Ratio of Optic Nerve Sheath Diameter to Eyeball Transverse Diameter by Ultrasound Can Predict Intracranial Hypertension in Traumatic Brain Injury Patients: A Prospective Study.

BACKGROUND: Measuring optic nerve sheath diameter (ONSD), an indicator to predict intracranial hypertension, is noninvasive and convenient, but the reliability of ONSD needs to be improved. Instead of using ONSD alone, this study aimed to evaluate the reliability of the ratio of ONSD to eyeball transverse diameter (ONSD/ETD) in predicting intracranial hypertension in traumatic brain injury (TBI) patients. METHODS: We performed a prospective study on patients admitted to the Surgery Intensive Care Unit. The included 52 adults underwent craniotomy for TBI between March 2017 and September 2018. The ONSD and ETD of each eyeball were measured by ultrasound and computed tomography (CT) scan within 24 h after a fiber optic probe was placed into lateral ventricle. Intracranial pressure (ICP) > 20 mmHg was regarded as intracranial hypertension. The correlations between invasive ICP and ultrasound-ONSD/ETD ratio, ultrasound-ONSD, CT-ONSD/ETD ratio, and CT-ONSD were each analyzed separately. RESULTS: Ultrasound measurement was successfully performed in 94% (n = 49) of cases, and ultrasound and CT measurement were performed in 48% (n = 25) of cases. The correlation efficiencies between ultrasound-ONSD/ETD ratio, ultrasound-ONSD, CT-ONSD/ETD ratio, and ICP were 0.613, 0.498, and 0.688, respectively (P < 0.05). The area under the curve (AUC) values of the receiver operating characteristic (ROC) curve for the ultrasound-ONSD/ETD ratio and CT-ONSD/ETD ratio were 0.920 (95% CI 0.877-0.964) and 0.896 (95% CI 0.856-0.931), respectively. The corresponding threshold values were 0.25 (sensitivity of 90%, specificity of 82.3%) and 0.25 (sensitivity of 85.7%, specificity of 83.3%), respectively. CONCLUSION: The ratio of ONSD to ETD tested by ultrasound may be a reliable indicator for predicting intracranial hypertension in TBI patients.

Acute post-traumatic hydrocephalus in children due to aqueductal obstruction by blood clot: a series of 6 patients.

INTRODUCTION: Post-traumatic hydrocephalus following head injury is a well-known entity. Most cases occur in patients with severe head injuries, often following decompressive craniectomy. On the contrary, acute post-traumatic hydrocephalus, caused by aqueductal obstruction by a blood clot, following mild head injury is uncommon. CLINICAL MATERIAL: Six patients aged between 6 and 15 months presented hydrocephalus secondary to a blood clot in the aqueduct. Because of intracranial hypertension at presentation, 4 patients were urgently treated with external ventricular drains (EVDs). Post-operative course was uneventful. In 2 cases, EVDs were removed without further treatments. In 2 cases, hydrocephalus recurred. These patients were successfully treated with endoscopic third ventriculostomy. The remaining two patients developed symptoms a few days after the trauma. One, that presented hydrocephalus at imaging, was managed with a ventriculo-peritoneal shunt; the other, that presented subdural hygroma, was managed with subduro-peritoneal shunt that was removed later. All patients had complete recovery. DISCUSSION AND CONCLUSION: Hydrocephalus secondary to clot in the aqueduct may rarely be the result of mild head injury in young children. Usually, prompt surgical management warrants a very good outcome. Most children may be treated without a permanent shunt, by using external drains and endoscopic third ventriculostomy.

Traumatic Microbleeds in the Hippocampus and Corpus Callosum Predict Duration of Posttraumatic Amnesia.

OBJECTIVE: Radiologic predictors of posttraumatic amnesia (PTA) duration are lacking. We hypothesized that the number and distribution of traumatic microbleeds (TMBs) detected by gradient recalled echo (GRE) magnetic resonance imaging (MRI) predicts PTA duration. SETTING: Academic, tertiary medical center. PARTICIPANTS: Adults with traumatic brain injury (TBI). DESIGN: We identified 65 TBI patients with acute GRE MRI. PTA duration was determined with the Galveston Orientation and Amnesia Test, Orientation Log, or chart review. TMBs were identified within memory regions (hippocampus, corpus callosum, fornix, thalamus, and temporal lobe) and control regions (internal capsule and global). Regression tree analysis was performed to identify radiologic predictors of PTA duration, controlling for clinical PTA predictors. MAIN MEASURES: TMB distribution, PTA duration. RESULTS: Sixteen patients (25%) had complicated mild, 4 (6%) had moderate, and 45 (69%) had severe TBI. Median PTA duration was 43 days (range, 0-240 days). In univariate analysis, PTA duration correlated with TMBs in the corpus callosum (R = 0.29, P = .02) and admission Glasgow Coma Scale (GCS) score (R = -0.34, P = .01). In multivariate regression analysis, admission GCS score was the only significant contributor to PTA duration. However, in regression tree analysis, hippocampal TMBs, callosal TMBs, age, and admission GCS score explained 26% of PTA duration variance and distinguished a subgroup with prolonged PTA. CONCLUSIONS: Hippocampal and callosal TMBs are potential radiologic predictors of PTA duration.

