Estimating intracranial parameters using an inverse mathematical model with viscoelastic elements that closely predicts complex ICP morphologies.

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.

Limitation of cerebral blood flow by increased venous outflow resistance in elevated ICP.

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.

Mechanisms of reduced cerebral blood flow in cerebral edema and elevated intracranial pressure.

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.

Rationale and Methods for Updated Guidelines for the Management of Penetrating Traumatic Brain Injury.

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.

Intracranial Pulsating Balloon-Based Cardiac-Gated ICP Modulation Impact on Brain Oxygenation: A Proof-of-Concept Study in a Swine Model.

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.

A Case Report of Mycoplasma hominis Subdural Empyema Following Decompressive Craniotomy, and a Review of Central Nervous System Mycoplasma hominis Infections.

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.

Improved Pressure Equalization Ratio Following Mannitol Administration in Patients With Severe TBI: A Preliminary Study of a Potential Bedside Marker for Response to Therapy.

BACKGROUND: 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). METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

Interactions of brain, blood, and CSF: a novel mathematical model of cerebral edema.

BACKGROUND: 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. We sought to develop a mathematical model that incorporates resistance to the bulk flow of cerebral ISF to better simulate the physiological changes that occur in pathologies in which brain swelling predominates and to assess the model's ability to depict changes in cerebral physiology associated with cerebral edema. 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 cerebral blood flow (CBF). The model is based on an electrical analog circuit with four intracranial compartments: the (1) subarachnoid space, (2) brain, (3) ventricles, (4) cerebral vasculature and the extracranial spinal thecal sac. We determined changes in pressure and volume within cerebral compartments at steady-state and simulated physiological perturbations including rapid injection of fluid into the intracranial space, hyperventilation, and hypoventilation. We simulated changes in resistance to flow or absorption of CSF and cerebral ISF to model hydrocephalus, cerebral edema, and to simulate disruption of the blood-brain barrier (BBB). RESULTS: The model accurately replicates well-accepted features of intracranial physiology including the exponential-like pressure-volume curve with rapid fluid injection, increased ICP pulse pressure with rising ICP, hydrocephalus resulting from increased resistance to CSF outflow, and changes associated with hyperventilation and hypoventilation. Importantly, modeling cerebral edema with increased resistance to cerebral ISF flow mimics key features of brain swelling including elevated ICP, increased brain volume, markedly reduced ventricular volume, and a contracted subarachnoid space. Similarly, a 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.

Early identification of acute kidney injury in the ICU with real-time urine output monitoring: a clinical investigation.

BACKGROUND: KDIGO (Kidney Disease: Improving Global Outcomes) provides two sets of criteria to identify and classify acute kidney injury (AKI): serum creatinine (SCr) and urine output (UO). Inconsistencies in the application of KDIGO UO criteria, as well as collecting and classifying UO data, have prevented an accurate assessment of the role this easily available biomarker can play in the early identification of AKI. STUDY GOAL: To assess and compare the performance of the two KDIGO criteria (SCr and UO) for identification of AKI in the intensive care unit (ICU) by comparing the standard SCr criteria to consistent, real-time, consecutive, electronic urine output measurements. METHODS: Ninety five catheterized patients in the General ICU (GICU) of Hadassah Medical Center, Israel, were connected to the RenalSense™ Clarity RMS™ device to automatically monitor UO electronically (UOelec). UOelec and SCr were recorded for 24-48 h and up to 1 week, respectively, after ICU admission. RESULTS: Real-time consecutive UO measurements identified significantly more AKI patients than SCr in the patient population, 57.9% (N = 55) versus 26.4% (N = 25), respectively (P < 0.0001). In 20 patients that had AKI according to both criteria, time to AKI identification was significantly earlier using the UOelec criteria as compared to the SCr criteria (P < 0.0001). Among this population, the median (interquartile range (IQR)) identification time of AKI UOelec was 12.75 (8.75, 26.25) hours from ICU admission versus 39.06 (25.8, 108.64) hours for AKI SCr. CONCLUSION: Application of KDIGO criteria for AKI using continuous electronic monitoring of UO identifies more AKI patients, and identifies them earlier, than using the SCr criteria alone. This can enable the clinician to set protocol goals for earlier intervention for the prevention or treatment of AKI.

