The outcome with aggressive treatment in severe head injuries

1979 ◽  
Vol 50 (1) ◽  
pp. 26-30 ◽  
Author(s):  
Lawrence F. Marshall ◽  
Randall W. Smith ◽  
Harvey M. Shapiro
Keyword(s):  
Intracranial Hypertension ◽  
Head Injuries ◽  
High Rate ◽  
High Dose ◽  
Content Type ◽  
Diffuse Brain Injury ◽  
High Dose Dexamethasone ◽  
Brain Injured ◽  
Injured Patients ◽  
Fine Print

✓ In a series of 100 consecutive patients with severe head injuries, uncontrolled intracranial hypertension, which was defined as occurring when intracranial pressure (ICP) exceeded 40 mm Hg for 15 minutes or more, occurred in 25 patients. This was despite high-dose dexamethasone, hyperventilation, mannitol, normothermia, appropriate surgical evacuation, and cerebrospinal fluid drainage when possible. Persistently elevated ICP occurred in 19 patients with diffuse brain injury, and in six patients uncontrolled intracranial hypertension followed evacuation of a surgical mass. All of these patients received intravenous barbiturates to control the ICP. At the time of initial barbiturate administration, 11 of the 25 had bilaterally unreactive pupils and 12 were decerebrate. The initial pentobarbital loading dose (3 to 5 mg/kg) effectively reduced the ICP in 76% of the patients. Prolonged pentobarbital treatment with blood barbiturate levels from 2.5 to 3.5 mg% was associated with normalization of the ICP (ICP less than 15 mm Hg) in 13 patients. In those patients responding to barbiturates, the daily mannitol requirement was reduced from 4.5 to 0.5 gm/kg/day (p < 0.01). In six nonresponders to barbiturates, mannitol requirements increased to 5.9 gm/kg/day; five of these died and one remains vegetative. Ten of the 19 barbiturate responders have returned to a productive life, two remain moderately disabled, two are severely disabled, one is vegetative, and four are dead. The high rate of good quality survival in this series of severely brain-injured patients indicates that barbiturates are useful in the treatment of uncontrolled intracranial hypertension and that a broader investigation of the clinical application of barbiturates is indicated.

Role of intracranial pressure monitoring in severely head-injured patients without signs of intracranial hypertension on initial computerized tomography

1994 ◽  
Vol 80 (1) ◽  
pp. 46-50 ◽  
Author(s):  
Michael G. O'Sullivan ◽  
Patrick F. Statham ◽  
Patricia A. Jones ◽  
J. Douglas Miller ◽  
N. Mark Dearden ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Ct Scan ◽  
Intracranial Hypertension ◽  
Mass Lesion ◽  
Midline Shift ◽  
Pressure Monitoring ◽  
Content Type ◽  
Head Injured ◽  
Injured Patients ◽  
Fine Print

✓ Previous studies have suggested that only a small proportion (< 15%) of comatose head-injured patients whose initial computerized tomography (CT) scan was normal or did not show a mass lesion, midline shift, or abnormal basal cisterns develop intracranial hypertension. The aim of the present study was to re-examine this finding against a background of more intensive monitoring and data acquisition. Eight severely head-injured patients with a Glasgow Coma Scale score of 8 or less, whose admission CT scan did not show a mass lesion, midline shift, or effaced basal cisterns, underwent minute-to-minute recordings of arterial blood pressure, intracranial pressure (ICP), and cerebral perfusion pressure (CPP) derived from blood pressure minus ICP. Intracranial hypertension (ICP ≥ 20 mm Hg lasting longer than 5 minutes) was recorded in seven of the eight patients; in five cases the rise was pronounced in terms of both magnitude (ICP ≥ 30 mm Hg) and duration. Reduced CPP (≤ 60 mm Hg lasting longer than 5 minutes) was recorded in five patients. Severely head-injured (comatose) patients whose initial CT scan is normal or does not show a mass lesion, midline shift, or abnormal cisterns nevertheless remain at substantial risk of developing significant secondary cerebral insults due to elevated ICP and reduced CPP. The authors recommend continuous ICP and blood pressure monitoring with derivation of CPP in all comatose head-injured patients.