Vessel Wall Magnetic Resonance Imaging in a Case of Post-traumatic Multifocal Striatocapsular Hemorrhagic Infarction.

Post-traumatic striatocapsular infarction is extremely rare and has been described only within the vascular territory of the perforating arteries originating from the middle cerebral artery (MCA). We recently encountered a patient presenting with unilateral multifocal striatocapsular hemorrhagic infarctions following mild head injury. This 25-year-old female was admitted to our trauma center after a motorcycle accident. Initial brain computed tomography and magnetic resonance (MR) imaging showed multifocal acute hemorrhagic infarctions with a clustering in the right caudate head, anterior limb of internal capsule, and globus pallidus. MR angiography and digital subtraction angiography showed suspicious luminal irregularities of the lenticulostriate arteries of the right MCA. Vessel wall MR images (VWI) did neither indicate intramural hematoma nor wall enhancement in the right MCA, suggesting dissection. However, VWI showed the passages of each lenticulostriate artery supplying each infarction site. Therefore, based on both conventional images and VWI, we postulate that this patient's post-traumatic multifocal striatocapsular hemorrhagic infarctions were caused by damage to multiple lenticulostriate arteries.

Effects of Deferoxamine Mesylate on Hematoma and Perihematoma Edema after Traumatic Intracerebral Hemorrhage.

Deferoxamine mesylate can cross the blood-brain barrier and reduce iron accumulation in nervous tissue; moreover, it has a variety of neuroprotective functions in addition to complexing with iron ions. Such iron chelators are expected to become a new treatment option for intracerebral hemorrhage. This study evaluated the effects of deferoxamine mesylate on hematoma and edema absorption after traumatic intracerebral hemorrhage (TICH), and it provides clinical evidence for TICH treatment with deferoxamine mesylate. Patients with isolated TICH, confirmed by head computed tomography, were enrolled prospectively from January 2013 to December 2016. Patients were divided non-randomly into an experimental or control group as decided by the attending neurosurgeon. Patients in the experimental group received intravenous deferoxamine mesylate (20 mg/kg daily) from the day of admission for 5 consecutive days. We evaluated the impact of deferoxamine mesylate on the change in edema volume and the absorption of hematoma volume using a propensity score-matched analysis. In total, 190 patients were included. After matching, 94 patients were included in the final analysis (47 per group); no variable differed significantly between the two groups. The hematoma volume on the 7th day in the control group was higher than that at the same time-point in the experimental group (9.4 ± 7.2 vs. 5.2 ± 4.8 mL; p = 0.001). There was no difference in hematoma volume on Day 1 (12.6 ± 7.8 vs. 12.8 ± 6.4 mL; p = 0.896), Day 3 (12.4 ± 7.4 vs. 11.4 ± 4.9 mL; p = 0.442), and Day 14 (3.2 ± 3.0 vs. 2.5 ± 2.6 mL; p = 0.215) between the groups. The absorption of hematoma volume between the 1st and 3rd days and the 1st and 7th days in the experimental group was higher than that during the same periods in the control group. The edema volumes on the 3rd, 7th, and 14th days in the control group were higher than those at the same time-points in the experimental group. There was no difference in edema volume on the 1st day. The changes in edema volume between the 1st and 3rd days, the 1st and 7th days, and the 1st and 14th days in the control group were higher than those during the same periods in the experimental group. Deferoxamine mesylate may accelerate hematoma absorption and inhibit edema after TICH; however, further investigation is required to reach definitive conclusions.

Spreading depolarizations in patients with spontaneous intracerebral hemorrhage: Association with perihematomal edema progression.

