BACKGROUND:Penetrating traumatic brain injury (pTBI) affects civilian and military populations resulting in significant morbidity, mortality, and health care costs. No up-to-date and evidence-based guidelines exist to assist modern medical and surgical management of these complex injuries. METHODS:A preliminary literature search informed a need for updated guidelines. Methodologists experienced in TBI guidelines supported 2 co-chairs, a diverse steering committee and three expert working groups. Over half of our panelists were active service military or military veterans and they addressed twenty-six Key Questions (KQs). We searched Ovid MEDLINE®, EMBASE, and Cochrane CENTRAL from inception to August 31, 2022, reference lists, and clinical trial registries. Penetrating, perforating and tangential penetrating brain injuries were included. Predefined criteria were used to identify studies; pre-specified methods were used to assess study quality and strength of evidence for key outcomes. Effects were analyzed qualitatively and quantitatively where appropriate. RESULTS:125 studies provided evidence and another 80 studies provided contextual data for these guidelines. In general there was a paucity of literature and most of the identified evidence was judged to be high risk of bias due to study design. We did not identify any studies meeting inclusion criteria for 12 KQs. The highest quality evidence, rated moderate in strength, was identified for four KQs that covered: cerebral angiography vs computed tomography angiography, the relationship between bihemispheric injury in adult pTBI and mortality, the ability of the Surviving Penetrating Injury to the Brain (SPIN) score to predict mortality, and the relationship between infection and cerebrospinal fluid fistula. Evidence for most KQs came from case series. CONCLUSIONS:The development of up-to-date evidence and consensus based clinical care guidelines and algorithms for pTBI provide guidance to care providers in the prehospital and emergency medicine, surgical and intensive care settings. Few moderately strong conclusions on the benefit of specific management strategies for penetrating brain injury could be made. Detailed reporting of patient outcomes in future studies could advance the field by providing greater evidence for specific treatments by patient population, mechanism of injury, severity of injury, and specific interventions employed.

BACKGROUND:An External Ventricular Drain (EVD) is a catheter inserted into one or both of the lateral ventricles of the brain. The indications for inserting this drain include intracranial haemorrhage, severe traumatic brain injury, to monitor intracranial pressure and to drain excess Cerebral Spinal Fluid. To ensure safe care for patients with an EVD, nurses need evidence-based knowledge in providing quality care. AIM:The purpose of this study was to describe and compare nursing knowledge and practices regarding patients with EVDs between nurses in General Intensive (GICU) and Neurosurgical Intensive Care Units (NICU). STUDY DESIGN:A convenience sample and snowball sample of General and Neurosurgical Intensive Care Unit nurses completed a structured questionnaire measuring the level of knowledge and describing nursing practices for patients with an EVD. Descriptive statistics, t-tests and correlations were used to analyse data. RESULTS:The final sample included 154 nurses from eight Israeli medical centres, divided almost equally between NICUs (n = 78, 51%) and GICUs (n = 76, 49%). The majority of nurses were female (71.4%), and the ages ranged between 23 and 65 years, with the average being 38.8 years. NICU nurses' mean total knowledge and practices score was significantly higher than that of the GICU nurses (NICU: mean = 16.9 [SD 3.22], GICU: mean = 14.07 [SD 3.71]), p ≤ 0.00001. CONCLUSION:The level of knowledge and self-perceived knowledge application of the nursing care of patients with an EVD was higher among NICU compared to GICU nurses. Mean GICU nurse scores were low. Therefore, it is preferred that patients with an EVD be hospitalised in neurosurgical units if possible. RELEVANCE TO CLINICAL PRACTICE:This study provides additional evidence that patients receiving specialised treatments or having unique diseases or injuries should receive care from nurses with specialised experience and training.