Mannitol dose requirements in brain-injured patients

1978 ◽  
Vol 48 (2) ◽  
pp. 169-172 ◽  
Author(s):  
Lawrence F. Marshall ◽  
Randall W. Smith ◽  
L. Andrew Rauscher ◽  
Harvey M. Shapiro
Keyword(s):  
Time Course ◽  
Osmotic Gradient ◽  
Intracranial Volume ◽  
Severe Dehydration ◽  
Dose Response Relationship ◽  
Content Type ◽  
Acute Head Injury ◽  
Brain Injured ◽  
Injured Patients ◽  
Fine Print

✓ There is little information as to the optimal use of mannitol. To determine the dose-response relationship, the osmotic gradient required, and the time course of intracranial pressure (ICP) reduction produced by mannitol, eight patients with acute head injury were studied in whom ICP was monitored with a ventriculostomy and found to be elevated. Ventilation was controlled to a pCO2 of 25 ± 3 mm Hg and all were paralyzed with Pavulon. None had received barbiturates. Before mannitol administration the intracranial volume-pressure response was determined. Mannitol was administered as a bolus of 0.25 gm/kg, 0.5 gm/kg, and in six patients, 1 gm/kg, separated by at least 8 hours. In all patients the ICP reduction with 0.25 gm/kg (41.3 ± 10.2 mm Hg→16.4 ± 5.6, p < 0.01) was equivalent to that achieved with the larger doses. Serum osmolality rises of 10 mOsm or more were associated with a reduction in ICP. Much smaller doses than those previously recommended were effective in reducing the ICP acutely, although at 5 hours there was a trend toward persistent reduction when the larger dose is used. This trend was small and indicates that smaller and more frequent doses are as effective in reducing the ICP while avoiding the risk of osmotic disequilibrium and severe dehydration.

Head-injured patients who talk and deteriorate into coma

1991 ◽  
Vol 75 (2) ◽  
pp. 256-261 ◽  
Author(s):  
Ramiro D. Lobato ◽  
Juan J. Rivas ◽  
Pedro A. Gomez ◽  
Mario Castañeda ◽  
José M. Cañizal ◽  
...  
Keyword(s):  
Glasgow Coma Scale ◽  
Scale Score ◽  
Glasgow Coma Scale Score ◽  
Epidural Hematoma ◽  
Head Injuries ◽  
Mass Lesion ◽  
Content Type ◽  
Coma Scale ◽  
Injured Patients ◽  
Fine Print

✓ Of 838 patients with severe head injuries admitted since the introduction of computerized tomography, 211 (25.1%) talked at some time between trauma and subsequent deterioration into coma. Of these 211 patients, 89 (42.2%) had brain contusion/hematoma, 46 (21.8%) an epidural hematoma, 35 (16.6%) a subdural hematoma, and 41 (19.4%) did not show focal mass lesions. Thus, four of every five patients who deteriorated into coma after suffering an apparently nonsevere head injury had a mass lesion potentially requiring surgery; the mass was intracerebral in 52.3% of the cases and extracerebral in 47.6%. Patients aged 20 years or less had a 39% chance of having a nonfocal mass lesion (diffuse brain damage), a 29% chance of having an epidural hematoma, and a 32% chance of having an intradural mass lesion; patients over 40 years had only a 3% chance of having a nonfocal mass lesion, an 18% chance of having an epidural hematoma, and a 79% chance of having a intradural mass lesion. Sixty-eight (32.2%) patients died and 143 (67.8%) survived. The following were independent outcome predictors (in order of significance): Glasgow Coma Scale score following deterioration into coma, the highest intracranial pressure during the patient's course, the degree of midline shift, the type of intracranial lesion, and the age of the patient. In contrast, the mechanism of injury, the verbal Glasgow Coma Scale score during the lucid interval, and the length of time until deterioration or until operative intervention did not influence the final result.

