Critical Care Management and Monitoring of Intracranial Pressure
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Driving Cerebral Perfusion Pressure with Pressors: How, Which, When?
Driving Cerebral Perfusion Pressure with Pressors: How, Which, When? J. A. MYBURGH Department of Intensive Care Medicine, The St George Hospital, Sydney, NEW SOUTH WALES ABSTRACT In traumatic brain injury, cerebral hypoperfusion is associated with adverse outcome, particularly in the early phases of management. This has resulted in the increased use of drugs such as adrenaline, noradrenaline, dopamine and phenylephrine to augment or maintain systemic blood pressures at near normal levels. This is now part of standard practice and is endorsed by the Brain Trauma Foundation guidelines. It probably matters little which agent is used, provided appropriate monitoring is in place and those reversible causes of hypotension are promptly excluded and treated. However, blindly applying management guidelines to all patients may negate these early benefits. The time has come move away from artificially separated concepts of “intracranial pressure” versus “cerebral perfusion pressure” based strategies. These should be considered in parallel and applied to an individual patient, rather than making the patient fit into an all-encompassing treatment algorithm. A paradigm shift from a “set and forget” philosophy to one of “titration against time” to achieve appropriate therapeutic targets is now required. In this context the rational use of vasoactive agents to optimise cerebral perfusion pressure may be employed. On the basis of limited animal and human evidence, noradrenaline appears to be the most appropriate catecholamine for traumatic brain injury, although definitive, targeted trials are required. (Critical Care and Resuscitation 2005; 7: 200-205) Key words: Cerebral perfusion, inotropic agents, resuscitation, head injury, review The recognition of the importance of defending simplistic. -
DIAGNOSTICS and THERAPY of INCREASED INTRACRANIAL PRESSURE in ISCHEMIC STROKE
DIAGNOSTICS and THERAPY of INCREASED INTRACRANIAL PRESSURE in ISCHEMIC STROKE Erich Schmutzhard INNSBRUCK, AUSTRIA e - mail: erich.schmutzhard@i - med.ac.at Neuro - ICU Innsbruck Conflict of interest : Speaker‘s honoraria from ZOLL Medical and Honoraria for manuscripts from Pfizer Neuro - ICU Innsbruck OUTLINE Introduction Definition: ICP, CPP, PbtiO2, metabolic monitoring, lactate , pyruvate , brain temperature etc Epidemiology of ischemic stroke and ICP elevation in ischemic stroke ACM infarction and the role of collaterals and/ or lack of collaterals for ICP etc Hydrocephalus in posterioir fossa ( mainly cerebellar ) infarction Diagnosis of ICP etc Monitoring of ICP etc Therapeutic management : decompressive craniectomy – meta - analysis of DESTINY HAMLET und co deepening of analgosedation , ventilation , hyperventilation , osmotherapy , CPP - oriented th , MAP management , hypothermia , prophylactic normothermia , external ventricular drainage Neuro - ICU Innsbruck Introduction - Malignant cerebral edema following ischemic stroke is life threatening. - The pathophysiology of brain edema involves failure of the sodium - potassium adenosine triphosphatase pump and disruption of the blood - brain barrier, leading to cytotoxic edema and cellular death. - The Monro - Kellie doctrine clearlc states that - since the brain is encased in a finite space - increased intracranial pressure (ICP) due to cerebral edema can result in herniation through the foramen magnum and openings formed by the falx and tentorium. - Moreover, elevated ICP can cause secondary brain ischemia through decreased cerebral perfusion and blood flow, brain tissue hypoxia, and metabolic crisis. - Direct cerebrovascular compression caused by brain tissue shifting can lead to secondary infarction, especially in the territories of the anterior and posterior cerebral artery. - Tissue shifts can also stretch and tear cerebral vessels, causing intracranial hemorrhage such as Duret’s hemorrhage of the brainstem. -
Stroke Intracranial Hypertension Cerebral Edema Roman Gardlík, MD, Phd