Pathophysiologic mechanisms of secondary brain injury after intracerebral hemorrhage and in particular mechanisms of perihematomal-edema progression remain incompletely understood. Recently, the role of spreading depolarizations in secondary brain injury was established in ischemic stroke, subarachnoid hemorrhage and traumatic brain injury patients. Its role in intracerebral hemorrhage patients and in particular the association with perihematomal-edema is not known. A total of 27 comatose intracerebral hemorrhage patients in whom hematoma evacuation and subdural electrocorticography was performed were studied prospectively. Hematoma evacuation and subdural strip electrode placement was performed within the first 24 h in 18 patients (67%). Electrocorticography recordings started 3 h after surgery (IQR, 3-5 h) and lasted 157 h (median) per patient and 4876 h in all 27 patients. In 18 patients (67%), a total of 650 spreading depolarizations were observed. Spreading depolarizations were more common in the initial days with a peak incidence on day 2. Median electrocorticography depression time was longer than previously reported (14.7 min, IQR, 9-22 min). Postoperative perihematomal-edema progression (85% of patients) was significantly associated with occurrence of isolated and clustered spreading depolarizations. Monitoring of spreading depolarizations may help to better understand pathophysiologic mechanisms of secondary insults after intracerebral hemorrhage. Whether they may serve as target in the treatment of intracerebral hemorrhage deserves further research.

Progressive hemorrhagic injury in patients with traumatic intracerebral hemorrhage: characteristics, risk factors and impact on management.

BACKGROUND: Progressive hemorrhagic injury (PHI) is a common occurrence in clinical practice; however, how PHI affects clinical management remains unclear. We attempt to evaluate the characteristics and risk factors of PHI and also investigate how PHI influences clinical management in traumatic intracerebral hemorrhage (TICH) patients. METHODS: This retrospective study included a cohort of 181 patients with TICH who initially underwent conservative treatment and they were dichotomized into a PHI group and a non-PHI group. Clinical data were reviewed for comparison. Multivariate logistic regression analysis was applied to identify predictors of PHI and delayed operation. RESULTS: Overall, 68 patients (37.6%) experienced PHI and 27 (14.9%) patients required delayed surgery. In the PHI group, 17 patients needed late operation; in the non-PHI group, 10 patients received decompressive craniectomy. Compared to patients with non-PHI, the PHI group was more likely to require late operation (P = 0.005, 25.0 vs 8.8%), which took place within 48 h (P = 0.01, 70.6 vs 30%). Multivariate logistic regression identified past medical history of hypertension (odds ratio [OR] = 4.56; 95% confidence interval [CI] = 2.04-10.45), elevated international normalized ratio (INR) (OR = 20.93; 95% CI 7.72-71.73) and linear bone fracture (OR = 2.11; 95% CI = 1.15-3.91) as independent risk factors for PHI. Hematoma volume of initial CT scan >5 mL (OR = 3.80; 95% CI = 1.79-8.44), linear bone fracture (OR = 3.21; 95% CI = 1.47-7.53) and PHI (OR = 3.49; 95% CI = 1.63-7.77) were found to be independently associated with delayed operation. CONCLUSIONS: Past medical history of hypertension, elevated INR and linear bone fracture were predictors for PHI. Additionally, the latter was strongly predictive of delayed operation in the studied cohort.

Attitudes in 2013 to Monitoring Intracranial Pressure for Traumatic Intracerebral Haemorrhage.

INTRODUCTION: Recent research has been equivocal regarding the usefulness of intracranial pressure (ICP) monitoring for traumatic intracerebral haemorrhage (ICH). We aimed to investigate attitudes of clinicians from as wide an international audience as possible. MATERIALS AND METHODS: A SurveyMonkey® questionnaire was distributed to individuals, including members of the Society of British Neurological Surgeons, the European Brain Injury Consortium, the Euroacademia Multidisciplinaria Neurotraumatologica and the neurotrauma committee of the World Federation of Neurosurgical Societies. RESULTS: Ninety-eight participants from at least 25 different countries completed the survey (86 surgeons). ICP was routinely monitored by 76 % and would be monitored by 5 % more if they had equipment. ICP monitoring was valued (0 = not at all important, 10 = critically important) as 10 by 21 % (median = 8; Q1 = 7, Q3 = 9). Responders were aware of 16 trials that investigated the value of ICP monitoring in neurotrauma, including BEST TRIP (n = 35), Rescue ICP (n = 13) and DECRA (n = 8). Other results are discussed. DISCUSSION: Despite equivocation in the literature, we found that ICP monitoring continues to be routinely performed and is highly valued. Interestingly, only 36 % of responders were aware of the BEST TRIP trial, which found no difference in outcome between patients with a head injury managed with or without ICP monitoring.

Delayed Deterioration in Isolated Traumatic Subarachnoid Hemorrhage.

