Optimization Of Cerebral Perfusion Pressure Research Articles

Basic principle in the management of brain edema and elevated intracranial pressure

Background: Brain edema is a well-recognized pathophysiological secondary change after primary brain injury. The mechanism of brain edema may differ based on the types of brain edema. However, numerous ion channels are involved in its development and are therefore currently a hot target for anti-edema therapy. Here, this paper reviews the clinically important differences among the types of brain edema and a step-wise management strategy for brain edema and elevated intracranial pressure (ICP).Current Concepts: Brain edema can be classified as cytotoxic, ionic, vasogenic, and interstitial edema. Although the underlying mechanisms may differ among the various types of brain edema, multiple ion channels and the integrity of tight junctions are associated with the development of brain edema. If brain edema aggravates, the intracranial volume expands and leads to an elevation of ICP. A basic principle in the management of ICP includes proper positioning, screening for a need for extraventricular drainage, proper sedation, transient hyperventilation, assessing the intracranial water status with the serum sodium level, optimization of cerebral perfusion pressure, hyperosmolar therapy, targeted temperature management, and induction of a pharmacological coma with sedatives.Discussion and Conclusion: Stepwise treatment strategies are recommended in the management of patients with ICP crisis. Based on the principle, detailed management plans need to be adjusted based on the status of an individual patient.

THE THE EFFECT OF BOWEL MASSAGE ON BODY NOISE FREQUENCY IN POST TREPANATION PATIENTS

Trepanation is one of the most serious and soul-critical traumas. The main goal of anesthetic management for patients with brain injury is optimization of cerebral perfusion pressure and brain oxygenation. As a result of anesthetic drugs reduce peristalsis in the large intestine and small intestine. Bowel massage is a mechanism of action to reduce contractions and tension in the abdominal muscles, increase motility in the digestive system, increase secretions in the intestinal system and have an effect on sphincter relaxation so that this mechanism of action will facilitate and facilitate expulsion of feces. The universal aim of this research is to identify the comparison of bowel sounds frequency in post trepanation patients between being treated and not being treated in the ICU room at RSUD dr. Saiful Anwar Malang. This study uses a quantitative approach with a Quasi Experimental design with a Non Equivalent Control Group Design approach. The sampling technique used in this research is accidental sampling. Linear regression test between time and bowel sounds in the treatment group obtained a p value of 0.048 (p <0.05), it can be concluded that time has a significant effect on bowel sounds in the treatment group. Test the difference in bowel bissing between the control group with the Mann Whitney test at 3 different times. The p value is (p < 0.05), meaning that there is a difference in bowel sounds after bowel massage.

Neurocritical care management of poor-grade subarachnoid hemorrhage: Unjustified nihilism to reasonable optimism.

Historically, overall outcomes for patients with high-grade subarachnoid hemorrhage (SAH) have been poor. Generally, between physicians, either reluctance to treat, or selectivity in treating such patients has been the paradigm. Recent studies have shown that early and aggressive care leads to significant improvement in survival rates and favorable outcomes of grade V SAH patients. With advancements in both neurocritical care and end-of-life care, non-treatment or selective treatment of grade V SAH patients is rarely justified. Current paradigm shifts towards early and aggressive care in such cases may lead to improved outcomes for many more patients. We performed a detailed review of the current literature regarding neurointensive management strategies in high-grade SAH, discussing multiple aspects. We discussed the neurointensive care management protocols for grade V SAH patients. Acutely, intracranial pressure control is of utmost importance with external ventricular drain placement, sedation, optimization of cerebral perfusion pressure, osmotherapy and hyperventilation, as well as cardiopulmonary support through management of hypotension and hypertension. Advancements of care in SAH patients make it unethical to deny treatment to poor Hunt and Hess grade patients. Early and aggressive treatment results in a significant improvement in survival rate and favorable outcome in such patients.

Transcranial Doppler Waveforms During Intra-aortic Balloon Pump Counterpulsation for Vasospasm Detection After Subarachnoid Hemorrhage.