Stroke Intracranial hypertension Cerebral edema Roman Gardlík, MD, PhD. Institute of Pathological Physiology Institute of Molecular Biomedicine [email protected] Books • Silbernagl 356 • Other book 667 Brain • The most complex structure in the body • Anatomically • Functionally • Signals to and from various part of the body are controlled by very specific areas within the brain • Brain is more vulnerable to focal lesions than other organs • Renal infarct does not have a significant effect on kidney function • Brain infarct of the same size can produce complete paralysis on one side of the body Brain • 2% of body weight • Receives 1/6 of resting cardiac output • 20% of oxygen consumption Blood-brain barrier Mechanisms of brain injury • Various causes: • trauma • tumors • stroke • metabolic dysbalance • Common pathways of injury: • Hypoxia • Ischemia • Cerebral edema • Increased intracranial pressure Hypoxia • Deprivation of oxygen with maintained blood flow • Causes: • Exposure to reduced atmospheric pressure • Carbon monoxide poisoning • Severe anemia • Failure to ogygenate blood • Well tolerated, particularly if chronic • Neurons capable of anaerobic metabolism • Euphoria, listlessness, drowsiness, impaired problem solving • Acute and severe hypoxia – unconsciousness and convulsions • Brain anoxia can result to cardiac arrest Ischemia • Reduced blood flow • Focal / global ischemia • Energy sources (glucose and glycogen) are exhausted in 2 to 4 minutes • Cellular ATP stores are depleted in 4 to 5 minutes • 50% - 75% of energy is -
Idiopathic Intracranial Hypertension
IDIOPATHIC INTRACRANIAL HYPERTENSION William L Hills, MD Neuro-ophthalmology Oregon Neurology Associates Affiliated Assistant Professor Ophthalmology and Neurology Casey Eye Institute, OHSU No disclosures CASE - 19 YO WOMAN WITH HEADACHES X 3 MONTHS Headaches frontal PMHx: obesity Worse lying down Meds: takes ibuprofen for headaches Wake from sleep Pulsatile tinnitus x 1 month. Vision blacks out transiently when she bends over or sits down EXAMINATION Vision: 20/20 R eye, 20/25 L eye. Neuro: PERRL, no APD, EOMI, VF full to confrontation. Dilated fundoscopic exam: 360 degree blurring of disc margins in both eyes, absent SVP. Formal visual field testing: Enlargement of the blind spot, generalized constriction both eyes. MRI brain: Lumbar puncture: Posterior flattening of Opening pressure 39 the globes cm H20 Empty sella Normal CSF studies otherwise normal Headache improved after LP IDIOPATHIC INTRACRANIAL HYPERTENSION SYNDROME: Increased intracranial pressure without ventriculomegaly or mass lesion Normal CSF composition NOMENCLATURE Idiopathic intracranial hypertension (IIH) Benign intracranial hypertension Pseudotumor cerebri Intracranial hypertension secondary to… DIAGNOSTIC CRITERIA Original criteria have been updated to reflect new imaging modalities: 1492 Friedman and Jacobsen. Neurology 2002; 59: Symptoms and signs reflect only those of - increased ICP or papilledema 1495 Documented increased ICP during LP in lateral decubitus position Normal CSF composition No evidence of mass, hydrocephalus, structural -
Sodium-Based Osmotherapy in Continuous Renal Replacement Therapy: a Mathematical Approach
Review Article Sodium-Based Osmotherapy in Continuous Renal Replacement Therapy: a Mathematical Approach Jerry Yee ,1 Naushaba Mohiuddin,2 Tudor Gradinariu,1 Junior Uduman,1 and Stanley Frinak1 Abstract Cerebral edema, in a variety of circumstances, may be accompanied by states of hyponatremia. The threat of brain injury from hypotonic stress-induced astrocyte demyelination is more common when vulnerable patients with hyponatremia who have end stage liver disease, traumatic brain injury, heart failure, or other conditions undergo overly rapid correction of hyponatremia. These scenarios, in the context of declining urinary output from CKD and/or AKI, may require controlled elevations of plasma tonicity vis-a`-vis increases of the plasma sodium concentration. We offer a strategic solution to this problem via sodium-based osmotherapy applied through a conventional continuous RRT modality: predilution continuous venovenous hemofiltration. KIDNEY360 1: 281–291, 2020. doi: https://doi.org/10.34067/KID.0000382019 Introduction continuous venovenous hemofiltration (CVVH) (11,12), Generally, sodium-based osmotherapy (SBO) is tonicity continuous venovenous hemodialysis (13), or con- therapy with the aim of reducing cerebral edema during tinuous venovenous hemodiafiltration (14). states of hypotonic hyponatremia. Depending on the circumstance, plasma tonicity may be increased or decreased. Because the sodium concentration ([Na]) General Principles of SBO in the plasma at any time (t), PNa(t), and accompa- SBO can be implemented as a stepwise approach nying anions constitute the bulk of plasma tonicity, based on established biophysical principles govern- SBOispredicatedongradualalterationofPNa,in ing sodium transit via predilution CVVH. The follow- contrast to the relatively rapid PNa increases imposed ing urea- and sodium-based kinetic methodology by steep dialysate-to-plasma [Na] gradients associ- involves six steps: (1) establishing a time-dependent ∇ ated with conventional hemodialysis. -
