Acute Elevation Of Intracranial Pressure Research Articles

Laparoscopic Ovarian Cystectomy in A Patient With Vetriculoperitoneal Shunt: a case report

Ventriculoperitoneal shunt (VPS) is often the best treatment modality for neurologic disorders such as hydrocephalus and pseudotumor cerebri. In recent years, laparoscopic surgery has emerged as a preferred method of accessing and treating a variety of abdominopelvic pathology. Laparoscopic procedures were previously contraindicated in patients of hydrocephalus having a Ventriculoperitoneal (VP) shunt due to shunt obstruction, shunt malfunction, infection and acute elevation of intracranial pressure. Now, conclusive evidence indicating that it is safe to perform laparoscopic surgery in a patient with VP shunt using routine anaesthetic monitoring and without any shunt manipulation. We report a case of successfully performing laparoscopic ovarian cystectomy in a patient with VP shunt.

Intracranial Pressure Influences the Behavior of the Optic Nerve Head.

In this work, the biomechanical responses of the optic nerve head (ONH) to acute elevations in intracranial pressure (ICP) were systematically investigated through numerical modeling. An orthogonal experimental design was developed to quantify the influence of ten input factors that govern the anatomy and material properties of the ONH on the peak maximum principal strain (MPS) in the lamina cribrosa (LC) and postlaminar neural tissue (PLNT). Results showed that the sensitivity of ONH responses to various input factors was region-specific. In the LC, the peak MPS was most strongly dependent on the sclera thickness, LC modulus, and scleral canal size, whereas in the PLNT, the peak MPS was more sensitive to the scleral canal size, neural tissue modulus, and pia mater modulus. The enforcement of clinically relevant ICP in the retro-orbital subarachnoid space influenced the sensitivity analysis. It also induced much larger strains in the PLNT than in the LC. Moreover, acute elevation of ICP leads to dramatic strain distribution changes in the PLNT, but had minimal impact on the LC. This work could help to better understand patient-specific responses, to provide guidance on biomechanical factors resulting in optic nerve diseases, such as glaucoma, papilledema, and ischemic optic neuropathy, and to illuminate the possibilities for exploiting their potential to treat and prevent ONH diseases.

Subarachnoid Hemorrhage (SAH) Triggers Arrest of Cerebral Spinal Fluid (CSF) Circulation

SAH, blood accumulation in subarachnoid space (SS), is caused by rupture of intracranial aneurisms or by TBI. CSF circulating throughout SS and brain parenchyma forms glymphatic pathways for waste removal. We explored alterations to CSF circulation following SAH in C57BL mice at various time after perforation SAH. Fluorescent microspheres (μS, 0.02, 1.0 mm) were injected into the cisterna magna (CM). One hour later, their spread across the brain was monitored using in vivo multiphoton or ex vivo fluorescence microscopy. In naive mice, from CM μS spread to the brain stem, paraarterially along Willis circle, and further along middle cerebral artery and the ventral surface vessels toward the olfactory bulb. Caudally μS spread down the spinal cord. One hour after SAH, μS were confined to the CM and brain stem region limited by the rostral pons border indicating significant CSF flow impairment. The number of μS distributed to the spinal cord was also greatly reduced. Four days post SAH CSF flow remained arrested, indicating long‐lasting CSF flow blockade and its independence from acute elevation of intracranial pressure. In vivo examination of vasculature before and after SAH showed significant vasoconstriction as early as 15 minutes post SAH, and suppression of the slow high amplitude vasomotion. The mitigation of vasomotion, in conjunction with the vasoconstriction may contribute to the CSF flow blockade. Acute and prolonged arrest of CSF flow may play an important role in SAH‐induced brain pathology. Supported by The Ting Tsung and Wei Fong Chao Center for BRAIN, John S Dunn Research Foundation, and the Oden Brain Aneurysm Research Foundation.

Perioperative estimation of the intracranial pressure using the optic nerve sheath diameter during liver transplantation

An elevation of the intracranial pressure (ICP) secondary to cerebral edema is a major contributor to morbidity and mortality in acute liver failure. In addition, invasive ICP monitoring in this setting is controversial because coagulopathy predisposes patients to hemorrhagic complications. In this case report, we describe the novel use of optic nerve sheath diameter monitoring as a noninvasive modality for checking for acute elevations in ICP in this setting. Because of the merits of rapidly evolving ultrasound technologies, this may serve as a safe method for improving patient care in this setting.

Use of Near Infrared Transillumination / Back Scattering Sounding (NIR-T/BSS) to assess effects of elevated intracranial pressure on width of subarachnoid space and cerebrovascular pulsation in animals.

