EFFECTS OF TRANEXAMIC ACID ON NEUROPATHOLOGY, ELECTROENCEPHALOGRAPHY, AND CEREBRAL FIBRIN DEPOSITION IN A RAT MODEL OF POLYTRAUMA WITH CONCOMITANT PENETRATING TRAUMATIC BRAIN INJURY.

ABSTRACT: Several studies have demonstrated the clinical utility of tranexamic acid (TXA) for use in trauma patients presenting with significant hemorrhage. Tranexamic acid is an antifibrinolytic that inhibits plasminogen activation, and plasmin activity has been shown to mitigate blood loss and reduce all-cause mortality in the absence of adverse vascular occlusive events. Recent clinical developments indicate TXA is safe to use in patients with concomitant traumatic brain injury (TBI); however, the prehospital effects are not well understood. Importantly, TXA has been associated with seizure activity. Therefore, this study sought to evaluate the effects of early administration of TXA on neurological recovery and electroencephalogram (EEG) abnormalities following penetrating TBI with concomitant hypoxemia and hemorrhagic shock. We hypothesized that early administration of TXA will provide hemodynamic stabilization and reduce intracerebral hemorrhage, which will result in improved neurological function. To test this hypothesis, Sprague-Dawley rats received a unilateral, frontal penetrating ballistic-like brain injury by inserting a probe into the frontal cortex of the anesthetized rat. Five minutes following brain injury, animals underwent 30 min of respiratory distress and 30 min of hemorrhage. Upon completion of the hemorrhage phase, animals received the initial dose of drug intravenously over 10 min after which the prehospital phase was initiated. During the prehospital phase, animals received autologous shed whole blood as needed to maintain a MAP of 65 mm Hg. After 90 min, "in-hospital" resuscitation was performed by administering the remaining shed whole blood providing 100% oxygen for 15 min. Upon recovery from surgery, animals were administered their second dose of vehicle or TXA intravenously over 8 h. Tranexamic acid induced an early improvement in neurologic deficit, which was statistically significant compared with vehicle at 24, 48, and 72 h at three doses tested. Analysis of cerebral hemoglobin content and intracerebral lesion progression revealed 100 mg/kg provided the optimal effects for improvement of neuropathology and was continued for determination of adverse treatment effects. We observed no exacerbation of cerebral thrombosis, but TXA treatment caused an increased risk of EEG abnormalities. These results suggest that TXA following polytrauma with concomitant brain injury may provide mild neuroprotective effects by preventing lesion progression, but this may be associated with an increased risk of abnormal EEG patterns. This risk may be associated with TXA inhibition of glycine receptors and may warrant additional considerations during the use of TXA in patients with severe TBI.

Respuesta de los autores: Acerca del papel del ácido tranexámico en pacientes con traumatismo en urgencias y emergencias / Authors' reply: On the role of tranexamic acid in emergency department patients with trauma

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Differential Effects of Caffeine on Motor and Cognitive Outcomes of Penetrating Ballistic-Like Brain Injury.

This study assessed the effect of caffeine on neurobehavioral recovery in the WRAIR penetrating ballistic-like brain injury (PBBI) model. Unilateral frontal PBBI was produced in the right hemisphere of anesthetized rats at moderate (7%-PBBI) or severe (10%-PBBI) injury levels. Animals were randomly assigned to pretreatment groups: acute caffeine (25 mg/kg CAF gavage, 1 h prior to PBBI), or chronic caffeine (0.25 g/L CAF drinking water, 30 days prior to PBBI). Motor function was evaluated on the rotarod at fixed-speed increments of 10, 15, and 20 RPM. Cognitive performance was evaluated on the Morris water maze. Acute caffeine showed no significant treatment effect on motor or cognitive outcome. Acute caffeine exposure prior to 10%-PBBI resulted in a significantly higher thigmotaxic response compared to vehicle-PBBI groups, which may indicate caffeine exacerbates post-injury anxiety/attention decrements. Results of the chronic caffeine study revealed a significant improvement in motor outcome at 7 and 10 days post-injury in the 7%-PBBI group. However, chronic caffeine exposure significantly increased the latency to locate the platform in the Morris water maze task at all injury levels. Results indicate that chronic caffeine consumption prior to a penetrating TBI may provide moderate beneficial effects to motor recovery, but may worsen the neurocognitive outcome.

Exogenous progesterone is neuroprotective following injury to the male zebra finch brain.