Spinal Cerebrospinal Fluid Leak
Spinal Cerebrospinal Fluid Leak –An Under-recognized Cause of Headache More common than expected, why is this type of headache so often misdiagnosed or the diagnosis is delayed? Challenging the “One Size Fits All” Approach in Modern Medicine As research becomes more patient-centric, it is time to recognize individual variations in response to treatment and determine why these differences occur. Newly Approved CGRP Blocker, Aimovig™, the First Ever Migraine- Specific Preventive Medicine The approval of erenumab and eventually, other drugs in this class heralds a new dawn for migraine therapy. But will it be accessible for patients who could respond to it? Remembering Donald J. Dalessio, MD $6.99 Volume 7, Issue 1 •2018 The Headache Clinic www.headaches.org Featuring the Baylor Scott & White Headache Clinic in Temple, Texas. An Excerpt from the New Book – Headache Solutions at the Diamond Headache Clinic Written by Doctor Diamond in collaboration with Brad Torphy, MD. Spinal Cerebrospinal Fluid Leak – An Under-recognized Cause of Headache Connie Deline, MD, Spinal CSF Leak Foundation Spontaneous intracranial hypotension, or low cerebrospinal fluid (CSF) pressure inside the head, is an under-recognized cause of headache that is treatable and in many cases, curable. Although misdiagnosis and delayed diagnosis remain common, increasing awareness of this condition is improving the situation for those afflicted. Frequently, patients with a confirmed diagnosis of intracranial hypotension will report that they have been treated for chronic migraine or another headache disorder for months or years. This type of headache rarely responds to medications; however, when treatment is directed at the appropriate underlying cause, most patients respond well. -
Arginine-Vasopressin Receptor Blocker Conivaptan Reduces Brain Edema and Blood- Brain Barrier Disruption After Experimental Stroke in Mice
RESEARCH ARTICLE Arginine-Vasopressin Receptor Blocker Conivaptan Reduces Brain Edema and Blood- Brain Barrier Disruption after Experimental Stroke in Mice Emil Zeynalov1*, Susan M. Jones1, Jeong-Woo Seo1, Lawrence D. Snell2, J. Paul Elliott3 1 Swedish Medical Center, Neurotrauma Research, Englewood, Colorado, United States of America, 2 Colorado Neurological Institute, Englewood, Colorado, United States of America, 3 Colorado Brain and Spine Institute, Englewood, Colorado, United States of America a11111 * [email protected] Abstract OPEN ACCESS Background Citation: Zeynalov E, Jones SM, Seo J-W, Snell LD, Stroke is a major cause of morbidity and mortality. Stroke is complicated by brain edema Elliott JP (2015) Arginine-Vasopressin Receptor and blood-brain barrier (BBB) disruption, and is often accompanied by increased release of Blocker Conivaptan Reduces Brain Edema and arginine-vasopressin (AVP). AVP acts through V1a and V2 receptors to trigger hyponatre- Blood-Brain Barrier Disruption after Experimental Stroke in Mice. PLoS ONE 10(8): e0136121. mia, vasospasm, and platelet aggregation which can exacerbate brain edema. The AVP doi:10.1371/journal.pone.0136121 receptor blockers conivaptan (V1a and V2) and tolvaptan (V2) are used to correct hypona- Editor: Muzamil Ahmad, Indian Institute of Integrative tremia, but their effect on post-ischemic brain edema and BBB disruption remains to be elu- Medicine, INDIA cidated. Therefore, we conducted this study to investigate if these drugs can prevent brain Received: May 25, 2015 edema and BBB disruption in mice after stroke. Accepted: July 29, 2015 Methods Published: August 14, 2015 Experimental mice underwent the filament model of middle cerebral artery occlusion Copyright: © 2015 Zeynalov et al. -
Cerebral Hemodynamics and Intracranial Compliance Impairment in Critically Ill COVID-19 Patients: a Pilot Study