Little benefit from mild hypothermia therapy for severely head injured patients with low intracranial pressure

1999 ◽  
Vol 91 (2) ◽  
pp. 185-191 ◽  
Author(s):  
Tadahiko Shiozaki ◽  
Amami Kato ◽  
Mamoru Taneda ◽  
Toshiaki Hayakata ◽  
Naoyuki Hashiguchi ◽  
...  
Keyword(s):  
Intracranial Pressure ◽  
Mild Hypothermia ◽  
Neurological Status ◽  
High Dose ◽  
Fluid Restriction ◽  
Content Type ◽  
Head Injured ◽  
Factor Α ◽  
Injured Patients ◽  
Fine Print

Object. This study was performed to determine whether mild hypothermia therapy is essential for the treatment of severely head injured patients in whom intracranial pressure (ICP) can be maintained below 20 mm Hg by using conventional therapies.Methods. Sixteen consecutive severely head injured patients fulfilled the following criteria: the patient's ICP was maintained below 20 mm Hg by using fluid restriction, hyperventilation, and high-dose barbiturate therapy; and the patient had a Glasgow Coma Scale score of 8 or less on admission. After conventional therapies had been applied, the patients were divided randomly into two groups: the mild hypothermia group (HT group; eight patients) and the normothermia group (NT group; eight patients). The HT group received mild hypothermia (intracranial temperature 34°C) therapy for 48 hours followed by rewarming at 1°C per day for 3 days, whereas the NT group received normothermia (intracranial temperature 37°C) therapy for 5 days. Specimens of cerebrospinal fluid (CSF) taken from an intraventricular catheter every 24 hours were analyzed for the presence of excitatory amino acids ([EAAs] glutamate, aspartate, and glycine) and cytokines (tumor necrosis factor—α, interleukin [IL]-1β, IL-6, IL-8, and IL-10). The two groups did not differ significantly in patient age, neurological status, or level of ICP. There were no significant differences in daily changes in CSF concentrations of EAAs and cytokines between the two groups. The incidence of pneumonia was slightly higher in the HT group compared with the NT group (p = 0.059). The incidence of diabetes insipidus associated with hypernatremia was significantly higher in the HT group compared with that in the NT group (p < 0.01). The two groups did not differ with respect to their clinical outcomes.Conclusions. The authors recommend normothermia therapy for the treatment of severely head injured patients in whom ICP can be maintained at lower than 20 mm Hg by using conventional therapies, because mild hypothermia therapy does not convey any advantage over normothermia therapy in such patients.

Proton magnetic resonance spectroscopy for detection of axonal injury in the splenium of the corpus callosum of brain-injured patients

1998 ◽  
Vol 88 (5) ◽  
pp. 795-801 ◽  
Author(s):  
Kim M. Cecil ◽  
Everett C. Hills ◽  
M. Elizabeth Sandel ◽  
Douglas H. Smith ◽  
Tracy K. McIntosh ◽  
...  
Keyword(s):  
White Matter ◽  
Proton Magnetic Resonance ◽  
Axonal Injury ◽  
Diffuse Axonal Injury ◽  
Resonance Spectroscopy ◽  
Proton Mrs ◽  
Content Type ◽  
Brain Injured ◽  
Injured Patients ◽  
Fine Print

Object. This study was conducted to determine whether proton magnetic resonance spectroscopy (MRS) is a sensitive method for detecting diffuse axonal injury, which is a primary sequela of traumatic brain injury (TBI). Diffuse axonal injury is characterized by selective damage to white matter tracts that is caused in part by the severe inertial strain created by rotational acceleration and deceleration, which is often associated with motor vehicle accidents. This axonal injury is typically difficult to detect by using conventional imaging techniques because it is microscopic in nature. The splenium was selected because it is a site vulnerable to shearing forces that produce diffuse axonal injury. Methods. The authors used proton MRS to evaluate the splenium, the posterior commissure of the corpus callosum, in normal control volunteers and in patients with TBI. Proton MRS provided an index of neuronal and axonal viability by measuring levels of N-acetyl aspartate (NAA). Conclusions. A majority of mildly brain injured patients, as well as those more severely injured, showed diminished NAA/creatine (Cr) levels in the splenium compared with normal control volunteers. The patients displaying lowered NAA/Cr in the splenium were also likely to exhibit lowered NAA/Cr in lobar white matter. Also, the levels of NAA/Cr in the splenium of normal volunteers were higher compared with those found in lobar white matter. Decreases in NAA/Cr levels in the splenium may be a marker for diffuse injury. A proton MRS examination may be particularly useful in evaluating mildly injured patients with unexplained neurological and cognitive deficits. It is concluded that MRS is a sensitive tool in detecting axonal injury.