BACKGROUND: Isolated traumatic subarachnoid hemorrhage (SAH) in association with mild traumatic brain injury is considered to be a less severe finding that is not likely to require surgical intervention. No previous reports have described cases warranting craniotomy for isolated traumatic SAH by itself. CASE DESCRIPTION: We report 2 cases of minor head trauma with isolated traumatic SAH that showed delayed clinical deterioration requiring immediate surgical intervention. Initial computed tomography showed isolated traumatic SAH in the basal cistern and Sylvian fissure in both cases. Angiography showed no aneurysmal source. Within 24 hours of each accident, both disturbance of consciousness and hemiparesis deteriorated. Follow-up computed tomography showed formation of intracerebral hematoma adjacent to the Sylvian fissure. Intraoperative findings showed abruption injury of a perforating branch arising from the middle cerebral artery (MCA) as the cause of bleeding. Impact at the time of injury could have caused traction on the MCA in the Sylvian fissure, resulting in abruption of the perforator. CONCLUSIONS: Isolated traumatic SAH seen in the basal cistern and Sylvian fissure carries a risk of late deterioration. A possible cause of hematoma expansion is abruption of a perforating branch arising from the MCA at the time of head injury. When hematoma expansion is identified, surgical evacuation of the hematoma is indicated. Surgical evacuation should be safely performed with the knowledge of the point of bleeding in such patients.

Decreasing the Cerebral Edema Associated with Traumatic Intracerebral Hemorrhages: Use of a Minimally Invasive Technique.

Traumatic brain injury (TBI) is a major public health problem worldwide that affects all age groups. In the United States alone, there are approximately 50,000 deaths from severe traumatic brain injuries each year. In most studies, about 40 % of severe TBI have associated traumatic intracerebral hemorrhages (tICHs). The surgical treatment of tICH is debated largely because of its invasive nature, particularly in reaching deep tICHs. tICHs have a clear contribution to mass effect and exacerbate cerebral edema and ICP because of the break-down products of hemorrhage. We introduce a modification of the Mi SPACE technique (Minimally Invasive Subcortical Parafascicular Transsulcal Access for Clot Evacuation) that is applicable to tICH. In brief, this technique utilizes a trans-sulcal, stereotactic-guided technique in which a specially designed cannula is used to introduce a 13.5-mm-diameter tube into the epicenter of the tICH. We identified eight tICHs that were treated entirely or in part with the modified Mi SPACE technique during the time period from August 15, 2014 to December 15, 2014. This modified technique was readily deployed safely and efficaciously with significant removal of the tICH as demonstrated by postoperative CT scans. The removal of tICH using this minimally invasive technique may help with the control of ICP and cerebral edema.

[SEPTIC SHOCK IN PATIENT WITH SEVERE HEAD TRAUMA].

The clinical observation illustrates the role of screening of inflammatory markers and advanced hemodynamic monitoring in optimization of the treatment of the patient with severe traumatic brain injury (sTBI). The level of consciousness by the Glasgow Coma Scale at admission was 5 points. From the first day of stay the patient suffered hyperthermia to 39,0° C° The diagnosis of the aspiration pneumonia was determined by radiological signs, bronchoscopy and inflammatory blood markers, C-reactive protein, leukocytosis. From the second day the constant infusion of norepinephrine was necessary to maintain mean ABP above 80 mmHg. On the 10th day the patient's condition deteriorated sharply. Developed hyperthermia to 40, 2° and cardiovascular collapse (in spite of the high level of norepinephrine support a sharp decline in ABP up to 49/20 mmHg). Invasive advanced hemodynamic PiCCO monitoring (transpulmonary thermodilution) was started Septic shock was suspected. Standard laboratory tests did not meet the criteria for septic shock. Witnessed a slight increase in CRP and procalcitonin (PCT) was within normal limits. Diagnostic search was supplemented by a study of interleukins (IL-6 and IL-2R) in the blood plasma. The significant increase in their values, was regarded as the initial manifestations of the systemic inflammatory response. Sepsis was confirmed. The extended antibiotic therapy started Continuous Veno-Venous hemofiltration was used as part of treatment of the inflammatory-toxic condition. In two days of the therapy the patient's condition has stabilized, the patient recovered consciousness in the form of opening the eyes, simple instructions. At discharge, the patient's condition according to the Glasgow outcome scale was estimated at 4 points.

Memory impairment caused by cerebral hematoma in the left medial temporal lobe due to ruptured posterior cerebral artery aneurysm.

