Rise In Intracranial Pressure Research Articles

Changes of cortical perfusion in the early phase of subarachnoid bleeding in a rat model and the role of intracranial hypertension.

Brain perfusion is reduced early after subarachnoid hemorrhage (SAH) due to intracranial hypertension and early vasospasm. The contribution of these two mechanisms is unknown. By performing a prophylactic decompressive craniectomy (DC) in a rat model of SAH we aimed to study brain perfusion after the component of intracranial hypertension has been eliminated. We used 2x2 factorial design, where rats received either decompressive craniectomy or sham operation followed by injection of 250 microl of blood or normal saline into prechiasmatic cistern. The cortical perfusion has been continually measured by laser speckle-contrast analysis for 30 min. Injection of blood caused a sudden increase of intracranial pressure (ICP) and drop of cerebral perfusion, which returned to baseline within 6 min. DC effectively prevented the rise of ICP, but brain perfusion after SAH was significantly lower and took longer to normalize compared to non-DC animals due to increased cerebral vascular resistance, which lasted throughout 30 min experimental period. Our findings suggest that intracranial hypertension plays dominant role in the very early hypoperfusion after SAH whilst the role of early vasospasm is only minor. Prophylactic DC effectively maintained cerebral perfusion pressure, but worsened cerebral perfusion by increased vascular resistance.

Effect of intravenous midazolam on intracranial pressure during endotracheal suctioning in patients with severe head injury

Abstract Background: Patients with severe traumatic brain injury (TBI) require elective ventilation and sedation to decrease intracranial pressure (ICP) and any increase in ICP may be detrimental for the outcome in these patients. Methods: This prospective study was done in a neurotrauma intensive care unit ( ICU )of a level 1 trauma centre in India over a one month period. All adult male patients with severe TBI on mechanical ventilation and monitored for ICP were included in this study. Baseline ICP was measured before starting endotracheal (ET) suctioning and serial readings were taken during and after ET suctioning. Patients were divided into two groups (control and intervention) with intervention group receiving intravenous bolus dose of 2 mg of midazolam before ET suction. Results: A total of 20 patients were enrolled during the study period. Both groups were well matched with regards to age and admission Glasgow coma scale (GCS). There were 10 patients in the midazolam group and 10 patients in the control group. The mean rise of ICP following ET suctioning in control group was found to be 24.1mm Hg ±11.1 as compared to 18.25 mm Hg ±-9.29 in the midazolam group ( P< 0.05). Conclusions: Significant rise in ICP from baseline occurs following ET suctioning in ventilated, severe TBI patients. Our study suggests that additional intravenous bolus of midazolam prior to suctioning may significantly reduce the rise in ICP and should be practiced by ICU nurses.

Pathophysiological central nervous system changes in a porcine model of acetaminophen-induced acute liver failure

BackgroundCritical care management of patients suffering from acute liver failure (ALF) continues to be challenging. Animal models studying the pathophysiological central nervous system alterations during the course of ALF provide an opportunity to improve diagnostic and therapeutic strategies. The aim of this study was to analyse the course of cerebral oxygenation in addition to conventional neuromonitoring during the course of acetaminophen-induced ALF. MethodsALF was induced by intrajejunal acetaminophen administration in 20 German landrace pigs. All animals underwent invasive hemodynamic and neuromonitoring and were maintained under standardized intensive care support. Neuromonitoring consisted of continuous intraparenchymatous recording of intracranial pressure and brain partial oxygen pressure. Hemodynamic and ventilation parameters were continuously recorded; laboratory parameters were analysed every eight hours. Mean values were compared using the Wilcoxon test. ResultsAcute liver failure occurred in all intoxicated animals after 23±2h, resulting in death due to ALF after further 15±2h. Continuous neuromonitoring was performed in all animals during the whole experiment without observing signs of intracranial haemorrhage. Two hours after manifestation of ALF an increase in brain tissue oxygen (PtiO2) was observed. Brain oxygenation stayed stable until nine hours before death. Intracranial pressure (ICP) remained basically at a plateau level until manifestation of ALF. In the following ten hours a linear and slow increase was observed until five hours before death, followed by a fast and continuous rise in ICP to a final level of 35±1mmHg. Cerebral perfusion pressure (CPP) began to decrease 25h prior to exitus, further decreasing to 18±2mmHg at the end of the experiment. A strong negative linear correlation was found between PtiO2 and ICP (R=0.97). Arterial partial pressure of oxygen (PaO2) below 100mmHg was associated with lower PtiO2 levels. Changes in arterial partial pressure of carbon dioxide (PaC02) did not influence PtiO2 values. Hemoglobin values below 7g/dl were associated with lower PtiO2 values. ConclusionsThe results of our experiments demonstrate that ICP and PtiO2 measurements indicate impending damage well before serious complications occur and their use should be considered in order to protect endangered brain function in the presence of acetaminophen-induced ALF.