The effect of changes in cerebral perfusion pressure upon middle cerebral artery blood flow velocity and jugular bulb venous oxygen saturation after severe brain injury

1992 ◽  
Vol 77 (1) ◽  
pp. 55-61 ◽  
Author(s):  
Kwan-Hon Chan ◽  
J. Douglas Miller ◽  
N. Mark Dearden ◽  
Peter J. D. Andrews ◽  
Susan Midgley
Keyword(s):  
Blood Flow ◽  
Flow Velocity ◽  
Perfusion Pressure ◽  
Jugular Bulb ◽  
Artery Blood Flow ◽  
Content Type ◽  
Brain Injured ◽  
Venous Oxygen Saturation ◽  
Injured Patients ◽  
Fine Print

✓ Middle cerebral artery blood flow velocity and jugular bulb venous oxygen saturation (SJO2) were measured by transcranial Doppler (TCD) ultrasonography and continuous venous oximetry, respectively, in 41 severely brain-injured patients. The purpose of the study was to examine the relationships between TCD flow velocity, SJO2, and alterations in blood pressure (BP), intracranial pressure (ICP), and cerebral perfusion pressure (CPP). In these patients, CPP was reduced either by rising ICP or by falling BP. Both forms of reduction of CPP resulted in a greater fall in diastolic flow velocity than other flow parameters. As CPP decreased below a critical value of 70 mm Hg, a progressive increase in TCD pulsatility index (PI) was observed (r = −0.942, p < 0.0001), accompanied by a fall in SJO2 (r = 0.78, p < 0.0001). At pressures above 70 mm Hg, there was no correlation of either PI or SJO2 with CPP. The relationship between PI and CPP held true in patients with both focal and diffuse pathologies and was the same whether changes in CPP resulted from alterations in ICP or BP. The PI and SJO2 correlated better with CPP than with ICP or BP. Transcranial Doppler ultrasonography can identify states of reduced CPP. Decreases in SJO2 with falling CPP suggested progressive failure of cerebral blood flow to meet metabolic demands. Monitoring of TCD and SJO2 may be used to define the optimum CPP level for management of severely brain-injured patients.

Efficacy of moderate hypothermia in patients with severe head injury and intracranial hypertension refractory to mild hypothermia

2003 ◽  
Vol 99 (1) ◽  
pp. 47-51 ◽  
Author(s):  
Tadahiko Shiozaki ◽  
Yoshikazu Nakajima ◽  
Mamoru Taneda ◽  
Osamu Tasaki ◽  
Yoshiaki Inoue ◽  
...  
Keyword(s):  
Intracranial Hypertension ◽  
Mild Hypothermia ◽  
Brain Temperature ◽  
Moderate Hypothermia ◽  
Content Type ◽  
Arterial Blood ◽  
Cell Counts ◽  
Head Injured ◽  
Injured Patients ◽  
Fine Print

Object. This study was performed to determine whether moderate hypothermia (31°C) improves clinical outcome in severely head injured patients whose intracranial hypertension cannot be controlled using mild hypothermia (34°C). Methods. Twenty-two consecutive severely head injured patients who fulfilled the following criteria were included in this study: an intracranial pressure (ICP) that remained higher than 40 mm Hg despite the use of mild hypothermia combined with conventional therapies; and a Glasgow Coma Scale score of 8 or less on admission. After the failure of mild hypothermia in combination with conventional therapies; patients were exposed to moderate hypothermia as quickly as possible. As brain temperature was reduced from 34 to 31°C, the volume of intravenous fluid infusion was increased significantly from 1.9 ± 0.9 to 2.6 ± 1.2 mg/kg/hr (p < 0.01), and the dose of dopamine infusion increased significantly from 4.3 ± 3.1 to 8.2 ± 4.4 µg/kg/min (p < 0.01). Nevertheless, mean arterial blood pressure and heart rate decreased significantly from 97.1 ± 13.1 to 85.1 ± 10.5 mm Hg (p < 0.01) and from 92.2 ± 13.8 to 72.2 ± 14.3 beats/minute at (p < 0.01) at 34 and 31°C, respectively. Arterial base excess was significantly aggravated from −3.3 ± 4 at 34°C to −5.6 ± 5.4 mEq/L (at 31°C; p < 0.05). Likewise, serum potassium concentration, white blood cell counts, and platelet counts at 31°C decreased significantly compared with those at 34°C (p < 0.01). In 19 (86%) of 22 patients, elevation of ICP could not be prevented using moderate hypothermia. In the remaining three patients, ICP was maintained below 40 mm Hg by inducing moderate hypothermia; however, these three patients died of multiple organ failure. These results clearly indicate that moderate hypothermia induces complications more severe than those induced by mild hypothermia without improving outcomes. Conclusions. The authors concluded that moderate hypothermia is not effective in improving clinical outcomes in severely head injured patients whose ICP remains higher than 40 mm Hg after treatment with mild hypothermia combined with conventional therapies.