BACKGROUND: Cognitive disorders, such as memory disturbances, are often observed following a subarachnoid hemorrhage. We present a very rare case where rupture of a posterior cerebral artery aneurysm caused restricted damage to the hippocampus unilaterally, and caused memory disturbances. CASE PRESENTATION: A 56-year-old, right-handed man, with a formal education history of 16 years and company employees was admitted to our hospital because of a consciousness disturbance. He was diagnosed as having a subarachnoid hemorrhage due to a left posterior cerebral artery dissecting aneurysm, and coil embolization was performed. Subsequently, he had neither motor paresis nor sensory disturbances, but he showed disorientation, and both retrograde and anterograde amnesia. Although immediate recall and remote memory were almost intact, his recent memory was moderately impaired. Both verbal and non-verbal memories were impaired. Brain computed tomography (CT) and magnetic resonance imaging (MRI) revealed a cerebral hematoma in the left temporal lobe involving the hippocampus and parahippocampal gyrus, and single-photon emission computed tomography (SPECT) demonstrated low perfusion areas in the left medial temporal lobe. CONCLUSIONS: We suggest that the memory impairment was caused by local tissue destruction of Papez's circuit in the dominant hemisphere due to the cerebral hematoma.

Attitudes to intracranial pressure monitoring of traumatic intracerebral haemorrhage.

INTRODUCTION: Recent research has been equivocal regarding the usefulness of intracranial pressure (ICP) monitoring for traumatic intracerebral haemorrhage (ICH). We aimed to investigate attitudes of clinicians from as wide an international audience as possible. MATERIALS AND METHODS: A SurveyMonkey(®) questionnaire was distributed to individuals, including members of the Society of British Neurological Surgeons, the European Brain Injury Consortium, the neurotrauma committee of the Euroacademia Multidisciplinaria Neurotraumatologica and the World Federation of Neurosurgical Societies. RESULTS: N = 98 completed the survey (surgeons n = 86) from at least 25 different countries. ICP was routinely monitored by 76% and would be monitored by 5% more if they had equipment. ICP monitoring was valued (0 = not at all important, 10 = critically important) as 10 by 21% (median = 8, Q1 = 7, Q3 = 9). Triggers to begin ICP monitoring included midline shift (n = 48), contusion (n = 47), ICH (n = 46), subdural haemorrhage (n = 42), Glasgow coma scale reduction of median 2 for eye, verbal or motor, and one reactive pupil (30%). Responders stated that intervention would begin for adults with an ICP median of 25 mmHg and for children 20 mmHg. Most favourable treatments of raised ICP included Mannitol and ventriculostomy, which were ranked as most favourable (out of 10) by n = 31 each. Responders claimed to be aware of 16 different trials that investigated the value of ICP monitoring in neurotrauma, including BEST TRIP (n = 35), Rescue ICP (n = 13) and DECRA (n = 8). CONCLUSION: ICP monitoring continues to be a highly valued and clinically desirable technique for managing traumatic ICH patients.

Effect of erythrocytes on brain water content and haem oxygenase-1 expression in rats with traumatic intracerebral haemorrhage.

BACKGROUND: Studies have demonstrated that brain oedema formation following spontaneous intracerebral haemorrhage is associated with substances derived from blood clots or blood components. However, these studies did not completely reveal the role of blood components in brain oedema formation following traumatic intracerebral haemorrhage (TICH). Here, we explore the role of erythrocytes in brain oedema development by studying the effect of erythrocytes on brain water content (BWC) and expression of haem oxygenase-1 (HO-1) in rats with TICH. METHODS: A total of 120 Sprague-Dawley rats were randomly divided into four experimental treatment groups: traumatic brain injury (TBI), TBI plus whole blood (WB), TBI plus lysed red blood cells (RBCs; LRBC) and TBI plus packed RBCs (PRBC). Following TBI, which was established by applying a free-falling device, WB, LRBC or PRBC were infused with stereotactic guidance into the injured cortex to produce a model of TICH. All rats were killed at 1, 3 or 5 days after TBI or TICH. BWC was measured, and immunohistochemistry for HO-1 was performed. RESULTS: In the WB, PRBC and TBI groups, BWC at 3 days post-TBI or post-TICH was the greatest. However, BWC in the LRBC group at 1 day was markedly higher than that at 3 and 5 days. Comparisons among the four groups showed that BWC in the LRBC group was the highest at 1 day, and the highest at 3 days in the WB and PRBC groups; there was no significant difference at 5 days. Positive expression of HO-1 in the WB, PRBC and LRBC groups coincided with changes in BWC. CONCLUSIONS: Our results indicate that erythrocytes play an important role in delayed brain oedema formation (3 days post-injury) following TICH, but have no significant influence on brain oedema at early stages (1 day post-injury), and that the mechanisms of delayed brain oedema involve RBC breakdown products.