Proteomic Expression Changes in Large Cerebral Arteries After Experimental Subarachnoid Hemorrhage in Rat Are Regulated by the MEK-ERK1/2 Pathway

Subarachnoid hemorrhage (SAH) is a serious clinical condition where leakage of blood into the subarachnoid space causes an acute rise in intracranial pressure and reduces cerebral blood flow, which may lead to delayed cerebral ischemia and poor outcome. In experimental SAH, we have previously shown that the outcome can be significantly improved by early inhibition of the MAPK/ERK kinase/extracellular signal-regulated kinase (MEK/ERK1/2) pathway. The aim of this study was to apply mass spectrometry to investigate the overall late effects of experimental SAH on cerebrovascular protein expression. SAH was induced in rats that were treated with the MEK1/2 inhibitor U0126 or vehicle. Neurological outcome was assessed using a battery of behavioral tests. Specific protein expression of large cerebral arteries was analyzed quantitatively with high-throughput tandem mass spectrometry. SAH resulted in a marked reduction of neurological scores, which was counteracted by U0126 treatment. Mass spectrometry analysis demonstrated regulation of 184 proteins after SAH, regulations that were in part prevented by U0126 treatment. Network analysis identified several protein networks including a strong structural network centered around 14-3-3. Additionally, protein networks with functions in mRNA metabolism and protein folding were identified. Treatment with U0126 inhibited cerebral vessel wall pERK1/2 expression and significantly improved outcome of the rats. In conclusion, we show that SAH induces a broad array of specific changes in the overall protein networks in cerebral artery smooth muscle cells and suggest that this is essential for understanding the vascular pathophysiology after SAH.

Intravenous mannitol in status migrainosus treatment: a clinical case series

Status migrainosus (SM) is defined as a severe migraine attack, usually poorly responsive to treatments, lasting more than 72h. Recurrent SM predicts chronic migraine (CM) development in 83.7% of cases. There is evidence that in most unresponsive CM patients a sinus stenosis-associated raised intracranial pressure is causatively involved in migraine chronification. To test the hypothesis that SM may reflect a sustained rise in intracranial pressure, we tested the efficacy of a 3-day treatment with intravenous mannitol 18% 250ml b.i.d. in seven subjects presenting with a SM unresponsive to common treatments, showing unilateral or bilateral sinus stenosis at magnetic resonance venography. Mannitol infusion induced the abrupt reduction or the disappearance of pain in all patients, at least along the 3days of treatment. While the benefit was only observed during the days of treatment in two subjects, in the remaining five patients the time to the next headache was delayed between 20days to 5weeks after mannitol infusion. Due to the lack of any analgesic property of mannitol, our data indicate that in this series a rise in intracranial pressure was involved in SM causative mechanisms.

Use of Dexmedetomidine in Patients Undergoing Craniotomies.

The neuroanaesthesia ensures stable perioperative cerebral haemodynamics, avoids sudden rise in intracranial pressure and prevents acute brain swelling. The clinical characteristics of dexmeditomidine make this intravenous agent a potentially attractive adjunct for neuroanaesthesia and in the neurological intensive care unit. This study aimed to assess the effect of dexmedetomidine on intraoperative haemodynamic stability and to assess the intraoperative requirements of analgesic and other anaesthetic agents, and also to assess postoperative sedation, respiratory depression and any other side effects of dexmedetomidine as compared to placebo. This prospective randomized study was done in 60 patients of either sex, age between 18 to 60 years and American Society of Anaesthesiologist (ASA) Grade I and II undergoing elective craniotomies under General Anaesthesia (GA) for intracranial Space Occupying Lesion (SOL). These 60 patients underwent thorough history, clinical examination and laboratory investigations. They were randomly divided into two groups, Group D (received Inj. Dexmedetomidine) and Group P (received Inj. Placebo). During bolus and infusion Heart Rate (HR), Systolic Blood Pressure (SBP), Diastolic Blood Pressure (DBP), Mean Arterial Pressure (MAP), Peripheral oxygen saturation (SPO2) was recorded at every five minutes interval for first 20 minute. The mean age in Group D was 39.5 years and in Group P was 40 years. The sex distribution in two groups was in Group D, 12 patients (40%) were females and 18 (60%) patients were males. While in Group P 10 (33.3%) were females and 20 (66.7%) patients were males. The two groups were comparable with respect to diagnosis and type of surgery of patients and difference was not statistically significant. The mean HR, the mean DBP and the mean MAP was lower in Group D as compared to Group P and the difference was statistically significant. Dexmedetomidine provided intraoperative haemodynamic stability. It attenuates the haemodynamic responses to laryngoscopy, intubation, at pin fixation and the emergence from anaesthesia.