Transcranial Doppler ultrasound is a standard screening tool for vasospasm after subarachnoid hemorrhage. Prevention of vasospasm-induced delayed cerebral ischemia after subarachnoid hemorrhage depends on optimization of cerebral perfusion pressure, which can be challenged by neurogenic stress cardiomyopathy. Intra-aortic balloon pumps have been utilized to augment cerebral perfusion, but they change the transcranial Doppler waveform, altering its interpretability for vasospasm screening. To assess the features of the transcranial Doppler waveform that correlate with vasospasm. We retrospectively reviewed cases of subarachnoid hemorrhage that underwent same-day transcranial Doppler ultrasound and angiography. Transcranial Doppler waveforms were assessed for mean velocity, peak systolic velocity, balloon pump-augmented diastolic velocity, and a novel feature, "delta velocity" (balloon pump-augmented velocity - systolic velocity). Relationship of flow velocity features to vasospasm was estimated by generalized estimating equation models using a Gaussian distribution and an exchangeable correlation structure. There were 31 transcranial Doppler and angiography pairings (12 CT angiography/19 digital subtraction angiography) from 4 patients. Fourteen pairings had proximal vasospasm by angiography. Delta velocity was associated with proximal vasospasm (coefficient -6.8 [95% CI -9.8 to -3.8], P<.001). There was no significant correlation with proximal vasospasm for mean velocity (coefficient -13.0 [95% CI -29.3 to 3.4], P=.12), systolic velocity (coefficient -8.7 [95% CI -24.8 to 7.3], P=.29), or balloon pump-augmented velocity (coefficient -15.3 [95% CI -31.3 to 0.71], P=.06). Delta velocity, a novel transcranial Doppler flow velocity feature, may reflect vasospasm in patients with subarachnoid hemorrhage and intra-aortic balloon pumps.

Cerebral Microdialysis Monitoring to Improve Individualized Neurointensive Care Therapy: An Update of Recent Clinical Data.

Cerebral microdialysis (CMD) allows bedside semicontinuous monitoring of patient brain extracellular fluid. Clinical indications of CMD monitoring are focused on the management of secondary cerebral and systemic insults in acute brain injury (ABI) patients [mainly, traumatic brain injury (TBI), subarachnoid hemorrhage, and intracerebral hemorrhage (ICH)], specifically to tailor several routine interventions—such as optimization of cerebral perfusion pressure, blood transfusion, glycemic control and oxygen therapy—in the individual patient. Using CMD as clinical research tool has greatly contributed to identify and better understand important post-injury mechanisms—such as energy dysfunction, posttraumatic glycolysis, post-aneurysmal early brain injury, cortical spreading depressions, and subclinical seizures. Main CMD metabolites (namely, lactate/pyruvate ratio, and glucose) can be used to monitor the brain response to specific interventions, to assess the extent of injury, and to inform about prognosis. Recent consensus statements have provided guidelines and recommendations for CMD monitoring in neurocritical care. Here, we summarize recent clinical investigation conducted in ABI patients, specifically focusing on the role of CMD to guide individualized intensive care therapy and to improve our understanding of the complex disease mechanisms occurring in the immediate phase following ABI. Promising brain biomarkers will also be described.

ABSTRACT 383

Background and aims: Urgent craniotomy is often indicated in pediatric patients due to traumatic brain injury and occasionally for arterio-venous malformation and brain abscess. Aims: To discuss the perioperative management of urgent craniotomy in pediatric patients. Methods: Experience of our institute as well as the recently published articles in the same field. Results: Urgent craniotomy is indicated mainly to evacuate extra- or subdural hematoma causing intra-cranial mass effects. Less common indications include brain abscess and decompression after bleeding form AVM. The main perioperative goal is optimization of cerebral perfusion pressure (CPP), prevention and early management of secondary brain injury. Secondary brain injury may result from hypotension, hypovolemia, hypoxia, fever, high intra-cranial pressure (ICP), anemia, hypo- or hyperglycemia, acidosis and seizure. ICP should be monitored in patients with severe brain injury, CPP should be maintained according to the age (usually 40 -50 mmHg). Hyperosmolar therapy may be used if indicated. Hypothermia may be used in patients with TBI within 8 hours. Arterial carbon dioxide pressure should maintained within normal range and Prophylactic hyperventilation should be not be used. High ICP is managed initially with medical measures, but if it is failed or the patient has early signs of herniation decompression craniectomy should be done. Conclusions: The main therapeutic goals are limitation the effects of primary injury, prevention and aggressive management of factors which may cause secondary brain injury. Medical treatment of high ICP and maintenance of CPP are paramount. Early surgical intervention may limits the adverse effects of high ICP and mass occupying lesions.