The use of progesterone following brain injury has a controversial history. On one hand, some lab-based models have showed progesterone as being neuroprotective, but on the other, clinical trials have showed quite the opposite. One of many complaints that arose from this discrepancy was the lack of a diverse pool of animal models and paradigms employed during the preclinical phase. However, over the past decade, the zebra finch has emerged as an optimal organism for the study of steroid-mediated neuroprotection. Following an injury, steroid hormones and receptors are upregulated, serving to decrease neuroinflammation and overall damage to the brain. As compared to other vertebrate models, zebra finches can upregulate expression of both estrogens and androgens at a faster and more robust response, suggesting that vertebrates differ in their neuroprotective mechanisms and timing following injury. Therefore, to expand the types organisms studied in pre-clinical trials, we chose to use zebra finches. While the majority of work in the zebra finch brain has focused on estrogens and androgens, we sought to clarify the role of progesterone following injury. Adult male zebra finches were given daily injections of progesterone following a penetrating injury and then were assessed for the size of injury and expression of various genes associated with neuroinflammation and cell survival. Treatment with progesterone decreased the injury size in zebra finches over controls and increased expression of various genes associated with cell survival and neuroinflammation. These data suggest that progesterone does mediate neuroprotection, most likely through the alteration of neuroinflammatory and cell survival pathways.

Dexamethasone retrodialysis attenuates microglial response to implanted probes in vivo.

Intracortical neural probes enable researchers to measure electrical and chemical signals in the brain. However, penetration injury from probe insertion into living brain tissue leads to an inflammatory tissue response. In turn, microglia are activated, which leads to encapsulation of the probe and release of pro-inflammatory cytokines. This inflammatory tissue response alters the electrical and chemical microenvironment surrounding the implanted probe, which may in turn interfere with signal acquisition. Dexamethasone (Dex), a potent anti-inflammatory steroid, can be used to prevent and diminish tissue disruptions caused by probe implantation. Herein, we report retrodialysis administration of dexamethasone while using in vivo two-photon microscopy to observe real-time microglial reaction to the implanted probe. Microdialysis probes under artificial cerebrospinal fluid (aCSF) perfusion with or without Dex were implanted into the cortex of transgenic mice that express GFP in microglia under the CX3CR1 promoter and imaged for 6 h. Acute morphological changes in microglia were evident around the microdialysis probe. The radius of microglia activation was 177.1 µm with aCSF control compared to 93.0 µm with Dex perfusion. T-stage morphology and microglia directionality indices were also used to quantify the microglial response to implanted probes as a function of distance. Dexamethasone had a profound effect on the microglia morphology and reduced the acute activation of these cells.

Neuroprotection and anti-seizure effects of levetiracetam in a rat model of penetrating ballistic-like brain injury.

PURPOSE: We assessed the therapeutic efficacy of FDA-approved anti-epileptic drug Levetiracetam (LEV) to reduce post-traumatic nonconvulsive seizure (NCS) activity and promote neurobehavioral recovery following 10% frontal penetrating ballistic-like brain injury (PBBI) in male Sprague-Dawley rats. METHODS: Experiment 1 anti-seizure study: 50 mg/kg LEV (25 mg/kg maintenance doses) was given twice daily for 3 days (LEV3D) following PBBI; outcome measures included seizures incidence, frequency, duration, and onset. Experiment 2 neuroprotection studies: 50 mg/kg LEV was given twice daily for either 3 (LEV3D) or 10 days (LEV10D) post-injury; outcome measures include motor (rotarod) and cognitive (water maze) functions. RESULTS: LEV3D treatment attenuated seizure activity with significant reductions in NCS incidence (54%), frequency, duration, and delayed latency to seizure onset compared to vehicle treatment. LEV3D treatment failed to improve cognitive or motor performance; however extending the dosing regimen through 10 days post-injury afforded significant neuroprotective benefit. Animals treated with the extended LEV10D dosing regimen showed a twofold improvement in rotarod task latency to fall as well as significantly improved spatial learning performance (24%) in the MWM task. CONCLUSIONS: These findings support the dual anti- seizure and neuroprotective role of LEV, but more importantly identify the importance of an extended dosing protocol which was specific to the therapeutic targets studied.