BACKGROUND:Penetrating traumatic brain injury (pTBI) is an important wounding mechanism which is seen increasingly as a result of violent crime and armed conflicts. pTBI is very challenging to manage as it is often highly complex yet requires expeditious treatment. Treatment algorithms thus can assist even experienced clinicians to avoid pitfalls while caring for these patients. METHODS:To supplement the evidence-based recommendations produced in conjunction with the Brain Trauma Foundation Guidelines for the Management of Penetrating Brain Injury, Second Edition, we developed protocols for care to help bridge limitations of published evidence with care decisions required at the bedside. Our working group of over 30 diverse expert panelists identified care, care pathways and key decisions relevant to pTBI care through discussion. A rigorous, blinded Delphi consensus process was then applied. Items achieving at least an 80% consensus vote were incorporated into the treatment algorithms. Consensus voting also approved the final versions of the care pathways. RESULTS:To meet the needs of diverse pTBI patients we created a Master Care Pathway relevant to all patients. We also created 'Toolkits' designed to address care issues that only some patients will have. Toolkits for surgical management, protruding foreign bodies, severe injury, skull base injury and vascular injury were developed. In addition, a futility assessment is provided to assist with delineating the small proportion of patients for whom initial non-aggressive care might be considered with the recognition that avoidance of nihilism is critical to achieving best outcomes in pTBI victims. CONCLUSIONS:Care pathways are presented which reflect suggestions for care that aim to inspire thoughtful management. The algorithms also aim to avoids potential pitfalls in management to help achieve best possible outcomes for pTBI patients.

The intracranial pressure (ICP) waveform conveys important information regarding the state of intracranial physiology, but in clinical practice it is typically analyzed in a qualitative fashion. We sought to develop a minimized model of intracranial physiology that describes intracranial dynamics occurring in a single cardiac cycle. By using an abridged model to which inputs of measured arterial and ICP waveforms from patients with brain injury can be applied, we aimed to derive estimates of intracranial elastance and venous outflow resistance. The minimized model has two capacitor elements, representing arterial wall and intracranial compliance, and two resistance elements, representing intracranial viscoelasticity and venous outflow resistance. We use a parameter optimization method to achieve estimates of intracranial elastance and venous outflow resistance. We studied patients with brain injury in the neurointensive care unit who underwent ICP monitoring and analyzed data from periods of normal and elevated ICP. We studied 375 ICP waveforms in 15 patients. Model-derived waveforms corresponded closely to measured ICP waveforms at both normal and elevated ICP. Model-derived estimates of intracranial elastance and venous outflow resistance both increased significantly when ICP was elevated (mean increase of 1.0 mm Hg/mL and 0.9 mm Hg × s/mL, respectively). The minimized model closely replicates measured ICP waveforms and allows for estimation of intracranial elastance and venous outflow resistance in patients with brain injury from readily available clinical parameters.

IntroductionFunctional Near-Infrared Spectroscopy (fNIRS) is widely used to monitor cerebral hemodynamics, however, it is limited by shallow penetration depth and susceptibility to hemodynamic noise from the scalp. A novel intracranial fNIRS (ifNIRS) system, featuring depth optrodes (optode-electrodes) and optical anchor bolts (OABs), has been proposed to address these limitations. This study investigates the feasibility of ifNIRS in a swine model under controlled interventions.MethodsThree animals were implanted with ifNIRS. Each animal with three OABs, with depth optrodes (DO) inserted into two of the OABs. Hemodynamic changes were recorded using OAB-to-OAB (OAB-OAB) and DO-to-OAB (DO-OAB) channels. Two interventions were performed to generate hemodynamic changes: rapid infusion of hypotonic saline to induce cerebral edema and blood withdrawal. Postmortem assessment for tissue damage and hemorrhage was performed. Hemoglobin concentration changes were analyzed using the Beer-Lambert equation.ResultsA decrease in total hemoglobin (tHb) levels during blood withdrawal was observed in all channel configurations that displayed relevant signals. During hypotonic saline infusion, variable patterns of tHb were observed. Postmortem findings showed minor extra-axial hemorrhages near OABs, but no intracerebral or heat-related injuries.DiscussionThis study demonstrates the feasibility of the ifNIRS system in detecting hemodynamic changes in vivo. While technical refinements are needed, ifNIRS shows promise for improving cerebral hemodynamic monitoring and enhancing diagnostic accuracy in invasive monitoring of patients with epilepsy.