Critical care for patients with massive ischemic stroke.

Malignant cerebral edema following ischemic stroke is life threatening, as it can cause inadequate blood flow and perfusion leading to irreversible tissue hypoxia and metabolic crisis. Increased intracranial pressure and brain shift can cause herniation syndrome and finally brain death. Multiple randomized clinical trials have shown that preemptive decompressive hemicraniectomy effectively reduces mortality and morbidity in patients with malignant middle cerebral artery infarction. Another life-saving decompressive surgery is suboccipital craniectomy for patients with brainstem compression by edematous cerebellar infarction. In addition to decompressive surgery, cerebrospinal fluid drainage by ventriculostomy should be considered for patients with acute hydrocephalus following stroke. Medical treatment begins with sedation, analgesia, and general measures including ventilatory support, head elevation, maintaining a neutral neck position, and avoiding conditions associated with intracranial hypertension. Optimization of cerebral perfusion pressure and reduction of intracranial pressure should always be pursued simultaneously. Osmotherapy with mannitol is the standard treatment for intracranial hypertension, but hypertonic saline is also an effective alternative. Therapeutic hypothermia may also be considered for treatment of brain edema and intracranial hypertension, but its neuroprotective effects have not been demonstrated in stroke. Barbiturate coma therapy has been used to reduce metabolic demand, but has become less popular because of its systemic adverse effects. Furthermore, general medical care is critical because of the complex interactions between the brain and other organ systems. Some challenging aspects of critical care, including ventilator support, sedation and analgesia, and performing neurological examinations in the setting of a minimal stimulation protocol, are addressed in this review.

Optimal cerebral perfusion pressure: are we ready for it?

Objectives: Cerebral perfusion pressure (CPP)-oriented therapy and the Lund concept lie on opposite ends of the CPP scale, in the management of head injury. Optimization of CPP by monitoring cerebral vascular pressure reactivity is an alternative approach that may reconcile these two divergent approaches, preventing both injurious hypotension and hypertension with an individualized CPP target.Methods: Indices describing cerebral vascular reactivity or cerebral blood flow autoregulation, derived from intracranial pressure, near-infrared spectroscopy, or transcranial Doppler are reviewed in this manuscript.Results: Indices of cerebrovascular reactivity and autoregulation typically converge to a U-shape curve when viewed as a function of CPP, with the best reactivity metrics indicating optimal CPP. In a retrospective study of prospectively collected data from head-injured patients, Steiner et al. demonstrated that a greater distance between averaged over total monitoring time-CPP and optimal CPP, correlated with unfavourable outcome. A recent study of 300 head-injured patients (2003–2009) showed that hypotension below optimal CPP was associated with greater mortality rate, while hypertension above optimal CPP was associated with an increase in severe disability.Discussion: Pilot studies indicating feasibility of autoregulation-oriented CPP optimization have been performed in adult and paediatric traumatic brain injury, aneurysmal subarachnoid haemorrhage, and in patients undergoing cardiothoracic surgery. It remains to be prospectively demonstrated whether optimal CPP management is able to improve outcome.

