and death worldwide. The initial mechanical insult results in tissue and vascular disruption with hemorrhages and cellular necrosis that is followed by a dynamic secondary brain damage that presumably results in additional destruction of the brain. In order to minimize deleterious consequences of the secondary brain damage-such as inflammation, bleeding or reduced oxygen supply. The old concept of the -staircase approach- has been updated in recent years by most guidelines and should be followed as it is considered the only validated approach for the treatment of TBI. Besides, a variety of novel therapies have been proposed as neuroprotectants. The molecular mechanisms of each drug involved in inhibition of secondary brain injury can result as potential target for the early and late treatment of TBI. However, no specific recommendation is available on their use in clinical setting. The administration of both synthetic and natural compounds, which act on specific pathways involved in the destructive processes after TBI, even if usually employed for the treatment of other diseases, can show potential benefits. This review represents a massive effort towards current and novel therapies for TBI that have been investigated in both pre-clinical and clinical settings. This review aims to summarize the advancement in therapeutic strategies basing on specific and distinct -target of therapies-: brain edema, ICP control, neuronal activity and plasticity, anti-inflammatory and immunomodulatory effects, cerebral autoregulation, antioxidant properties, and future perspectives with the adoption of mesenchymal stromal cells.


PLoS ONE ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. e0245425
Author(s):  
Tomas Vilimovsky ◽  
Peii Chen ◽  
Kristyna Hoidekrova ◽  
Jakub Petioky ◽  
Pavel Harsa

Spatial neglect (SN) is a common cognitive disorder after brain injury. Prism adaptation treatment (PAT) is one of the promising interventions for SN albeit inconsistent results from previous studies. We carried out a comparison intervention (PAT vs. Sham) and aimed to evaluate the efficacy of PAT on visuospatial symptoms of SN in an inpatient rehabilitation setting that offered a highly intensive comprehensive brain injury rehabilitation program. A total of 34 patients with moderate-to-severe SN secondary to stroke or traumatic brain injury were randomized to the PAT group and the Sham group (an active control group). Both groups received 10 sessions of treatment, over two weeks, in addition to the rehabilitation therapies provided by their rehabilitation care teams. Outcomes were measured using an ecological instrument (the Catherine Bergego Scale) and paper-and-pencil tests (the Bells Test, the Line Bisection Test and the Scene Copying Test). Patients were assessed at baseline, immediately after treatment, two weeks after treatment, and four weeks after treatment. 23 (67.6%) patients completed treatment and all the assessment sessions and were included in the final analyses using mixed linear modeling. While SN symptoms reduced in both groups, we found no difference between the two groups in the degree of improvement. In addition, the average SN recovery rates were 39.1% and 28.6% in the PAT and Sham groups, respectively, but this discrepancy did not reach statistical significance. Thus, the present study suggests that PAT may contribute little to SN care in the context of a highly intensive inpatient rehabilitation program. Further large-scale investigation is required to uncover the mechanisms underlying PAT and Sham in order to refine the treatment or create new interventions.


2018 ◽  
Author(s):  
Jessica Bruijel ◽  
Sven Z Stapert ◽  
Annemiek Vermeeren ◽  
Jennie L Ponsford ◽  
Caroline M van Heugten

BACKGROUND Fatigue and sleep problems are common after a traumatic brain injury (TBI) and are experienced as highly distressing symptoms, playing a significant role in the recovery trajectory, and they can drastically impact the quality of life and societal participation of the patient and their family and friends. However, the etiology and development of these symptoms are still uncertain. OBJECTIVE The aim of this study is to examine the development of fatigue and sleep problems following moderate to severe TBI and to explore the changes in underlying biological (pain, brain damage), psychological (emotional state), and social (support family, participation) factors across time. METHODS This study is a longitudinal multicenter observational cohort study with 4 measurement points (3, 6, 12, and 18 months postinjury) including subjective questionnaires and cognitive tasks, preceded by 7 nights of actigraphy combined with a sleep diary. Recruitment of 137 moderate to severe TBI patients presenting at emergency and neurology departments or rehabilitation centers across the Netherlands is anticipated. The evolution of fatigue and sleep problems following TBI and their association with possible underlying biological (pain, brain damage), psychological (emotional state), and social (support family, participation) factors will be examined. RESULTS Recruitment of participants for this longitudinal cohort study started in October 2017, and the enrollment of participants is ongoing. The first results are expected at the end of 2020. CONCLUSIONS To the authors’ knowledge, this is the first study that examines the development of both post-TBI fatigue and sleep longitudinally within a biopsychosocial model in moderate to severe TBI using both subjective and objective measures. Identification of modifiable factors such as mood and psychosocial stressors may give direction to the development of interventions for fatigue and sleep problems post-TBI. CLINICALTRIAL Netherlands Trial Register NTR7162; http://www.trialregister.nl/trialreg/admin/rctview.asp?TC=7162 (Archived by WebCite at http://www.webcitation.org/6z3mvNLuy) INTERNATIONAL REGISTERED REPOR RR1-10.2196/11295


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