The quantitative relationship between arterial blood pressure (ABP) and intracranial pressure (ICP) waveforms has not been adequately explained. We hypothesized that the ICP waveform results from interferences between propagating and reflected pressure waves occurring in the cranium following the initiating arterial waveform. To demonstrate cranial effects on interferences between waves and generation of an ICP waveform morphology, we modified our previously reported mathematical model to include viscoelastic elements that affect propagation velocity. Using patient data, we implemented an inverse model methodology to generate simulated ICP waveforms in response to given ABP waveforms. We used an open database of traumatic brain injury patients and studied 65 pairs of ICP and ABP waveforms from 13 patients (five pairs from each). Incorporating viscoelastic elements into the model resulted in model-generated ICP waveforms that very closely resembled the measured waveforms with a 16-fold increase in similarity index relative to the model with only pure elasticity elements. The mean similarity index for the pure elasticity model was 0.06 +/- 0.12 SD, compared to 0.96 +/- 0.28 SD for the model with viscoelastic components. The normalized root mean squared error (NRMSE) improved substantially for the model with viscoelastic elements compared to the model with pure elastic elements (NRMSE of 2.09% +/- 0.62 vs. 15.2% +/- 4.8, respectively). The ability of the model to generate complex ICP waveforms indicates that the model may indeed reflect intracranial dynamics. Our results suggest that the model may allow the estimation of intracranial biomechanical parameters with potential clinical significance. It represents a first step in the estimation of inaccessible intracranial parameters.

Extensive investigation and modeling efforts have been dedicated to cerebral pressure autoregulation, which is primarily regulated by the ability of the cerebral arterioles to change their resistance and modulate cerebral blood flow (CBF). However, the mechanisms by which elevated intracranial pressure (ICP) leads to increased resistance to venous outflow have received less attention. We modified our previously described model of intracranial fluid interactions with a newly developed model of a partially collapsed blood vessel, which we termed the "flow control zone" (FCZ). We sought to determine the degree to which ICP elevation causing venous compression at the FCZ becomes the main parameter limiting CBF. The FCZ component was designed using nonlinear functions representing resistance as a function of cross-sectional area and the pressure-volume relations of the vessel wall. We used our previously described swine model of cerebral edema with graduated elevation of ICP to calculate venous outflow resistance and a newly defined parameter, the cerebral resistance index (CRI), which is the ratio between venous outflow resistance and cerebrovascular resistance. Model simulations of cerebral edema and increased ICP led to increased venous outflow resistance. There was a close similarity between model predictions of venous outflow resistance and experimental results in the swine model (cross-correlation coefficient of 0.97, a mean squared error of 0.087, and a mean absolute error of 0.15). CRI was strongly correlated to ICP in the swine model (r2 = 0.77, P = 0.00012, 95% confidence interval [0.15, 0.45]). A CRI value of 0.5 was associated with ICP values above clinically significant thresholds (24 mmHg) in the swine model and a diminished capacity of changes in arteriolar resistance to influence flow in the mathematical model. Our results demonstrate the importance of venous compression at the FCZ in determining CBF when ICP is elevated. The cerebral resistance index may provide an indication of when compression of venous outflow becomes the dominant factor in limiting CBF following brain injury.NEW & NOTEWORTHY The goal of this study was to investigate the effects of venous compression caused by elevated intracranial pressure (ICP) due to cerebral edema, validated through animal experiments. The flow control zone model highlights the impact of cerebral venous compression on cerebral blood flow (CBF) during elevated ICP. The cerebral venous outflow resistance-to-cerebrovascular resistance ratio may indicate when venous outflow compression becomes the dominant factor limiting CBF. CBF regulation descriptions should consider how arterial or venous factors may predominantly influence flow in different clinical scenarios.