Monitoring of cerebral oxygenation in patients with severe head injuries: brain tissue PO2 versus jugular vein oxygen saturation

1996 ◽  
Vol 85 (5) ◽  
pp. 751-757 ◽  
Author(s):  
Karl L. Kiening ◽  
Andreas W. Unterberg ◽  
Tillman F. Bardt ◽  
Gerd-Helge Schneider ◽  
Wolfgang R. Lanksch
Keyword(s):  
Oxygen Saturation ◽  
Cerebral Oxygenation ◽  
Jugular Vein ◽  
Head Injuries ◽  
Jugular Bulb ◽  
Cerebral White Matter ◽  
Content Type ◽  
Head Injured ◽  
Injured Patients ◽  
Fine Print

✓ Monitoring of cerebral oxygenation is considered to be of great importance in minimizing secondary hypoxic and ischemic brain damage following severe head injury. Although the threshold for cerebral hypoxia in jugular bulb oximetry (measurement of O2 saturation in the jugular vein (SjvO2)) is generally accepted to be 50% oxygen saturation, a comparable value in brain tissue PO2 (PtiO2) monitoring, a new method for direct assessment of PO2 in the cerebral white matter, has not yet been established. Hence, the purpose of this study was to compare brain PtiO2 with SjvO2 in severely head injured patients during phases of reduced cerebral perfusion pressure (CPP) to define a threshold in brain PtiO2 monitoring. In addition, the safety and data quality of both SjvO2 and brain PtiO2 monitoring were studied. In 15 patients with severe head injuries, SjvO2 and brain PtiO2 were monitored simultaneously. For brain PtiO2 monitoring a polarographic microcatheter was inserted in the frontal cerebral white matter, whereas for SjvO2 measurements were obtained by using a fiberoptic catheter placed in the jugular bulb. Intracranial pressure was monitored by means of an intraparenchymal catheter. Mean arterial blood pressure, CPP, end-tidal CO2, and arterial oxygen saturation (pulse oximetry) were continuously recorded. All data were simultaneously stored and analyzed using a multimodal computer system. For specific analysis, phases of marked deterioration in systemic blood pressure and consecutive reductions in CPP were investigated. There were no complications that could be attributed to the PtiO2 catheters, that is, no intracranial bleeding or infection. The “time of good data quality” was 95% in brain PtiO2 compared to 43% in SjvO2; PtiO2 monitoring could be performed twice as long as SjvO2 monitoring. During marked decreases in CPP, SjvO2 and brain PtiO2 correlated closely. A significant second-order regression curve of SjvO2 versus brain PtiO2 (p < 0.01) was plotted. At a threshold of 50% in SjvO2, brain PtiO2 was found to be within the range of 3 to 12 mm Hg, with a regression curve “best fit” value of 8.5 mm Hg. There was a close correlation between CPP and oxygenation parameters (PtiO2 and SjvO2) when CPP fell below a breakpoint of 60 mm Hg, suggesting intact cerebral autoregulation in most patients. This study demonstrates that monitoring brain PtiO2 is a safe, reliable, and sensitive diagnostic method to follow cerebral oxygenation. In comparison to SjvO2, PtiO2 is more suitable for long-term monitoring. It can be used to minimize episodes of secondary cerebral maloxygenation after severe head injury and may, hopefully, improve the outcome in severely head injured patients.