Cardiac-gated intracranial elastance in a swine model of raised intracranial pressure: a novel method to assess intracranial pressure-volume dynamics.

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.

Cerebral blood flow augmentation using a cardiac-gated intracranial pulsating balloon pump in a swine model of elevated ICP.

OBJECTIVE: Augmenting 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. METHODS: The 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. RESULTS: Eleven 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. CONCLUSIONS: The 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.

Characterizing the Response to Cerebrospinal Fluid Drainage in Patients with an External Ventricular Drain: The Pressure Equalization Ratio.

BACKGROUND: An external ventricular drain (EVD) is the gold standard for measurement of intracranial pressure (ICP) and allows for drainage of cerebrospinal fluid (CSF). Different causes of elevated ICP, such as CSF outflow obstruction or cerebral swelling, respond differently to CSF drainage. This is a widely recognized but seldom quantified distinction. We sought to define an index to characterize the response to CSF drainage in neurocritical care patients. METHODS: We studied consecutive patients admitted to the neurointensive care unit who had an EVD. The EVD was closed for 30 min prior to assessment. We documented pre-drainage ICP, opened EVD to drainage allowing CSF to drain until it ceased, and recorded post-drainage ICP at EVD closure. We calculated the pressure equalization (PE) ratio as the difference between pre-drainage ICP and post-drainage ICP divided by the difference between pre-drainage ICP and EVD height. RESULTS: We studied 60 patients (36 traumatic brain injury [TBI], 24 non-TBI). As expected, TBI patients had more signs of cerebral swelling on CT and smaller ventricles. Although TBI patients had significantly higher pre-drainage ICP (26 ± 10 mm Hg) than non-TBI patients (19 ± 5 mm Hg, p < 0.001) they drained less CSF (7 cc vs. 4 cc, p < 0.01). PE ratio was substantially higher in non-TBI than in TBI patients (0.86 ± 0.36 vs. 0.43 ± 0.31, p < 0.0001), indicating that non-TBI patients were better able to equalize pressure with EVD height than TBI patients. CONCLUSIONS: PE ratio reflects the ability to equalize pressure with the preset height of the EVD and differs substantially between TBI and non-TBI patients. A high PE ratio likely indicates CSF outflow obstruction effectively treated by CSF diversion, while a lower PE ratio occurs when cerebral swelling predominates. Further studies could assess whether the PE ratio would be useful as a surrogate marker for cerebral edema or the state of intracranial compliance.

A swine model of intracellular cerebral edema - Cerebral physiology and intracranial compliance.

Cerebral edema leading to elevated intracranial pressure (ICP) is a fundamental concern after severe traumatic brain injury (TBI), stroke, and severe acute hyponatremia. We describe a swine model of water intoxication and its cerebral histological and physiological sequela. We studied female swine weighing 35-45 kg. Four serum sodium intervals were designated: baseline, mild, moderate, and severe hyponatremia attained by infusing hypotonic saline. Intracranial fluid injections were performed to assess intracranial compliance. At baseline and following water intoxication wedge biopsy was obtained for pathological examination and electron microscopy. We studied 8 swine and found an increase in ICP that was strongly related to the decrease in serum sodium level. Mean ICP rose from a baseline of 6 ±â€¯2 to 28 ±â€¯6 mm Hg during severe hyponatremia, while cerebral perfusion pressure (CPP) decreased from 72 ±â€¯10 to 46 ±â€¯11 mm Hg. Brain tissue oxygen tension (PbtO2) decreased from 18.4 ±â€¯8.9 to 5.3 ±â€¯3.0 mm Hg. Electron microscopy demonstrated intracellular edema and astrocytic foot process swelling following water intoxication. With severe hyponatremia, 2 cc intracranial fluid injection resulted in progressively greater ICP dose, indicating a worsening intracranial compliance. Our model leads to graded and sustained elevation of ICP, lower CPP, and decreased PbtO2, all of which cross clinically relevant thresholds. Intracranial compliance worsens with increased cerebral swelling. This model may serve as a platform to study which therapeutic interventions best improve the cerebral physiological profile in the face of severe brain edema.

