Intracranial hypertension in Africans with cerebral malaria

The causes of death and neurological sequelae in African children with cerebral malaria are obscure. Intracranial pressure (ICP) was monitored and cerebral perfusion pressure (CPP) calculated in 23 Kenyan children with cerebral malaria. Four children had severe intracranial hypertension (ICP > 40 mm Hg, CPP < 40 mm Hg): two died, one with an ICP of 158 mm Hg and signs of transtentorial herniation, the other one with an ICP of 42 mm Hg and cardiorespiratory arrest. The other two survived with severe neurological sequelae. Nine had intermediate intracranial hypertension (ICP > 20 mm Hg, CPP < 50 mm Hg) and 10 had mild intracranial hypertension (maximum ICP 10-20 mm Hg); all survived without severe sequelae. Mannitol controlled the ICP in children with intermediate intracranial hypertension, but it did not prevent the development of intractable intracranial hypertension in children with severe intracranial hypertension. Intracranial hypertension is a feature of Kenyan children with cerebral malaria and severe intracranial hypertension is associated with a poor outcome.     

Emergency and intensive care management of a comatose patient with intracranial hypertension, current concepts

Altered mental status is a common occurrence in children with acute critical illness. The causes of non-traumatic coma are diverse ranging from neurological to systemic causes. Early appropriate supportive care is essential to avoid preventable secondary insults and optimize the neurological outcome. Evaluation and stabilization of the patient's airway, breathing and circulation (ABCs) must proceed simultaneously with assessments of the depth of coma and the presence of raised intracranial pressure (ICP). Any rapidly correctable cause of coma must be immediately corrected. Most patients with non-traumatic encephalopathies have raised ICP, although papilledema may be absent and the CT scan may be normal if ICP elevation occurs acutely. The most important early treatment for raised ICP is controlled intubation and ventilation followed by osmotherapy. Early control of seizures, including non-convulsive seizures is important. Urgent imaging is indicated in most cases particularly in the presence of afebrile coma, focal signs or papilledema. Following stabilization, isotonic fluids are administered, aiming for euvolemia and euglycaemia. Ventilation should aim for the lower end of eucapnia to avoid causing cerebral ischemia. Surgical options should be explored and, in refractory intracranial hypertension, barbiturates and mild hypothermia may have a role.     

Preliminary experience with controlled external lumbar drainage in diffuse pediatric head injury.

Our experience with the use of external lumbar subarachnoid drainage in 5 children with severe diffuse head injuries is presented. All patients had Glasgow Coma Scale scores of 8 or less at 24 h after injury and were initially treated with ventriculostomies. Two children required surgical evacuation of focal mass lesions. Within 72 h of admission, all children manifested high intracranial pressures (ICP) refractory to maximal therapy, including hyperventilation, furosemide, mannitol, and barbiturate coma. After the institution of lumbar drainage, 3 of the 5 children had an abrupt and lasting decrease in ICP, obviating the need for continued barbiturates and hyperventilation. Three children survived, 2 of whom made good recoveries; 1 child is functional with disability. ICP varied passively with the height of the drainage bag in these surviving patients. Two patients died, most likely from uncontrolled ICP before the lumbar drain was placed. We conclude that controlled external lumbar subarachnoid drainage is a potentially useful treatment for severe diffuse pediatric head injury when maximal medical therapy and ventricular cerebrospinal fluid (CSF) evacuation have failed to control high ICP. Posttraumatic CSF circulation disruption, white matter cerebral edema, and intracranial venous hypertension can be treated with this modality in the absence of focal mass lesions.     

Intracranial pressure monitoring in comatose children

Coma may be associated with raised intracranial pressure (ICP), with a causative relationship in some cases. ICP monitoring provides an objective measurement of intracranial pressure and allows the ICP response to specific interventions to be directly observed. A combination of ICP and invasive arterial pressure monitoring provides a measure of the cerebral perfusion pressure (CPP), which is an important parameter in determining cerebral blood flow. Despite widespread use of ICP monitoring in certain causes of coma, most notably traumatic brain injury, the use of ICP monitoring is not proven to improve outcome in any cause of coma. This review explores the current medical literature regarding the uses of ICP monitoring in the paediatric population.     