The objective was to assess changes in the width of the subarachnoid space (SAS) and amplitude of cerebrovascular pulsation (CVP) during acute elevation of intracranial pressure (ICP) using Near Infrared Transillumination/Back Scattering Sounding (NIR-T/BSS). Changes in the width of the SAS and amplitude of CVP were observed in rabbits during experimental ICP elevation induced by: (1) quick injections of saline into the subdural space of the spinal cord, and (2) distension of a surgical catheter balloon placed intracranially in the subdural space. The amplitude of CVP was also assessed during acute elevation of blood pressure in the intracranial portion of the internal carotid artery (ICA) induced by adrenaline. Each of the injections of saline caused a transient rise in the width of the SAS and amplitude of CVP. The amplitude of the increase in CVP was dependent on changes in blood pressure in the ICA (r=-0.82, P<0.01). Distension of the intracranial balloon resulted in elimination of the respiratory oscillations in the CVP and increased its systolic-diastolic amplitude. An increase in the amplitude of CVP was evoked by adrenaline without an increase in the carotid blood flow. We demonstrated that during elevation of ICP the amplitude of CVP depends on blood pressure rather than on blood flow in large cerebral vessels. Elimination of the respiratory oscillations by a minute ("sub-critical") ICP increase may be used as an early indicator of rising ICP. The direction of changes recorded using NIR-T/BSS was consistent with changes recorded using tensometric transducers.

Dependence of the optic nerve sheath diameter on acutely applied subarachnoidal pressure - an experimental ultrasound study

To determine the distensibility and elastic characteristics of the optic nerve sheath for development of a basic understanding of ultrasound studies aimed to measure optic nerve sheath diameter (ONSD) for detection of acutely elevated intracranial pressure (ICP). Isolated human optic nerves preparations obtained from autopsies were submitted to predefined pressure alterations, and consecutive changes in ONSD were measured by B-scan ultrasound under defined conditions. Following submission to pressure, the diameter of the nerve sheath increased up to 140% of its baseline value. The increase (mean 1.97 mm, SD 0.52 mm) corresponded to the magnitude of pressure steps measured in the perineural subarachnoidal space (SAS). Similarly, the ONSD declined in each of the preparations within a few minutes after the optic nerve was decompressed. However, it did not reach its baseline value again when pressure loads of 45-55 mmHg or more had been applied. The elasticity of the anterior sheath of the optic nerve is sufficient for the detection of pressure changes in the SAS especially for upward pressure steps. This is basically important for the application of clinical monitoring of the sheath diameter to facilitate the identification of patients with elevated ICP non-invasively (screening). However, further implementation of this procedure in neurointensive care and emergency medicine has to consider that the sheath diameter reversibility may be impaired after episodes of prolonged intracranial hypertension and a model for hysteresis is proposed.

P-007 Initial experience with a combined multi-detector row CT and a biplane angiography suite with a single interactive table for the evaluation and treatment of vascular disease involving the head and neck

Introduction and purposeThe purpose of this study is to present our initial experience with the usefulness of a combined multi-detector row CT and biplane angiographic system with a single interactive...

HYPERTONIC SALINE AND ITS EFFECT ON INTRACRANIAL PRESSURE, CEREBRAL PERFUSION PRESSURE, AND BRAIN TISSUE OXYGEN

Hypertonic saline is emerging as a potentially effective single osmotic agent for control of acute elevations in intracranial pressure (ICP) caused by severe traumatic brain injury. This study examines its effect on ICP, cerebral perfusion pressure (CPP), and brain tissue oxygen tension (PbtO2). Twenty-five consecutive patients with severe traumatic brain injury who were treated with 23.4% NaCl for elevated ICP were evaluated. Bolt catheter probes were placed in the noninjured hemisphere, and hourly ICP, mean arterial pressure, CPP, and PbtO2 values were recorded. Thirty milliliters of 23.4% NaCl was infused over 15 minutes for intracranial hypertension, defined as ICP greater than 20 mm Hg. Twenty-one male patients and 4 female patients aged 16 to 64 years were included. The mean presenting Glasgow Coma Scale score was 5.7. Mean pretreatment values included an ICP level of 25.9 mm Hg and a PbtO2 value of 32 mm Hg. The posttreatment ICP level was decreased by a mean of 8.3 mm Hg (P < 0.0001), and there was an improvement in PbtO2 of 3.1 mm Hg (P < 0.01). ICP of more than 31 mm Hg decreased by 14.2 mm Hg. Pretreatment CPP values of less than 70 mm Hg increased by a mean of 6 mm Hg (P < 0.0001). No complications occurred from this treatment, with the exception of electrolyte and chemistry abnormalities. At 6 months postinjury, the mortality rate was 28%, with 48% of patients achieving a favorable outcome by the dichotomized Glasgow Outcome Scale. Hypertonic saline as a single osmotic agent decreased ICP while improving CPP and PbtO2 in patients with severe traumatic brain injury. Patients with higher baseline ICP and lower CPP levels responded to hypertonic saline more significantly.