Static Autoregulation Is Intact Early After Severe Unilateral Brain Injury in a Neonatal Swine Model

Autoregulation is impaired by traumatic brain injury. Cerebral blood flow disturbances are spatially heterogeneous, but autoregulation is often reported as a global metric. We tested lateralization of autoregulatory responses in the neonatal piglet brain during hypotension early after unilateral injury. Neonatal piglets (5-7 days old) had controlled cortical impact (severe, n = 12; moderate, n = 13; sham, n = 13) and recovery for 6 hours. The lower limit of autoregulation (LLA) and static rate of autoregulation (SRoR) were determined for each subject and compared among groups and between the ipsilateral and contralateral hemispheres. The LLA was not increased by injury (sham, 34 mm Hg [29-39 mm Hg]; moderate injury, 37 mm Hg [33-41 mm Hg]; severe injury, 35 mm Hg [32-38 mm Hg]; P = .93, mean [95% confidence interval]). SRoR, when measured ipsilateral to injury and above the LLA, showed intact autoregulation and was not lower than SRoR in uninjured subjects (sham, 0.82 [0.53-1.1]; moderate injury, 1.0 [0.60-1.5]; severe, 0.91 [0.33-1.5]; P = .44). The average hemispheric LLA difference was 2.7 mm Hg, (95% limits of agreement, -7.5 to 7.0; bias, -0.25; Spearman r = 0.73; P < .0001). Ipsilateral and contralateral SRoR measurements also showed correlation in the injured groups (Spearman r = 0.85, P < .0001). LLA was not increased by controlled cortical impact, nor did SRoR measurements demonstrate ineffective autoregulation when cerebral perfusion pressure was greater than and within 10 mm Hg of the LLA. Cerebral perfusion pressure optimization, indicated by autoregulation measurements, was significantly similar in the 2 hemispheres despite severe unilateral injury.

Critical care of poor-grade subarachnoid hemorrhage

Early aggressive treatment of poor-grade subarachnoid hemorrhage patients has resulted in more favorable long-term outcomes. This article covers the aspects of neurocritical care management directed to the patient with poor-grade subarachnoid hemorrhage (Hunt and Hess 4 and 5) and outlines important prognostic features. Immediate cardiopulmonary and neurological support, early aneurysm repair, neuromodality and multimodality monitoring under the care of neurointensivists, treatment of medical complications, prevention and appropriate management of delayed cerebral ischemia have improved long-term outcomes after poor-grade subarachnoid hemorrhage. This includes control of intracranial hypertension, optimization of cerebral perfusion pressure and cardiac hemodynamics, correction of electrolyte abnormalities, and management of complications. Global cerebral edema, acute ischemic injury seen on diffusion-weighted imaging, and early vasospasm are disease states in the poor-grade patients that require attention and further investigation. Monitoring techniques such as surface and intracortical continuous electroencephalography, brain tissue oxygen monitoring, and microdialysis may detect secondary brain injury in a potentially reversible state. Poor-grade subarachnoid hemorrhage patients have the potential to recover and should therefore be fully resuscitated and treated aggressively with the available standards and monitoring techniques.

Effects of cerebrovascular pressure reactivity-guided optimization of cerebral perfusion pressure on brain tissue oxygenation after traumatic brain injury*

To evaluate the concept of a cerebrovascular pressure reactivity-guided optimal cerebral perfusion pressure after traumatic brain injury by analyzing the relationship between optimal cerebral perfusion pressure and brain tissue oxygen. Prospective observational cohort study. Neurosurgical intensive care unit of a university hospital. Thirty-eight patients after head injury. Continuous computerized monitoring of mean arterial pressure, intracranial pressure, and brain tissue oxygen for 5.3 +/- 2.6 days. The index of cerebrovascular pressure reactivity was calculated as a moving correlation coefficient between spontaneous low-frequency fluctuations of mean arterial pressure and intracranial pressure. Optimal cerebral perfusion pressure was defined as the cerebral perfusion pressure level with the lowest average index of cerebrovascular pressure reactivity. Optimal cerebral perfusion pressure could be identified in 32 of 38 patients. Median optimal cerebral perfusion pressure was between 70 and 75 mm Hg (range, 60-100 mm Hg). Below the level of optimal cerebral perfusion pressure, brain tissue oxygen decreased in parallel to cerebral perfusion pressure, whereas brain tissue oxygen reached a plateau above optimal cerebral perfusion pressure. Optimal cerebral perfusion pressure correlated significantly with the cerebral perfusion pressure level, where brain tissue oxygen reached its plateau (r = .79; p < .01). Average brain tissue oxygen at optimal cerebral perfusion pressure was 24.5 +/- 6.0 mm Hg. This study supports the concept of cerebrovascular pressure reactivity-based individual optimal cerebral perfusion pressure. Driving cerebral perfusion pressure in excess of optimal cerebral perfusion pressure does not yield improvements in brain tissue oxygen after head injury and should be avoided, whereas cerebral perfusion pressure below optimal cerebral perfusion pressure may result in secondary cerebral ischemia.