Comentarios al artículo «Tratamiento anestesiológico de la fractura de pelvis "en libro abierto" secundaria a explosión» / Comment on article «Anesthesiology treatment of an "open book" pelvic fracture due to an explosión»

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Réplica a «Comentarios al artículo "Tratamiento anestesiológico de la fractura de pelvis 'en libro abierto' secundario a explosión"» / Reply to «Comment on article "Anesthesiology treatment of an 'open book' pelvic fracture due to an explosión"»

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Dual Therapeutic Effects of C-10068, a Dextromethorphan Derivative, Against Post-Traumatic Nonconvulsive Seizures and Neuroinflammation in a Rat Model of Penetrating Ballistic-Like Brain Injury.

Post-traumatic seizures can exacerbate injurious outcomes of severe brain trauma, yet effective treatments are limited owing to the complexity of the pathology underlying the concomitant occurrence of both events. In this study, we tested C-10068, a novel deuterium-containing analog of (+)-N-methyl-3-ethoxymorphinan, in a rat model of penetrating ballistic-like brain injury (PBBI) and evaluated the effects of C-10068 on PBBI-induced nonconvulsive seizures (NCS), acute neuroinflammation, and neurofunctional outcomes. NCS were detected by electroencephalographic monitoring. Neuroinflammation was evaluated by immunohistochemical markers, for example, glial fibrillary acidic protein and major histocompatibility complex class I, for activation of astrocytes and microglia, respectively. Neurofunction was tested using rotarod and Morris water maze tasks. Three infusion doses of C-10068 (1.0, 2.5, and 5.0 mg/kg/h × 72 h) were tested in the antiseizure study. Neuroinflammation and neurofunction were evaluated in animals treated with 5.0 mg/kg/h × 72 h C-10068. Compared to vehicle treatment, C-10068 dose dependently reduced PBBI-induced NCS incidence (40-50%), frequency (20-70%), and duration (30-82%). The most effective antiseizure dose of C-10068 (5.0 mg/kg/h × 72 h) also significantly attenuated hippocampal astrocyte activation and perilesional microglial reactivity post-PBBI. Within C-10068-treated animals, a positive correlation was observed in reduction in NCS frequency and reduction in hippocampal astrocyte activation. Further, C-10068 treatment significantly attenuated astrocyte activation in seizure-free animals. However, C-10068 failed to improve PBBI-induced motor and cognitive functions with the dosing regimen used in this study. Overall, the results indicating that C-10068 exerts both potent antiseizure and antiinflammatory effects are promising and warrant further investigation.

Treatment with amnion-derived cellular cytokine solution (ACCS) induces persistent motor improvement and ameliorates neuroinflammation in a rat model of penetrating ballistic-like brain injury.

PURPOSE: The present work compared the behavioral outcomes of ACCS therapy delivered either intravenously (i.v.) or intracerebroventricularly (i.c.v.) after penetrating ballistic-like brain injury (PBBI). Histological markers for neuroinflammation and neurodegeneration were employed to investigate the potential therapeutic mechanism of ACCS. METHODS: Experiment-1, ACCS was administered either i.v. or i.c.v. for 1 week post-PBBI. Outcome metrics included behavioral (rotarod and Morris water maze) and gross morphological assessments. Experiment-2, rats received ACCS i.c.v for either 1 or 2 weeks post-PBBI. The inflammatory response was determined by immunohistochemistry for neutrophils and microglia reactivity. Neurodegeneration was visualized using silver staining. RESULTS: Both i.v. and i.c.v. delivery of ACCS improved motor outcome but failed to improve cognitive outcome or tissue sparing. Importantly, only i.c.v. ACCS treatment produced persistent motor improvements at a later endpoint. The i.c.v. ACCS treatment significantly reduced PBBI-induced increase in myeloperoxidase (MPO) and ionized calcium binding adaptor molecule 1 (Iba1) expression. Concomitant reduction of both Iba1 and silver staining were detected in corpus callosum with i.c.v. ACCS treatment. CONCLUSIONS: ACCS, as a treatment for TBI, showed promise with regard to functional (motor) recovery and demonstrated strong capability to modulate neuroinflammatory responses that may underline functional recovery. However, the majority of beneficial effects appear restricted to the i.c.v. route of ACCS delivery, which warrants future studies examining delivery routes (e.g. intranasal delivery) which are more clinically viable for the treatment of TBI.