The Effect of Etomidate on Intracranial Pressure and Systemic Blood Pressure in Pediatric Patients with Severe Traumatic Brain Injury

To evaluate the effects of single-dose etomidate in pediatric patients with intracranial hypertension after severe traumatic brain injury. Patients admitted to the pediatric intensive care unit with severe traumatic brain injury were enrolled with the informed consent of their guardians. The experimental intervention was a single dose of etomidate 0.3 mg/kg intravenously. This dosage was administered only when enrolled patients had acute elevations of intracranial pressure (ICP) to over 20 mm Hg for over 5 minutes. ICP and mean arterial pressure (MAP) were monitored continuously. ICP and MAP values for 6 consecutive 5-minute intervals after etomidate administration were averaged for all patients and compared with baseline. Eight patients were enrolled. Mean ICP after etomidate administration was significantly lower than baseline ICP for each 5-minute interval (P < 0.05). The mean MAP for all patients increased from baseline during the first 5-minute interval, but this change was not statistically significant. No patient's MAP decreased below baseline at any time point. In pediatric patients with severe traumatic brain injury, single-dose etomidate administration resulted in statistically significant reductions in ICP and improvement in cerebral perfusion pressure without significantly altering MAP.

Interpretation of Approximate Entropy: Analysis of Intracranial Pressure Approximate Entropy During Acute Intracranial Hypertension

We studied changes in intracranial pressure (ICP) complexity, estimated by the approximate entropy (ApEn) of the ICP signal, as subjects progressed from a state of normal ICP (< 20-25 mmHg) to acutely elevated ICP (an ICP "spike" defined as ICP > 25 mmHg for < or = 5 min). We hypothesized that the measures of intracranial pressure (ICP) complexity and irregularity would decrease during acute elevations in ICP. To test this hypothesis we studied ICP spikes in pediatric subjects with severe traumatic brain injury (TBI). We conclude that decreased complexity of ICP coincides with episodes of intracranial hypertension (ICH) in TBI. This suggests that the complex regulatory mechanisms that govern intracranial pressure are disrupted during acute rises in ICP. Furthermore, we carried out a series of experiments where ApEn was used to analyze synthetic signals of different characteristics with the objective of gaining a better understanding of ApEn itself, especially its interpretation in biomedical signal analysis.

Influence of acute elevation of intracranial pressure on duodenal motility activity and mucosal blood flow

Influence of acute elevation of intracranial pressure on duodenal motility activity and mucosal blood flow

The use of hyperventilation in the treatment of plateau waves in two patients with severe traumatic brain injury: contrasting effects on cerebral oxygenation.

We present the case reports of two patients with severe traumatic brain injury who, in the absence of external stimuli, developed episodes of acute elevation of intracranial pressure (plateau waves) associated with jugular bulb oxyhemoglobin (SjO2) desaturation, severe reduction of cerebral tissue PO2 (PbrO2), and deterioration of neurological status. In all of these episodes hyperventilation was successful in extinguishing plateau waves, but in one patient it was associated with an improvement of both the global (increased SjO2) and local (increased PbrO2) cerebral perfusion, while in the other patient it was associated with a reduction of both SjO2 and PbrO2. In both patients the effects of hyperventilation (and other pharmacological treatments) were short-lived; plateau waves reappeared and the patients had to be submitted to decompressive craniotomy (first patient) and cerebrospinal fluid (CSF) drainage (second patient). We conclude that hyperventilation can be useful as a temporary measure to treat plateau waves, but cerebral oxygenation should always be monitored to avoid iatrogenic cerebral ischemia.

Gastroesophageal Reflux in Infants with Hydrocephalus before and after Ventriculo-Peritoneal Shunt Operation

Gastroesophageal reflux (GER) is common in neurologically impaired children, especially those with central nervous system disorders. The cause of GER in these children has not yet been defined, but in animal studies, acute elevation of intracranial pressure (ICP) has been shown to result in a decrease in lower esophageal sphincter pressure. Ten infants with hydrocephalus underwent esophageal pH monitoring prior to and after a ventriculoperitoneal (V-P) shunt operation. A significant degree of reflux was present in 5 patients with hydrocephalus prior to shunt operation and reverted to normal in 2. In the other 3 infants, the degree of reflux decreased as evidenced by fewer abnormal parameters and lower scoring in each of the parameters measured. Our study supports the contention that increased ICP in infants is indeed associated with GER. As 4 of the 5 infants with significant reflux suffered from an Arnold-Chiari malformation, a causal relation between increased ICP due to defects involving the fourth ventricle floor and GER is suggested.