Acute Subdural Hematoma after Carotid Artery Stenting

Cerebral hyperperfusion syndrome is a major cause of morbidity and mortality following carotid artery stenting (CAS). We present a case of acute subdural hematoma (SDH) 2 hours after CAS. In this case, arterial origin of bleeding was verified during operation. To our knowledge, there is no prior case report of SDH without intraparenchymal nor subarachnoid hemorrhage subsequent to CAS. We postulate that SDH was caused by sudden rise in intracranial pressure due to the hyperperfusion which disrupted a corticodural bridging artery. Key Words: Carotid artery stenting, Cerebral hyperperfusion syndrome, Subdural hematoma

Central neurogenic hyperventilation with acute respiratory alkalosis, transient lactic acidosis and tachycardia following endoscopic third ventriculostomy in a child

Endoscopic third ventriculostomy (ETV) is a common minimal-invasive neurosurgical procedure with well-documented complications. We report the case of a 6-year-old female child who underwent ETV, external ventricular drainage (EVD) catheter insertion and biopsy for a tumour arising from the pineal gland causing obstructive hydrocephalus and raised intra cranial pressure (ICP). Vital signs were stable pre-operatively and anaesthesia was maintained using propofol infusion. The operative bed was irrigated with normal saline under pressure after ETV, which immediately resulted in sinus tachycardia intra-operatively and central neurogenic hyperventilation (CNH) with respiratory alkalosis and transient lactic acidosis an hour after the surgery. Only few case reports have been reported in adults with CNH and respiratory alkalosis. Hyperventilation resulting in lactic acidosis is a well-known entity but lactic acidosis following CNH due to transient hypothalamic dysfunction after endoscopic third ventriculostomy has not been reported previously. Our patient was managed with benzodiazepines and oxygen delivered by a rebreathing mask, which resulted in complete recovery within 12 hours. This case highlights the importance of ICP measurement and monitoring and assessment of the type, volume and pressure of fluid used for brain irrigation during ETV, to prevent complications. ETV may cause intra-operative hemodynamic disturbances such as tachycardia, hypertension and hyperthermia followed by post-operative transient hypothalamic dysfunction and CSF acidosis leading to sequelae of CNH with acute respiratory alkalosis and transient lactic acidosis. We emphasize the importance of ICP monitoring during neuroendoscopic procedures, as an inadvertant rise in ICP appears to be the central factor leading to the various ill effects encountered both intra and post-operatively. Moreover, although normal saline has been the irrigation fluid of choice for neurosurgeons, a multitude of laboratory studies suggest it being less ideal and it might be prudent to look into alternatives, namely artificial CSF and Ringer's Lactate.

Comparison of rocuronium bromide and succinylcholine chloride for use during rapid sequence intubation in adult patients

The introduction of endotracheal intubation during First World War and introduction of balanced anaesthesia in 1926, urged the search for a drug which could cause Jaw relaxation to facilitate endotracheal intubation.Succinylcholine chloride introduced in 1951, was a synthetic depolarising muscle relaxant. It fulfilled both of the above requirements and soon became the drug of choice for endotracheal intubation especially in rapid sequence intubation in emergency cases. Because of its adverse effects like hyperkalemia, rise in intragastric, intraocular, intracranial pressures and cardiovascular effects, a quest began for a safer substitute for Succinylcholine chloride. The new non depolarising muscle relaxant drug rocuronium bromide introduced in 1994 became the first competitor for Succinylcholine chloride. Rocuronium bromide when given in two to three times the ED95 dose is said to produce excellent to good intubating conditions in 60 seconds. Further rocuronium bromide is said to be devoid of the adverse effects that are seen with Succinylcholine chloride. Hence the present study was undertaken to evaluate the intubating conditions with rocuronium bromide 1 mg/kg body weight and to compare the intubating conditions with that of Succinylcholine chloride 1.5 mg/kg body weight, for use during rapid sequence intubation in adult patients. Rocuronium bromide 1 mg/kg body weight produces excellent intubating conditions in 96.67% of patients and good to excellent intubating conditions in 100% of patients at 60 seonds with an average clinical duration of action of 49 minute and 10 seonds.