Hipertensión endocraneal asociada a la sedación con sevoflurano mediante el dispositivo AnaConDa ®en un paciente con traumatismo craneoencefálico severo / Intracranial hypertension related to sedation with sevoflurane using the AnaConDa ® device in a patient with severe traumatic brain injury

La sedación en los pacientes neurocríticos es difícil, debido a que ningún fármaco cumple todos los requisitos. Desde la aparición del dispositivo AnaConDa® y según las últimas recomendaciones, el sevoflurano se ha convertido en una alternativa para el paciente neurocrítico. Una de las consecuencias de la utilización del dispositivo es el aumento del espacio muerto anatómico instrumental que produce una disminución de la ventilación alveolar. Si la disminución de la ventilación alveolar no se compensa con un aumento del volumen minuto se producirá un aumento de la PaCO2. Presentamos el caso de un paciente con traumatismo craneoencefálico severo en el que se produjo un aumento de la presión endocraneal como consecuencia del aumento de la PaCO2 tras colocar el dispositivo AnaConDa® para sedación (AU)

Pharmacological mitigation of tissue damage during brain microdialysis.

Microdialysis sampling in the brain is employed frequently in the chemical analysis of neurological function and disease, but implanting the probes, which are substantially larger than the size and spacing of brain cells and blood vessels, is injurious and triggers ischemia, gliosis, and cell death at the sampling site. The nature of the interface between the brain and the microdialysis probe is critical to the use of microdialysis as a neurochemical analysis technique. The objective of the work reported here was to investigate the potential of two compounds, dexamethasone, a glucocorticoid anti-inflammatory agent, and XJB-5-131, a mitochondrially targeted reactive oxygen species scavenger, to mitigate the penetration injury. Measurements were performed in the rat brain striatum, which is densely innervated by axons that release dopamine, an electroactive neurotransmitter. We used voltammetry to measure electrically evoked dopamine release next to microdialysis probes during the retrodialysis of dexamethasone or XJB-5-131. After the in vivo measurements, the brain tissue containing the microdialysis probe tracks was examined by fluorescence microscopy using markers for ischemia, neuronal nuclei, macrophages, and dopamine axons and terminals. Dexamethasone and XJB-5-131 each diminished the loss of evoked dopamine activity, diminished ischemia, diminished the loss of neuronal nuclei, diminished the appearance of extravasated macrophages, and diminished the loss of dopamine axons and terminals next to the probes. Our findings confirm the ability of dexamethasone and XJB-5-131 to mitigate, but not eliminate, the effects of the penetration injury caused by implanting microdialysis probes into brain tissue.

Tamoxifen favoured the rat sensorial cortex regeneration after a penetrating brain injury.

A penetrating brain injury produces a glial scar formed by astrocytes, oligodendrocytes, microglia and NG2 cells. Glial scar is a barrier preventing the extent of damage but it has deleterious effects in the regeneration of the axons. Estradiol and tamoxifen reduce gliosis and have neuroprotective effects in the hippocampus and the spinal cord. We evaluated the proliferation of glia and the electrocorticogram in the sensorial cortex in a brain injury model. At seven days post-injury, estradiol, tamoxifen and estradiol plus tamoxifen reduced the number of resident and proliferative NG2 and reactive astrocyte vimentin+ cells. Estradiol and tamoxifen effects on NG2 cells could be produced by the classical oestrogen receptors found in these cells. The glial scar was also reduced by tamoxifen. At thirty days post-injury, the amount of resident and proliferative astrocytes increased significantly, except in the estradiol plus tamoxifen group, whilst the oligodendrocytes proliferation in the glial scar was reduced in treated animals. Tamoxifen promotes the survival of FOX-3+ neurons in the injured area and a recovery in the amplitude of electrocorticogram waves. At thirty days, estradiol did not favour the survival of neurons but produced a greater number of reactive astrocytes. In contrast, the number of oligodendrocytes was reduced. Tamoxifen could favour brain repair promoting neuron survival and adjusting glial cell number. It seems to recover adequate neural communication.

Mechanism of action for NNZ-2566 anti-inflammatory effects following PBBI involves upregulation of immunomodulator ATF3.

