Intracranial pressure

Microvascular shunts in the pathogenesis of high intracranial pressure

Authors: Nemoto EM, Bragin D, Stippler M, Pappu S, Kraynik J, Berlin T, Yonas H.

Hyperemia in the infarcted brain has been -suggested for years by "red veins" reported by neurosurgeons, shunt peaks in radioactive blood flow clearance curves, and quantitative cerebral blood flow using stable xenon CT. Histological characterization of infarcted brain revealed capillary rarefaction with prominent microvascular shunts (MVS). Despite abundant histological evidence, the presence of cerebrovascular shunts have been largely ignored, perhaps because of a lack of physiological evidence demonstrating the transition from capillary flow to MVS flow. Our studies have shown that high intracranial pressure induces a transition from capillary to microvascular shunt flow resulting in cerebral hypoperfusion, tissue hypoxia and brain edema, which could be delayed by increasing cerebral perfusion pressure. The transition from capillary to microvascular shunt flow provides for the first time a physiological basis for evaluating the optimal cerebral perfusion pressure with increased intracranial pressure. It also provides a physiological basis for evaluating the effectiveness of various drugs and therapies in reducing intracranial pressure and the development of brain edema and tissue hypoxia after brain injury and ischemia. In summary, the clear-cut demonstration of the transition from capillary to MVS flow provides an important method for evaluating various therapies for the treatment of brain edema and loss of autoregulation.

Review and recommendations on management of refractory raised intracranial pressure in aneurysmal subarachnoid hemorrhage

Authors: Mak CH, Lu YY, Wong GK.

Intracranial hypertension is commonly encountered in poor-grade aneurysmal subarachnoid hemorrhage patients. Refractory raised intracranial pressure is associated with poor prognosis. The management of raised intracranial pressure is commonly referenced to experiences in traumatic brain injury. However, pathophysiologically, aneurysmal subarachnoid hemorrhage is different from traumatic brain injury. Currently, there is a paucity of consensus on the management of refractory raised intracranial pressure in spontaneous subarachnoid hemorrhage. We discuss in this paper the role of hyperosmolar agents, hypothermia, barbiturates, and decompressive craniectomy in managing raised intracranial pressure refractory to first-line treatment, in which preliminary data supported the use of hypertonic saline and secondary decompressive craniectomy. Future clinical trials should be carried out to delineate better their roles in management of raised intracranial pressure in aneurysmal subarachnoid hemorrhage patients.

Pressure is only part of the story in traumatic brain injured patients; focal cerebral blood flow goes to zero in some patients with adequate cerebral perfusion pressure

Authors: Chovanes G, Richards RM.

INTRODUCTION: The pathophysiology of traumatic brain injury (TBI) is still not clearly understood. Recently, a decompressive craniectomy trial (1) and a trial of intracranial pressure (ICP) treatment with ICP monitoring vs no monitoring (2) failed to support the concept that increases in ICP are exclusively responsible for TBI mortality and morbidity. To analyze the role ICP, cerebral perfusion pressure (CPP = BP-ICP), and cerebral blood flow (CBF) play in head injury, we monitored brain injured patients' ICP, blood pressure (BP), CPP, and focal cerebral blood flow (fCBF), recording the real-time data for computer analysis.
METHODS: 20 patients with severe brain injury were monitored with recordings of ICP, BP, CPP, and fCBF every minute. 17 patients had severe closed TBI, 1 gunshot wound, and 2 intracerebral hemorrhages. 13 patients lived (GCS 3-9, average 5), 7 died (GCS 3-7, average 5). Of the 7 patients who died, 5 had technically adequate recordings before and as death supervened. Graphs were prepared of time vs CPP, ICP and fCBF and reviewed for the time course of fCBF deterioration vs CPP elevation. If CPP obviously and substantially decreased before fCBF decreased, that was termed a pressure death. However, if CPP stayed adequate and fCBF still decreased to zero, that was termed a non-pressure death.
RESULTS: Three patients had a pressure death (Fig 1), and 2 patients had a non-pressure death (Fig 2).
CONCLUSION: This may be the first real-time documentation of non-CPP dependent brain death as expressed by fCBF. There are pathological processes in the injured brain that do not directly involve increases in ICP and decreases in CPP. Heretofore clinical treatment efforts in brain injury have focused on ICP: other mechanisms are also extant and should be further investigated so as to more successfully treat brain injury.

Mathematical Modelling of Near-Infrared Spectroscopy Signals and Intracranial Pressure in Brain-Injured Patients

Authors: Highton D, Panovska-Griffiths J, Smith M, Elwell CE.