Intracranial Pressure Elevation 24 h after Ischemic Stroke in Aged Rats Is Prevented by Early, Short Hypothermia Treatment.

Stroke is predominantly a senescent disease, yet most preclinical studies investigate treatment in young animals. We recently demonstrated that short-duration hypothermia-treatment completely prevented the dramatic intracranial pressure (ICP) rise seen post-stroke in young rats. Here, our aim was to investigate whether a similar ICP rise occurs in aged rats and to determine whether short-duration hypothermia is an effective treatment in aged animals. Experimental middle cerebral artery occlusion (MCAo-3 h occlusion) was performed on male Wistar rats aged 19–20 months. At 1 h after stroke-onset, rats were randomized to 2.5 h hypothermia-treatment (32.5°C) or normothermia (37°C). ICP was monitored at baseline, for 3.5 h post-occlusion, and at 24 h post-stroke. Infarct and edema volumes were calculated from histology. Baseline pre-stroke ICP was 11.2 ± 3.3 mmHg across all animals. Twenty-four hours post-stroke, ICP was significantly higher in normothermic animals compared to hypothermia-treated animals (27.4 ± 18.2 mmHg vs. 8.0 ± 5.0 mmHg, p = 0.03). Infarct and edema volumes were not significantly different between groups. These data demonstrate ICP may also increase 24 h post-stroke in aged rats, and that short-duration hypothermia treatment has a profound and sustained preventative effect. These findings may have important implications for the use of hypothermia in clinical trials of aged stroke patients.

Intracranial pressure and cerebral perfusion pressure in patients developing brain death

PurposeWe investigated whether a critical rise of intracranial pressure (ICP) leading to a loss of cerebral perfusion pressure (CPP) could serve as a surrogate marker of brain death (BD). Materials and methodsWe retrospectively analyzed ICP and CPP of patients in whom BD was diagnosed (n = 32, 16-79 years). Intracranial pressure and CPP were recorded using parenchymal (n = 27) and ventricular probes (n = 5). Data were analyzed from admission until BD was diagnosed. ResultsIntracranial pressure was severely elevated (mean ± SD, 95.5 ± 9.8 mm Hg) in all patients when BD was diagnosed. In 28 patients, CPP was negative at the time of diagnosis (−8.2 ± 6.5 mm Hg). In 4 patients (12.5%), CPP was reduced but not negative. In these patients, minimal CPP was 4 to 18 mm Hg. In 1 patient, loss of CPP occurred 4 hours before apnea completed the BD syndrome. ConclusionsBrain death was universally preceded by a severe reduction of CPP, supporting loss of cerebral perfusion as a critical step in BD development. Our data show that a negative CPP is neither sufficient nor a prerequisite to diagnose BD. In BD cases with positive CPP, we speculate that arterial blood pressure dropped below a critical closing pressure, thereby causing cessation of cerebral blood flow.

Intracranial Pressure and Collateral Blood Flow.

Leptomeningeal collateral vessels, linking the 3 major arterial territories over the surface of the brain, have been recognized for >140 years.1 More widespread use of advanced clinical imaging in the past decade has led to increasing recognition of the key importance of collaterals in ischemic stroke outcome.2 However, recent studies from several groups indicate that failure of initially good collateral supply is a key feature of patients with delayed infarct expansion.3,4 This clinically challenging problem typically occurs in the first 1 to 2 days after hospital admission in patients with initially mild stroke symptoms. Rethrombosis of reperfused vessels was previously thought to be the likely cause of delayed infarct expansion in most patients. However, this theory is not supported by more recent evidence from imaging studies. Despite the important recent observations, there is limited understanding of the dynamic control of the collateral circulation, in particular, the cause of collateral blood flow failure. In this article, we will discuss recent observations from our experimental stroke model, indicating a dramatic increase in intracranial pressure (ICP) occurring around 24 hours after onset of even small stroke.5,6 We have also shown a significant linear reduction of collateral blood flow in response to progressive ICP elevation.7 We believe that a similar transient ICP elevation occurring during the first 1 to 2 days post stroke is a likely mechanism to explain delayed infarct expansion in patients with minor stroke. Perhaps surprisingly, we can find no published data on ICP at 24 hours in patients with minor stroke. The preclinical findings suggest that gathering such data should be a priority. ### Human Stroke There is a strong association between the extent of leptomeningeal collaterals and clinical stroke outcome. Initial studies using digital subtraction angiography permitted direct visualization of collateral vessels and …