间断静脉滴注3%高渗盐水与20%甘露醇治疗小儿急性脑水肿的疗效对比

目的 比较3%高渗盐水和20%甘露醇治疗小儿急性脑水肿的疗效.方法 将20例急性脑水肿患儿随机分为高渗盐水组和甘露醇组(每组各10例),接受3%高渗盐水或20%甘露醇治疗.用药前及用药后30 min,1、2、3、4、5、6 h,观察颅内压(ICP)、平均动脉压(MAP)、中心静脉压(CVP)、脑灌注压(CPP)、血电解质、血浆渗透压、肾功能以及尿量的变化.结果 3%高渗盐水和20%甘露醇均可显著降低ICP(P＜0.05).3%高渗盐水有效降ICP时间持续(4.5±1.2)h,20%甘露醇有效降ICP时间持续(3.2±1.5)h,差异有显著性(P＜0.05).且在用药2 h后,高渗盐水组MAP和CPP明显高于甘露醇组(P＜0.05).结论 3%高渗盐水与20%甘露醇均可迅速降低ICP,但3%高渗盐水作用持续时间比20%甘露醇更长,且可更好地稳定循环和提高脑血流灌注.     

A piglet model for evaluation of cerebral blood flow and brain oxidative metabolism during gradual cerebral perfusion pressure decrease.

A piglet model was developed to study the effect of epidural volume expansion on cerebral perfusion pressure (CPP) by stepwise elevating intracranial pressure (ICP). Mean arterial blood pressure (ABP) was strictly maintained using an extracorporeal ABP controller. Two-week-old piglets (n = 10) were studied by surgically placing an epidural balloon over the right parietal region and gradually increasing the inflation to increase ICP to 25, 35 and 45 mm Hg, maintaining each pressure level for 30 min. Regional cerebral blood flow was measured using the colored microsphere technique, and cerebral oxygen delivery and cerebral metabolic rate of oxygen were calculated at baseline conditions and after reaching ICP levels of 25, 35 and 45 mm Hg. The results showed that this model of epidural volume expansion reproducibly reduces CPP to 70, 50 and 33% of baseline CPP values with elevation of ICP, and that the physiological variables remained stable throughout each increase in ICP. We conclude that the model simulates the effects of an acute intracranial focal mass expansion and is well suited for the evaluation of different therapeutical strategies for increased ICP in newborns and infants.     

Neuropsychiatric disorders in very-low-birthweight newborn infants (VLBW-infants)--before and after the introduction of modern perinatal medicine. 3. Discussion of trends in quality of survival (CNS morbidity) and conclusions

The reduction of both the severe CNS-disturbances (major CNS-handicaps) as a whole and the infantile cerebral palsies (ICP), epilepsies, and mental retardations (oligophrenias) especially, can be attributed to the comprehensively improved pre-, intra- and postnatal care since the 60/70-ies. The best indicator is the decreasing ICP, because 60% of this disturbance is caused perinatally. It is closely associated with cerebral hemorrhages. In several centers, in Sweden and in West-Australia, an isolated recrudescence of ICP was noted. This fact is probably caused by a very active management of respirator therapy in some perinatological centers. However, today there is an effective therapy of several potential causes of perinatal cerebral lesions, i.e. hypoglycemia, hypothermia, asphyxia, RDS, and hyperbilirubinemia. The therapy of these diseases is simultaneously a prevention of the possible consecutive cerebral lesion as well. In the past, only two causes for CNS-disturbances have scarcely been influenced: cerebral hemorrhage, and nosocomial infections. Conclusions for the strategy of the further perinatal care can be deduced from these analyses: prevention of the extremely preterm deliveries, improvement of the perinatal care, prevention of cerebral hemorrhages and nosocomial infections, and responsible ethical decision about the application of the respirator therapy in the individual case.     

Reliability of cranial CT versus intracerebral pressure measurement for the evaluation of generalised cerebral oedema in children

Objective. To examine the extent to which intracranial pressure (ICP) in children after severe brain trauma can be determined by cranial CT.¶Materials and methods. Two experienced paediatric radiologists, without any knowledge of the clinical symptoms, evaluated 124 CT scans from 65 children (average age 5.4 years) who underwent intracranial measurement of their cerebral pressure.¶Results. CT had high sensitivity (99.1 %) for ’high cerebral pressure' but a much lower specificity (78.1 %). The examiners tended to estimate ICP as ’high' even when actual ICP was low. Since therapy for lowering cerebral pressure involves potential risks, actual cerebral pressure measurement, particularly in children, should be considered before intervention (e. g. hyperventilation or trepanation). We report the change in different intracerebral fluid compartments with varying cerebral pressure and modifications of the density of the brain tissue in an inter- and intraobserver comparison.¶Conclusion. The radiologist cannot differentiate, for methodological reasons, between a change in the intracranial fluid compartments not associated with a change in ICP and one in which it is critically elevated. Before any interventional treatments such as decompression-trepanation or hyperventilation are instituted, measurement of ICP should be considered, especially in children.     