Posttraumatic epilepsy: long-term follow-up of children with mild traumatic brain injury.

OBJECTIVE Posttraumatic epilepsy (PTE) is a known complication of traumatic brain injury (TBI). The true incidence of PTE in children is still uncertain, because most research has been based primarily on adults. This study aimed to determine the true incidence of PTE in a pediatric population with mild TBI (MTBI) and to identify risk factors for the development of epileptic events. METHODS Data were collected from electronic medical records of children 0-17 years of age, who were admitted to a single medical center between 2007 and 2009 with a diagnosis of MTBI. This prospective research consisted of a telephone survey between 2015 and 2016 of children or their caregivers, querying for information about epileptic episodes and current seizure and neurological status. The primary outcome measure was the incidence of epilepsy following TBI, which was defined as ≥ 2 unprovoked seizure episodes. Posttraumatic seizure (PTS) was defined as a single, nonrecurrent convulsive episode that occurred > 24 hours following injury. Seizures within 24 hours of the injury were defined as immediate PTS. RESULTS Of 290 children eligible for this study, 191 of them or their caregivers were reached by telephone survey and were included in the analysis. Most injuries (80.6%) were due to falls. Six children had immediate PTS. All children underwent CT imaging; of them, 72.8% demonstrated fractures and 10.5% did not demonstrate acute findings. The mean follow-up was 7.4 years. Seven children (3.7%) experienced PTS; of them, 6 (85.7%) developed epilepsy and 3 (42.9%) developed intractable epilepsy. The overall incidence of epilepsy and intractable epilepsy in this cohort was 3.1% and 1.6%, respectively. None of the children who had immediate PTS developed epilepsy. Children who developed epilepsy spent an average of 2 extra days in the hospital at the time of the injury. The mean time between trauma and onset of seizures was 3.1 years. Immediate PTS was not correlated with PTE. CONCLUSIONS In this analysis of data from medical records and long-term follow-up, MTBI was found to confer increased risk for the development of PTE and intractable PTE, of 4.5 and 8 times higher, respectively. As has been established in adults, these findings confirm that MTBI increases the risk for PTE in the pediatric population.

Clinical Significance of Long-Term Follow-Up of Children with Posttraumatic Skull Base Fracture.

OBJECTIVE: To assess the incidence of cerebrospinal fluid (CSF) leak and meningitis, and the need for prophylactic antibiotics, antipneumococcal vaccination, and surgical interventions, in children with a skull base fracture. METHODS: We reviewed the records of children with a skull base fracture who were admitted to our tertiary care center between 2009 and 2014. RESULTS: A total of 196 children (153 males), age 1 month to 18 years (mean age, 6 ± 4 years), were hospitalized with skull base fracture. Causes of injury were falls (n = 143), motor vehicle accidents (n = 34), and other (n = 19). Fracture locations were the middle skull base in 112 patients, frontal base in 62, and occipital base in 13. Fifty-four children (28%) had a CSF leak. In 34 of these children (63%), spontaneous resolution occurred within 3 days. Three children underwent surgery on admission owing to a CSF leak from an open wound, 3 underwent CSF diversion by spinal drainage, and 4 (2%) required surgery to repair a dural tear after failure of continuous spinal drainage and acetazolamide treatment. Twenty-eight children (14%) received prophylactic antibiotic therapy, usually due to other injuries, and 11 received pneumococcal vaccination. Two children developed meningitis, and 3 children died. Long-term follow up in 124 children revealed 12 children with delayed hearing loss and 3 with delayed facial paralysis. CONCLUSIONS: This is the largest pediatric series of skull base fractures reporting rates of morbidity and long-term outcomes published to date. The rate of meningitis following skull base fracture in children is low, supporting a policy of not administering prophylactic antibiotics or pneumococcal vaccine. Long-term follow up is important to identify delayed complications.

Vertebral artery pseudoaneurysms secondary to blunt trauma: Endovascular management by means of neurostents and flow diverters.