Ischemic penumbra as a trigger for intracranial pressure rise – A potential cause for collateral failure and infarct progression?

We have recently shown that intracranial pressure (ICP) increases dramatically 24 h after minor intraluminal thread occlusion with reperfusion, independent of edema. Some of the largest ICP rises were observed in rats with the smallest final infarcts. A possible alternate mechanism for this ICP rise is an increase of cerebrospinal fluid (CSF) volume secondary to choroid plexus damage (a known complication of the intraluminal stroke model used). Alternatively, submaximal injury may be needed to induce ICP elevation. Therefore, we aimed to determine (a) if choroid plexus damage contributes to the ICP elevation, (b) if varying the patency of an important internal collateral supply to the middle cerebral artery (MCA), the anterior choroidal artery (AChA), produces different volumes of ischemic penumbra and (c) if presence of ischemic penumbra (submaximal injury) is associated with ICP elevation. We found (a) no association between choroid plexus damage and ICP elevation, (b) animals with a good internal collateral supply through the AChA during MCAo had significantly larger penumbra volumes and (c) ICP elevation at ≈24 h post-stroke only occurred in rats with submaximal injury, shown in two different stroke models. We conclude that active cellular processes within the ischemic penumbra may be required for edema-independent ICP elevation.

Dandy Walker syndrome with giant occipital meningocele with craniovertebral anomalies: Challenges faced during anaesthesia.