brain sciences Article Cerebral Hemodynamics and Intracranial Compliance Impairment in Critically Ill COVID-19 Patients: A Pilot Study Sérgio Brasil 1,*, Fabio Silvio Taccone 2,Sâmia Yasin Wayhs 1, Bruno Martins Tomazini 3, Filippo Annoni 2, Sérgio Fonseca 3, Estevão Bassi 3, Bruno Lucena 3, Ricardo De Carvalho Nogueira 1, Marcelo De-Lima-Oliveira 1, Edson Bor-Seng-Shu 1, Wellingson Paiva 1 , Alexis Fournier Turgeon 4 , Manoel Jacobsen Teixeira 1 and Luiz Marcelo Sá Malbouisson 3 1 Division of Neurosurgery, Department of Neurology, Universidade de São Paulo, São Paulo 05403-000, Brazil; [email protected] (S.Y.W.); [email protected] (R.D.C.N.); [email protected] (M.D.-L.-O.); [email protected] (E.B.-S.-S.); [email protected] (W.P.); [email protected] (M.J.T.) 2 Department of Intensive Care, Universitè Libre de Bruxelles, 1000 Brussels, Belgium; [email protected] (F.S.T.); fi[email protected] (F.A.) 3 Department of Intensive Care, Universidade de São Paulo, São Paulo 05403-000, Brazil; [email protected] (B.M.T.); [email protected] (S.F.); [email protected] (E.B.); [email protected] (B.L.); [email protected] (L.M.S.M.) 4 Division of Critical Care Medicine and the Department of Anesthesiology, Université Laval, Québec City, QC G1V 0A6, Canada; [email protected] * Correspondence: [email protected] Abstract: Introduction: One of the possible mechanisms by which the new coronavirus (SARS- Citation: Brasil, S.; Taccone, F.S.; Cov2) could induce brain damage is the impairment of cerebrovascular hemodynamics (CVH) and Wayhs, S.Y.; Tomazini, B.M.; Annoni, intracranial compliance (ICC) due to the elevation of intracranial pressure (ICP). -
Critical Care and Resuscitation • Volume 11 Number 2 • June 2009 151 POINTS of VIEW
POINTS OF VIEW Mannitol or hypertonic saline for intracranial hypertension? A point of view Luis B Castillo, Guillermo A Bugedo and Jorge L Paranhos Osmotically active solutions have been used for more than ABSTRACT 30 years in the treatment of intracranial hypertension. The traditional agent of choice has been mannitol, but hyper- Osmotically active solutions, particularly mannitol, have tonicCrit saline Care has Resusc recently ISSN: emerged 1441-2772 as an1 Junealternative. Here, been used for more than 30 years in the treatment of we discuss2009 11 the2 151-154 systemic and cerebral effects of these two intracranial hypertension. Recently hypertonic saline has ©Crit Care Resusc 2009 substances,www.jficm.anzca.edu.au/aaccm/journal/publi- as well as their side effects and complications, emerged as an alternative to mannitol. Both solutions are and cations.htmmake recommendations about their clinical use. used worldwide, and their indications and long-term side Points of View effects are well known. More recently, knowledge about their effects has increased, both limiting and expanding Mannitol their clinical use. Here, we compare the systemic and Mannitol has been the agent of choice in osmotherapy for cerebral effects of mannitol and hypertonic saline, as well as cerebral injury since the 1960s. It is a mannose-derived their side effects and complications. Finally, we make simple alcohol, which is easy to prepare and use, stable in recommendations about their clinical use. solution, inert, not metabolised, freely filtered by the kidneys without being reabsorbed, and low in toxicity. Its Crit Care Resusc 2009; 11: 151–154 distribution volume corresponds to the extracellular com- partment.1-7 The effects of mannitol on the central nervous For editorial comment, see page 94 system have been well described, but the mechanisms are still not completely understood. -
7. Headache Attributed to Non-Vascular Intracranial Disorder
Classification and Diagnosis of Secondary Headaches, Part II- Altered Intracerebral Pressure, Neoplasms, and Infections Lawrence C. Newman, M.D. Director, The Headache Institute Roosevelt Hospital Center New York, N.Y. 7. Headache7. Headache attributed attributed to to non-vascularnon-vascular intracranial intracranial disorder 7.1 Headache attributed to high cerebrospinal fluid pressure 7.2 Headache attributed to low cerebrospinaldisorder fluid pressure 7.3 Headache attributed to non-infectious inflammatory disease 7.4 Headache attributed to intracranial neoplasm 7.5 Headache attributed to intrathecal injection 7.6 Headache attributed to epileptic seizure 7.7 Headache attributed to Chiari malformation type I 7.8 Syndrome of transient Headache and Neurological Deficits with cerebrospinal fluid Lymphocytosis (HaNDL) 7.9 Headache attributed to other non-vascular intracranial disorder ICHD-II. Cephalalgia 2004; 24 (Suppl 1) ©International Headache Society 2003/4 Headaches attributed to alterations in CSF pressure: • Headache frequently accompanies alteration of CSF pressure, either high or low • Pressure alterations may be the result of disruptions of CSF production, flow, or absorption • Major source of CSF is choroid plexus; some also formed extra-choroidal • CSF absorbed primarily in pacchionian granulations arachnoid villi and vessels of subarachnoid space over hemispheres ® American Headache Society Increased Intracranial Pressure: Secondary Causes • Venous sinus occlusion • Medications (naladixic • Radical neck dissection acid,danocrine, -