The oval pupil: clinical significance and relationship to intracranial hypertension

1983 ◽  
Vol 58 (4) ◽  
pp. 566-568 ◽  
Author(s):  
Lawrence F. Marshall ◽  
David Barba ◽  
Belinda M. Toole ◽  
Sharon A. Bowers
Keyword(s):  
Intracranial Hypertension ◽  
Head Injuries ◽  
Transitional Stage ◽  
Content Type ◽  
Closed Head Injuries ◽  
Transtentorial Herniation ◽  
Neurosurgical Patients ◽  
Closed Head ◽  
Third Nerve ◽  
Fine Print

✓ The oval pupil, or what has also been termed the “oblong” or “football” pupil, has been observed in 15 neurosurgical patients over a 2-year period. In 14 of the 15 patients, the intracranial pressure (ICP) was elevated, ranging from 18 to 38 mm Hg. While the oval pupil was primarily seen in patients suffering closed head injuries (11 cases), it was also observed in two patients with elevated ICP following hemorrhage from an arteriovenous malformation. In nine of the 14 patients in whom the pupillary abnormality was associated with intracranial hypertension, the oval pupil disappeared when the ICP was reduced to below 20 mm Hg. In four cases, the ICP could not be controlled and the pupil became progressively larger, and finally fixed and unreactive. The oval pupil represents a transitional stage indicating transtentorial herniation with third nerve compression. Although it may be seen in the absence of intracranial hypertension (one case in this series), this appears to be relatively uncommon. The presence of such a pupil on examination in a patient suffering an intracranial catastrophe, be it head injury, subarachnoid hemorrhage, or intracerebral hemorrhage, suggests impending transtentorial herniation with brain-stem compression.

Effects of hyperbaric oxygenation therapy on cerebral metabolism and intracranial pressure in severely brain injured patients

2001 ◽  
Vol 94 (3) ◽  
pp. 403-411 ◽  
Author(s):  
Sarah B. Rockswold ◽  
Gaylan L. Rockswold ◽  
Janet M. Vargo ◽  
Carla A. Erickson ◽  
Richard L. Sutton ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Hyperbaric Oxygenation ◽  
Cerebral Metabolism ◽  
Content Type ◽  
Brain Injured ◽  
Csf Lactate ◽  
Injured Patients ◽  
Fine Print

Object. Hyperbaric oxygenation (HBO) therapy has been shown to reduce mortality by 50% in a prospective randomized trial of severely brain injured patients conducted at the authors' institution. The purpose of the present study was to determine the effects of HBO on cerebral blood flow (CBF), cerebral metabolism, and intracranial pressure (ICP), and to determine the optimal HBO treatment paradigm. Methods. Oxygen (100% O2, 1.5 atm absolute) was delivered to 37 patients in a hyperbaric chamber for 60 minutes every 24 hours (maximum of seven treatments/patient). Cerebral blood flow, arteriovenous oxygen difference (AVDO2), cerebral metabolic rate of oxygen (CMRO2), ventricular cerebrospinal fluid (CSF) lactate, and ICP values were obtained 1 hour before and 1 hour and 6 hours after a session in an HBO chamber. Patients were assigned to one of three categories according to whether they had reduced, normal, or raised CBF before HBO. In patients in whom CBF levels were reduced before HBO sessions, both CBF and CMRO2 levels were raised 1 hour and 6 hours after HBO (p < 0.05). In patients in whom CBF levels were normal before HBO sessions, both CBF and CMRO2 levels were increased at 1 hour (p < 0.05), but were decreased by 6 hours after HBO. Cerebral blood flow was reduced 1 hour and 6 hours after HBO (p < 0.05), but CMRO2 was unchanged in patients who had exhibited a raised CBF before an HBO session. In all patients AVDO2 remained constant both before and after HBO. Levels of CSF lactate were consistently decreased 1 hour and 6 hours after HBO, regardless of the patient's CBF category before undergoing HBO (p < 0.05). Intracranial pressure values higher than 15 mm Hg before HBO were decreased 1 hour and 6 hours after HBO (p < 0.05). The effects of each HBO treatment did not last until the next session in the hyperbaric chamber. Conclusions. The increased CMRO2 and decreased CSF lactate levels after treatment indicate that HBO may improve aerobic metabolism in severely brain injured patients. This is the first study to demonstrate a prolonged effect of HBO treatment on CBF and cerebral metabolism. On the basis of their data the authors assert that shorter, more frequent exposure to HBO may optimize treatment.

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