Sir, The coexistence of rare congenital neurodevelopmental and craniofacial abnormalities make proper positioning for endotracheal intubation difficult and alternative methods of positioning and intubation must be sought for. Although difficult airway cart should be in hand, one must give emphasis on proper positioning of patient. A sound knowledge and proper laryngoscopy by experienced anaesthesiologist results in successful intubation even in cases of anticipated difficult airway and thus, prevents the need of surgical airway. We report a rare case of an 8-month-old child weighing 5 kg with Dandy–Walker syndrome (DWS) associated with a giant occipito-cervical meningocele and craniovertebral anomalies, and posted for shunt surgery. Pre-anaesthetic check-up suggested no history of seizure, vomiting, difficulty in feeding, cyanosis or respiratory distress. There were no cardiac or respiratory signs. Power in all limbs was equal. The child had a large head and a giant occipital cervical meningocele measuring 10 cm × 10 cm, extending from occipital protuberance to mid scapula, causing fixed flexion of the neck [Figure 1]. Magnetic resonance imaging (MRI) of the brain showed enlarged posterior fossa with multiple craniovertebral anomalies with meningocele in occipital and upper cervical region communicating with fourth ventricle, hypoplasia of inferior vermis coupled with hypoplasia of cerebellar hemisphere, suggestive of DWS with occipital meningocele. MRI spine [Figure 2] showed multiple craniovertebral anomalies such as cranial bifida and spina bifida in upper cervical vertebrae coupled with occipito-cervical meningocoele. Figure 1 Extension of occipita cervical swelling along with large head Figure 2 Magnetic resonance imaging spine showing huge occipita cervical meningocele On arrival of the child in the operation theatre, monitoring was established with an electrocardiogram pulse oximeter non-invasive blood pressure (BP) and temperature probe. Baseline parameters included BP of 94/70 mmHg pulse rate of 118/min and oxygen saturation of 100%. Injection glycopyrrolate 0.02 mg intravenous (IV) and injection fentanyl 5 μg was given in the cannula in situ. As there was a large and firm swelling at occipito-cervical region along with flexed neck with no neck movement, supine positioning could not be done in our case. The patient was positioned in the left lateral position with head beyond the edge of the table with an assistant stabilising the head of the baby from below and other supporting the body. After pre-oxygenation with 100% oxygen, injection thiopentone IV was administered in titrated manner, and a total of 20 mg was injected. Check laryngoscopy in lateral position was done with Miller's straight blade one by the senior anaesthesiologist. Laryngoscopy revealed Cormack–Lehane laryngeal view Grade 2. Injection succinylcholine, 10 mg IV was administered and eventually trachea was intubated with no. 3.5 mm uncuffed endotracheal tube. After confirmation of bilateral equal air entry, the endotracheal tube was fixed. Injection atracurium 2.5 mg was given, and anaesthesia was maintained with nitrous oxide-oxygen and sevoflurane (1%). Paracetamol 80 mg suppository was placed for post-operative analgesia. Once the tube was properly fixed, the patient was positioned supine by placing large ring under the head and large cotton roll under shoulder for proper surgical field view. All the pressure points were adequately padded. Intraoperative course was uneventful. After completion of surgery, neuromuscular blockade was reversed with injection neostigmine 0.4 mg and injection glycopyrrolate 0.008 mg. Extubation was performed once the patient became awake. After satisfactory recovery, the patient was shifted to paediatric Intensive Care Unit. DWS although a rare clinical entity with incidence being about 1 in 25000-30000 live births with a slight female predominance.[1,2] It is often associated with other congenital anomalies such as cleft lip, cleft palate, hypertelorism and micrognathia making airway management challenging.[3] Ewart and Oh reported a case of 2 weeks old DWS patient with micrognathia and anterior larynx in whom they found difficulty in awake intubation.[4] Our child was positioned laterally during induction and intubation. An alternative technique such was suggested by Mowafi et al.[5] in which child was placed supine in silicon platform so that height of silicon platform equals the size of the sac. We did not go for this technique as the occipital swelling was extending until mid-scapula, making positioning more difficult. Other major concern in patients of DWS is avoidance of further rise in intracranial pressure (ICP). Endotracheal intubation should be as gentle as possible. Inhalational agent causes a dose-dependent rise in intracranial pressure and so better avoided. However, it has been shown that isoflurane and sevoflurane in <1 MAC concentration do not cause a significant rise in ICP.[6] In conclusion, patients with DWS with other associated anomalies can be successfully managed by a thorough evaluation of airway, emphasis on proper positioning during laryngoscopy, preparation for difficult intubation, avoidance of rise in ICP during anaesthesia and proper post-operative care. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.

Improved Neurological Outcome With Mild Hypothermia in Surviving Patients With Massive Cerebral Hemispheric Infarction

We conducted this randomized controlled trial to investigate the effects of therapeutic hypothermia on mortality and neurological outcome in patients with massive cerebral hemispheric infarction. Patients within 48 hours of symptom onset were randomized to either a hypothermia group or a control group. Patients in the hypothermia group were given standard medical treatment plus endovascular hypothermia with a target temperature of 33 or 34°C. Hypothermia was maintained for a minimum of 24 hours. Patients in the control group were given standard medical treatment only with a target temperature of normothermia. The primary end points were mortality and the modified Rankin Scale score at 6 months. There were 16 patients in the hypothermia group and 17 patients in the control group. At 6 months, 8 patients had died in the hypothermia group versus 7 patients in the control group (P=0.732). The main cause of death was fatal herniation caused by a pronounced rise in intracranial pressure. Seven patients (43.8%) had a modified Rankin Scale of 1 to 3 in the hypothermia group versus 4 patients (23.5%) in the control group (P=0.282). Additionally, of the survivors, patients in the hypothermia group achieved better neurological outcomes compared with those in the control group (7/8, 87.5% versus 4/10, 40.0%; P=0.066; odds ratio=10.5; 95% confidence interval, 0.9-121.4). Mild hypothermia seems to not reduce mortality in patients with massive cerebral hemispheric infarction but may improve the neurological outcome in survivors. An adequately powered multicenter randomized controlled trial seems warranted. URL: http://www.chictr.org.cn. Unique identifier: ChiCTR-TCS-12002680.

Gasless laparoscopy in patients with prior ventriculoperitoneal shunt: yet another option!