A mechanism of elevated intracranial pressure (ICP) in cerebral edema and its effects on cerebral blood flow (CBF) are presented in this paper. To study and demonstrate these effects, a mathematical model of intracranial hydrodynamics was developed. The model simulates the intracranial hydrodynamics and the changes that occur when cerebral edema predominates. To account for an edema pathology, the model includes resistances to cerebrospinal fluid (CSF) and interstitial fluid (ISF) flows within the parenchyma. The resistances change as the intercellular space becomes smaller due to swelling of brain cells. The model demonstrates the effect of changes in these resistances on ICP and venous resistance to blood flow by accounting for the key interactions between pressure, volume, and flow in the intracranial compartments in pathophysiological conditions. The model represents normal intracranial physiology as well as pathological conditions. Simulating cerebral edema with increased resistance to cerebral ISF flow resulted in elevated ICP, increased brain volume, markedly reduced ventricular volume, and decreased CBF as observed in the neurointensive care patients. The model indicates that in high ICP values, alternation of the arterial-arteriolar resistance to flow minimally affects CBF, whereas at low ICP they have a much greater effect on CBF. The model demonstrates and elucidates intracranial mechanisms related to elevated ICP. NEW & NOTEWORTHY Study goal was to elucidate the role of "bulk flow" of ISF through brain parenchyma. A model was developed to simulate fluid shifts in brain edema, ICP elevation, and their effect on CBF. Bulk flow resistance affected by edema elevates ICP and reduces CBF. Bulk flow affects transmural pressure and volume distribution in brain compartments. Changes in bulk flow resistance result in increase of venous resistance to flow and decrease in CBF.

BACKGROUND:Brain oxygenation improvement is a sought-after goal in neurocritical care patients. Previously, we have shown that cerebral blood flow improvement by cardiac-gated intracranial pressure (ICP) modulation using an intracranial pulsating balloon is feasible in a swine model. We sought to explore specific ICP modulation protocols to assess the feasibility of influencing brain oxygenation. METHODS:A previously presented electrocardiogram (ECG)-gated intracranial balloon pump in which volume, timing, and duty cycle of balloon inflation could be altered was used. Different protocols were tested in a swine model of normal and elevated ICP attained by intracranial fluid infusion with continuous monitoring of physiological parameters, and brain tissue oxygen tension (PbtO2) was measured at baseline and after device activation. RESULTS:We studied five swine, subjected to two main protocols differing in their phase relative to the cardiac cycle. In reduced brain perfusion status (ICP > 20 mm Hg, PbtO2 < 15 mm Hg), the late-diastolic-early-systolic (Inflation/deflation) protocol showed consistent elevation in PbtO2 (+ 9%, p < 0.01), coupled with ICP reduction (- 12%, p < 0.01), whereas the early-systolic-late-diastolic (inflation/deflation) protocol resulted in PbtO2 reduction (- 4%, p < 0.01), coupled with ICP increase (+ 5% above baseline, p < 0.01). No significant changes in brain oxygenation or ICP were observed at normal perfusion status (ICP < 20 mm Hg, PbtO2 > 15 mm Hg). CONCLUSIONS:Intracranial cardiac-gated balloon pump activation can influence cerebral oxygenation and raise PbtO2 above threshold values. This study supports the concept of late-diastolic pressure rise, coupled with early-systolic pressure drop, as a potential effector of flow augmentation leading to improve brain tissue oxygenation. Further studies are warranted to assess the translational potential of using an intracranial cardiac-gated balloon pump device to improve brain tissue oxygenation.

Background Mycoplasma hominis is a small cell-wall-free organism, part of the normal microbiota of the genitourinary tract. It is rarely involved in extragenital infections, mainly joint, surgical-site, and respiratory infections. Methods We describe a case of M. hominis subdural empyema and lower limb surgical site infections, following decompressive craniotomy, after traumatic brain and extremities injury. In addition, a literature review of 34 cases M. hominis CNS infections was done. Results Our case depicts a 25-years old patient who developed subdural empyema and surgical site infections in his cranium and fibula. Both sites were cultured, and small pinpoint colonies grew on blood agar. MALDI-TOF MS identified M. hominis. Simultaneously 16S-rDNA PCR from CSF detected M. hominis. Antimicrobial treatment was switched to doxycycline with improvement. Literature review revealed 21 adults and 13 pediatric cases of M. hominis CNS infection. Risk factors in adults were head trauma, neurosurgery, or post-partum period. Conclusions Based upon the literature reviewed, we postulate that adult patients with head trauma or neurosurgical procedure, rarely are infected either through direct contamination during the trauma, or by undergoing urgent, urinary catheterization, and may experience distant infection due to translocation of M. hominis into the bloodstream. In such cases diagnosis is delayed due to difficulties in growing and identifying the bacteria. Empiric antimicrobials are usually not effective against mycoplasmas. These factors contributed to the mortality in adult cases (15%). Our rare case highlights the necessity of combining classical microbiology routines with advanced molecular techniques to establish a diagnosis in complicated cases.