Elevated intracranial pressure stimulates gastric contractility in the rat

The gastric contractile response to elevated intracranial pressure (ICP) was studied in conscious rats. Elevation of intracranial pressure to 20 mm Hg was associated with a marked increase in the amplitude of gastric contractions (70–90% over baseline) without any change in contractile frequency (5.2 ± .5 contractions per min). The increase in contractility continued for 45 min following release of the pressure. Vagotomy completely blocked the increase in gastric contractility seen with elevation in ICP. We conclude that acute elevation of intracranial pressure in rats results in increased force of gastric contractions. The forceful contractions persist despite release of the pressure and the increased contractile force is vagally mediated.

FUNCTION OF KIDNEY GRAFTS FROM BRAIN-DEAD DONOR PIGS

There are conflicting reports about the effects of administration of dopamine to brain-dead donors upon posttransplant organ function. This study compared the survival and serum creatinine levels in pigs that received renal grafts from untreated controls, from controls in which either the donor or donor and recipient received dopamine or from animals rendered brain dead for 16 hr by acute elevation of intracranial pressure, and given standard supportive treatment. In two additional groups, brain-dead donors were given dopamine or dopamine with triiodothyronine. Recipients of grafts from control animals or from brain-dead donors survived the 7-day period of study and showed minimal changes in serum creatinine. Recipients of grafts from brain-dead donors given dopamine however showed reduced survival and progressive increase in serum creatinine. This did not occur in the group given triiodothyronine concurrently with dopamine. It is suggested that if administration of dopamine is essential to treat donor hypotension, concurrent use of triiodothyronine may preserve posttransplant renal function.

Continuous recording of intracranial pressure in the awake, drug-free cat

A simple and quantitatively reliable technique for continuous recording of intracranial pressure in awake, drug-free cats is presented. In addition, behavioral responses to acute elevation of intracranial pressure by slow intraventricular infusion in awake cats are described.

Acute Elevation of Intracranial Pressure Following Transection of Non-functional Spinal Cord

A spinal cord which is neurologically nonfunctional may be functioning as a conduit for CSF between the ventricular system and the spinal subarachnoid space. Interruption of this pathway can have catastrophic consequences unless there is an adequately functioning shunt.

A Pharmacological Analysis of Cushing's Response in Rats

Cushing demonstrated that acute elevation of intracranial pressure (ICP) to levels above the initial mean arterial pressure (MAP) provokes an increase in blood pressure. This effect, now known as the Cushing response, is accompanied by tachycardia. The pressor response during the Cushing reflex is a result of a strong sympathetic discharge. This chapter presents a pharmacological analysis of Cushing's response in rats. The blood pressure response after acute elevation of the intercranial pressure is studied in anaesthetized rats. After establishing an ICP/blood pressure curve, the chapter studies the influence on this response of bilateral vagotomy, with and without atropine pretreatment and that of L(—)propranolol, practolol, phentolamine, piperoxane, clonidine, and hydralazine. The influence of reserpine, 6-hydroxydopamine (6-OHDA), and guanethidine, with or without bilateral adrenalectomy, is studied as well. The results suggest that in order to be able to inhibit a pressor response due to a rise in ICP, both the peripheral sympathetic system and the adrenal medulla should be dysfunctional.

Acute intraoperative intracranial hypertension in neurosurgical patients: mechanical and pharmacologic factors.

Intracranial pressure (ICP) and cardiovascular changes were studied intraoperatively in eight neurosurgical patients undergoing craniotomy. Four patients with preoperative signs of increased ICP had acute elevations in ICP (34–83 torr). These occurred during intubation with thiopental and succinylch

Localization of regions mediating the Cushing response in CNS of cat.

THAT an acute elevation of intracranial pressure results in a rise of the systemic blood pressure and a fall of heart rate has been known for many years. 1-3 In 1902, Cushing 4,5 first demonstrated the quantitative nature of this response, showing that it was graded and occurred when the pressure within the head exceeded that of the systolic blood pressure. Furthermore, the response he observed was reversibly abolished by instilling cocaine into the cisterna magna. Cushing speculated that ischemia of the brain stem was the stimulus for the response and that it was in some manner mediated by the caudal brain stem. Since his report, the vasomotor phenomenon he described has become known as the Cushing reflex. Because the reflex nature of the response has never been clearly established, however, in this paper it will be referred to as the Cushing response. It was never proved by Cushing, nor