Continuous intracranial pressure monitoring and serial electroencephalographic recordings in severely asphyxiated term neonates

We report our observations from intensive intracranial pressure (ICP) monitoring and serial clinical neurologic and electroencephalographic examinations in ten asphyxiated full-term neonates, of whom five died and at least two survivors had multiple severe neurologic handicaps. Direct measurements of ICP were obtained by a newly developed infant subarachnoid bolt and/or a transfontanelle pressure transducer. Simultaneous ICPs were recorded and correlated when possible. We noted a dependence of transfontanelle ICP values on application technique and force. In infants with no bleeding diathesis, the subarachnoid bolt was safe and no complications were encountered. Only six infants experienced pathologic elevations of ICP following birth asphyxia, and of these infants only two had sustained, marked increases of ICP. We also noted abundant fluctuations of cerebral perfusion pressure (mean arterial blood pressure minus ICP), but the majority of fluctuations were accounted for by mean arterial pressure changes rather than ICP changes. We found no deterioration of clinical neurologic function as measured by serial mental status examinations and electroencephalogram samples at the time the maximum ICP was measured. We also noted very little change in ICP during most electrographic seizures. In these infants ICP did increase after birth but major ICP elevations were uncommon and did not appear to introduce any acute functional neurologic disturbances. Most changes in cerebral perfusion pressure were attributed to blood pressure rather than ICP changes. It appears unlikely that cerebral edema and elevated ICP play a major role in determining neurologic outcome in some asphyxiated term infants.     

Assessment of childhood intracranial pressure recordings using a new method of processing intracranial pressure signals

BACKGROUND: Intracranial compliance may be more reliably predicted by the pulsatile component (pulse pressure) than the steady (mean pressure) component of intracranial pressure (ICP). A new method of processing continuous ICP signals assessing both components of ICP is described and applied to the ICP recordings of 6 pediatric cases. METHOD: The new method was applied to each subsequent 6-second time sequence window of a continuous ICP signal. For time sequence windows including single ICP waves, the following time sequence (TS.x)-related parameters were computed: (a) mean ICP (i.e. TS.MeanP) was computed according to the currently used and known technology; (b) the mean ICP wave was computed according to the new method, characterized by mean wave amplitude (i.e. TS.MeanWavedP) and mean wave latency (i.e. TS.MeanWavedT). Cases No. 1-4 were treated for hydrocephalus and cases No. 5 and 6 for craniosynostosis. RESULTS: In 5 children, clinical intracranial hypertension was associated with elevations of mean ICP above 15-20 mm Hg of variable durations. The ICP recordings of the 5 children with intracranial hypertension and successful outcome after surgery revealed mean wave amplitude values above 5 mm Hg. Mean wave latency was more variable, ranging between 0.10 and 0.25 s. CONCLUSIONS: In the children with intracranial hypertension and successful outcome after surgery, mean wave amplitude was variably above 5 mm Hg. It is suggested that mean wave amplitude may be a useful parameter by more directly predicting cerebral compliance than mean ICP.     

儿童颅内压监测研究进展

颅内高压是儿科较常见的急危重症,颅内压(intracranial pressure,ICP)监测能动态评估脑损伤患者的病情变化,计算脑灌注压,指导临床治疗.ICP监测有其局限性,不能及时反映大脑微血管功能障碍和细胞功能障碍,因此需要在ICP监测的基础上开展多模态监测(multimodality monitoring).ICP监测和多模态监测的信息整合有助于进一步理解脑损伤的病理生理机制,有助于对患者进行针对性个体化治疗.     