Penetrating traumatic brain injury (pTBI) affects civilian and military populations resulting in significant morbidity, mortality, and healthcare costs. No up-to-date and evidence-based guidelines exist to assist modern medical and surgical management of these complex injuries. A preliminary literature search revealed a need for updated guidelines, supported by the Brain Trauma Foundation. Methodologists experienced in TBI guidelines were recruited to support project development alongside two cochairs and a diverse steering committee. An expert multi-disciplinary workgroup was established and vetted to inform key clinical questions, to perform an evidence review and the development of recommendations relevant to pTBI. The methodological approach for the project was finalized. The development of up-to-date evidence- and consensus-based clinical care guidelines and algorithms for pTBI will provide critical guidance to care providers in the pre-hospital and emergent, medical, and surgical settings.

INTRODUCTION: Previous models of intracranial pressure (ICP) dynamics have not included flow of cerebral interstitial fluid (ISF) and changes in resistance to its flow when brain swelling occurs. METHODS: We developed a lumped parameter model which includes a representation of cerebral ISF flow within brain tissue and its interactions with CSF flow and CBF. The model is based on an electrical analog circuit with four intracranial compartments: the (1) subarachnoid space, (2) brain, (3) ventricles and (4) cerebral vasculature. We determined changes in pressure and volume within cerebral compartments at steady-state and simulated perturbations: Rapid injection into the intracranial space, hyper-and hypoventilation. We simulated changes in resistance to flow or absorption of CSF and cerebral ISF to model hydrocephalus and cerebral edema. RESULTS: The model accurately replicates features of intracranial physiology including the pressure–volume curve, increased ICP pulse pressure with rising ICP, hydrocephalus from increased resistance to CSF outflow, and changes associated with ventilation. Importantly, modeling edema with increased resistance to ISF flow mimics key features of brain swelling including elevated ICP, increased brain volume, effaced ventricles, and a contracted subarachnoid space. Similarly, decreased resistance to flow of fluid across the BBB leads to an exponential-like rise in ICP and ventricular collapse. CONCLUSIONS: The model accurately depicts the complex interactions that occur between pressure, volume, and resistances to flow in the different intracranial compartments under specific pathophysiological conditions. In modelling resistance to bulk flow of cerebral ISF, it may serve as a platform for improved modelling of cerebral edema and blood–brain barrier disruption that occur following brain injury.

Performing a cerebrospinal fluid (CSF) drainage challenge can be used to measure the pressure equalization (PE) ratio, which describes the extent to which CSF drainage can equalize pressure to the height of the external ventricular drain and may serve as a correlate of cerebral edema. We sought to assess whether treatment with mannitol improves PE ratio in patients with severe traumatic brain injury (TBI) with elevated intracranial pressure (ICP). We studied consecutive patients with TBI and brain edema on computed tomography scan and an external ventricular drain (EVD), admitted to the neurointensive care unit. PE ratio, defined as ICP prior to CSF drainage minus ICP after CSF drainage divided by ICP prior to CSF drainage minus EVD height, was measured as previously described. Patients were treated with mannitol for raised ICP based on clinical indication and PE ratio measured before and after mannitol administration. We studied 20 patients with severe TBI with raised ICP. Mean ICP prior to mannitol treatment was 29 ± 7 mm Hg. PE ratio rose substantially after mannitol treatment (0.62 ± 0.24 vs. 0.29 ± 0.20, p < 0.0001), indicating an improved ability to drain CSF and equalize ICP with the preset height of the EVD. The combination of mannitol and CSF drainage led to an improved reduction in ICP compared with that seen before mannitol therapy (11 ± 2 mm Hg vs. 6 ± 2 mm Hg, p < 0.01), and led to a decrease in ICP below the 20 mm Hg threshold in 77% of cases. Treatment with mannitol leads to a substantial improvement in PE ratio that reflects the ability to achieve a greater decrease in ICP when CSF drainage is performed after mannitol administration. This preliminary study raises the possibility that PE ratio may be useful to follow response to therapy in patients with cerebral edema and raised ICP. Further studies to determine whether PE ratio may serve as an easily obtained and clinically useful surrogate marker for the extent of brain edema are warranted.