Raised intracranial pressure (ICP) is a key concern following acute brain injury as it may be associated with cerebral hypoperfusion and poor outcome. In this research we describe a mathematical physiological model designed to interpret cerebral physiology from neuromonitoring: ICP, near-infrared spectroscopy and transcranial Doppler flow velocity. This aims to characterise the complex dynamics of cerebral compliance, cerebral blood volume, cerebral blood flow and their regulation in individual patients. Analysis of data from six brain-injured patients produces cohesive predictions of cerebral biomechanics suggesting reduced cerebral compliance, reduced volume compensation and impaired blood flow autoregulation. Patient-specific physiological modelling has the potential to predict the key biomechanical and haemodynamic changes following brain injury in individual patients, and might be used to inform individualised treatment strategies.

Beyond intracranial pressure: optimization of cerebral blood flow, oxygen, and substrate delivery after traumatic brain injury

Authors: Bouzat P, Sala N, Payen JF, Oddo M.

Monitoring and management of intracranial pressure (ICP) and cerebral perfusion pressure (CPP) is a standard of care after traumatic brain injury (TBI). However, the pathophysiology of so-called secondary brain injury, i.e., the cascade of potentially deleterious events that occur in the early phase following initial cerebral insult---after TBI, is complex, involving a subtle interplay between cerebral blood flow (CBF), oxygen delivery and utilization, and supply of main cerebral energy substrates (glucose) to the injured brain. Regulation of this interplay depends on the type of injury and may vary individually and over time. In this setting, patient management can be a challenging task, where standard ICP/CPP monitoring may become insufficient to prevent secondary brain injury. Growing clinical evidence demonstrates that so-called multimodal brain monitoring, including brain tissue oxygen (PbtO2), cerebral microdialysis and transcranial Doppler among others, might help to optimize CBF and the delivery of oxygen/energy substrate at the bedside, thereby improving the management of secondary brain injury. Looking beyond ICP and CPP, and applying a multimodal therapeutic approach for the optimization of CBF, oxygen delivery, and brain energy supply may eventually improve overall care of patients with head injury. This review summarizes some of the important pathophysiological determinants of secondary cerebral damage after TBI and discusses novel approaches to optimize CBF and provide adequate oxygen and energy supply to the injured brain using multimodal brain monitoring.

Complications associated with prolonged hypertonic saline therapy in children with elevated intracranial pressure

Authors: Gonda DD, Meltzer HS, Crawford JR, Hilfiker ML, Shellington DK, Peterson BM, Levy ML.

OBJECTIVES: Safe upper limits for therapeutic hypernatremia in the treatment of intracranial hypertension have not been well established. We investigated complications associated with hypernatremia in children who were treated with prolonged infusions of hypertonic saline.
DESIGN: Retrospective chart analysis.
SETTING: PICU in university-affiliated children's hospital.
PATIENTS: All children from 2004 to 2009 requiring intracranial pressure monitoring (external ventricular drain or fiberoptic intraparenchymal monitor) for at least 4 days who were treated with hypertonic saline infusion for elevated intracranial pressure and did not meet exclusion criteria.
INTERVENTION: Continuous hypertonic saline infusion on a sliding scale was used to achieve target sodium levels that would keep intracranial pressure less than 20 mm Hg once the conventional therapies failed.
MEASUREMENTS AND MAIN RESULTS: Eighty-eight children met inclusion criteria. Etiologies of elevated intracranial pressure included trauma (n = 48), ischemic or hemorrhagic stroke (n = 20), infection (n = 8), acute disseminated encephalomyelitis (n = 5), neoplasm (n = 2), and others (n = 5). The mean peak serum sodium was 171.3 mEq/L (range, 150-202). The mean Glasgow Outcome Score was 2.8 (± 1.1) at time of discharge from the hospital. Overall mortality was 15.9%. Children with sustained (> 72 hr) serum sodium levels above 170 mEq/L had a significantly higher occurrence of thrombocytopenia (p < 0.001), renal failure (p < 0.001), neutropenia (p = 0.006), and acute respiratory distress syndrome (p = 0.029) after controlling for variables of age, gender, Pediatric Risk of Mortality score, duration of barbiturate-induced coma, duration of intracranial pressure monitoring, vasopressor requirements, and underlying pathology. Children with sustained serum sodium levels greater than 165 mEq/L had a significantly higher prevalence of anemia (p < 0.001).
CONCLUSIONS: Children treated by continuous hypertonic saline infusion for intracranial hypertension whose serum sodium levels exceeded certain thresholds experienced significantly more events of acute renal failure, thrombocytopenia, neutropenia, anemia, and acute respiratory distress syndrome than those whose sodium level was maintained below these thresholds.

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