Anaesthetic management of patients with ventriculoperitoneal shunt (VPS) undergoing laparoscopic surgeries remains controversial for its safety concerns. At present, no standardized protocol exists for managing these patients during perioperative period. The prime concerns are the rise in intracranial pressure (ICP) and shunt dysfunction due to carbon dioxide insufflation. Anaesthetic considerations in these patients should focus primarily on the intrinsic characteristics and functioning of the VP shunt, the insufflation pressures for pneumoperitoneum creation and techniques to monitor the function of shunt. Gasless laparoscopy may be an option by warding off the complications associated with pneumoperitoneum. In our institution, surgeon improvises the laparoscopic technique to create a gasless condition. We discuss the anaesthetic concerns and considerations in this subset of patients for laparoscopy surgeries.Bangladesh Journal of Medical Science Vol.14(4) 2015 p.420-421

Pathogenesis of optic disc edema in raised intracranial pressure.

Optic disc edema in raised intracranial pressure was first described in 1853. Ever since, there has been a plethora of controversial hypotheses to explain its pathogenesis. I have explored the subject comprehensively by doing basic, experimental and clinical studies. My objective was to investigate the fundamentals of the subject, to test the validity of the previous theories, and finally, based on all these studies, to find a logical explanation for the pathogenesis. My studies included the following issues pertinent to the pathogenesis of optic disc edema in raised intracranial pressure: the anatomy and blood supply of the optic nerve, the roles of the sheath of the optic nerve, of the centripetal flow of fluids along the optic nerve, of compression of the central retinal vein, and of acute intracranial hypertension and its associated effects. I found that, contrary to some previous claims, an acute rise of intracranial pressure was not quickly followed by production of optic disc edema. Then, in rhesus monkeys, I produced experimentally chronic intracranial hypertension by slowly increasing in size space-occupying lesions, in different parts of the brain. Those produced raised cerebrospinal fluid pressure (CSFP) and optic disc edema, identical to those seen in patients with elevated CSFP. Having achieved that, I investigated various aspects of optic disc edema by ophthalmoscopy, stereoscopic color fundus photography and fluorescein fundus angiography, and light microscopic, electron microscopic, horseradish peroxidase and axoplasmic transport studies, and evaluated the effect of opening the sheath of the optic nerve on the optic disc edema. This latter study showed that opening the sheath resulted in resolution of optic disc edema on the side of the sheath fenestration, in spite of high intracranial CSFP, proving that a rise of CSFP in the sheath was the essential pre-requisite for the development of optic disc edema. I also investigated optic disc edema with raised CSFP in patients, by evaluating optic disc and fundus changes by stereoscopic fundus photography and fluorescein fundus angiography. Based on the combined information from all the studies discussed above, it is clear that the pathogenesis of optic disc edema in raised intracranial pressure is a mechanical phenomenon. It is primarily due to a rise of CSFP in the optic nerve sheath, which produces axoplasmic flow stasis in the optic nerve fibers in the surface nerve fiber layer and prelaminar region of the optic nerve head. Axoplasmic flow stasis then results in swelling of the nerve fibers, and consequently of the optic disc. Swelling of the nerve fibers and of the optic disc secondarily compresses the fine, low-pressure venules in that region, resulting in venous stasis and fluid leakage; that leads to the accumulation of extracellular fluid. Contrary to the previous theories, the various vascular changes seen in optic disc edema are secondary and not primary. Thus, optic disc edema in raised CSFP is due to a combination of swollen nerve fibers and the accumulation of extracellular fluid. My studies also provided information about the pathogeneses of visual disturbances in raised intracranial pressure.

Human Albumin Improves Long-Term Behavioral Sequelae After Subarachnoid Hemorrhage Through Neurovascular Remodeling.

Subarachnoid hemorrhage results in significant long-lasting neurologic sequelae. Here, we investigated whether human albumin improves long-term outcomes in experimental subarachnoid hemorrhage and whether neurovascular remodeling is involved in the protection of albumin. Laboratory investigation. Hospital research laboratory. Male Sprague-Dawley rats. Rats underwent subarachnoid hemorrhage by endovascular perforation. Albumin of either 0.63 or 1.25 g/kg was injected IV immediately after the surgery. Modified Garcia test, beam-walking test, novel object recognition, and Morris water maze were employed to determine the behavioral deficits. The effects of albumin on early neurovascular dysfunction and chronic synaptic plasticity were also studied. Both doses of albumin significantly improved the sensorimotor scores (F = 31.277; p = 0.001) and cognitive performance (F = 7.982; p = 0.001 in novel object recognition test; and F = 3.431; p = 0.026 in the latency analysis of Morris water maze test) for at least 40 days after subarachnoid hemorrhage. There were remarkable microvasculature hypoperfusion, intracranial pressure rise, early vasoconstriction, neural apoptosis, and degeneration in subarachnoid hemorrhage rats, with albumin significantly attenuating such neurovascular dysfunction. Furthermore, albumin markedly prevented blood-brain barrier disruption, as indicated by less blood-brain barrier leakage, preserved blood-brain barrier-related proteins, and dampened gelatinase activities. The expressions of key synaptic elements were up-regulated with albumin supplementation in both acute and chronic phases. Accordingly, a higher dendritic spine density was observed in the prefrontal and hippocampal areas of albumin-treated subarachnoid hemorrhage animals. Albumin at low-to-moderate doses markedly improves long-term neurobehavioral sequelae after subarachnoid hemorrhage, which may involve an integrated process of neurovascular remodeling.