The tripeptide glycine-proline-glutamate analogue NNZ-2566 (Neuren Pharmaceuticals) demonstrates neuroprotective efficacy in models of traumatic brain injury. In penetrating ballistic-like brain injury (PBBI), it significantly decreases injury-induced upregulation of inflammatory cytokines including TNF-α, IFN-γ, and IL-6. However, the mechanism by which NNZ-2566 acts has yet to be determined. The activating transcription factor-3 (ATF3) is known to repress expression of these inflammatory cytokines and was increased at the mRNA and protein level 24-h post-PBBI. This study investigated whether 12 h of NNZ-2566 treatment following PBBI alters atf3 expression. PBBI alone significantly increased atf3 mRNA levels by 13-fold at 12 h and these levels were increased by an additional fourfold with NNZ-2566 treatment. To confirm that changes in mRNA translated to changes in protein expression, ATF3 expression levels were determined in vivo in microglia/macrophages, T cells, natural killer cells (NKCs), astrocytes, and neurons. PBBI alone significantly increased ATF3 in microglia/macrophages (820%), NKCs (58%), and astrocytes (51%), but decreased levels in T cells (48%). NNZ-2566 treatment further increased ATF3 protein expression in microglia/macrophages (102%), NKCs (308%), and astrocytes (13%), while reversing ATF3 decreases in T cells. Finally, PBBI increased ATF3 levels by 55% in neurons and NNZ-2566 treatment further increased these levels an additional 33%. Since increased ATF3 may be an innate protective mechanism to limit inflammation following injury, these results demonstrating that the anti-inflammatory and neuroprotective drug NNZ-2566 increase both mRNA and protein levels of ATF3 in multiple cell types provide a cellular mechanism for NNZ-2566 modulation of neuroinflammation following PBBI.

Long-term administration of amnion-derived cellular cytokine suspension promotes functional recovery in a model of penetrating ballistic-like brain injury.

BACKGROUND: Previous work has shown that human amnion-derived progenitor (AMP) cell therapy is neuroprotective in a penetrating ballistic-like brain injury (PBBI) model. However, the neuroprotective capacity of AMP cells seemed to be mediated by the sustained secretion of AMP cell-derived neurotrophic factors, which are abundant in the amnion-derived cellular cytokine suspension (ACCS). To test this theory, the current study assessed the neuroprotective efficacy of long-term ACCS delivery in the PBBI model. METHODS: Experiment 1 assessed the bioactive stability and neuroprotective capacity of ACCS in an in vitro model of neurodegeneration. Experiment 2 evaluated the therapeutic effects of ACCS delivery initiated 15 minutes after PBBI and continued for 2 weeks after injury. Experiment 3 was designed to identify the therapeutic window for long-term ACCS delivery in the PBBI model. Outcome metrics included neurobehavioral assessments and neuropathologic measures of neuroinflammation and axonal/neuronal degeneration. RESULTS: Experiment 1 demonstrated that ACCS is thermally stable for 1 week at 37°C and that ACCS treatment protected neurite against staurosporine toxicity. Experiment 2 identified the optimal infusion rate of ACCS (1 µL/h) and demonstrated that long-term infusion of ACCS was capable of promoting significant protection against PBBI-induced neuropathology and motor abnormalities, but was not sufficient for reducing cognitive deficits. Finally, the results of Experiment 3 showed that ACCS is effective in promoting significant neuroprotection even when onset of treatment is delayed out to 24 hours (but not 48 hours) after PBBI. CONCLUSIONS: Collectively, our results support the hypothesis that the neuroprotective effects of AMP cells are mediated through a sustained delivery of ACCS, which implicates ACCS as a promising neuroprotection agent for clinical study.

[Optimization of medical-diagnostic process in patients with traumatic brain injury during early rehabilitation].

The problem of cardiovascular disease and cancer, the effects of traumatic brain injury is now one of the major health and social problems. Every year in Ukraine registered 200 thousand cases of the victims of traumatic brain injury. Of these, 30% of people then have persistent signs of disability that results in a disability, sometimes painful existence the patient and his relatives. Therefore, in order to bring man back into society after a traumatic brain injury, to the rehabilitation phase of treatment, immediately after the stabilization of the patient.

Tromboprofilaxis en el paciente politraumatizado y con traumatismo craneoencefálico / Thromboprophylaxis in multiple trauma and head injury patients

La enfermedad tromboembólica venosa (ETV) es una importante entidad clínica (epidemiológica, por su gravedad y costes), con elevada mortalidad por infradiagnóstico o tratamiento inadecuado, especialmente en pacientes como la población traumática. La incidencia de la ETV en estos pacientes varía de un 5 a 58% y se considera esencial la tromboprofilaxis para su correcto manejo. Tradicionalmente, las fracturas de pelvis y extremidad inferior, presencia de trauma craneal y la inmovilización prolongada han sido considerados factores de riesgo de ETV, sin embargo no está claro qué combinación de estos factores y otros puedan ser predictores de alto riesgo. En la actualidad, la estrategia óptima de profilaxis de la ETV para los pacientes politraumatizados es desconocida. La tromboprofilaxis se puede realizar con medidas mecánicas y con tratamientos farmacológicos. En la mayoría de estos pacientes, las principales guías recomienda la tromboprofilaxis con heparina de bajo peso molecular (HBPM) que se puede iniciar a las 48 horas y en pacientes con hemorragia activa debe ser considerada la compresión mecánica, a pesar de su eficacia limitada, hasta que el riesgo de hemorragia haya disminuido. No existen datos suficientes para justificar la realización rutinaria de ecografía o flebografía en todos estos pacientes. En el caso de los pacientes con traumatismo craneoencefálico y riesgo de hemorragia intracraneal, se recomienda retrasar el inicio de la tromboprofilaxis con HBPM hasta la desaparición de dicho riesgo pero se puede valorar la utilización de las medidas mecánicas según la situación clínica (AU)