Intracerebral hemorrhage: getting ready for effective treatments

Spontaneous intracerebral hemorrhage (ICH) is the most devastating type of stroke and a leading cause of disability and mortality in the United States and the rest of the world. The purpose of this article is to review recent advances in the management of spontaneous intracerebral hemorrhage. Although no interventions have consistently shown an improvement of mortality or functional outcomes after ICH, results from multicenter prospective randomized controlled trials have shown that early hemostasis to prevent hematoma growth, removal of clot by surgical or minimally invasive interventions, clearance of intraventricular hemorrhage, and adequate blood pressure control for the optimization of cerebral perfusion pressure may constitute the most important therapeutic goals to ameliorate secondary neurological damage, decrease mortality, and improve functional outcomes after ICH. Several promising methods may be ready for routine clinical use in a few years to decrease disability and mortality from ICH.

Management of Patients with Fulminant Hepatic Failure and Brain Edema

Cerebral edema in acute liver failure is associated with a poor prognosis. Optimization of cerebral perfusion pressure and blood flow plays a key role in contemporary management of these patients. However, understanding of the pathophysiology of brain edema is required for optimal patient management. This review explains the relationships between cerebral perfusion and edema and summarizes therapies that are currently used in patients with acute liver failure to prevent and reduce intracranial pressure.

New therapies for intracranial hypertension

The main concepts involved in the therapeutic management of intracranial hypertension are revisited, including pathophysiology, monitoring, the traditional approach, and also the presentation of recently proposed therapies. The main medical literature data bases (especially Medline and Lilacs) were searched for articles published in the last 10 years, and traditional text books and dissertations focusing the subject were consulted. Intracranial hypertension may be associated with several cerebral neurologic lesions from traumatic, infectious or metabolic origin, and in severe cases may represent an important factor for morbidity and mortality. Increases in intracranial pressure interfere with cerebral blood flow; in order to maintain an adequate cerebral perfusion pressure, it is necessary to both reduce and control intracranial hypertension and combat low blood pressure from the very beginning of treatment. Adequate monitoring is essential, and the main points addressed in conventional management include elevation of the head of bed to 30 degrees C, central positioning of the head, optimization of hypocapnia, perfect metabolic and hydro-electrolyte balance, sedation, anti-convulsive therapy, liquor drainage, and the use of barbiturics, mannitol and furosemide. New therapies currently under investigation include the use of dexanabinol, hypertonic saline solutions, moderate hypothermia, decompressive craniectomy, optimization of cerebral perfusion pressure, and reduction in cerebral microvasculature pressure (Lund therapy). The use of new therapies to effectively control intracranial hypertension, especially in cases that are refractory to the usual treatment, represent a promising scenario in the management of this problem.

CURRENT TRENDS IN THE MANAGEMENT OF HEAD INJURY

The importance of cerebral perfusion pressure (CPP) optimization has been recognized in the neurosurgical community in the United States as part of the recently published Guidelines for Management of Severe Head Injury. Although further basic and clinical research is needed before a CPP-directed head injury management standard of care is formulated, optimization of CPP is practical with present personnel and equipment resources in many emergency departments. Emergency Department physicians should be familiar with CPP management principles to facilitate interactions with neurosurgical colleagues and improve patient outcomes.

MANAGEMENT OF COMPLICATED NEUROLOGIC INJURIES

Despite measures based on the Monro-Kellie principles for ICP reduction and optimization of cerebral perfusion pressure, the outcome from complicated neurologic injuries remains unsatisfactory. Many patients are "pulled through" the acute event only to remain minimally functional or vegetative for the remainder of their lives. Pharmacologic interventions to protect the brain against the toxic and metabolic consequences of neurologic injury seem to be the future of neurotrauma.