Anesthetic management of pediatric patients with Sturge-Weber syndrome: our experience and a review of the literature.

Sturge-Weber syndrome (SWS) is a rare sporadic congenital neurocutaneous syndrome which is characterized by vascular malformation involving the brain, face and eye. The anesthetic management is complicated by its localized as well as systemic manifestations, associated anomalies and difficult airway due to the presence of angiomas of the oral cavity and airway. We retrospective analyzed the perioperative anesthetic management of children with SWS undergoing ophthalmic surgery and reviewed the literature. Medical records and anesthetic charts of all the children with SWS who had undergone an ophthalmic procedure under general anesthesia during the past 6 years were reviewed. Information related to the demographic profile, preoperative evaluation, anesthetic techniques, and perioperative complications were collected and analyzed. Forty children with SWS received general anesthesia for an ophthalmic procedure within the 6-year period. The median age of the children was 3 years. 30 (92.5%) children had facial port-wine staining, 10 (25%) had facial hypertrophy, 15 (37.5%) had a history of convulsion and 4 (10%) children had mental retardation. Inhalational induction was performed in 34 (85%) children (sevoflurane 82.8%). A laryngeal mask airway (LMA) and endotracheal tube were used in 32 (80%) and 5 (12.5%) cases, respectively. One patient had difficult mask ventilation and difficult LMA insertion. There was no significant problem in any of the other children. Preoperative evaluation with airway assessment should be performed with the knowledge of local and systemic manifestation of the syndrome. Proconvulsant and anticonvulsant properties of the anesthetics, as well as drug interactions of antiepileptic medications should be considered when planning anesthesia. Avoiding a rise in intracranial and intraocular pressures, vigilant intraoperative monitoring and postoperative care are the key for conducting safe anesthesia in these children. For ophthalmic procedures, LMAs can be used for airway maintenance with minimal complications in children with SWS.

Principles of cerebral hemodynamics when intracranial pressure is raised: lessons from the peripheral circulation.

Background: The brain is highly vascular and richly perfused, and dependent on continuous flow for normal function. Although confined within the skull, pressure within the brain is usually less than 15 mmHg, and shows small pulsations related to arterial pulse under normal circumstances. Pulsatile arterial hemodynamics in the brain have been studied before, but are still inadequately understood, especially during changes of intracranial pressure (ICP) after head injury.Method: In seeking cohesive explanations, we measured ICP and radial artery pressure (RAP) invasively with high-fidelity manometer systems, together with middle cerebral artery flow velocity (MCAFV) (transcranial Doppler) and central aortic pressure (CAP) generated from RAP, using a generalized transfer function technique, in eight young unconscious, ventilated adults following closed head trauma. We focused on vascular effects of spontaneous rises of ICP (‘plateau waves’).Results: A rise in mean ICP from 29 to 53 mmHg caused no consistent change in pressure outside the cranium, or in heart rate, but ICP pulsations increased in amplitude from 8 to 20 mmHg, and ICP waveform came to resemble that in the aorta. Cerebral perfusion pressure (=central aortic pressure – ICP), which equates with transmural pressure, fell from 61 to 36 mmHg. Mean MCAFV fell from 53 to 40 cm/s, whereas pulsatile MCAFV increased from 77 to 98 cm/s. These significant changes (all P < 0.01) may be explained using the Monro–Kellie doctrine, because of compression of the brain, as occurs in a limb when external pressure is applied.Conclusion: The findings emphasize importance of reducing ICP, when raised, and on the additional benefits of reducing wave reflection from the lower body.