Extracranial vertebral pseudoaneurysms that develop following blunt trauma to the cervical area may have a benign course; however, embolic or ischemic stroke and progressive pseudoaneurysm enlargement may occur. We review the presentation and endovascular management of pseudoaneurysms of the cervical vertebral artery (VA) due to blunt trauma in nine patients (eight male, mean age 27years). Pseudoaneurysms occurred in dominant vessels in seven patients and coexisted with segmental narrowing in six. We favored endovascular intervention during the acute phase only in cases with significant narrowing of a dominant VA, especially when anticoagulation was contraindicated. Four patients were treated during the acute stage (contraindication to anticoagulation, mass effect, severely injured dominant VA/impending stroke); five during the chronic phase (pseudoaneurysm growth, ischemic stroke on aspirin prophylaxis, patient preference). Reconstructive techniques were favored over deliberate endovascular occlusion when dominant vessels were involved. Arterial reconstruction was performed in eight of nine patients using a flow-diverter implant (5 patients), stent-assisted coiling (1), overlapping stent implant (1), or implantation of a balloon-expandable stent (1). Deliberate VA occlusion with coils was performed in one of nine patients due to suboptimal expansion of the stented artery after flow-diverter implant. No neurological complications occurred during follow-up. All cases treated by reconstructive techniques showed complete, persistent pseudoaneurysm occlusion and full arterial patency. Endovascular therapy of traumatic VA pseudoaneurysms using neurostents and flow-diverters resulted in occlusion of the pseudoaneurysms, preservation of the parent vessel, and no periprocedural or delayed clinical complications, supporting the feasibility and safety of the approach.

Evaluation of the necessity of hospitalization in children with an isolated linear skull fracture (ISF).

OBJECTIVE: The prevalence of skull fractures after mild head trauma is 2 % in children of all ages and 11 % in children younger than 2 years. The current standard management for a child diagnosed with an isolated skull fracture (ISF), in our institute, is hospitalization for a 24-h observation period. Based on data from the literature, less than 1 % of all minor head injuries require neurosurgical intervention. The main objective of this study was to evaluate the risk of neurological deterioration of ISF cases, in order to assess the need for hospitalization. METHODS: We reviewed the medical charts of 222 children who were hospitalized from 2006 to 2012 with ISF and Glascow Coma Scale-15 at the time of arrival. We collected data regarding demographic characteristics, mechanism of injury, fracture location, clinical symptoms and signs, need for hospitalization, and need for repeated imaging. Data was collected at three time points: at presentation to the emergency room, during hospitalization, and 1 month after admission, when the patients' parents were asked about the course of the month following discharge. RESULTS: None of the 222 children included in the study needed neurosurgical intervention. All were asymptomatic 1 month after the injury. Two children underwent repeated head CT due to persistence or worsening of symptoms; these CT scans did not reveal any new findings and did not lead to any intervention whatsoever. CONCLUSION: Children arriving at the emergency room with a minor head injury and isolated skull fracture on imaging studies may be considered for discharge after a short period of observation. Discharge should be considered in these cases provided the child has a reliable social environment and responsible caregivers who are able to return to the hospital if necessary. Hospital admission should be reserved for children with neurologic deficits, persistent symptoms, suspected child abuse, or when the parent is unreliable or is unable to return to the hospital if necessary. Reducing unnecessary hospitalizations can prevent emotional stress, in addition to saving costs for the child's family and the health care system.

Brain tissue oxygen tension and its response to physiological manipulations: influence of distance from injury site in a swine model of traumatic brain injury.