OBJECTIVE:Previous studies have demonstrated the importance of intracranial elastance; however, methodological difficulties have limited widespread clinical use. Measuring elastance may offer potential benefit in helping to identify patients at risk for untoward intracranial pressure (ICP) elevation from small rises in intracranial volume. The authors sought to develop an easily used method that accounts for the changing ICP that occurs over a cardiac cycle and to assess this method in a large-animal model over a broad range of ICPs. METHODS:The authors used their previously described cardiac-gated intracranial balloon pump and swine model of cerebral edema. In the present experiment they measured elastance at 4 points along the cardiac cycle-early systole, peak systole, mid-diastole, and end diastole-by using rapid balloon inflation to 1 ml over an ICP range of 10-30 mm Hg. RESULTS:The authors studied 7 swine with increasing cerebral edema. Intracranial elastance rose progressively with increasing ICP. Peak-systolic and end-diastolic elastance demonstrated the most consistent rise in elastance as ICP increased. Cardiac-gated elastance measurements had markedly lower variance within swine compared with non-cardiac-gated measures. The slope of the ICP-elastance curve differed between swine. At ICP between 20 and 25 mm Hg, elastance varied between 8.7 and 15.8 mm Hg/ml, indicating that ICP alone cannot accurately predict intracranial elastance. CONCLUSIONS:Measuring intracranial elastance in a cardiac-gated manner is feasible and may offer an improved precision of measure. The authors' preliminary data suggest that because elastance values may vary at similar ICP levels, ICP alone may not necessarily best reflect the state of intracranial volume reserve capacity. Paired ICP-elastance measurements may offer benefit as an adjunct "early warning monitor" alerting to the risk of untoward ICP elevation in brain-injured patients that is induced by small increases in intracranial volume.

OBJECTIVEAugmenting brain perfusion or reducing intracranial pressure (ICP) dose is the end target of many therapies in the neuro-critical care unit. Many present therapies rely on aggressive systemic interventions that may lead to untoward effects. Previous studies have used a cardiac-gated intracranial balloon pump (ICBP) to model hydrocephalus or to flatten the ICP waveform. The authors sought to sought to optimize ICBP activation parameters to improve cerebral physiological parameters in a swine model of raised ICP.METHODSThe authors developed a cardiac-gated ICBP in which the volume, timing, and duty cycle (time relative to a single cardiac cycle) of balloon inflation could be altered. They studied the ICBP in a swine model of elevated ICP attained by continuous intracranial fluid infusion with continuous monitoring of systemic and cerebral physiological parameters, and defined two specific protocols of ICBP activation.RESULTSEleven swine were studied, 3 of which were studied to define the optimal timing, volume, and duty cycle of balloon inflation. Eight swine were studied with two defined protocols at baseline and with ICP gradually raised to a mean of 30.5 mm Hg. ICBP activation caused a consistent modification of the ICP waveform. Two ICBP activation protocols were used. Balloon activation protocol A led to a consistent elevation in cerebral blood flow (8%-25% above baseline, p < 0.00001). Protocol B resulted in a modest reduction of ICP over time (8%-11%, p < 0.0001) at all ICP levels. Neither protocol significantly affected systemic physiological parameters.CONCLUSIONSThe preliminary results indicate that optimized protocols of ICBP activation may have beneficial effects on cerebral physiological parameters, with minimal effect on systemic parameters. Further studies are warranted to explore whether ICBP protocols may be of clinical benefit in patients with brain injuries with increased ICP.