Venous thromboembolic disease (VTD) is a frequent condition with serious clinical consequences and elevated mortality related to underdiagnosis or undertreatment, especially in patients with multiple trauma. The incidence of VTD in these patients ranges from 5% to 58% and thromboprophylaxis is considered essential for proper management. Traditionally, pelvic and lower extremity fractures, head injury, and prolonged immobilization have been cited as risk factors for VTD; however, how these factors combine with others to predict high risk is still unclear. The best way to approach VTD prophylaxis in multiple trauma patients is currently unclear. Both mechanical and pharmacologic means are available. The main clinical practice guidelines recommend thromboprophylaxis with low-molecular weight heparin, which can be started 48 hours after trauma, unless patients are still bleeding, in which case mechanical compression is recommended in spite of the limited effectiveness of that measure. Compression is maintained until the risk of hemorrhage has diminished. There is insufficient evidence to support routine use of ultrasound imaging or venography. In patients with head injury who are at risk for intracranial bleeding, the use of low-molecular weight heparin should be delayed until risk disappears but mechanical prophylaxis (compression) can be considered according to clinical status (AU)

Orbitocerebral injury by a knife: case report.

Orbital penetrating injuries may cause significant harm to the optic nerves and eyeball as well as to the brain and cerebral vessels. Management of orbital foreign bodies should include prompt recognition of the extent of the injury, broad-spectrum parenteral antibiotics, tetanus prophylaxis, anticonvulsant medication and early surgical intervention under direct vision to remove the foreign body and to avoid immediate and long-term complications. We report a penetrating orbital injury caused by a bread knife that extended from the orbit to the tegmental dura mater of the temporal bone. The knife's main trajectory coursed through the temporal lobe. Adjacent cerebral structures were explored before removal of the knife.

Orbitocerebral injury by a knife: case report

Orbital penetrating injuries may cause significantharm to the optic nerves and eyeball as well as to thebrain and cerebral vessels. Management of orbitalforeign bodies should include prompt recognition of theextent of the injury, broad-spectrum parenteral antibiotics,tetanus prophylaxis, anticonvulsant medicationand early surgical intervention under direct vision toremove the foreign body and to avoid immediate andlong-term complications. We report a penetrating orbitalinjury caused by a bread knife that extended fromthe orbit to the tegmental dura mater of the temporalbone. The knife’s main trajectory coursed through thetemporal lobe. Adjacent cerebral structures were exploredbefore removal of the knife (AU)

Los traumatismos perforantes orbitarios suelencausar un daño importante al nervio óptico y globoocular, así como al cerebro y vasos cerebrales. Laórbita permite un acceso fácil hacia la cavidad cranealdebido a que tiene una pared ósea delgada y a la presenciadel agujero óptico. El enfoque terapéutico de lostraumatismos orbitarios por cuerpo extraño dependefundamentalmente del tipo de traumatismo y delcuerpo extraño. El tratamiento de este tipo de lesionesincluirá un rápido diagnostico de la magnitud del dañoocasionado, el empleo por vía parenteral de antibióticosde amplio espectro, profilaxis del tétanos, medicaciónanticonvulsivante y cirugía urgente que permita, bajovisión directa, la extracción del cuerpo extraño, a fin de evitar complicaciones inmediatas o a largo plazo. Presentamosel caso de un traumatismo perforante ocularocasionado por un cuchillo de pan que se extendíadesde la órbita hasta el tegmentum del hueso temporal.El cuchillo seguía una trayectoria directa a través dellóbulo temporal. Se practicó una exploración quirúrgicade las estructuras cerebrales adyacentes para poderextirpar el cuchillo. Se revisan y analizan las opcionesde tratamiento de los traumatismos perforantes de laórbita (AU)