Emergency management of increased intracranial pressure

Primary neurological injury in children can be induced by diverse intrinsic and extrinsic factors including brain trauma, tumors, and intracranial infections. Regardless of etiology, increased intracranial pressure (ICP) as a result of the primary injury or delays in treatment may lead to secondary (preventable) brain injury. Therefore, early diagnosis and aggressive treatment of increased ICP is vital in preventing or limiting secondary brain injury in children with a neurological insult. Present management strategies to improve survival and neurological outcome focus on reducing ICP while optimizing cerebral perfusion and meeting cerebral metabolic demands. Targeted therapies for increased ICP must be considered and implemented as early as possible during and after the initial stabilization of the child. Thus, the emergency physician has a critical role to play in early identification and treatment of increased ICP. This article intends to identify those patients at risk of intracranial hypertension and present a framework for the emergency department investigation and treatment, in keeping with contemporary guidelines. Intensive care management and the treatment of refractory increases in ICP are also outlined.     

Evaluation of change of cerebral circulation by SpO2 in preterm infants with apneic episodes using near infrared spectroscopy

BACKGROUND: In the neonatal intensive care unit (NICU), hemodynamics in very low-birthweight infants are generally examined for oxygen saturation (SpO2), heart rate, respiration rate, and blood pressure. The present study examined how changes in cerebral circulation in preterm infants can be evaluated by the SpO2 monitoring method with near infrared spectroscopy (NIRS) to detect the cerebral circulation. METHODS: The study was conducted in 11 low-birthweight neonates with a mean weight of 1252 g (940-1948 g), mean post-conceptional age of 28.9 weeks (28-31 weeks) and in whom a total of 145 apneic episodes were examined. Changes in cerebral circulation at the apneic attack were evaluated by two parameters of Delta HbD ( micro mol/L) for reduction in cerebral oxygenation and Delta cHb (mL/100 g brain) for variation in cerebral blood volume using the near infrared spectroscopy (NIRS). RESULTS: There was a tendency for a reduction in cerebral oxygenation and a change in cerebral blood volume as SpO2 was reduced. In the event of apneic attacks where SpO2 was reduced to <85%, cerebral oxygen saturation was extensively reduced. In addition, cerebral blood volume was also greatly changed when the SpO2 was reduced to <85%, and changed further still when SpO2 was reduced again to < or =75%. CONCLUSION: Reduction in SpO2 (<85%) was suggested to be an effective indication to changes in cerebral circulation. In the case of apneic attacks where SpO2 was < or =85%, the cerebral circulation in preterm low-birthweight neonates was extensively changed and, therefore, attention should be paid to changes in the concentration of SpO2 when managing apnea of prematurity in NICU.     

Intracranial pressure and cerebral blood flow velocity in preterm infants with posthaemorrhagic ventricular dilatation

AIM: To determine the volume of cerebrospinal fluid (CSF) that should be tapped in preterm infants with posthaemorrhagic ventricular dilatation as guided by intracranial pressure (ICP) and cerebral blood flow velocity (CBFV). METHODS: The total number of measurements was 106 in 22 infants. Birth weights ranged from 630 to 2050 g, gestational age from 24.5 to 30.3 weeks, and age at insertion from 12 to 67 days. A subcutaneous ventricular catheter reservoir for repetitive CSF drainage was placed when the diameter of a ventricle was > 4 mm above the 97th centile. A volume of 5 ml/kg body weight was removed twice daily. ICP and CBFV were determined before and after CSF tapping. RESULTS: If the ICP after tapping exceeded 7 cm H(2)O, tapping did not result in a significant improvement in CBFV. If the ICP before tapping was less than 6 cm H(2)O, tapping also had no effect on CBFV. Longitudinal studies in individual infants showed a slight correlation between ICP and CBFV. CONCLUSION: Volume of repetitive CSF drainage in preterm infants with posthaemorrhagic ventricular dilatation guided by ICP and CBFV may be a useful technique. An ICP of about 6 cm H(2)O is the cut off point for CSF drainage.     

Noninvasive detection of changes in cerebral blood flow by near-infrared spectroscopy in a piglet model of hydrocephalus