Idiopathic Intracranial Hypertension: Consensus Guidelines On
General Neurology J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp-2017-317440 on 14 June 2018. Downloaded from REVIEW Idiopathic intracranial hypertension: consensus guidelines on management Susan P Mollan,1,2 Brendan Davies,3 Nick C Silver,4 Simon Shaw,5 Conor L Mallucci,6,7 Benjamin R Wakerley,8,9 Anita Krishnan,4 Swarupsinh V Chavda,10 Satheesh Ramalingam,10 Julie Edwards,11,12 Krystal Hemmings,13 Michelle Williamson,13 Michael A Burdon,2 Ghaniah Hassan-Smith,1,12 Kathleen Digre,14 Grant T Liu,15 Rigmor Højland Jensen,16 Alexandra J Sinclair1,2,12,17 ► Additional material is ABSTRact contains information that will be of interest to those published online only. To view The aim was to capture interdisciplinary expertise from a in primary care and other healthcare professionals. please visit the journal online large group of clinicians, reflecting practice from across The increasing economic burden of IIH has been (http:// dx. doi. org/ 10. 1136/ 1 2 jnnp- 2017- 317440). the UK and further, to inform subsequent development of highlighted by a number of groups. Clear guid- a national consensus guidance for optimal management ance will help educate the attending doctors to For numbered affiliations see of idiopathic intracranial hypertension (IIH). manage these patients appropriately. This will help end of article. Methods Between September 2015 and October reduce the repeat unsolicited emergency hospital 2017, a specialist interest group including neurology, attendances and reduce IIH-related disability. Correspondence to There are a number of ongoing clinical trials in IIH Dr Alexandra J Sinclair, neurosurgery, neuroradiology, ophthalmology, nursing, Metabolic Neurology, Institute primary care doctors and patient representatives (https://www. -
European Headache Federation Guideline on Idiopathic Intracranial
Hoffmann et al. The Journal of Headache and Pain (2018) 19:93 The Journal of Headache https://doi.org/10.1186/s10194-018-0919-2 and Pain CONSENSUSARTICLE Open Access European Headache Federation guideline on idiopathic intracranial hypertension Jan Hoffmann1* , Susan P Mollan2, Koen Paemeleire3, Christian Lampl4, Rigmor H Jensen5 and Alexandra J Sinclair6 Abstract Background: Idiopathic Intracranial Hypertension (IIH) is characterized by an elevation of intracranial pressure (ICP no identifiable cause. The aetiology remains largely unknown, however observations made in a number of recent clinical studies are increasing the understanding of the disease and now provide the basis for evidence-based treatment strategies. Methods: The Embase, CDSR, CENTRAL, DARE and MEDLINE databases were searched up to 1st June 2018. We analyzed randomized controlled trials and systematic reviews that investigate IIH. Results: Diagnostic uncertainty, headache morbidity and visual loss are among the highest concerns of clinicians and patients in this disease area. Research in this field is infrequent due to the rarity of the disease and the lack of understanding of the underlying pathology. Conclusions: This European Headache Federation consensus paper provides evidence-based recommendations and practical advice on the investigation and management of IIH. Objective Headache Society (IHS) [3] (Table 1). The term ‘pseudo- Idiopathic Intracranial Hypertension (IIH) is character- tumor cerebri’, in the past commonly used as a synonym ized by an elevation of intracranial pressure (ICP) with for IIH, is now used as an umbrella term that describes no identifiable cause [1]. Despite the fact that its aeti- the chronic elevation of ICP regardless of its aetiology ology remains largely unknown, the observations made and further subdivides in the primary (IIH) and second- in a significant number of recent clinical studies and the ary forms [2].