OBJECTIVE The optimal site for placement of tissue oxygen probes following traumatic brain injury (TBI) remains unresolved. The authors used a previously described swine model of focal TBI and studied brain tissue oxygen tension (PbtO2) at the sites of contusion, proximal and distal to contusion, and in the contralateral hemisphere to determine the effect of probe location on PbtO2 and to assess the effects of physiological interventions on PbtO2 at these different sites. METHODS A controlled cortical impact device was used to generate a focal lesion in the right frontal lobe in 12 anesthetized swine. PbtO2 was measured using Licox brain tissue oxygen probes placed at the site of contusion, in pericontusional tissue (proximal probe), in the right parietal region (distal probe), and in the contralateral hemisphere. PbtO2 was measured during normoxia, hyperoxia, hypoventilation, and hyperventilation. RESULTS Physiological interventions led to expected changes, including a large increase in partial pressure of oxygen in arterial blood with hyperoxia, increased intracranial pressure (ICP) with hypoventilation, and decreased ICP with hyperventilation. Importantly, PbtO2 decreased substantially with proximity to the focal injury (contusion and proximal probes), and this difference was maintained at different levels of fraction of inspired oxygen and partial pressure of carbon dioxide in arterial blood. In the distal and contralateral probes, hypoventilation and hyperventilation were associated with expected increased and decreased PbtO2 values, respectively. However, in the contusion and proximal probes, these effects were diminished, consistent with loss of cerebrovascular CO2 reactivity at and near the injury site. Similarly, hyperoxia led to the expected rise in PbtO2 only in the distal and contralateral probes, with little or no effect in the proximal and contusion probes, respectively. CONCLUSIONS PbtO2 measurements are strongly influenced by the distance from the site of focal injury. Physiological alterations, including hyperoxia, hyperventilation, and hypoventilation substantially affect PbtO2 values distal to the site of injury but have little effect in and around the site of contusion. Clinical interpretations of brain tissue oxygen measurements should take into account the spatial relation of probe position to the site of injury. The decision of where to place a brain tissue oxygen probe in TBI patients should also take these factors into consideration.

Supraciliary keyhole craniotomy for anterior frontal lesions in children.

Treatment for anterior frontal space occupying lesions such as epidural hematoma, vascular malformations or brain tumors, have typically involved invasive craniotomies. This method often requires large incisions with wide exposure and may be associated with high morbidity rates. The basis for the "keyhole" method is that a minimally invasive craniotomy is often sufficient for exposing large areas deep in tissue, and may limit exposure and decrease surgically related morbidity while enabling adequate removal and decompression. The supraciliary method includes a cut above the eyebrow and a small craniotomy to uncover the base of the frontal lobe and the orbital roof. We demonstrate our experience with this method. We identified children who were operated via the supraciliary approach between January 2009 and December 2013, and gathered their pre- and post-operative clinical and radiological statistics. Fourteen patients were identified. Pathologies included tumors, abscesses and epidural hematomas. Nine were operated due to epidural hematoma, two due to tumors, two due to brain abscesses, and one for anterior encephalocele. No significant peri-operative or post-operative complications were observed. Long-term follow-up shows that the surgical scars were nearly invisible. The supraciliary approach is a safe, effective and elegant technique for treating lesions in the anterior skull base. The method should be weighed alongside traditional methods on a case-by-case basis.

Intracranial pressure monitoring following decompressive hemicraniectomy for malignant cerebral infarction.

Randomized controlled trials have demonstrated the efficacy of decompressive craniectomy in substantially decreasing mortality and improving functional outcome in middle cerebral artery infarction. The role of intracranial pressure (ICP) monitoring following decompressive craniectomy for stroke has not been well studied. We present a retrospective review of our experience with postoperative ICP monitoring in 12 stroke patients who underwent decompressive craniectomy. All elevations of ICP above a 20 mm Hg threshold were noted. ICP was recorded for 1417 hours during which 68 ICP elevations were seen. Nine out of 12 patients had events of raised ICP, including eight with more than three elevations. A total of 81 interventions were employed to treat elevated ICP; 71 were effective in reducing ICP below the 20 mm Hg threshold. The most frequent intervention was cerebrospinal fluid drainage via an external ventricular drain, which was effective in 85.4% of cases. Eleven out of 12 patients survived (92%) and attained a median modified Rankin Scale score of 4 (interquartile range 4-5) at a mean 15 month follow-up. In our experience, elevated ICP may commonly occur following decompressive craniectomy for stroke. Monitoring ICP influenced postoperative management and standard measures for reducing ICP were usually effective in the current series.