Formulation of rational interventions in infantile hydrocephalus is limited by the inability to monitor cerebral hemodynamics quantitatively, continuously, and noninvasively. Near-infrared spectroscopy (NIRS) measures changes in cerebral concentration of oxygenated and deoxygenated hemoglobin (HbO(2) and Hb); HbD is the derived difference between HbO(2) and Hb. Our previous work showed that HbD reflected cerebral blood flow (CBF) measured by radioactive microspheres in a piglet model of systemic hypotension. This study was designed to determine whether NIRS detected important changes in cerebral perfusion and oxygenation in a piglet model of hydrocephalus and whether changes in HbD accurately reflected changes in CBF. Acute hydrocephalus was produced in neonatal piglets by intraventricular infusion of "mock cerebrospinal fluid." Intracranial pressure (ICP) was maintained for several minutes at approximately 10, 20, and 30 mm Hg above the baseline ICP. CBF was measured in cerebral cortex, white matter, and basal ganglia at each ICP by radioactive microspheres. Changes in HbO(2) and Hb were measured continuously by NIRS. Cerebral perfusion pressure declined with increasing ICP, and this decline was accompanied by significant decreases in HbD measured by NIRS and CBF measured by radioactive microspheres. There was a strong correlation between changes in HbD and individual changes in CBF in cerebral cortex, white matter, and basal ganglia (all p < 0.0001). This study demonstrates that changes in HbD reflect changes in CBF over a wide range of ICP in a model of acute hydrocephalus. This reproducible and easily obtained measurement by NIRS could facilitate considerably decisions concerning therapeutic interventions.     

Cerebral oedema complicating diabetic ketoacidosis

Signs of raised intracranial pressure (ICP) developed during treatment of diabetic ketoacidosis in a young child. A CT scan revealed cerebral oedema and direct measurement confirmed elevated ICP. Aggressive treatment was successful in maintaining cerebral perfusion pressure. The child survived with mild handicap in contrast to the poor outcome of previous reports.     

Intracranial pressure during procedural pain

Physiological changes provoked by pain may threaten the integrity of the CNS. In particular, intracranial pressure (ICP) regulates brain perfusion, and its sudden increase may trigger brain haemorrhage. We measured ICP in 51 healthy newborns (gestational age: 35-41 weeks) during blood sampling, by means of a tonometer applied to the anterior fontanelle. Peak ICP values were compared during 3 different types of blood sampling: from the external jugular vein (JV), by heel prick and by heel prick with sensorial saturation. Sensorial saturation consists in giving sensorial stimuli during pain to arrest the transmission of pain to the cerebral cortex. ICP peak values during heel prick were higher than during JV sampling (mean=26.22 vs. 21.036 mm Hg; p<0.0001), though babies who underwent the latter procedure had high ICP values before sampling due to the body position required. Heel prick with sensorial saturation was associated with a lower ICP peak (mean=11.75 mm Hg) than sampling from JV (p<0.0001). We concluded that heel prick caused a greater rise in ICP than sampling from JV and that sensorial saturation moderated the rise associated with heel prick.     

Cerebral Oedema Complicating Diabetic Ketoacidosis

ABSTRACT. Signs of raised intracranial pressure (ICP) developed during treatment of diabetic ketoacidosis in a young child. A CT scan revealed cerebral oedema and direct measurement conlirmed elevated ICP. Aggressive treatment was successful in maintaining cerebral perfusion pressure. The child survived with mild handicap in contrast to the poor outcome of previous reports.     

Management of intracranial hypertension

Raised intracranial pressure (ICP) is a life threatening condition that is common to many neurological and non-neurological illnesses. Unless recognized and treated early it may cause secondary brain injury due to reduced cerebral perfusion pressure (CPP), and progress to brain herniation and death. Management of raised ICP includes care of airway, ventilation and oxygenation, adequate sedation and analgesia, neutral neck position, head end elevation by 20°–30°, and short-term hyperventilation (to achieve PCO₂ 32–35 mm Hg) and hyperosmolar therapy (mannitol or hypertonic saline) in critically raised ICP. Barbiturate coma, moderate hypothermia and surgical decompression may be helpful in refractory cases. Therapies aimed directly at keeping ICP <20 mmHg have resulted in improved survival and neurological outcome. Emerging evidence suggests that cerebral perfusion pressure targeted therapy may offer better outcome than ICP targeted therapies.     

Head position affects intracranial pressure in newborn infants

We studied the effects of six different head positions on intracranial pressure and cerebral blood flow velocity in six infants with a recent history of asphyxia and eight without. ICP was measured noninvasively using a transfontanel pressure transducer, and CBF was assessed using the continuous-wave Doppler method. We found that ICP was lowest with the head elevated and in the midline (P less than 0.01), and that ICP was higher in all infants in the dependent position (P less than 0.001). This increase was significantly greater in those who had had an episode of asphyxia during the 48 to 72 hours prior to the study (P less than 0.02). Therefore, we recommend a head elevation of 30 degrees in the midline in any infant with increased ICP or at high risk for cerebral injury, and caution against the use of the dependent position in these infants.